Researchers Database

SHIBASAKI Manabu

    Faculty Division of Engineering Research Group of Engineering Professor
Contact:
shibacc.nara-wu.ac.jp
Last Updated :2021/06/02

researchmap

Degree

  • Ph.D, Kobe University
  • MS, Kobe University

Research Areas

  • Life sciences, Physiology
  • Humanities & social sciences, Home economics, lifestyle science
  • Life sciences, Physical and health education

Research Experience

  • Apr. 2017 Mar. - 2021, 奈良女子大学研究院生活環境科学系
  • Apr. 2012 Mar. - 2017, 奈良女子大学研究院生活環境科学系准教授
  • Apr. 2009 Mar. - 2012, 奈良女子大学大学院人間文化研究科准教授
  • Mar. 2008 Mar. - 2009, 奈良女子大学生活環境学部生活健康・衣環境学科准教授
  • Apr. 2007 Feb. - 2008, 奈良女子大学生活環境学部生活健康・衣環境学科助教
  • Apr. 1999 Mar. - 2007, 奈良女子大学生活環境学部生活環境学科生活健康学講座助手
  • Mar. 2004 Mar. - 2005, University of Texas Southwestern Medical center at Dallas, Visiting Scientist
  • Aug. 1998 Mar. - 1999, Institute for Exercise & Environmental Medicine, Presbyterian Hospital of Dallas, Research Associate
  • Apr. 1998 Mar. - 1999, Research Fellow of the Japan Society for the Promotion of Science
  • Apr. 2021, 奈良女子大学研究院工学系工学領域

Education

  • Apr. 1995, Mar. - 1998, Kobe University, Graduate School, Division of National Science and Technology (except Gakushuin University, Konan University), 知能科学
  • - 1993, Kobe University, Faculty of Education, 初等教育

Committee Memberships

  • Jan. 2011 Jun.2015日本繊維製品消費科学会編集委員
  • Aug. 2015日本体力医学会評議員
  • Sep. 2015日本体力医学会将来構想計画委員会
  • Apr. 2008日本運動生理学会評議員

Awards

  • 久野寧記念賞, 日本生理学会, 2006

Published Papers

  • An assessment of hypercapnia-induced elevations in regional cerebral perfusion during combined orthostatic and heat stresses

    Manabu Shibasaki; Kohei Sato; Ai Hirasawa; Tomoko Sadamoto; Craig G. Crandall; Shigehiko Ogoh

    Springer Science and Business Media LLC, May 2020, The Journal of Physiological Sciences, 70 (1), doi;url;url

    Scientific journal

  • 圧衝撃緩和性からみたゴールボール用プロテクター素材の検討

    坂下 理穂; 加藤 礼菜; 諸岡 晴美; 渡邊 敬子; 芝﨑 学

    Apr. 2020, 繊維製品消費科学, 61 (4), 308 - 316

    Scientific journal

  • Differences in characteristics of somatosensory evoked potentials between children and adults

    Miho Takezawa; Keita Kamijo; Manabu Shibasaki; Hiroki Nakata

    Ovid Technologies (Wolters Kluwer Health), Dec. 2019, NeuroReport, 30 (18), 1284 - 1288, doi;url

    Scientific journal

  • 認知機能と環境ストレス

    中田大貴; 芝﨑学

    Oct. 2019, 日本生気象学会雑誌, 56 (1), 3 - 11

    Scientific journal

  • Effects of whole body skin cooling on human cognitive processing: a study using SEPs and ERPs

    Hiroki Nakata; Fumino Kobayashi; Justin S. Lawley; Ryusuke Kakigi; Manabu Shibasaki

    The present study investigated the effect of whole body skin cooling on somatosensory ascending processing by utilizing somatosensory-evoked potentials (SEPs) and motor execution, as well as inhibitory processing by event-related potentials (ERPs). Fourteen healthy participants wearing a water-perfused suit performed two sessions ( sessions 1 and 2) consisting of SEPs and ERPs with somatosensory Go/No-go paradigms under two conditions (cold stress and control) on different days. In session 2, under the cold stress condition, whole body skin cooling was achieved by circulating 20°C water through the suit for 40 min, whereas 34°C water was perfused in the other sessions. The mean skin temperature decreased from 35.0 ± 0.5°C ( session 1) to 30.4 ± 0.9°C ( session 2) during whole body skin cooling, but the internal temperature was maintained. Whole body skin cooling delayed the peak latencies of N20, P25, and P45 components at C4′ of SEPs (all: P < 0.05). Moreover, the peak latencies of P14, N18, and P22 components at Fz of SEPs and the Go-P300 component of ERPs were delayed (all: P < 0.05). In contrast, the peak amplitudes of all individual components of SEPs as well as N140 and P300 of ERPs remained unchanged. These results suggest that passive whole body skin cooling delays neural activities on somatosensory processing and higher cognitive function., American Physiological Society, 01 Sep. 2019, American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 317 (3), R432 - R441, doi;url

    Scientific journal

  • Effects of repetitive exercise and thermal stress on human cognitive processing

    Manabu Shibasaki; Mari Namba; Yoshi-Ichiro Kamijo; Tomoyuki Ito; Ryusuke Kakigi; Hiroki Nakata

    Wiley, Feb. 2019, Physiological Reports, 7 (4), e14003 - e14003, doi;url;url

    Scientific journal

  • Differences in serum IL-6 response after 1 °C rise in core body temperature in individuals with spinal cord injury and cervical spinal cord injury during local heat stress

    Takamasa Hashizaki; Yukihide Nishimura; Kenzo Teramura; Yasunori Umemoto; Manabu Shibasaki; C. A. Leicht; Ken Kouda; Fumihiro Tajima

    Informa UK Limited, 31 Dec. 2018, International Journal of Hyperthermia, 35 (1), 541 - 547, doi;url

    Scientific journal

  • Warm-, hot- and pain-related neural activities depending on baseline skin temperatures

    H. Nakata; R. Kakigi; M. Shibasaki

    Wiley, Nov. 2018, European Journal of Pain, 22 (10), 1791 - 1799, doi;url

    Scientific journal

  • 暑熱環境下の循環調節とトレーニング適応

    芝﨑学

    Jul. 2018, 体育の科学, 68 (7), 519 - 525

    In book

  • Dynamic cerebral autoregulation during cognitive task: effect of hypoxia

    Shigehiko Ogoh; Hiroki Nakata; Tadayoshi Miyamoto; Damian Miles Bailey; Manabu Shibasaki

    Changes in cerebral blood flow (CBF) subsequent to alterations in the partial pressures of oxygen and carbon dioxide can modify dynamic cerebral autoregulation (CA). While cognitive activity increases CBF, the extent to which it impacts CA remains to be established. In the present study we determined whether dynamic CA would decrease during a cognitive task and whether hypoxia would further compound impairment. Fourteen young healthy subjects performed a simple Go/No-go task during normoxia and hypoxia (inspired O2 fraction = 12%), and the corresponding relationship between mean arterial pressure (MAP) and mean middle cerebral artery blood velocity (MCA Vmean) was examined. Dynamic CA and steady-state changes in MCA V in relation to changes in arterial pressure were evaluated with transfer function analysis. While MCA Vmean increased during the cognitive activity ( P < 0.001), hypoxia did not cause any additional changes ( P = 0.804 vs. normoxia). Cognitive performance was also unaffected by hypoxia (reaction time, P = 0.712; error, P = 0.653). A decrease in the very low- and low-frequency phase shift (VLF and LF; P = 0.021 and P = 0.01) and an increase in LF gain were observed ( P = 0.037) during cognitive activity, implying impaired dynamic CA. While hypoxia also increased VLF gain ( P < 0.001), it failed to cause any additional modifications in dynamic CA. Collectively, our findings suggest that dynamic CA is impaired during cognitive activity independent of altered systemic O2 availability, although we acknowledge the interpretive complications associated with additional competing, albeit undefined, inputs that could potentially distort the MAP-MCA Vmean relationship. NEW & NOTEWORTHY During normoxia, cognitive activity while increasing cerebral perfusion was shown to attenuate dynamic cerebral autoregulation (CA) yet failed to alter reaction time, thereby questioning its functional significance. No further changes were observed during hypoxia, suggesting that impaired dynamic CA occurs independently of altered systemic O2 availability. However, impaired dynamic CA may reflect a technical artifact, given the confounding influence of additional inputs that could potentially distort the mean arterial pressure-mean middle cerebral artery blood velocity relationship., American Physiological Society, 01 Jun. 2018, Journal of Applied Physiology, 124 (6), 1413 - 1419, doi;url

    Scientific journal

  • A comparison of static and dynamic cerebral autoregulation during mild whole-body cold stress in individuals with and without cervical spinal cord injury: a pilot study

    Jan W. van der Scheer; Yoshi-Ichiro Kamijo; Christof A. Leicht; Philip J. Millar; Manabu Shibasaki; Victoria L. Goosey-Tolfrey; Fumihiro Tajima

    Springer Science and Business Media LLC, May 2018, Spinal Cord, 56 (5), 469 - 477, doi;pubmed;url;url

    Scientific journal

  • Effect of increases in cardiac contractility on cerebral blood flow in humans

    Shigehiko Ogoh; Gilbert Moralez; Takuro Washio; Satyam Sarma; Michinari Hieda; Steven A. Romero; Matthew N. Cramer; Manabu Shibasaki; Craig G. Crandall

    The effect of acute increases in cardiac contractility on cerebral blood flow (CBF) remains unknown. We hypothesized that the external carotid artery (ECA) downstream vasculature modifies the direct influence of acute increases in heart rate and cardiac function on CBF regulation. Twelve healthy subjects received two infusions of dobutamine [first a low dose (5 μg·kg−1·min−1) and then a high dose (15 μg·kg−1·min−1)] for 12 min each. Cardiac output, blood flow through the internal carotid artery (ICA) and ECA, and echocardiographic measurements were performed during dobutamine infusions. Despite increases in cardiac contractility, cardiac output, and arterial pressure with dobutamine, ICA blood flow and conductance slightly decreased from resting baseline during both low- and high-dose infusions. In contrast, ECA blood flow and conductance increased appreciably during both low- and high-dose infusions. Greater ECA vascular conductance and corresponding increases in blood flow may protect overperfusion of intracranial cerebral arteries during enhanced cardiac contractility and associated increases in cardiac output and perfusion pressure. Importantly, these findings suggest that the acute increase of blood perfusion attributable to dobutamine administration does not cause cerebral overperfusion or an associated risk of cerebral vascular damage. NEW & NOTEWORTHY A dobutamine-induced increase in cardiac contractility did not increase internal carotid artery blood flow despite an increase in cardiac output and arterial blood pressure. In contrast, external carotid artery blood flow and conductance increased. This external cerebral blood flow response may assist with protecting from overperfusion of intracranial blood flow., American Physiological Society, 01 Dec. 2017, American Journal of Physiology-Heart and Circulatory Physiology, 313 (6), H1155 - H1161, doi;web_of_science;url

    Scientific journal

  • Effects of acute hypoxia on human cognitive processing: a study using ERPs and SEPs

    Hiroki Nakata; Tadayoshi Miyamoto; Shigehiko Ogoh; Ryusuke Kakigi; Manabu Shibasaki

    Although hypoxia has the potential to impair the cognitive function, the effects of acute hypoxia on the high-order brain function (executive and/or inhibitory processing) and somatosensory ascending processing remain unknown. We tested the hypothesis that acute hypoxia impairs both motor executive and inhibitory processing and somatosensory ascending processing. Fifteen healthy subjects performed two sessions ( sessions 1 and 2), consisting of electroencephalographic event-related potentials with somatosensory Go/No-go paradigms and somatosensory-evoked potentials (SEPs) under two conditions (hypoxia and normoxia) on different days. On 1 day, participants breathed room air in the first and second sessions of the experiment; on the other day, participants breathed room air in the first session, and 12% O2 in the second session. Acute hypoxia reduced the peak amplitudes of Go-P300 and No-go-P300, and delayed the peak latency of Go-P300. However, no significant differences were observed in the peak amplitude or latency of N140, behavioral data, or the amplitudes and latencies of individual SEP components between the two conditions. These results suggest that acute hypoxia impaired neural activity in motor executive and inhibitory processing, and delayed higher cognitive processing for motor execution, whereas neural activity in somatosensory processing was not affected by acute hypoxia. NEW & NOTEWORTHY Hypoxia has the potential to impair the cognitive function, but the effects of acute hypoxia on the cognitive function remain debatable. We investigated the effects of acute hypoxia on human cognitive processing using electroencephalographic event-related potentials and somatosensory-evoked potentials. Acute normobaric hypoxia impaired neural activity in motor executive and inhibitory processing, but no significant differences were observed in neural activity in somatosensory processing., American Physiological Society, 01 Nov. 2017, Journal of Applied Physiology, 123 (5), 1246 - 1255, doi;web_of_science;url

    Scientific journal

  • Effects of face/head and whole body cooling during passive heat stress on human somatosensory processing

    Hiroki Nakata; Mari Namba; Ryusuke Kakigi; Manabu Shibasaki

    We herein investigated the effects of face/head and whole body cooling during passive heat stress on human somatosensory processing recorded by somatosensory-evoked potentials (SEPs) at C4′ and Fz electrodes. Fourteen healthy subjects received a median nerve stimulation at the left wrist. SEPs were recorded at normothermic baseline (Rest), when esophageal temperature had increased by ~1.2°C (heat stress: HS) during passive heating, face/head cooling during passive heating (face/head cooling: FHC), and after HS (whole body cooling: WBC). The latencies and amplitudes of P14, N20, P25, N35, P45, and N60 at C4′ and P14, N18, P22, and N30 at Fz were evaluated. Latency indicated speed of the subcortical and cortical somatosensory processing, while amplitude reflected the strength of neural activity. Blood flow in the internal and common carotid arteries (ICA and CCA, respectively) and psychological comfort were recorded in each session. Increases in esophageal temperature due to HS significantly decreased the amplitude of N60, psychological comfort, and ICA blood flow in the HS session, and also shortened the latencies of SEPs (all, P < 0.05). While esophageal temperature remained elevated, FHC recovered the peak amplitude of N60, psychological comfort, and ICA blood flow toward preheat baseline levels as well as WBC. However, the latencies of SEPs did not recover in the FHC and WBC sessions. These results suggest that impaired neural activity in cortical somatosensory processing during passive HS was recovered by FHC, whereas conduction velocity in the ascending somatosensory input was accelerated by increases in body temperature., American Physiological Society, 01 Jun. 2017, American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 312 (6), R996 - R1003, doi;url

    Scientific journal

  • Suppression of cognitive function in hyperthermia; From the viewpoint of executive and inhibitive cognitive processing

    Manabu Shibasaki; Mari Namba; Misaki Oshiro; Ryusuke Kakigi; Hiroki Nakata

    Springer Science and Business Media LLC, Apr. 2017, Scientific Reports, 7 (1), doi;web_of_science;url;url

    Scientific journal

  • 暑熱環境下における認知機能

    芝﨑学; 中田大貴

    Jan. 2017, 繊維製品消費科学, 58 (1), 50 - 54

    Scientific journal

  • Effects of aerobic exercise under different thermal conditions on human somatosensory processing

    Hiroki Nakata; Misaki Oshiro; Mari Namba; Manabu Shibasaki

    The present study aimed to investigate the effects of aerobic exercise on human somatosensory processing recorded by somatosensory evoked potentials (SEPs) under temperate [TEMP, 20°C and 40% relative humidity (RH)] and hot (HOT, 35°C and 30% RH) environments. Fifteen healthy subjects performed 4 × 15-min bouts of a moderate cycling exercise [mean power output: 156.5 ± 7.7 (SE) W], with a 10-min rest period and received a posterior tibial nerve stimulation at the left ankle before and after each exercise bout; SEPs were recorded in five sessions; 1st (pre), 2nd (post-1st exercise bout), 3rd (post-2nd exercise bout), 4th (post-3rd exercise bout), and 5th (post-4th exercise bout). The peak latencies and amplitudes of the P37, N50, P60, and N70 components at Cz were evaluated. The latencies of P37, N50, P60, and N70 were significantly shorter with the repetition of aerobic exercise, and these shortened latencies were significantly greater in the HOT condition than in the TEMP condition (P37: 3rd, P < 0.05, and 5th, P < 0.01; P60: 4th, P < 0.05, and 5th, P < 0.01; N70: 4th, P < 0.05, and 5th, P < 0.001). No significant differences were observed in the amplitudes of any SEP component under either thermal condition. These results suggest that the conduction velocity of the ascending somatosensory input was accelerated by increases in body temperature, and aerobic exercise did not alter the strength of neural activity in cortical somatosensory processing., American Physiological Society, 01 Oct. 2016, American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 311 (4), R629 - R636, doi;web_of_science;url

    Scientific journal

  • The effect of elevations in internal temperature on event-related potentials during a simple cognitive task in humans

    Manabu Shibasaki; Mari Namba; Misaki Oshiro; Craig G. Crandall; Hiroki Nakata

    The effect of hyperthermia on cognitive function remains equivocal, perhaps because of methodological discrepancy. Using electroencephalographic event-related potentials (ERPs), we tested the hypothesis that a passive heat stress impairs cognitive processing. Thirteen volunteers performed repeated auditory oddball paradigms under two thermal conditions, normothermic time control and heat stress, on different days. For the heat stress trial, these paradigms were performed at preheat stress (i.e., normothermic) baseline, when esophageal temperature had increased by ∼0.8°C, when esophageal temperature had increased by ∼2.0°C, and during cooling following the heat stress. The reaction time and ERPs were recorded in each session. For the time control trial, subjects performed the auditory oddball paradigms at approximately the same time interval as they did in the heat stress trial. The peak latency and amplitude of an indicator of auditory processing (N100) were not altered regardless of thermal conditions. An indicator of stimulus classification/evaluation time (latency of P300) and the reaction time were shortened during heat stress; moreover an indicator of cognitive processing (the amplitude of P300) was significantly reduced during severe heat stress (8.3 ± 1.3 μV) relative to the baseline (12.2 ± 1.0 μV, P < 0.01). No changes in these indexes occurred during the time control trial. During subsequent whole body cooling, the amplitude of P300 remained reduced, and the reaction time and latency of P300 remained shortened. These results suggest that excessive elevations in internal temperature reduce cognitive processing but promote classification time., American Physiological Society, 01 Jul. 2016, American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 311 (1), R33 - R38, doi;web_of_science;url

    Scientific journal

  • Effects of passive heat stress on human somatosensory processing

    Hiroki Nakata; Misaki Oshiro; Mari Namba; Manabu Shibasaki

    Herein, we investigated the effects of passive heat stress on human somatosensory processing recorded by somatosensory-evoked potentials (SEPs). Fifteen healthy subjects received a median nerve stimulation at the left wrist under two thermal conditions: Heat Stress and normothermic Time Control. The latencies and amplitudes of P14, N20, P25, N35, P45, and N60 at C4′ and P14, N18, P22, and N30 at Fz were evaluated. Under the Heat Stress condition, SEPs were recorded at normothermic baseline (1st), early in heat stress (2nd), when esophageal temperature had increased by ∼1.0°C (3rd) and ∼2.0°C (4th), and after heat stress (5th). In the Time Control condition, SEPs were measured at the same time intervals as those in the Heat Stress condition. The peak latencies and amplitudes of SEPs did not change early in heat stress. However, the latencies of P14, N20, and N60 at C4′ and P14, N18, and P22 at Fz were significantly shorter in the 4th session than in the 1st session. Furthermore, the peak amplitudes of P25 and N60 at C4′, and P22 and N30 at Fz decreased with increases in body temperature. On the other hand, under the Time Control condition, no significant differences were observed in the amplitudes or latencies of any component of SEPs. These results suggested that the conduction velocity of the ascending somatosensory input was accelerated by increases in body temperature, and hyperthermia impaired the neural activity of cortical somatosensory processing., American Physiological Society, 01 Dec. 2015, American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 309 (11), R1387 - R1396, doi;web_of_science;url

    Scientific journal

  • The role of cardiac sympathetic innervation and skin thermoreceptors on cardiac responses during heat stress

    Manabu Shibasaki; Yasunori Umemoto; Tokio Kinoshita; Ken Kouda; Tomoyuki Ito; Takeshi Nakamura; Craig G. Crandall; Fumihiro Tajima

    The mechanism(s) for the changes in cardiac function during heat stress remain unknown. This study tested two unique hypotheses. First, sympathetic innervation to the heart is required for increases in cardiac systolic function during heat stress. This was accomplished by comparing responses during heat stress between paraplegics versus tetraplegics, with tetraplegics having reduced/absent cardiac sympathetic innervation. Second, stimulation of skin thermoreceptors contributes to cardiovascular adjustments that occur during heat stress in humans. This was accomplished by comparing responses during leg only heating between paraplegic versus able-bodied individuals. Nine healthy able-bodied, nine paraplegics, and eight tetraplegics participated in this study. Lower body (i.e., nonsensed area for para/tetraplegics) was heated until esophageal temperature had increased by ∼1.0°C. Echocardiographic indexes of diastolic and systolic function were performed before and at the end of heat stress. The heat stress increased cardiac output in all groups, but the magnitude of this increase was attenuated in the tetraplegics relative to the able-bodied (1.3 ± 0.4 vs. 2.3 ± 1.0 l/min; P < 0.05). Diastolic function was maintained in all groups. Indexes of left atrial and ventricular systolic function were enhanced in the able-bodied, but did not change in tetraplegics, while these changes in paraplegics were attenuated relative to the able-bodied. These data suggest that the cardiac sympathetic innervation is required to achieve normal increases in cardiac systolic function during heat stress but not required to maintain diastolic function during this exposure. Second, elevated systolic function during heat stress primarily occurs as a result of increases in internal temperature, although stimulation of skin thermoreceptors may contribute., American Physiological Society, 01 Jun. 2015, American Journal of Physiology-Heart and Circulatory Physiology, 308 (11), H1336 - H1342, doi;web_of_science;url

    Scientific journal

  • Blood flow in internal carotid and vertebral arteries during graded lower body negative pressure in humans

    Shigehiko Ogoh; Kohei Sato; Kazunobu Okazaki; Tadayoshi Miyamoto; Ai Hirasawa; Tomoko Sadamoto; Manabu Shibasaki

    New Findings What is the central question of this study? Recently, the heterogeneity of the cerebral arterial circulation has been argued. Orthostatic tolerance may be associated with an orthostatic stress-induced change in blood flow in vertebral arteries rather than in internal carotid arteries, because vertebral arteries supply blood to the medulla oblongata, which is the location of important cardiac, vasomotor and respiratory control centres. What is the main finding and its importance? The effect of graded orthostatic stress on vertebral artery blood flow is different from that on internal carotid artery blood flow. This response allows for the possibility that orthostatic tolerance may be associated with haemodynamic changes in posterior rather than anterior cerebral blood flow. Recently, the heterogeneity of the cerebral arterial circulation has been argued, but the characteristics of vertebral artery (VA) and internal carotid artery (ICA) blood flow during graded orthostatic stress remain unknown. We hypothesized that the change in blood flow in VA is not similar to that in ICA blood flow during graded orthostatic stress. We measured blood flows in both ICA and VA during graded lower body negative pressure (LBNP; -20, -35and -50mmHg) by using two colour-coded ultrasound systems. The effect of graded orthostatic stress on the VA blood flow was different from that on the ICA blood flow (LBNPxartery, P=0.006). The change in ICA blood flow was associated with the level of LBNP (r = 0.287, P=0.029), and a reduction in ICA blood flow from pre-LBNP was observed during -50mmHg LBNP (from 411 +/- 35 to 311 +/- 40mlmin(-1), P=0.044) without symptoms of presyncope. In contrast, VA blood flow was unchanged during graded LBNP compared with the baseline (P=0.597) relative to the reduction in ICA blood flow and thus there was no relationship between VA blood flow and the level of LBNP (r=0.167, P=0.219). These findings suggest that the change in ICA blood flow is due to the level of LBNP during graded orthostatic stress, but the change in VA blood flow is different from that in ICA blood flow across the different levels of LBNP. These findings provide the possibility that posterior cerebral blood flow decreases only during severe orthostatic stress and is therefore more likely to be linked with orthostatic tolerance., WILEY-BLACKWELL, Mar. 2015, EXPERIMENTAL PHYSIOLOGY, 100 (3), 259 - 266, doi;web_of_science

    Scientific journal

  • Hyperthermia modulates regional differences in cerebral blood flow to changes in CO2

    Shigehiko Ogoh; Kohei Sato; Kazunobu Okazaki; Tadayoshi Miyamoto; Ai Hirasawa; Manabu Shibasaki

    The purpose of this study was to assess blood flow responses to changes in carbon dioxide (CO2) in the internal carotid artery (ICA), external carotid artery (ECA), and vertebral artery (VA) during normothermic and hyperthermic conditions. Eleven healthy subjects aged 22 +/- 2 (SD) yr were exposed to passive whole body heating followed by spontaneous hypocapnic and hypercapnic challenges in normothermic and hyperthermic conditions. Right ICA, ECA, and VA blood flows, as well as left middle cerebral artery (MCA) mean blood velocity (V-mean), were measured. Esophageal temperature was elevated by 1.53 +/- 0.09 degrees C before hypocapnic and hypercapnic challenges during heat stress. Whole body heating increased ECA blood flow and cardiac output by 130 +/- 78 and 47 +/- 26%, respectively (P < 0.001), while blood flow (or velocity) in the ICA, MCA, and VA was reduced by 17 +/- 14, 24 +/- 18, and 12 +/- 7%, respectively (P < 0.001). Regardless of the thermal conditions, ICA and VA blood flows and MCA V-mean were decreased by hypocapnic challenges and increased by hypercapnic challenges. Similar responses in ECA blood flow were observed in hyperthermia but not in normothermia. Heat stress did not alter CO2 reactivity in the MCA and VA. However, CO2 reactivity in the ICA was decreased (3.04 +/- 1.17 vs. 2.23 +/- 1.03%/mmHg; P +/- 0.039) but that in the ECA was enhanced (0.45 +/- 0.47 vs. 0.95 +/- 0.61%/mmHg; P = 0.032). These results indicate that hyperthermia is capable of altering dynamic cerebral blood flow regulation., AMER PHYSIOLOGICAL SOC, Jul. 2014, JOURNAL OF APPLIED PHYSIOLOGY, 117 (1), 46 - 52, doi;web_of_science

    Scientific journal

  • Effects of acute hypoxia on cerebrovascular responses to carbon dioxide

    Shigehiko Ogoh; Hidehiro Nakahara; Shinya Ueda; Kazunobu Okazaki; Manabu Shibasaki; Andrew W. Subudhi; Tadayoshi Miyamoto

    New Findings What is the central question of this study? In acute hypoxia, the reduction in arterial CO2 tension due to the hypoxic ventilatory response (respiratory chemoreflex) stimulates cerebral vasoconstriction, which opposes the degree of hypoxic cerebral vasodilatation. The aim was to examine this interaction further. Specifically, we questioned whether arterial CO2 tension-mediated effects on cerebrovascular regulation are attenuated during acute hypoxia. What is the main finding and its importance? Cerebrovascular CO2 reactivity and CO2-mediated effects on dynamic cerebral autoregulation were attenuated during acute hypoxia. These findings suggest that blunted cerebrovascular responses to CO2 may limit the degree of CO2-mediated vasoconstriction to help maintain adequate cerebral blood flow for cerebral O2 homeostasis during acute hypoxia. In normoxic conditions, a reduction in arterial carbon dioxide tension causes cerebral vasoconstriction, thereby reducing cerebral blood flow and modifying dynamic cerebral autoregulation (dCA). It is unclear to what extent these effects are altered by acute hypoxia and the associated hypoxic ventilatory response (respiratory chemoreflex). This study tested the hypothesis that acute hypoxia attenuates arterial CO2 tension-mediated regulation of cerebral blood flow to help maintain cerebral O2 homeostasis. Eight subjects performed three randomly assigned respiratory interventions following a resting baseline period, as follows: (1) normoxia (21% O2); (2) hypoxia (12% O2); and (3) hypoxia with wilful restraint of the respiratory chemoreflex. During each intervention, 0, 2.0, 3.5 or 5.0% CO2 was sequentially added (8 min stages) to inspired gas mixtures to assess changes in steady-state cerebrovascular CO2 reactivity and dCA. During normoxia, the addition of CO2 increased internal carotid artery blood flow and middle cerebral artery mean blood velocity (MCAVmean), while reducing dCA (change in phase=-0.73 +/- 0.22rad, P=0.005). During acute hypoxia, internal carotid artery blood flow and MCAVmean remained unchanged, but cerebrovascular CO2 reactivity (internal carotid artery, P=0.003; MCAVmean, P=0.031) and CO2-mediated effects on dCA (P=0.008) were attenuated. The effects of hypoxia were not further altered when the respiratory chemoreflex was restrained. These findings support the hypothesis that arterial CO2 tension-mediated effects on the cerebral vasculature are reduced during acute hypoxia. These effects could limit the degree of hypocapnic vasoconstriction and may help to regulate cerebral blood flow and cerebral O2 homeostasis during acute periods of hypoxia., WILEY-BLACKWELL, Jun. 2014, EXPERIMENTAL PHYSIOLOGY, 99 (6), 849 - 858, doi;web_of_science

    Scientific journal

  • Blood flow distribution during heat stress: cerebral and systemic blood flow

    Shigehiko Ogoh; Kohei Sato; Kazunobu Okazaki; Tadayoshi Miyamoto; Ai Hirasawa; Keiko Morimoto; Manabu Shibasaki

    The purpose of the present study was to assess the effect of heat stress-induced changes in systemic circulation on intra- and extracranial blood flows and its distribution. Twelve healthy subjects with a mean age of 22 +/- 2 (s.d.) years dressed in a tube-lined suit and rested in a supine position. Cardiac output (Q), internal carotid artery (ICA), external carotid artery (ICA), and vertebral artery (VA) blood flows were measured by ultrasonography before and during whole body heating. Esophageal temperature increased from 37.0 +/- 0.2 degrees C to 38.4 +/- 0.2 degrees C during whole body heating. Despite an increase in Q (59 +/- 31%, P<0.001), ICA and VA decreased to 83 +/- 15% (P=0.001) and 87 +/- 8% (P=0.002), respectively, whereas ECA blood flow gradually increased from 188 +/- 72 to 422 +/- 189 mL/minute (135%, P<0.001). These findings indicate that heat stress modified the effect of Q on blood flows at each artery; the increased Q due to heat stress was redistributed to extracranial vascular beds., NATURE PUBLISHING GROUP, Dec. 2013, JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 33 (12), 1915 - 1920, doi;web_of_science

    Scientific journal

  • Aging and thermoregulation

    Manabu Shibasaki; Kazunobu Okazaki; Yoshimitsu Inoue

    The Japanese Society of Physical Fitness and Sports Medicine, Apr. 2013, The Journal of Physical Fitness and Sports Medicine, 2 (1), 37 - 47, doi

    Scientific journal

  • 那智勝浦町における被災地支援活動

    SHIBASAKI Manabu

    Mar. 2013, 繊維製品消費科学, 54 (3), 37-40

  • Muscle sympathetic responses during orthostasis in heat-stressed individuals

    Jian Cui; Manabu Shibasaki; David A. Low; David M. Keller; Scott L. Davis; Craig G. Crandall

    Whole-body heat stress compromises the control of blood pressure during an orthostatic challenge, although the extent to which this occurs can vary greatly between individuals. The mechanism(s) responsible for these varying responses remain unclear. This study tested the hypothesis that the individuals who are best able to tolerate an orthostatic challenge while heat stressed are the ones with the largest increase in sympathetic activity during orthostasis, indexed from recordings of muscle sympathetic nerve activity (MSNA). MSNA, arterial blood pressure, and heart rate were recorded from 11 healthy volunteers throughout passive whole-body heating and during 15 min of 60A degrees head-up tilt (HUT) or until the onset of pre-syncopal symptoms. Whole-body heating significantly increased core temperature (similar to 0.9A degrees C), supine heart rate and MSNA. Eight of 11 subjects developed pre-syncopal symptoms resulting in early termination of HUT. The HUT tolerance time was positively correlated (R = 0.82, P = 0.01) with the increase in MSNA by HUT. These data suggest that the individuals with the largest increase in MSNA during upright tilt have the greatest capacity to withstand the orthostatic challenge while heat stressed., SPRINGER HEIDELBERG, Dec. 2011, CLINICAL AUTONOMIC RESEARCH, 21 (6), 381 - 387, doi;web_of_science

    Scientific journal

  • Modelflow underestimates cardiac output in heat-stressed individuals

    Manabu Shibasaki; Thad E. Wilson; Morten Bundgaard-Nielsen; Thomas Seifert; Niels H. Secher; Craig G. Crandall

    An estimation of cardiac output can be obtained from arterial pressure waveforms using the Modelflow method. However, whether the assumptions associated with Modelflow calculations are accurate during whole body heating is unknown. This project tested the hypothesis that cardiac output obtained via Modelflow accurately tracks thermodilution-derived cardiac outputs during whole body heat stress. Acute changes of cardiac output were accomplished via lower-body negative pressure (LBNP) during normothermic and heat-stressed conditions. In nine healthy normotensive subjects, arterial pressure was measured via brachial artery cannulation and the volume-clamp method of the Finometer. Cardiac output was estimated from both pressure waveforms using the Modeflow method. In normothermic conditions, cardiac outputs estimated via Modelflow (arterial cannulation: 6.1 +/- 1.0 l/min; Finometer 6.3 +/- 1.3 l/min) were similar with cardiac outputs measured by thermodilution (6.4 +/- 0.8 l/min). The subsequent reduction in cardiac output during LBNP was also similar among these methods. Whole body heat stress elevated internal temperature from 36.6 +/- 0.3 to 37.8 +/- 0.4 degrees C and increased cardiac output from 6.4 +/- 0.8 to 10.9 +/- 2.0 l/min when evaluated with thermodilution (P < 0.001). However, the increase in cardiac output estimated from the Modelflow method for both arterial cannulation (2.3 +/- 1.1 l/min) and Finometer (1.5 +/- 1.2 l/min) was attenuated compared with thermodilution (4.5 +/- 1.4 l/min, both P < 0.01). Finally, the reduction in cardiac output during LBNP while heat stressed was significantly attenuated for both Modelflow methods (cannulation: -1.8 +/- 1.2 l/min, Finometer: -1.5 +/- 0.9 l/min) compared with thermodilution (-3.8 +/- 1.19 l/min). These results demonstrate that the Modelflow method, regardless of Finometer or direct arterial waveforms, underestimates cardiac output during heat stress and during subsequent reductions in cardiac output via LBNP., AMER PHYSIOLOGICAL SOC, Feb. 2011, AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY, 300 (2), R486 - R491, doi;web_of_science

    Scientific journal

  • Skin blood flow and local temperature independently modify sweat rate during passive heat stress in humans

    Jonathan E. Wingo; David A. Low; David M. Keller; R. Matthew Brothers; Manabu Shibasaki; Craig G. Crandall

    Sweat rate (SR) is reduced in locally cooled skin, which may result from decreased temperature and/or parallel reductions in skin blood flow. The purpose of this study was to test the hypotheses that decreased skin blood flow and decreased local temperature each independently attenuate sweating. In protocols I and II, eight subjects rested supine while wearing a water-perfused suit for the control of whole body skin and internal temperatures. While 34 C water perfused the suit, four microdialysis membranes were placed in posterior forearm skin not covered by the suit to manipulate skin blood flow using vasoactive agents. Each site was instrumented for control of local temperature and measurement of local SR (capacitance hygrometry) and skin blood flow (laser-Doppler flowmetry). In protocol I, two sites received norepinephrine to reduce skin blood flow, while two sites received Ringer solution (control). All sites were maintained at 34 degrees C. In protocol II, all sites received 28 mM sodium nitroprusside to equalize skin blood flow between sites before local cooling to 20 degrees C (2 sites) or maintenance at 34 degrees C (2 sites). In both protocols, individuals were then passively heated to increase core temperature similar to 1 degrees C. Both decreased skin blood flow and decreased local temperature attenuated the slope of the SR to mean body temperature relationship (2.0 +/- 1.2 vs. 1.0 +/- 0.7 mg.cm(-2).min(-1).degrees C(-1) for the effect of decreased skin blood flow, P = 0.01; 1.2 +/- 0.9 vs. 0.07 +/- 0.05 mg.cm(-2).min(-1).degrees C(-1) for the effect of decreased local temperature, P = 0.02). Furthermore, local cooling delayed the onset of sweating (mean body temperature of 37.5 +/- 0.4 vs. 37.6 +/- 0.4 degrees C, P = 0.03). These data demonstrate that local cooling attenuates sweating by independent effects of decreased skin blood flow and decreased local skin temperature., AMER PHYSIOLOGICAL SOC, Nov. 2010, JOURNAL OF APPLIED PHYSIOLOGY, 109 (5), 1301 - 1306, doi;web_of_science

    Scientific journal

  • Heat stress attenuates the increase in arterial blood pressure during the cold pressor test

    Jian Cui; Manabu Shibasaki; David A. Low; David M. Keller; Scott L. Davis; Craig G. Crandall

    The mechanisms by which heat stress impairs the control of blood pressure leading to compromised orthostatic tolerance are not thoroughly understood. A possible mechanism may be an attenuated blood pressure response to a given increase in sympathetic activity. This study tested the hypothesis that whole body heating attenuates the blood pressure response to a non-baroreflex-mediated sympathoexcitatory stimulus. Ten healthy subjects were instrumented for the measurement of integrated muscle sympathetic nerve activity (MSNA), mean arterial blood pressure (MAP), heart rate, sweat rate, and forearm skin blood flow. Subjects were exposed to a cold pressor test (CPT) by immersing a hand in an ice water slurry for 3 min while otherwise normothermic and while heat stressed (i.e., increase core temperature similar to 0.7 degrees C via water-perfused suit). Mean responses from the final minute of the CPT were evaluated. In both thermal conditions CPT induced significant increases in MSNA and MAP without altering heart rate. Although the increase in MSNA to the CPT was similar between thermal conditions (normothermia: Delta 14.0 +/- 2.6; heat stress: Delta 19.1 +/- 2.6 bursts/min; P = 0.09), the accompanying increase in MAP was attenuated when subjects were heat stressed (normothermia: Delta 25.6 +/- 2.3, heat stress: Delta 13.4 +/- 3.0 mmHg; P < 0.001). The results demonstrate that heat stress can attenuate the pressor response to a sympathoexcitatory stimulus., AMER PHYSIOLOGICAL SOC, Nov. 2010, JOURNAL OF APPLIED PHYSIOLOGY, 109 (5), 1354 - 1359, doi;web_of_science

    Scientific journal

  • Insufficient cutaneous vasoconstriction leading up to and during syncopal symptoms in the heat stressed human

    C. G. Crandall; M. Shibasaki; T. E. Wilson

    Crandall CG, Shibasaki M, Wilson TE. Insufficient cutaneous vasoconstriction leading up to and during syncopal symptoms in the heat stressed human. Am J Physiol Heart Circ Physiol 299: H1168-H1173, 2010. First published August 6, 2010; doi:10.1152/ajpheart.00290.2010.-As much as 50% of cardiac output can be distributed to the skin in the hyperthermic human, and therefore the control of cutaneous vascular conductance (CVC) becomes critical for the maintenance of blood pressure. Little is known regarding the magnitude of cutaneous vasoconstriction in profoundly hypotensive individuals while heat stressed. This project investigated the hypothesis that leading up to and during syncopal symptoms associated with combined heat and orthostatic stress, reductions in CVC are inadequate to prevent syncope. Using a retrospective study design, we evaluated data from subjects who experienced syncopal symptoms during lower body negative pressure (N = 41) and head-up tilt (N = 5). Subjects were instrumented for measures of internal temperature, forearm skin blood flow, arterial pressure, and heart rate. CVC was calculated as skin blood flow/mean arterial pressure x 100. Data were obtained while subjects were normothermic, immediately before an orthostatic challenge while heat stressed, and at 5-s averages for the 2 min preceding the cessation of the orthostatic challenge due to syncopal symptoms. Whole body heat stress increased internal temperature (1.25 +/- 0.3 degrees C; P < 0.001) and CVC (29 +/- 20 to 160 +/- 58 CVC units; P < 0.001) without altering mean arterial pressure (83 +/- 7 to 82 +/- 6 mmHg). Mean arterial pressure was reduced to 57 +/- 9 mmHg (P < 0.001) immediately before the termination of the orthostatic challenge. At test termination, CVC decreased to 138 +/- 61 CVC units (P < 0.001) relative to before the orthostatic challenge but remained approximately fourfold greater than when subjects were normothermic. This negligible reduction in CVC during pronounced hypotension likely contributes to reduced orthostatic tolerance in heat-stressed humans. Given that lower body negative pressure and head-up tilt are models of acute hemorrhage, these findings have important implications with respect to mechanisms of compromised blood pressure control in the hemorrhagic individual who is also hyperthermic (e.g., military personnel, firefighters, etc.)., AMER PHYSIOLOGICAL SOC, Oct. 2010, AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 299 (4), H1168 - H1173, doi;web_of_science

    Scientific journal

  • Mechanisms and controllers of eccrine sweating in humans

    Manabu Shibasaki; Craig G. Crandall

    Human body temperature is regulated within a very narrow range. When exposed to hyperthermic conditions, via environmental factors and/or increased metabolism, heat dissipation becomes vital for survival. In humans, the primary mechanism of heat dissipation, particularly when ambient temperature is higher than skin temperature, is evaporative heat loss secondary to sweat secretion from eccrine glands. While the primary controller of sweating is the integration between internal and skin temperatures, a number of non-thermal factors modulate the sweating response. In addition to summarizing the current understanding of the neural pathways from the brain to the sweat gland, as well as responses at the sweat gland, this review will highlight findings pertaining to studies of proposed non-thermal modifiers of sweating, namely, exercise, baroreceptor loading state, and body fluid status. Information from these studies not only provides important insight pertaining to the basic mechanisms of sweating, but also perhaps could be useful towards a greater understanding of potential mechanisms and consequences of disease states as well as aging in altering sweating responses and thus temperature regulation., 01 Jan. 2010, Frontiers in Bioscience - Scholar, 2 (2), 685 - 696, pubmed

    Scientific journal

  • Plasma hyperosmolality elevates the internal temperature threshold for active thermoregulatory vasodilation during heat stress in humans

    Manabu Shibasaki; Ken Aoki; Keiko Morimoto; John M. Johnson; Akira Takamata

    Shibasaki M, Aoki K, Morimoto K, Johnson JM, Takamata A. Plasma hyperosmolality elevates the internal temperature threshold for active thermoregulatory vasodilation during heat stress in humans. Am J Physiol Regul Integr Comp Physiol 297: R1706-R1712, 2009. First published October 7, 2009; doi:10.1152/ajpregu.00242.2009.Plasma hyperosmolality delays the response in skin blood flow to heat stress by elevating the internal temperature threshold for cutaneous vasodilation. This elevation could be because of a delayed onset of cutaneous active vasodilation and/or to persistent cutaneous active vasoconstriction. Seven healthy men were infused with either hypertonic (3% NaCl) or isotonic (0.9% NaCl) saline and passively heated by immersing their lower legs in 42 C water for 60 min (room temperature, 28 C; relative humidity, 40%). Skin blood flow was monitored via laser-Doppler flowmetry at sites pretreated with bretylium tosylate (BT) to block sympathetic vasoconstriction selectively and at adjacent control sites. Plasma osmolality was increased by similar to 13 mosmol/kgH(2)O following hypertonic saline infusion and was unchanged following isotonic saline infusion. The esophageal temperature (T(es)) threshold for cutaneous vasodilation at untreated sites was significantly elevated in the hyperosmotic state (37.73 +/- 0.11 degrees C) relative to the isosmotic state (36.63 +/- 0.12 degrees C, P < 0.001). A similar elevation of the Tes threshold for cutaneous vasodilation was observed between osmotic conditions at the BT-treated sites (37.74 +/- 0.18 vs. 36.67 +/- 0.07 degrees C, P < 0.001) as well as sweating. These results suggest that the hyperosmotically induced elevation of the internal temperature threshold for cutaneous vasodilation is due primarily to an elevation in the internal temperature threshold for the onset of active vasodilation, and not to an enhancement of vasoconstrictor activity., AMER PHYSIOLOGICAL SOC, Dec. 2009, AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY, 297 (6), R1706 - R1712, doi;web_of_science

    Scientific journal

  • Botulinum toxin abolishes sweating via impaired sweat gland responsiveness to exogenous acetylcholine

    M. Shibasaki; S. L. Davis; J. Cui; D. A. Low; D. M. Keller; C. G. Crandall

    Background Botulinum toxin A (BTX) disrupts neurotransmitter release from cholinergic nerves. The effective duration of impaired sweat secretion with BTX is longer relative to that of impaired muscle contraction, suggesting different mechanisms in these tissues. Objectives The aim of this study was to test the hypothesis that BTX is capable of altering sweating by reducing the responsiveness of the sweat gland to acetylcholine. Methods BTX was injected into the dorsal forearm skin of healthy subjects at least 3 days before subsequent assessment. On the day of the experiment, intradermal microdialysis probes were placed within the BTX-treated area and in an adjacent untreated area. Incremental doses of acetylcholine were administered through the microdialysis membranes while the sweat rate (protocol 1; n = 8) or a combination of sweat rate and skin blood flow (protocol 2; n = 8) were assessed. Results A relative absence of sweating was observed at the BTX site for both protocols (protocol 1: 0.05 +/- 0.09 mg cm(-2) min(-1); protocol 2: 0.03 +/- 0.04 mg cm(-2) min(-1), both at the highest dose of acetylcholine), while the sweat rate increased appropriately at the control sites (protocol 1: 0 90 +/- 0 46 mg cm(-2) min(-1); protocol 2: 1 07 +/- 0 67 mg cm(-2) min(-1)). Cutaneous vascular conductance increased to a similar level at both the BTX and control sites. Conclusions These results demonstrate that BTX is capable of inhibiting sweat secretion by reducing the responsiveness of the sweat gland to acetylcholine, while not altering acetylcholine-mediated cutaneous vasodilatation., WILEY-BLACKWELL PUBLISHING, INC, Oct. 2009, BRITISH JOURNAL OF DERMATOLOGY, 161 (4), 757 - 761, doi;web_of_science

    Scientific journal

  • Early activation of the coagulation system during lower body negative pressure

    SHIBASAKI Manabu; Zaar M; Johansson PI; Nielsen LB; Crandall CG; Shibasaki M; Hilsted L; Secher NH

    Oct. 2009, Clinical physiology and functional imaging, 29 (6), 427-430

  • Sustained impairments in cutaneous vasodilation and sweating in grafted skin following long-term recovery

    Scott L. Davis; Manabu Shibasaki; David A. Low; Jian Cui; David M. Keller; Jonathan E. Wingo; Gary F. Purdue; John L. Hunt; Brett D. Arnoldo; Karen J. Kowalske; Craig G. Crandall

    We previously identified impaired cutaneous vasodilation and sweating in grafted skin 5 to 9 months postsurgery. The aim of this investigation was to test the hypothesis that cutaneous vasodilation, but not sweating, is restored as the graft heals. Skin blood flow and sweat rate were assessed from grafted skin and adjacent noninjured skin in three groups of subjects: 5 to 9 months postsurgery (n = 13), 2 to 3 years postsurgery (n = 13), and 4 to 8 years postsurgery (n = 13) during three separate protocols: 1) whole-body heating and cooling, 2) local administration of vasoactive drugs, and 3) local heating and cooling. Cutaneous vasodilation and sweating during whole-body heating were significantly lower (P < .001) in grafted skin when compared with noninjured skin across all groups and demonstrated no improvements with recovery time postsurgery. Maximal endothelial-dependent (acetylcholine) and endothelial-independent (sodium nitroprusside) cutaneous vasodilation remained attenuated (P < .001) in grafted skin up to 4 to 8 years postsurgery, indicating postsynaptic impairments. In grafted skin, cutaneous vasoconstriction during whole-body and local cooling was preserved, whereas vasodilation to local heating was impaired, regardless of the duration postsurgery. Split-thickness skin grafts have impaired cutaneous vasodilation and sweating up to 4 to 8 years postsurgery, thereby limiting the capability of this skin's contribution to thermoregulation during a heats stress. In contrast, grafted skin has preserved vasoconstrictor capacity. Copyright © 2009 by the American Burn Association., Jul. 2009, Journal of Burn Care and Research, 30 (4), 675 - 685, doi;pubmed

    Scientific journal

  • Neural and non-neural control of skin blood flow during isometric handgrip exercise in the heat stressed human

    Manabu Shibasaki; Peter Rasmussen; Niels H. Secher; Craig G. Crandall

    During heat stress, isometric handgrip (IHG) exercise causes cutaneous vasoconstriction, but it remains controversial whether neural mechanisms are responsible for this observation. The objective of this study was to test the hypothesis that cutaneous vasoconstriction during IHG exercise in heat stressed individuals occurs via a neural mechanism. An axillary nerve blockade was performed to block efferent nerve traffic to the left forearm in seven healthy subjects. Two intradermal microdialysis probes were placed within forearm skin of the blocked area. Forearm skin blood flow was measured by laser-Doppler flowmetry over the microdialysis probes as well as from skin of the contralateral (unblocked) forearm. Cutaneous vascular conductance (CVC) was calculated from the ratio of skin blood flow to mean arterial pressure. Effectiveness of nerve blockade was verified by the absence of tactile sensation, as well as an absence of sweating and cutaneous vasodilatation during a whole-body heat stress. Upon this confirmation, adenosine was perfused through one of the microdialysis probes to increase skin blood flow similar to that of the unblocked site. After internal temperature increased similar to 0.7 degrees C, subjects performed 2 min of IHG exercise at 35% of maximal voluntary contraction using the non-blocked arm. IHG exercise significantly decreased CVC at the unblocked site (82.3 +/- 5.7 to 70.9 +/- 5.4%max, P = 0.005, means +/- s.e.m.) and the adenosine treated site of the blocked arm (75.2 +/- 7.2 to 68.3 +/- 6.6%max, P = 0.005), whereas CVC was unchanged at the blocked site that did not receive adenosine (15.7 +/- 2.8 to 13.7 +/- 2.0%max, P = 0.10). Importantly, the reduction in CVC was greater at the unblocked site than at the adenosine treated site (11.4 +/- 2.6 vs. 6.9 +/- 1.6%max, respectively, P = 0.01). These findings suggest that neural and non-neural mechanisms contribute to the reduction in forearm CVC during IHG exercise in heat stressed humans., WILEY-BLACKWELL PUBLISHING, INC, May 2009, JOURNAL OF PHYSIOLOGY-LONDON, 587 (9), 2101 - 2107, doi;web_of_science

    Scientific journal

  • Whole body heat stress attenuates baroreflex control of muscle sympathetic nerve activity during postexercise muscle ischemia

    Jian Cui; Manabu Shibasaki; Scott L. Davis; David A. Low; David M. Keller; Craig G. Crandall

    Cui J, Shibasaki M, Davis SL, Low DA, Keller DM, Crandall CG. Whole body heat stress attenuates baroreflex control of muscle sympathetic nerve activity during postexercise muscle ischemia. J Appl Physiol 106: 1125-1131, 2009. First published February 12, 2009; doi: 10.1152/japplphysiol.00135.2008.-Both whole body heat stress and stimulation of muscle metabolic receptors activate muscle sympathetic nerve activity (MSNA) through nonbaroreflex pathways. In addition to stimulating muscle metaboreceptors, exercise has the potential to increase internal temperature. Although we and others report that passive whole body heating does not alter the gain of the arterial baroreflex, it is unknown whether increased body temperature, often accompanying exercise, affects baroreflex function when muscle metaboreceptors are stimulated. This project tested the hypothesis that whole body heating alters the gain of baroreflex control of muscle sympathetic nerve activity (MSNA) and heart rate during muscle metaboreceptor stimulation engaged via postexercise muscle ischemia (PEMI). MSNA, blood pressure (BP, Finometer), and heart rate were recorded from 11 healthy volunteers. The volunteers performed isometric handgrip exercise until fatigue, followed by 2.5 min of PEMI. During PEMI, BP was acutely reduced and then raised pharmacologically using the modified Oxford technique. This protocol was repeated two to three times when volunteers were normothermic, and again during heat stress (increase core temperature similar to 0.7 degrees C) conditions. The slope of the relationship between MSNA and BP during PEMI was less negative (i.e., decreased baroreflex gain) during whole body heating when compared with the normothermic condition (-4.34 +/- 0.40 to -3.57 +/- 0.31 units.beat(-1).mmHg(-1), respectively; P = 0.015). The gain of baroreflex control of heart rate during PEMI was also decreased during whole body heating (P < 0.001). These findings indicate that whole body heat stress reduces baroreflex control of MSNA and heart rate during muscle metaboreceptor stimulation., AMER PHYSIOLOGICAL SOC, Apr. 2009, JOURNAL OF APPLIED PHYSIOLOGY, 106 (4), 1125 - 1131, doi;web_of_science

    Scientific journal

  • Effect of elevated local temperature on cutaneous vasoconstrictor responsiveness in humans

    Jonathan E. Wingo; David A. Low; David M. Keller; R. Matthew Brothers; Manabu Shibasaki; Craig G. Crandall

    Wingo JE, Low DA, Keller DM, Brothers RM, Shibasaki M, Crandall CG. Effect of elevated local temperature on cutaneous vasoconstrictor responsiveness in humans. J Appl Physiol 106: 571-575, 2009. First published December 4, 2008; doi: 10.1152/japplphysiol.91249.2008.-Cutaneous vascular conductance (CVC) increases in response to local skin heating. Although attenuation of vasoconstrictor responsiveness due to local heating has been demonstrated, the mechanism(s) responsible for this attenuation remains unclear. Nitric oxide has been shown to at least partially contribute to this response, but other mechanisms also may be involved. The purpose of this study was to test the hypothesis that local heating diminishes cutaneous vasoconstrictor responsiveness through a nitric oxide-independent mechanism by altering postsynaptic reactivity to norepinephrine. A follow-up protocol tested the hypothesis that local heating attenuates the presynaptic release of neurotransmitters that cause vasoconstriction, also via non-nitric oxide mechanisms. In protocol I, CVC was assessed in eight subjects during administration of increasing doses of norepinephrine (via intradermal microdialysis) at adjacent sites separately heated to 34 degrees C and 40 degrees C. In protocol II, which was identical to, but separate from, protocol I, CVC was assessed in seven subjects during administration of increasing doses of tyramine, which causes release of neurotransmitters from adrenergic nerves. At each site for both protocols, nitric oxide synthesis was inhibited (via microdialysis administration of N(G)-nitro-L-arginine methyl ester) and flow was matched (via microdialysis administration of adenosine); therefore, temperature was the only variable that differed between the sites. For both protocols, nonlinear regression analysis revealed no difference (P > 0.05) in the effective drug concentration causing 50% of the vasoconstrictor response. Minimum CVC [6.3 +/- 2.0 and 9.0 +/- 4.0% of peak CVC (mean +/- SD) for protocol 1 and 19.3 +/- 9.3 and 20.5 +/- 11.9% of peak CVC for protocol II at 34 degrees C and 40 degrees C sites, respectively] was not different between sites. Independent of nitric oxide, local skin heating to 40 degrees C does not attenuate adrenergically mediated cutaneous vasoconstriction through pre- or postsynaptic mechanisms., AMER PHYSIOLOGICAL SOC, Feb. 2009, JOURNAL OF APPLIED PHYSIOLOGY, 106 (2), 571 - 575, doi;web_of_science

    Scientific journal

  • Thermoregulatory adaptation in humans and its modifying factors

    SHIBASAKI Manabu; Kondo N; Taylor NAS; Shibasaki M; Aoki K; Muhamed AMC

    2009, Global Environmental Research, 13 (1), 35-41

  • Nitric oxide inhibits cutaneous vasoconstriction to exogenous norepinephrine

    Manabu Shibasaki; David A. Low; Scott L. Davis; Craig G. Crandall

    Shibasaki M, Low DA, Davis SL, Crandall CG. Nitric oxide inhibits cutaneous vasoconstriction to exogenous norepinephrine. J Appl Physiol 105: 1504-1508, 2008. First published September 18, 2008; doi:10.1152/japplphysiol.91017.2008.-Previously, we found that nitric oxide (NO) inhibits cutaneous vasoconstrictor responsiveness evoked by whole body cooling, as well as an orthostatic stress in the heat-stressed human (Shibasaki M, Durand S, Davis SL, Cui J, Low DA, Keller DM, Crandall CG. J Physiol 585: 627-634, 2007). However, it remains unknown whether this response occurs via NO acting through presynaptic or postsynaptic mechanisms. The aim of this study was to test the hypothesis that NO is capable of impairing cutaneous vasoconstriction via postsynaptic mechanisms. Skin blood flow was monitored over two forearm sites where intradermal micro-dialysis membranes were previously placed. Skin blood flow was elevated four-to fivefold through perfusion of the NO donor sodium nitroprusside at one site and through perfusion of adenosine (primarily non-NO mechanisms) at a second site. Once a plateau in vasodilation was evident, increasing concentrations of norepinephrine (1 x 10(-8) to 1 x 10(-2) M) were administrated through both microdialysis probes, while the aforementioned vasodilator agents continued to be perfused. Cutaneous vascular conductance was calculated by dividing skin blood flow by mean arterial blood pressure. The administration of norepinephrine decreased cutaneous vascular conductance at both sites. However, the dose of norepinephrine at the onset of vasoconstriction (-5.9 +/- 1.3 vs.-7.2 +/- 0.7 log M norepinephrine, P = 0.021) and the concentration of norepinephrine resulting in 50% of the maximal vasoconstrictor response (-4.9 +/- 1.2 vs. -6.1 +/- 0.2 log M norepinephrine dose; P = 0.012) occurred at significantly higher norepinephrine concentrations for the sodium nitroprusside site relative to the adenosine site, respectively. These results suggested that NO is capable of attenuating cutaneous vasoconstrictor responsiveness to norepinephrine via postsynaptic mechanisms., AMER PHYSIOLOGICAL SOC, Nov. 2008, JOURNAL OF APPLIED PHYSIOLOGY, 105 (5), 1504 - 1508, doi;web_of_science

    Scientific journal

  • Cutaneous and hemodynamic responses during hot flashes in symptomatic postmenopausal women

    David A. Low; Scott L. Davis; David M. Keller; Manabu Shibasaki; Craig G. Crandall

    Objective: The aim of this study was to test the hypothesis that the postmenopausal hot flash is accompanied by rapid decreases in arterial blood pressure and increases in cutaneous vascular conductance (CVC), as evaluated by continuous measurements of these variables in symptomatic women. Design: Twelve healthy, normotensive, postmenopausal women rested in a temperature-controlled laboratory (26 degrees C) for approximately 90 minutes. The onset of a hot flash was objectively identified as a transient and pronounced elevation of sternal sweat rate (capacitance hygrometry). Results: Twenty-three hot flashes were recorded during the experimental sessions (3.4 +/- 1.4 min; range, 1.3-6.5 min). Mean arterial blood pressure decreased 13 2 min Hg during 11 hot flashes in five participants. Data from these participants, categorized as responders, were analyzed separately from data for those participants whose blood pressure did not change during their hot flashes (n = 7, 12 hot flashes). Heart rate (obtained from an electrocardiogram) significantly increased during the hot flashes, but there was no difference between the responder and nonresponder groups (9 +/- 2 vs 10 +/- 1 beats/min, respectively; P > 0.05). The increase in CVC was not different between groups at either the forearm (15% +/- 3% vs 12% +/- 3% maximal CVC, P > 0.05) or sternum (24% +/- 5% vs 21% +/- 3% maximal CVC, P > 0.05). Conclusions: These data demonstrate that in a subset of participants, the hot flash is accompanied by a significant reduction in blood pressure, but there is no difference in CVC between these women and women with no drop in blood pressure., LIPPINCOTT WILLIAMS & WILKINS, Mar. 2008, MENOPAUSE-THE JOURNAL OF THE NORTH AMERICAN MENOPAUSE SOCIETY, 15 (2), 290 - 295, doi;web_of_science

    Scientific journal

  • Cutaneous vasoconstriction during whole-body and local cooling in grafted skin 5-9 months post-surgery

    SHIBASAKI Manabu; Davis SL; Shibasaki M; Low DA; Cui J; Keller DM; Purdue GF; Hunt JL; Arnoldo BD; Kowalske KJ; Crandall CG

    Jan. 2008, Journal of Burn Care & Research, 29 (1), 36-41

  • Endogenous nitric oxide attenuates neutrally mediated cutaneous vasoconstriction

    Manabu Shibasaki; Sylvain Durand; Scott L. Davis; Jian Cui; David A. Low; David M. Keller; Craig G. Crandall

    Cutaneous vasoconstrictor responsiveness may be impaired by substance(s) directly or indirectly responsible for cutaneous active vasodilatation. In this study, we tested the hypothesis that endogenous nitric oxide (NO) attenuates the reduction in cutaneous vascular conductance (CVC) during an orthostatic challenge combined with whole-body heating, as well as during whole-body cooling. In protocol 1, healthy subjects were pretreated with an intradermal injection of botulinum toxin A (BTX) to block the release of neurotransmitters from nerves responsible for cutaneous active vasodilatation. On the experimental day, a microdialysis probe was placed at the BTX-treated site as well as at two adjacent untreated sites. N-G-nitro-L-arginine methyl ester (L-NAME, 10 mM) was perfused through the probe placed at the BTX-treated site and at one untreated site. After confirmation of the absence of cutaneous vasodilatation at the BTX site during whole-body heating, adenosine was infused through the microdialysis probe at this site to increase skin blood flow to a level similar to that at the untreated site. Subsequently, 30 and 40 mmHg lower-body negative pressures (LBNPs) were applied. The reduction in CVC to LBNP was greatest at the BTX-treated site (15.0 +/- 2.4% of the maximum level (% max)), followed by the L-NAME-treated site (11.3 +/- 2.6% max), and then the untreated site (3.8 +/- 3.0% max; P < 0.05 for all comparisons). In protocol 2, two microdialysis membranes were inserted in the dermal space of one forearm. Adenosine alone was infused at one site while the other site received adenosine and L-NAME. The reduction in CVC in response to whole-body cooling was significantly greater at the L-NAME-treated site than at the adjacent adenosine alone site. These results suggest that endogenous NO is capable of attenuating cutaneous vasoconstrictor responsiveness., BLACKWELL PUBLISHING, Dec. 2007, JOURNAL OF PHYSIOLOGY-LONDON, 585 (2), 627 - 634, doi;web_of_science

    Scientific journal

  • Does local heating-induced nitric oxide production attenuate vasoconstrictor responsiveness to lower body negative pressure in human skin?

    David A. Low; Manabu Shibasaki; Scott L. Davis; David M. Keller; Craig G. Crandall

    We tested the hypothesis that local heating-induced nitric oxide (NO) production attenuates cutaneous vasoconstrictor responsiveness. Eleven subjects (6 men, 5 women) had four microdialysis membranes placed in forearm skin. Two membranes were perfused with 10 mM of N-G-nitro-L-arginine (L-NAME) and two with Ringer solution (control), and all sites were locally heated to WC. Subjects then underwent 5 min of 60-mmHg lower body negative pressure (LBNP). Two sites (a control and an L-NAME site) were then heated to 39 degrees C, while the other two sites were heated to 42 degrees C. At the L-NAME sites, skin blood flow was elevated using 0.75-2 mg/ml of adenosine in the perfusate solution (Adn + L-NAME) to a similar level relative to control sites. Subjects then underwent another 5 min of 60-mmHg LBNP. At 34 degrees C, cutaneous vascular conductance (CVC) decreased (A) similarly at both control and L-NAME sites during LBNP (Delta 7.9 +/- 3.0 and Delta 3.4 +/- 0.8% maximum, respectively; P > 0.05). The reduction in CVC to LBNP was also similar between control and Adn + L-NAME sites at 39 degrees C (control Delta 11.4 +/- 2.5 vs. Adn + L-NAME Delta 7.9 +/- 2.0% maximum; P > 0.05) and 42 degrees C (control Delta 1.9 +/- 2.7 vs. Adn + L-NAME Delta 4.2 +/- 2.7% maximum; P > 0.05). However, the decrease in CVC at 42 degrees C, regardless of site, was smaller than at 39 degrees C (P < 0.05). These results do not support the hypothesis that local heating-induced NO production attenuates cutaneous vasoconstrictor responsiveness during high levels of LBNP. However, elevated local temperature, per se, attenuates cutaneous vasoconstrictor responsiveness to LBNP, presumably through non-nitric oxide mechanisms., AMER PHYSIOLOGICAL SOC, May 2007, JOURNAL OF APPLIED PHYSIOLOGY, 102 (5), 1839 - 1843, doi;web_of_science

    Scientific journal

  • Impaired cutaneous vasodilation and sweating in grafted skin during whole-body heating

    Scott L. Davis; Manabu Shibasaki; David A. Low; Jian Cui; David M. Keller; Gary F. Purdue; John L. Hunt; Brett D. Arnoldo; Karen J. Kowalske; Craig G. Crandall

    The aim of this investigation was to identify the consequences of skin grafting on cutaneous vasodilation and sweating in split-thickness grafted skin during indirect whole-body heating 5 to 9 months after surgery. In addition, thermoregulatory function was examined at donor skin sites on a separate day. Skin blood flow and sweat rate (SR) were assessed from both grafted (n = 14) or donor skin (n = 11) and compared with the respective adjacent control skin during indirect whole-body heating. Cutaneous vascular conductance (CVC) was calculated from the ratio of skin blood flow (arbitrary units; au) to mean arterial pressure. Whole-body heating significantly increased internal temperature (37.0 +/- 0.1 degrees C to 37.8 +/- 0.1 degrees C; P <.05). Cutaneous vasodilation (ie, the increase in CVC from baseline, Delta CVC) during whole-body heating was significantly attenuated in grafted skin (Delta CVC = 0.14 +/- 0.15 au/mm Hg) compared with adjacent control skin (Delta CVC = 0.84 +/- 0.11 au/mm Hg; P <.05). Increases in sweat rate (ASR) were also significantly lower in grafted skin (ASR = 0.08 +/- 0.08 mg/cm(2)/min) compared with adjacent control skin (ASR = 1.16 +/- 0.20 mg/ cm(2)/min; P <.05). Cutaneous vasodilation and sweating during heating were not significantly different between donor sites (Delta CVC = 0.71 +/- 0.19 au/mm Hg; ASR = 1.04 0.15 mg/cm2/min) and adjacent control skin (Delta CVC = 0.50 +/- 0.10 au/mm Hg; ASR = 0.83 +/- 0.17 mg/cm(2)/min). Greatly attenuated or absence of cutaneous vasodilation and sweating suggests impairment of thermoregulatory function in grafted skin, thereby, diminishing the contribution of this skin to overall temperature control during a heat stress., LIPPINCOTT WILLIAMS & WILKINS, May 2007, JOURNAL OF BURN CARE & RESEARCH, 28 (3), 427 - 434, doi;web_of_science

    Scientific journal

  • Skin grafting impairs postsynaptic cutaneous vasodilator and sweating responses

    Scott L. Davis; Manabu Shibasaki; David A. Low; Jian Cui; David M. Keller; Gary F. Purdue; John L. Hunt; Brett D. Arnoldo; Karen J. Kowalske; Craig G. Crandall

    This study tested the hypothesis that postsynaptic cutaneous vascular responses to endothelial-dependent and -independent vasodilators, as well as sweat gland function, are impaired in split-thickness grafted skin 5 to 9 months after surgery. Intradermal microdialysis membranes were placed in grafted and adjacent control skin, thereby allowing local delivery of the endothelial-dependent vasodilator, acetylcholine (ACh; 1 x 10(-7) to 1 x 10(-1) M at 10-fold increments) and the endothelial-independent nitric oxide donor, sodium nitroprusside (SNP; 5 x 10(-8) to 5 x 10(-2) M at 10-fold increments). Skin blood flow and sweat rate were simultaneously assessed over the semipermeable portion of the membrane. Cutaneous vascular conductance (CVC) was calculated from the ratio of laser Doppler-derived skin blood flow to mean arterial blood pressure. Delta CVC responses from baseline to these drugs were modeled via nonlinear regression curve fitting to identify the dose of ACh and SNP causing 50% of the maximal vasodilator response (EC50). A rightward shift in the CVC dose response curve for ACh was observed in grafted (EC50 = -2.61 +/- 0.44 log M) compared to adjacent control skin (EC50 = -3.34 +/- 0.46 log M; P =.003), whereas the mean EC50 for SNP was similar between grafted (EC50 = -4.21 +/- 0.94 log M) and adjacent control skin (EC50 = -3.87 +/- 0.65 log M; P = 0.332). Only minimal sweating to exogenous ACh was observed in grafted skin whereas normal sweating was observed in control skin. Increased EC50 and decreased maximal CVC responses to the exogenous administration of ACh suggest impairment of endothelial-dependent cutaneous vasodilator responses in grafted skin 5 to 9 months after surgery. Greatly attenuated sweating responses to ACh suggests either abnormal or an absence of functional sweat glands in the grafted skin., LIPPINCOTT WILLIAMS & WILKINS, May 2007, JOURNAL OF BURN CARE & RESEARCH, 28 (3), 435 - 441, doi;web_of_science

    Scientific journal

  • Carotid baroreceptor stimulation alters cutaneous vascular conductance during whole-body heating in humans

    David M. Keller; Scott L. Davis; David A. Low; Manabu Shibasaki; Peter B. Raven; Craig G. Crandall

    Prior studies investigating carotid baroreflex control of the cutaneous vasculature have yielded mixed findings. However, previously used methodological and analytical techniques may limit the ability to detect carotid baroreflex-mediated changes in cutaneous vascular conductance (CVC). The aim of this study was to test the hypothesis that dynamic carotid baroreceptor stimulation (i.e. 5 s trials) using neck pressure (NP, simulated carotid hypotension) and neck suction (NS, simulated carotid hypertension) will decrease and increase CVC, respectively, during normothermic and whole-body heating conditions in resting humans. Data were obtained from nine subjects (age, 31 +/- 2 year). The ratio of forearm skin blood flux (laser-Doppler flowmetry) and arterial blood pressure (Finapres) was used as an index of CVC. Multiple 5 s trials of NP (+40(Torr)) and NS (-60(Torr)), as well as breath-hold/airflow control trials, were applied during end-expiratory breath-holds while subjects were normotheric and heat stressed (change in core temperature similar to 0.75 degrees C). CVC responses to each NP and NS trial were averaged into 1 s intervals during the following periods: 3 s prestimulus, 5 s during stimulus, and 5 s poststimulus. Peak CVC responses (3 s average) to NP and NS were compared to prestimulus values using paired t test. During normothermia, NP decreased CVC by 0.032 +/- 0.007 arbitrary units (a.u.) mmHg(-1); (P < 0.05); however, breath-hold/airflow control trials resulted in similar decreases in CVC. NS did not change CVC (Delta= 0.002 +/- 0.005 a.u. mmHg(-1); P = 0.63). During whole-body heating, NP decreased CVC (by 0.16 +/- 0.04 a.u. mmHg(-1); (P < 0.05), whereas NS increased CVC by 0.07 +/- 0.03 a.u. mmHg(-1); (P < 0.05). Furthermore, these changes were greater than, or directionally different from, the breath-hold/airflow control trials. These findings indicate that carotid baroreceptor stimulation elicits dynamic changes in CVC and that these changes are more apparent during whole-body heating., BLACKWELL PUBLISHING, Dec. 2006, JOURNAL OF PHYSIOLOGY-LONDON, 577 (3), 925 - 933, doi;web_of_science

    Scientific journal

  • Neurally mediated vasoconstriction is capable of decreasing skin blood flow during orthostasis in the heat-stressed human

    Manabu Shibasaki; Scott L. Davis; Jian Cui; David A. Low; David M. Keller; Sylvain Durand; Craig G. Crandall

    Given the large increase in cutaneous vascular conductance (CVC) during whole-body heat stress, this vascular bed is important in the regulation of blood pressure during orthostatic stress. In this thermal state, changes in CVC are reported to be due to withdrawal of active vasodilator activity. The purpose of this study was to identify, contrary to the current line of thinking, whether cutaneous vasoconstrictor neural activity is enhanced and capable of contributing to reductions in CVC during an orthostatic challenge of heat-stressed individuals. Healthy normotensive subjects were pretreated, subcutaneously, with botulinum toxin A (BTX-A) to inhibit the release of neurotransmitters from cutaneous active vasodilator nerves. On the experimental day, microdialysis probes were placed in the BTX-A-treated site and in an adjacent untreated site. In protocol 1, internal temperature was elevated similar to 0.7 degrees C, followed by the application of lower body negative pressure (LBNP; -30 mmHg). LBNP reduced CVC at the BTX-A-treated sites (Delta 4.2 +/- 2.9%max), as well as at the control site (Delta 9.8 +/- 4.1%max). In protocol 2, after confirming the absence of cutaneous vasodilatation at the BTX-A-treated site during whole-body heating, CVC at this site was elevated to a similar level relative to the control site (55.4 +/- 13.4 versus 60.7 +/- 10.4%max, respectively) via intradermal administration of isoproterenol prior to LBNP. Similarly, when flow was matched between sites, LBNP reduced CVC at both the BTX-A-treated (Delta 15.3 +/- 4.6%max) and the control sites (Delta 8.8 +/- 5.6%max). These data suggest that the cutaneous vasoconstrictor system is engaged and is capable of decreasing CVC during an orthostatic challenge in heat-stressed individuals., BLACKWELL PUBLISHING, Sep. 2006, JOURNAL OF PHYSIOLOGY-LONDON, 575 (3), 953 - 959, doi;web_of_science

    Scientific journal

  • Neural control and mechanisms of eccrine sweating during heat stress and exercise

    M Shibasaki; TE Wilson; CG Crandall

    In humans, evaporative heat loss from eccrine sweat glands is critical for thermoregulation during exercise and/or exposure to hot environmental conditions, particularly when environmental temperature is greater than skin temperature. Since the time of the ancient Greeks, the significance of sweating has been recognized, whereas our understanding of the mechanisms and controllers of sweating has largely developed during the past century. This review initially focuses on the basic mechanisms of eccrine sweat secretion during heat stress and/or exercise along with a review of the primary controllers of thermoregulatory sweating (i.e., internal and skin temperatures). This is followed by a review of key nonthermal factors associated with prolonged heat stress and exercise that have been proposed to modulate the sweating response. Finally, mechanisms pertaining to the effects of heat acclimation and microgravity exposure are presented., AMER PHYSIOLOGICAL SOC, May 2006, JOURNAL OF APPLIED PHYSIOLOGY, 100 (5), 1692 - 1701, doi;web_of_science

  • Spectral characteristics of skin sympathetic nerve activity in heat-stressed humans

    J Cui; M Sathishkumar; TE Wilson; M Shibasaki; SL Davis; CG Crandall

    Skin sympathetic nerve activity (SSNA) exhibits low- and high-frequency spectral components in normothermic subjects. However, spectral characteristics of SSNA in heat-stressed subjects are unknown. Because the main components of the integrated SSNA during heat stress (sudomotor/vasodilator activities) are different from those during normothermia and cooling (vasoconstrictor activity), we hypothesize that spectral characteristics of SSNA in heat-stressed subjects will be different from those in subjects subjected to normothermia or cooling. In 17 healthy subjects, SSNA, electrocardiogram, arterial blood pressure (via Finapres), respiratory activity, and skin blood flow were recorded during normothermia and heat stress. In 7 of the 17 subjects, these variables were also recorded during cooling. Spectral characteristics of integrated SSNA, R-R interval, beat-by-beat mean blood pressure, skin blood flow variability, and respiratory excursions were assessed. Heat stress and cooling significantly increased total SSNA. SSNA spectral power in the low- frequency (0.03-0.15 Hz), high-frequency (0.15-0.45 Hz), and very-high-frequency (0.45-2.5 Hz) regions was significantly elevated by heat stress and cooling. Interestingly, heat stress caused a greater relative increase of SSNA spectral power within the 0.45- to 2.5-Hz region than in the other spectral ranges; cooling did not show this effect. Differences in the SSNA spectral distribution between normothermia/cooling and heat stress may reflect different characteristics of central modulation of vasoconstrictor and sudomotor/vasodilator activities., AMER PHYSIOLOGICAL SOC, Apr. 2006, AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 290 (4), H1601 - H1609, doi;web_of_science

    Scientific journal

  • Central command and the cutaneous vascular response to isometric exercise in heated humans

    M Shibasaki; NH Secher; JM Johnson; CG Crandall

    Cutaneous vascular conductance (CVC) decreases during isometric handgrip, exercise in heat stressed individuals, and we hypothesized that central command is involved in this response. Seven subjects performed 2 min of isometric handgrip exercise (35% of maximal voluntary contraction) followed by postexercise ischaemia in normothermia and during heat stress (increase in internal temperature similar to 1 degrees C). To augment the contribution of central command independent of force generation, on a separate day the protocol was repeated following partial neuromuscular blockade (PNB; i.v. cisatracurium). Forearm skin blood flow was measured by laser-Doppler flowmetry, and CVC was the ratio of skin blood flow to mean arterial pressure. The PNB attenuated force production despite encouragement to attain the same workload. During the heat stress trials, isometric exercise decreased CVC by similar to 12% for both conditions, but did not change CVC in either of the normothermic trials. During isometric exercise in the heat, the increase in mean arterial pressure (MAP) was greater during the control trial relative to the PNB trial (31.0 +/- 9.8 versus 18.6 +/- 6.4 mmHg, P < 0.01), while the elevation of heart rate tended to be lower (19.4 +/- 10.4 versus 27.4 +/- 8.1 b.p.m., P = 0.15). During postexercise ischaemia, CVC and MAP returned to pre-exercise levels in the PNB trial but remained reduced in the control trial. These findings suggest that central command, as well as muscle metabo-sensitive afferent stimulation, contributes to forearm cutaneous vascular responses in heat stressed humans., BLACKWELL PUBLISHING, Jun. 2005, JOURNAL OF PHYSIOLOGY-LONDON, 565 (2), 667 - 673, doi;web_of_science

    Scientific journal

  • Muscle mechanoreceptor modulation of sweat rate during recovery from moderate exercise

    M Shibasaki; M Sakai; M Oda; CG Crandall

    The objective of this study was to identify whether muscle mechanoreceptor stimulation is capable of modulating sweat rate. Seven healthy subjects performed two 20-min bouts of supine exercise on a tandem cycle ergometer (60 rpm at 65% of maximal heart rate). After one bout, the subject stopped exercising (i.e., no pedaling), whereas, after the other bout, the subject's legs were passively cycled (at 60 rpm) via a second person cycling the tandem ergometer. This allows for mechanical stimulation of muscle with minimal activation of central command. Esophageal temperature (T-es), mean skin temperature ((T) over bar (sk)), heart rate, mean arterial blood pressure, oxygen consumption, cutaneous vascular conductance (CVC), and sweat rate were not different during the two exercise bouts. Regardless of the mode of exercise recovery, there were no differences in T-es, (T) over bar (sk), or CVC. In contrast, early in the recovery period, chest and forearm sweat rate were significantly greater in the passive cycling recovery mode relative to the no-pedaling condition (chest: 0.57 +/- 0.13 vs. 0.39 +/- 0.14, forearm: 0.30 +/- 0.05 vs. 0.12 +/- 0.02 mg.cm(-2).min(-1); both P < 0.05). These results suggested that muscle mechanoreceptor stimulation to the previously activated muscle is capable of modulating sweat rate., AMER PHYSIOLOGICAL SOC, Jun. 2004, JOURNAL OF APPLIED PHYSIOLOGY, 96 (6), 2115 - 2119, doi;web_of_science

    Scientific journal

  • Central command is capable of modulating sweating from non-glabrous human skin

    M Shibasaki; NH Secher; C Selmer; N Kondo; CG Crandall

    Isometric handgrip, exercise (IHG) increases sweating rate without changing core or skin temperatures. The contribution of central command resulting in increases in sweating rate during IHG is unknown. To investigate this question, seven subjects performed IHG (35% maximum voluntary contraction (MVC) for 2 min) followed by 2-min of post-exercise ischaemia (PEI), with and without partial neuromuscular blockade (PNB). PNB was performed to augment central command during the IHG bout. These trials were conducted while the subject was normothermic, mildly heated, and moderately heated. On the non-exercising arm, forearm sweating rate was monitored over a microdialysis membrane perfused with neostigmine (acetylcholinesterase inhibitor), and at an adjacent untreated site. In normothermia with PNB, despite reduced force production during IHG (17 +/- 9 versus 157 +/- 13 N; P < 0.001), the elevation in sweating rate at the neostigmine-treated site was greater relative to the control IHG bout (P < 0.05). During subsequent PEI, for the PNB trial mean arterial blood pressure (MAP) and sweating rate returned towards pre-IHG levels, while during the control trial these variables remained elevated. During IHG while mildly heated, the elevation in sweating rate was greater during the PNB trial relative to the control trial. In contrast, during moderate heating sweating increased during IHG for both trials, however the elevation in sweating rate during the PNB trial was not greater than during the control trial. These results suggest that central command is capable of modulating sweating rate in all thermal conditions, however its effect is reduced when body temperatures and/or sweating rate are substantially elevated., CAMBRIDGE UNIV PRESS, Dec. 2003, JOURNAL OF PHYSIOLOGY-LONDON, 553 (3), 999 - 1004, doi;web_of_science

    Scientific journal

  • Exercise throughout 6 degrees head-down tilt bed rest preserves thermoregulatory responses

    M Shibasaki; TE Wilson; J Cui; BD Levine; CG Crandall

    Spaceflight and its bed rest analog [6degrees head-down tilt (HDT)]decrease plasma and blood volume and aerobic capacity. These responses may be associated with impaired thermoregulatory responses observed during exercise and passive heating after HDT exposure. This project tested the hypothesis that dynamic exercise during 13 days of HDT bed rest preserves thermoregulatory responses. Throughout HDT bed rest, 10 subjects exercised for 90 min/day (75% of pre-HDT maximum heart rate; supine). Before and after HDT bed rest, each subject exercised in the supine position at the same workload in a 28degreesC room. The internal temperature (T-core) threshold for the onset of sweating and cutaneous vasodilation, as well as the slope of the relationship between the elevation in T-core relative to the elevation in sweat rate (SR) and cutaneous vascular conductance (CVC; normalized to local heating maximum), were quantified pre- and post-HDT. T-core thresholds for the onset of cutaneous vasodilation on the chest and forearm (chest: 36.79 +/- 0.12 to 36.94 +/- 0.13degreesC, P = 0.28; forearm: 36.76 +/- 0.12 to 36.91 +/- 0.11degreesC, P = 0.16) and slope of the elevation in CVC relative to T-core (chest: 77.9 +/- 14.2 to 80.6 +/- 17.2% max/degreesC; P = 0.75; forearm: 76.3 +/- 11.8 to 67.5 +/- 14.3% max/degreesC, P = 0.39) were preserved post-HDT. Moreover, the T-core threshold for the onset of SR (36.66 +/- 0.12 to 36.74 +/- 0.10degreesC; P = 0.36) and the slope of the relationship between the elevation in SR and the elevation in T-core (1.23 +/- 0.19 to 1.01 +/- 0.14 mg.cm(-2).min(-1).degreesC(-1); P = 0.16) were also maintained. Finally, after HDT bed rest, peak oxygen uptake and plasma and blood volumes were not different relative to pre- HDT bed rest values. These data suggest that dynamic exercise during this short period of HDT bed rest preserves thermoregulatory responses., AMER PHYSIOLOGICAL SOC, Nov. 2003, JOURNAL OF APPLIED PHYSIOLOGY, 95 (5), 1817 - 1823, doi;web_of_science

    Scientific journal

  • Prolonged head-down tilt exposure reduces maximal cutaneous vasodilator and sweating capacity in humans

    CG Crandall; M Shibasaki; TE Wilson; J Cui; BD Levine

    Cutaneous vasodilation and sweat rate are reduced during a thermal challenge after simulated and actual microgravity exposure. The effects of microgravity exposure on cutaneous vasodilator capacity and on sweat gland function are unknown. The purpose of this study was to test the hypothesis that simulated microgravity exposure, using the 6degrees head-down tilt (HDT) bed rest model, reduces maximal forearm cutaneous vascular conductance (FVC) and sweat gland function and that exercise during HDT preserves these responses. To test these hypotheses, 20 subjects were exposed to 14 days of strict HDT bed rest. Twelve of those subjects exercised ( supine cycle ergometry) at 75% of pre-bed rest heart rate maximum for 90 min/day throughout HDT bed rest. Before and after HDT bed rest, maximal FVC was measured, via plethysmography, by heating the entire forearm to 42 degreesC for 45 min. Sweat gland function was assessed by administering 1 x 10(-6) to 2 M acetylcholine ( 9 doses) via intradermal microdialysis while simultaneously monitoring sweat rate over the microdialysis membranes. In the nonexercise group, maximal FVC and maximal stimulated sweat rate were significantly reduced after HDT bed rest. In contrast, these responses were unchanged in the exercise group. These data suggest that 14 days of simulated microgravity exposure, using the HDT bed rest model, reduces cutaneous vasodilator and sweating capacity, whereas aerobic exercise training during HDT bed rest preserves these responses., AMER PHYSIOLOGICAL SOC, Jun. 2003, JOURNAL OF APPLIED PHYSIOLOGY, 94 (6), 2330 - 2336, doi;web_of_science

    Scientific journal

  • Effects of 14 days of head-down tilt bed rest on cutaneous vasoconstrictor responses in humans

    TE Wilson; M Shibasaki; J Cui; BD Levine; CG Crandall

    This study tested the hypothesis that head-down tilt bed rest (HDBR) reduces adrenergic and nonadrenergic cutaneous vasoconstrictor responsiveness. Additionally, an exercise countermeasure group was included to identify whether exercise during bed rest might counteract any vasoconstrictor deficits that arose during HDBR. Twenty-two subjects underwent 14 days of strict 6degrees HDBR. Eight of these 22 subjects did not exercise during HDBR, while 14 of these subjects exercised on a supine cycle ergometer for 90 min a day at 75% of pre-bed rest heart rate maximum. To assess alpha-adrenergic vasoconstrictor responsiveness, intradermal microdialysis was used to locally administer norepinephrine ( NE), while forearm skin blood flow (SkBF; laser-Doppler flowmetry) was monitored over microdialysis membranes. Nonlinear regression modeling was used to identify the effective drug concentration that caused 50% of the cutaneous vasoconstrictor response (EC50) and minimum values from the SkBF-NE dose-response curves. In addition, the effects of HDBR on nonadrenergic cutaneous vasoconstriction were assessed via the venoarteriolar response of the forearm and leg. HDBR did not alter EC50 or the magnitude of cutaneous vasoconstriction to exogenous NE administration regardless of whether the subjects exercised during HDBR. Moreover, HDBR did not alter the forearm venoarteriolar response in either the control or exercise groups during HDBR. However, HDBR significantly reduced the magnitude of cutaneous vasoconstriction due to the venoarteriolar response in the leg, and this response was similarly reduced in the exercise group. These data suggest that HDBR does not alter cutaneous vasoconstrictor responses to exogenous NE administration, whereas cutaneous vasoconstriction of the leg due to the venoarteriolar response is reduced after HDBR. It remains unclear whether attenuated venoarteriolar responses in the lower limbs contribute to reduced orthostatic tolerance after bed rest and spaceflight., AMER PHYSIOLOGICAL SOC, Jun. 2003, JOURNAL OF APPLIED PHYSIOLOGY, 94 (6), 2113 - 2118, doi;web_of_science

    Scientific journal

  • Non-thermoregulatory modulation of sweating in humans

    M Shibasaki; N Kondo; CG Crandall

    SHIBASAKI, M., N. KONDO, and C.G. CRANDALL. Non-thermoregulatory modulation of sweating in humans. Exerc. Sport Sci. Rev., Vol. 31, No. 1, pp. 34-39, 2003. Sweating in humans is critical for appropriate thermoregulation during exercise and/or exposure to warm environmental temperatures. In addition to thermal controllers of sweating, a number of non-thermal factors modulate the sweating response. This review summarizes the primary non-thermal neural modifiers of sweating in humans., LIPPINCOTT WILLIAMS & WILKINS, Jan. 2003, EXERCISE AND SPORT SCIENCES REVIEWS, 31 (1), 34 - 39, web_of_science

  • Acetylcholine released from cholinergic nerves contributes to cutaneous vasodilation during heat stress

    M Shibasaki; TE Wilson; J Cui; CG Crandall

    Nitric oxide (NO) contributes to active cutaneous vasodilation during a heat stress in humans. Given that acetylcholine is released from cholinergic nerves during whole body heating, coupled with evidence that acetylcholine causes vasodilation via NO mechanisms, it is possible that release of acetylcholine in the dermal space contributes to cutaneous vasodilation during a heat stress. To test this hypothesis, in seven subjects skin blood flow (SkBF) and sweat rate were simultaneously monitored over three microdialysis membranes placed in the dermal space of dorsal forearm skin. One membrane was perfused with the acetyleholinesterase inhibitor neostigmine (10 muM), the second membrane was perfused with the NO synthase inhibitor NI-nitro-L-arginine methyl ester (L-NAME; 10 mM) dissolved in the aforementioned neostigmine solution (L-NAME(Neo)), and the third membrane was perfused with Ringer solution as a control site. Each subject was exposed to similar to20 min of whole body heating via a water-perfused suit, which increased mean body temperature from 36.4 +/- 0.1 to 37.5 +/- 0.1degreesC (P < 0.05). After the heat stress, SkBF at each site was normalized to its maximum value, identified by administration of 28 mM sodium nitroprusside. Mean body temperature threshold for cutaneous vasodilation was significantly lower at the neostigmine-treated site relative to the other sites (neostigmine: 36.6 &PLUSMN; 0.1&DEG;C, L-NAME(Neo): 37.1 &PLUSMN; 0.1&DEG;C, control: 36.9 &PLUSMN; 0.1&DEG;C), whereas no significant threshold difference was observed between the L-NAME(Neo)-treated and control sites. At the end of the heat stress, SkBF was not different between the neostigmine-treated and control sites, whereas SkBF at the L-NAME(Neo)-treated site was significantly lower than the other sites. These results suggest that acetylcholine released from cholinergic nerves is capable of modulating cutaneous vasodilation via NO synthase mechanisms early in the heat stress but not after substantial cutaneous vasodilation., AMER PHYSIOLOGICAL SOC, Dec. 2002, JOURNAL OF APPLIED PHYSIOLOGY, 93 (6), 1947 - 1951, doi;web_of_science

    Scientific journal

  • Sweating responses to a sustained static exercise is dependent on thermal load in humans

    N Kondo; N Horikawa; K Aoki; M Shibasaki; Y Inoue; T Nishiyasu; CG Crandall

    The purpose of this project was to test the hypothesis that internal temperature modulates the sweating response to sustained handgrip exercise. Ten healthy male subjects immersed their legs in 43 degreesC water for 30-40 min at an ambient temperatures of 30 degreesC and a relative humidity of 50%. Sweating responses to 50% maximal voluntary contraction isometric handgrip exercise (IH) were measured following the onset of sweating (i.e. following slight increases in internal temperature), and after more pronounced increases in internal temperature. Oesophageal temperature (T (es) ) was significantly lower during the first bout of exercise (37.54 +/- 0.07 degreesC) relative to the second bout (37.84 +/- 0.12 degreesC; P < 0.05). However, the increase in mean sweating rate (SR) from both the chest and forearm (non-glabrous skin) was significantly greater during the first IH bout relative to the second bout (P < 0.05). Increases in mean arterial blood pressure and palm SR (glabrous skin) did not differ significantly between exercise bouts, while heart rate and rating of perceived effort were significantly greater during the second bout of IH. As T (es) and mean skin temperature did not change during either bout of exercise, the changes in SR from non-glabrous skin between the bouts of IH were likely because of non-thermal factors. These data suggest that sweating responses from non-glabrous skin during IH vary depending on the magnitude of thermal input as indicated by differing internal temperatures between bouts of IH. Moreover, these data suggest that the contribution of non-thermal factors in governing sweating from non-glabrous skin may be greatest when internal temperature is moderate (37.54 degreesC), but has less of an effect after greater elevations in internal temperature (i.e. 37.84 degreesC)., WILEY, Aug. 2002, ACTA PHYSIOLOGICA SCANDINAVICA, 175 (4), 289 - 295, web_of_science

    Scientific journal

  • Evidence that the human cutaneous venoarteriolar response is not mediated by adrenergic mechanisms

    CG Crandall; M Shibasaki; TC Yen

    The venoarteriolar response causes vasoconstriction to skin and muscle via local mechanisms secondary to venous congestion. The purpose of this project was to investigate whether this response occurs through a-adrenergic mechanisms. In supine individuals, forearm skin blood flow was monitored via laser-Doppler flowmetry over sites following local administration of terazosin (alpha(1)-antagonist), yohimbine (alpha(2)-antagonist), phentolamine (non-selective a-antagonist) and bretylium tosylate (inhibits neurotransmission of adrenergic nerves) via intradermal microdialysis or intradermal injection. In addition, skin blood flow was monitored over an area of forearm skin that was locally anaesthetized via application of EMLA (2.5% lidocaine (lignocaine) and 2.5% prilocaine) cream. Skin blood flow was also monitored over adjacent sites that received the vehicle for the specified drug. Each trial was performed on a minimum of seven subjects and on separate days. The venoarteriolar response was engaged by lowering the subject's arm from heart level such that the sites of skin blood flow measurement were 34 1 cm below the heart. The arm remained in this position for 2 min. Selective and non-selective a-adrenoceptor antagonism and presynaptic inhibition of adrenergic neurotransmission did not abolish the venoarteriolar response. However, local anaesthesia blocked the venoarteriolar response without altering a-adrenergic mediated vasoconstriction. These data suggest that the venoarteriolar response does not occur through adrenergic mechanisms as previously reported. Rather, the venoarteriolar response may due to myogenic mechanisms associated with changes in vascular pressure or is mediated by a nonadrenergic, but neurally mediated, local mechanism., CAMBRIDGE UNIV PRESS, Jan. 2002, JOURNAL OF PHYSIOLOGY-LONDON, 538 (2), 599 - 605, doi;web_of_science

    Scientific journal

  • Sweating response in physically trained men to sustained handgrip exercise in mildly hyperthermic conditions

    S Yanagimoto; K Aoki; N Horikawa; M Shibasaki; Y Inoue; T Nishiyasu; N Kondo

    To investigate the effects of physical training on heat loss response to sustained handgrip exercise (non-thermal factors), we compared the sweating response during isometric handgrip exercise to mild hyperthermia in physically trained and untrained subjects. Seven trained and untrained male subjects (maximal oxygen uptake 62.7 +/- 2.4 and 42.7 +/- 1.6 mL kg(-1) min(-1), respectively, P < 0.05) performed isometric handgrip exercises at 20, 35 and 50% maximal voluntary contraction (MVC) for 60 s. The study was conducted in a climatic chamber with a regulated ambient temperature of 35 &DEG;C and relative humidity of 50% to induce sweating response at rest by rising skin temperature without a marked change in internal temperature. Sublingual and mean skin temperatures (thermal factors) in both trained and untrained groups were essentially constant throughout all exercise intensities. Changes in heart rate, mean arterial blood pressure, and rating of perceived exertion with increased exercise intensity were similar in both groups, Sweating rate (SR) on the limbs (mean value of forearm and thigh) was significantly greater in the trained group than in the untrained group at 50% MVC (P < 0.05). In addition, the slopes of the relationship between increased SR and exercise intensity (% MVC) on the trunk (chest) and limbs were significantly greater in the trained group than in the untrained group (P < 0.05). Our results suggest that the sweating response caused by non-thermal factors against a background of changing thermal factors was enhanced by physical training. It is also thought that the enhanced sweating response may be especially evident on the limbs than on the trunk, such as improvement of sweating response associated with thermal factors., BLACKWELL PUBLISHING LTD, Jan. 2002, ACTA PHYSIOLOGICA SCANDINAVICA, 174 (1), 31 - 39, web_of_science

    Scientific journal

  • Baroreflex modulation of muscle sympathetic nerve activity during posthandgrip muscle ischemia in humans

    J Cui; TE Wilson; M Shibasaki; NA Hodges; CG Crandall

    To identify whether muscle metaboreceptor stimulation alters baroreflex control of muscle sympathetic nerve activity (MSNA), MSNA, beat-by-beat arterial blood pressure (Finapres), and electrocardiogram were recorded in 11 healthy subjects in the supine position. Subjects performed 2 min of isometric handgrip exercise at 40% of maximal voluntary contraction followed by 2.5 min of posthandgrip muscle ischemia. During muscle ischemia, blood pressure was lowered and then raised by intravenous bolus infusions of sodium nitroprusside and phenylephrine HCl, respectively. The slope of the relationship between MSNA and diastolic blood pressure was more negative (P < 0.001) during posthandgrip muscle ischemia (-201.9 +/- 20.4 units.beat(-1).mmHg(-1)) when compared with control conditions (- 142.7 +/- 17.3 units.beat(-1).mmHg(-1)). No significant change in the slope of the relationship between heart rate and systolic blood pressure was observed. However, both curves shifted during postexercise ischemia to accommodate the elevation in blood pressure and MSNA that occurs with this condition. These data suggest that the sensitivity of baroreflex modulation of MSNA is elevated by muscle metaboreceptor stimulation, whereas the sensitivity of baroreflex of modulate heart rate is unchanged during posthandgrip muscle ischemia., AMER PHYSIOLOGICAL SOC, Oct. 2001, JOURNAL OF APPLIED PHYSIOLOGY, 91 (4), 1679 - 1686, web_of_science

    Scientific journal

  • Evidence for metaboreceptor stimulation of sweating in normothermic and heat-stressed humans

    M Shibasaki; N Kondo; CG Crandall

    1. Isometric handgrip (IHG) exercise increases sweat rate and arterial blood pressure, and both remain elevated during post-exercise ischaemia. The purpose of this study was to identify whether the elevation in arterial blood pressure during post-exercise ischaemia contributes to the increase in sweating. 2. In normothermia, and during whole-body heating, 2 min IHG exercise at 40 % maximal voluntary contraction, followed by 2 min post-exercise ischaemia, was performed with and without bolus intravenous administration of sodium nitroprusside during the ischaemic period. Sodium nitroprusside was administered to reduce blood pressure during post-exercise ischaemia to pre-exercise levels. Sweat rate was monitored over two microdialysis membranes placed in the dermal space of forearm skin. One membrane was perfused with the acetyleholinesterase inhibitor neostigmine, while the other was perfused with the vehicle. 3. In normothermia, IHG exercise increased sweat rate at the neostigmine-treated site but not at the control site. Sweat rate remained elevated during post-exercise ischaemia even after mean arterial blood pressure returned to the pre-IHG exercise baseline. Subsequent removal of the ischaemia stimulus returned sweat rate to pre-IHG exercise levels. Sweat rate during postexercise ischaemia without sodium nitroprusside administration followed a similar pattern. 4. During whole-body heating, IHG exercise increased sweat rate at both neostigmine-treated and untreated sites. Similarly, regardless of whether mean arterial blood pressure remained elevated or was reduced during post-exercise ischaemia, sweat rate remained elevated during the ischaemic period. 5. These results suggest that sweating in non-glabrous skin during post-IHG exercise ischaemia is activated by metaboreflex stimulation and not via baroreceptor loading., CAMBRIDGE UNIV PRESS, Jul. 2001, JOURNAL OF PHYSIOLOGY-LONDON, 534 (2), 605 - 611, web_of_science

    Scientific journal

  • Function of human eccrine sweat glands during dynamic exercise and passive heat stress

    N Kondo; M Shibasaki; K Aoki; S Koga; Y Inoue; CG Crandall

    The purpose of this study was to identify the pattern of change in the density of activated sweat glands (ASG) and sweat output per gland (SGO) during dynamic constant-workload exercise and passive heat stress. Eight male subjects (22.8 +/- 0.9 yr) exercised at a constant workload (117.5 +/- 4.8 W) and were also passively heated by lower-leg immersion into hot water of 42 degreesC under an ambient temperature of 25 degreesC and relative humidity of 50%. Esophageal temperature, mean skin temperature, sweating rate (SR), and heart rate were measured continuously during both trials. The number of ASG was determined every 4 min after the onset of sweating, whereas SGO was calculated by dividing SR by ASG. During both exercise and passive heating, SR increased abruptly during the first 8 min after onset of sweating, followed by a slower increase. Similarly for both protocols, the number of ASG increased rapidly during the first 8 min after the onset of sweating and then ceased to increase further (P > 0.05). Conversely, SGO increased linearly throughout both perturbations. Our results suggest that changes in forearm sweating rate rely on both ASG and SGO during the initial period of exercise and passive heating, whereas further increases in SR are dependent on increases in SGO., AMER PHYSIOLOGICAL SOC, May 2001, JOURNAL OF APPLIED PHYSIOLOGY, 90 (5), 1877 - 1881, web_of_science

    Scientific journal

  • Effect of local acetylcholinesterase inhibition on sweat rate in humans

    M Shibasaki; CG Crandall

    ACh is the neurotransmitter responsible for increasing sweat rate (SR) in humans. Because ACh is rapidly hydrolyzed by acetylcholinesterase (AChE), it is possible that AChE contributes to the modulation of SR. Thus the primary purpose of this project was to identify whether AChE around human sweat glands is capable of modulating SR during local application of various concentrations of ACh in vivo, as well as during a heat stress. In seven subjects, two microdialysis probes were placed in the intradermal space of the forearm. One probe was perfused with the AChE inhibitor neostigmine (10 muM); the adjacent membrane was perfused with the vehicle (Ringer solution). SR over both membranes was monitored via capacitance hygrometry during microdialysis administration of various concentrations of ACh (1 x 10(-7)-2 M) and during whole body heating. SR was significantly greater at the neostigmine-treated site than at the control site during administration of lower concentrations of ACh (1 x 10(-7)-1 x 10(-3) M, P < 0.05), but not during administration of higher concentrations of ACh (1 x 10(-2)-2 M, P > 0.05). Moreover, the core temperature threshold for the onset of sweating at the neostigmine-treated site was significantly reduced relative to that at the control site. However, no differences in SR were observed between sites after 35 min of whole body heating. These results suggest that AChE is capable of modulating SR when ACh concentrations are low to moderate (i.e., when sudomotor activity is low) but is less effective in governing SR after SR has increased substantially., AMER PHYSIOLOGICAL SOC, Mar. 2001, JOURNAL OF APPLIED PHYSIOLOGY, 90 (3), 757 - 762, web_of_science

    Scientific journal

  • Effect of muscle mass on Vo(2) kinetics at the onset of work

    S Koga; TJ Barstow; T Shiojiri; T Takaishi; Y Fukuba; N Kondo; M Shibasaki; DC Poole

    The dependence of O-2 uptake ((V) over dot o(2)) kinetics on the muscle mass recruited under conditions when fiber and muscle recruitment patterns are similar following the onset of exercise has not been determined. We developed a motorized cycle ergometer that facilitated one-leg (1L) cycling in which the electromyographic (EMG) profile of the active muscles was not discernibly altered from that during two-leg (2L) cycling. Six subjects performed 1L and 2L exercise transitions from unloaded cycling to moderate [<ventilatory threshold (VT)] and heavy (>VT) exercise. The 1L condition yielded kinetics that was unchanged from the 2L condition [the phase 2 time constants (tau (1), in s) for <VT were as follows: 1L = 16.8 +/- 8.4 (SD), 2L = 18.4 +/- 8.1, P > 0.05; for >VT: 1L = 26.8 +/- 12.0; 2L = 27.8 +/- 16.1, P > 0.05]. The overall (V) over dot o(2) kinetics (mean response time) was not significantly different for the two exercise conditions. However, the gain of the fast component (the amplitude/work rate) during the 1L exercise was significantly higher than that for the 2L exercise for both moderate and heavy work rates. The slow-component responses evident for heavy exercise were temporally and quantitatively unaffected by the 1L condition. These data demonstrate that, when leg muscle recruitment patterns are unchanged as assessed by EMC analysis, on-transient ire, kinetics for both moderate and heavy exercise are not dependent on the muscle mass recruited., AMER PHYSIOLOGICAL SOC, Feb. 2001, JOURNAL OF APPLIED PHYSIOLOGY, 90 (2), 461 - 468, web_of_science

    Scientific journal

  • Effects of exercise intensity on the sweating response to a sustained static exercise

    SHIBASAKI Manabu; Kondo N; Tominaga H; Shibasaki M; Aoki K; Okada S; Nishiyasu T

    Mar. 2000, Journal of Applied Physiology, 88 (3), 1590-1596

  • Relationship between skin blood flow and sweating rate in prepubertal boys and young men

    M Shibasaki; Y Inoue; N Kondo; K Aoki; K Hirata

    We sought the mechanisms in the maturation-related change of skin blood flow to heat stress. Eight prepubertal boys (7-11 years) and 11 young men (21-25 years) were exposed to a mild passive heating [by placing the lower legs and feet in a 42 degrees C water bath for 60 min while sitting in a neutral air condition (25 degrees C, 45% relative humidity)]. No age-related differences were observed for the increase in rectal temperature [0.61 +/- 0.05 (SEM) vs. 0.62 +/- 0.09 degrees C in the boys and men at the end of the passive heating, respectively], mean skin temperature (34.51 +/- 0.28 vs. 34.81 +/- 0.27 degrees C) or metabolic heat production (68 +/- 4 vs. 60 +/- 3 W m(-2)) during the passive heating. During the healing age-related differences in skin blood flow by laser Doppler flowmetry (LDF) and local sweating rate (m) over dot(sw)) varied by site; the boys had greater LDF on the chest and back, similar LDF on the forearm and thigh, lower (m) over dot(sw) on the chest and thigh, similar (m) over dot(sw) on the back, and greater (m) over dot(sw) on the forearm, compared with the men. The relationship between IDF and (m) over dot(sw) during the heat exposure was divided into three temporal phases: (a) an increase of LDF without an increase in (m) over dot(sw) (b) an increase of (m) over dot(sw) without the secondary increase of LDF, (c) a proportional increase of LDF and (m) over dot(sw). The increase of LDF in phase (a) and the slopes of the regression lines between the LDF and (m) over dot(sw) in phase (c) were significantly greater on the chest and back for the boys (P < 0.05), compared with the men, but not on the forearm and thigh. These results suggest: that the greater LDF observed on the trunk in the boys may be owing to a greater withdrawal of vasoconstrictor tone and a greater active vasodilation. Regional differences may exist in the maturation-related alterations in vasoconstriction and vasodilation., BLACKWELL SCIENCE LTD, Oct. 1999, ACTA PHYSIOLOGICA SCANDINAVICA, 167 (2), 105 - 110, web_of_science

    Scientific journal

  • Kinetics of oxygen uptake during supine and upright heavy exercise

    S Koga; T Shiojiri; M Shibasaki; N Kondo; Y Fukuba; TJ Barstow

    Kinetics of oxygen uptake during supine and upright heavy exercise. J. Appl. Physiol. 87(1). 253-260, 1999.-It is presently unclear how the fast and slow components of pulmonary oxygen uptake (V overdot O-2) kinetics would be altered by body posture during heavy exercise [i.e., above the lactate threshold (LT)]. Nine subjects performed transitions from unloaded cycling to work rates representing moderate (below the estimated LT) and heavy exercise (V overdot O-2 equal to 50% of the difference between LT and peak Vet) under conditions of upright and supine positions. During moderate exercise, the steady-state increase in V overdot O-2 was similar in the two positions, but V overdot O-2 kinetics were slower in the supine position. During heavy exercise, the rate of adjustment of V overdot O-2 to the B-min value was; also slower in the supine position but was characterized by a significant reduction in the amplitude of the fast component, of V overdot O-2 without a significant slowing of the phase 2 time constant. However, the amplitude of the slow component was significantly increased, such that the end-exercise V overdot O-2 was the same in the two positions. The changes in V overdot O-2 kinetics for the supine vs. upright position were paralleled by a blunted response of heart rate at 2 min into exercise during supine compared with upright heavy exercise. Thus the supine position was associated with not only a greater amplitude of the slow component for V overdot O-2 but also, concomitantly, with a reduced amplitude of the fast component; this latter effect may be due, at least in part, to an attenuated early rise in heart rate in the supine position., AMER PHYSIOLOGICAL SOC, Jul. 1999, JOURNAL OF APPLIED PHYSIOLOGY, 87 (1), 253 - 260, web_of_science

    Scientific journal

  • Modulation of the thermoregulatory sweating response to mild hyperthermia during activation of the muscle metaboreflex in humans

    N Kondo; H Tominaga; M Shibasaki; K Aoki; S Koga; T Nishiyasu

    1. To investigate the effect of the muscle metaboreflex on the thermoregulatory sweating response in humans, eight healthy male subjects performed sustained isometric handgrip exercise in an environmental chamber (35 degrees C and 50% relative humidity) at 30 or 45% maximal voluntary contraction (MVC), at the end of which the blood circulation to the forearm was occluded for 120 s. The environmental conditions were such as to produce sweating by increase in skin temperature without a marked change in oesophageal temperature. 2. During circulatory occlusion after handgrip exercise at 30% MVC for 120 s or at 45% MVC for 60 s, the sweating rate (SR) on the chest and forearm (hairy regions), and the mean arterial blood pressure were significantly above baseline values (P < 0.05). There were no changes from baseline values in the oesophageal temperature, mean skin temperature, or SR on the palm (hairless regions). 3. During the occlusion after handgrip exercise at 30% MVC for 60 s and during the occlusion alone, none of the measured parameters differed from baseline values. 4. It is concluded that, under mildly hyperthermic conditions, the thermoregulatory sweating response on the hairy regions is modulated by afferent signals from muscle metaboreceptors., WILEY, Mar. 1999, JOURNAL OF PHYSIOLOGY-LONDON, 515 (2), 591 - 598, web_of_science

    Scientific journal

  • Mechanisms underlying the age-related decrement in the human sweating response

    Y Inoue; M Shibasaki; H Ueda; H Ishizashi

    To examine the mechanisms underlying the age-related decrement in the ability to sweat, seven older (64-76 years) and seven younger (20-24 years) men participated in a 60-min sweating test. The test consisted of placing the subject's lower legs in a water bath at 42 degrees C while sitting in a controlled environment of 35 degrees C ambient temperature and 45% relative humidity. The rectal (T-re) and skin temperatures, local sweating rates ((m) over dot(sw): on the forehead, chest, back, forearm and thigh) and the frequency of sweat expulsion (f(sw)) were measured during the test. No group difference was observed in the mean body temperature ((T) over bar(b)) throughout the passive heating, although the older men had a higher T-re and a lower mean skin temperature during the last half of the 60-min test. There were no group differences in the (T) over bar(b) threshold for sweating, although the time to the onset of sweating tended to be longer for the older men regardless of body site. The (m) over dot(sw) increased gradually for approximately 35 min after the start of heat exposure in the older men and for 30 min in the younger men and then reached a steady state. During the first half of the test, the older men had a significantly lower (m) over dot(sw) at all sites. During the last half of the test, only (m) over dot(sw) on the thigh was significantly lower in the older men than in the younger men. There was no group difference in the slope of f(sw) versus (T) over bar(b) tan indicator of the change in the central sudomotor response to thermal input). The slope of (m) over dot(sw) versus f(sw) tan indicator of the change in peripheral activity in response to central sudomotor changes) was significantly lower on the thigh in the older men, but there were no differences for the other sites. These results suggest that in older men the lower thigh (m) over dot(sw) observed during the last half of the heat test was possibly due to age-related modifications of peripheral mechanisms involving the sweat glands and surrounding tissues. It was not due to a change in the central drive to sudomotor function. Furthermore, the sluggish (m) over dot(sw) responses in the older men appear to have been related to age-related modifications of the sensitivity of thermoreceptors in various body regions to thermal stimuli. They may also involve lower sweat glands' sensitivity to cholinergic stimulus or sluggish vasodilatation, and do not reflect age-related changes in the central drive., SPRINGER VERLAG, Jan. 1999, EUROPEAN JOURNAL OF APPLIED PHYSIOLOGY AND OCCUPATIONAL PHYSIOLOGY, 79 (2), 121 - 126, web_of_science

    Scientific journal

  • Relationship between skin blood flow and sweating rate, and age related regional differences

    Y Inoue; M Shibasaki; K Hirata; T Araki

    To examine the mechanisms and regional differences in the age-related decrement of skin blood flow, Il young (age 20-25 years) and 10 older (age 64-76 years) men were exposed to a mild heat stress by immersing their feet and lower legs in water at 42 degrees C for 60 min, while they were sitting in near thermoneutral conditions [25 degrees C and 45% relative humidity (rh)]. During the equilibrium period (25 degrees C and 45% rh) before the heat test, no group differences were observed in rectal (T-re) and mean skin (T-sk) temperatures or mean arterial pressure (MAP). During passive heating, T-sk was significantly lower in the older men 20 min after commencing exposure (P < 0.001), although there were similar increases in T-re in both groups. Exposure time and age did not affect MAP. The local sweating rate (liz,,) and the percentage change in skin blood flow by laser Doppler flowmetry (%LDF) relative to baseline values on the chest, back, forearm and thigh were significantly lower in the older men (P < 0.001), especially on the thigh. After starting the heat exposure, three temporal phases were observed in the relationship between %LDF and (m) over dot(sw) at most sites in each subject. In phase A, %LDF increased but with no increase in (m) over dot(sw). In phase B, (m) over dot(sw) increased but with no secondary increase in %LDF. Finally, in phase C, there were proportional increases in %LDF and (m) over dot(sw). The increase in %LDF in phase A was significantly lower on the forearm and thigh (P < 0.05) for the older men, but not on the chest and back. In phase C, the slopes of the regression lines between %LDF and (m) over dot(sw) were lower for the older men on the back (P < 0.03), forearm (P = 0.08) and thigh (P < 0.03), but not on the chest. These results would suggest that the age-related decrement in skin blood flow in response to passive heating may be due in part to a smaller release of vasoconstrictor tone and to less active vasodilatation once sweating begins. Regional differences exist in the impaired vasoconstriction and active vasodilatation systems., SPRINGER VERLAG, Dec. 1998, EUROPEAN JOURNAL OF APPLIED PHYSIOLOGY AND OCCUPATIONAL PHYSIOLOGY, 79 (1), 17 - 23, web_of_science

    Scientific journal

  • 赤外線透過ファイバを用いた非接触型鼓膜体温計の開発

    SHIBASAKI Manabu

    Oct. 1998, 人間工学, 34 (5), 247-253

  • Continuous measurement of tympanic temperature with a new infrared method using an optical fiber

    M Shibasaki; N Kondo; H Tominaga; K Aoki; E Hasegawa; Y Idota; T Moriwaki

    The purpose of this study was to investigate the utility of an infrared tympanic thermometry by using an optical fiber for measuring tympanic temperature (T-ty). In the head cooling and facial fanning tests during normothermia, right T-ty, measured by this method (infrared-T-ty) and esophageal temperature (T-es) were not affected by decreased temple and forehead skin temperatures, suggesting that the infrared sensor in this system measured the infrared radiation from the tympanic membrane selectively. Eight male subjects took part in passive-heat-stress and progressive-exercise tests. No significant differences among infrared-T-ty, the left T-ty measured by thermistor (contact-T-ty), and T-es were observed at rest or at the end of each experiment, and there was no significant difference in the increase in these core temperatures from rest to the end. Furthermore, there were no significant differences in the core temperature threshold at the onset of sweating and slope (the relationship of sweating rate vs. infrared-T-ty and vs. contact-T-ty). These results suggest that this method makes it possible to measure T-ty accurately, continuously, and more safely., AMER PHYSIOLOGICAL SOC, Sep. 1998, JOURNAL OF APPLIED PHYSIOLOGY, 85 (3), 921 - 926, web_of_science

    Scientific journal

  • Regional differences in the effect of exercise intensity on thermoregulatory sweating and cutaneous vasodilation

    N Kondo; S Takano; K Aoki; M Shibasaki; H Tominaga; Y Inoue

    To investigate regional body differences in the effect of exercise intensity on the thermoregulatory sweating response, nine healthy male subjects (23.2 +/- 0.4 year) cycled at 35, 50 and 65% of their maximal O-2 uptake ((V) over dot o(2max)) for 30 min at an ambient temperature of 28.3 +/- 0.2 degrees C and a relative humidity of 42.6 +/- 2.4%. Local sweating rate ((m) over dot(sw)) on the forehead, chest, back, forearm and thigh increased significantly with increases in the exercise intensity from 35 to 50% (V) over dot o(2max) and from 50 to 65% (V) over dot o(2max) (P < 0.05). The mean values for the density of activated sweat glands (ASG) at 50 and 65% (V) over dot o(2max) at the five sites were significantly greater than at 35% (V) over dot o(2max). The mean value of the sweat output per gland (SGO) also increased significantly with the increase in exercise intensity (P < 0.05). The patterns of changes in ASG and SGO with an increase in exercise intensity differed from one region of the body to another. Although esophageal temperature (T-es) threshold for the onset of sweating at each site was not altered by exercise intensity, the sensitivity of the sweating response on the forehead increased significantly from 35 to 50 and 65% (V) over dot o(2max) (P < 0.05). The threshold for cutaneous vasodilation lend to increase with exercise intensity, although the exercise intensity did not affect the sensitivity (the slope in the relationship T-es vs. percentage of the maximal skin blood flow) at each site. T-es threshold for cutaneous vasodilation on the forearm was significantly higher at 65% (V) over dot o(2max) than at either 35 or 50% (V) over dot o(2max). but this was not observed at the other sites, such as on the forehead and chest. These results suggest that the increase in (m) over dot(sw) seen with an increasing intensity of exercise depends first on ASG, and then on SGO, and the dependence of ASG and SGO on the increase in (m) over dot(sw) differs for different body sites. In addition, there are regional differences in the T-es threshold for vasodilation in response to an increase in exercise intensity., BLACKWELL SCIENCE LTD, Sep. 1998, ACTA PHYSIOLOGICA SCANDINAVICA, 164 (1), 71 - 78, web_of_science

    Scientific journal

  • Control of circadian variation in skin blood flow response to heat stress

    K Aoki; N Kondo; M Shibasaki; S Takano; T Katsuura; K Hirata

    Six male subjects had their lower legs immersed in water at 42 degrees C for 60 min at 4 different times of the day to study whether the skin blood flow response to passive heat stress shows circadian variation in the relationship between skin blood flow and local sweating rate. When skin blood flow was plotted against local sweating rate, three distinct phases were observed. Phase A, an increase in skin blood flow without sweating was maximal at night. But the slope of the regression line did not change over the day in Phase C. These findings suggest that there is circadian variation in the skin blood flow response before onset of sweating during passive heat stress. This variation might be related, in part, to the circadian rhythm in vasoconstrictor activity., CENTER ACADEMIC PUBL JAPAN, Feb. 1998, JAPANESE JOURNAL OF PHYSIOLOGY, 48 (1), 95 - 98, web_of_science

    Scientific journal

  • Circadian variation in skin blood flow responses to passive heat stress

    K Aoki; N Kondo; M Shibasaki; S Takano; T Katsuura

    To examine whether there is a circadian variation in skin blood flow response to passive heat stress and maximal skin brood flow, which was measured by local warming to 42 degrees C for 45 min, we studied six men at an ambient temperature of 28 degrees C at four different times of day [0400-0700 (morning), 1000-1300 (daytime), 1600-1900 (evening), and 2200-0100 hours (night)], each time of day being examined on separate days. Heat stress at rest was performed by immersing the legs below the knee in hot water (42 degrees C) for 60 min. The esophageal temperature (T-es) at rest was significantly higher in the evening than in the morning. The maximal skin blood flow (SkBF(max)) on both sites, back and forearm, did not show a significant difference among the four times of day. The variation in T-es thresholds for cutaneous vasodilation to heat stress was similar to the circadian rhythm in resting T-es. The relationship of the percentage of SkBF(max) (%SkBF) with T-es was significantly lower in the morning than in the evening. The results suggest that the maximal skin blood flow during local warming does not show variation over the day,but the sensitivity of vasodilation to passive heat stress shows a circadian variation. (C) 1998 Elsevier Science Inc., PERGAMON-ELSEVIER SCIENCE LTD, Dec. 1997, PHYSIOLOGY & BEHAVIOR, 63 (1), 1 - 5, web_of_science

    Scientific journal

  • Circadian variation of sweating responses to passive heat stress

    K Aoki; N Kondo; M Shibasaki; S Takano; H Tominaga; T Katsuura

    The aim of present study was to examine whether sweating responses to passive heat stress change with the circadian rhythm of internal temperature. Six men bad their legs immersed in water at 42 degrees C for 60 min in an ambient temperature of 29 degrees C on four separate days. Experiments were conducted at four different times [06.00 h (morning), 12.00 h (daytime), 18.00 h (evening) and 24.00 h (night)]. We measured oesophageal temperature (T-oes), mean body temperature ((T) over bar(b)) local sweating rate ((m) over dot (sw)) on the forehead, back, forearm and thigh, the densities of activated sweat gland (ASG) on the back, forearm and thigh, and the frequency of sweat expulsion per minute (F-SW) which has been suggested to represent central sudomotor activity. Sweat gland output (SGO) on each site was calculated by dividing (m) over dot (sw) by ASG. ASG was significantly higher on the forearm than on the back and thigh, and SGO was significantly lower on the forearm than cn the back and thigh. However, ASG and SGO did not significantly change over the day. (T) over bar(b) and T-oes thresholds for the onset of sweating showed a significant change with both the temperature rhythms at rest prior to each procedure, while the slopes of the relationships F-SW - (T) over bar(b) and (m) over bar (sw) - F-SW showed no significant difference over the day. We suggest that the circadian variation of sweating response to passive heat stress is regulated by a central sudomotor mechanism rather than by sweat gland function., BLACKWELL SCIENCE LTD, Nov. 1997, ACTA PHYSIOLOGICA SCANDINAVICA, 161 (3), 397 - 402, web_of_science

    Scientific journal

  • Mechanisms of underdeveloped sweating responses in prepubertal boys

    M Shibasaki; Y Inoue; N Kondo

    To approach the mechanisms underlying the underdeveloped sweating responses of prepubertal boys. 8 boys (7-11 years old) and 11 men (21-25 years old) were exposed to a standard heat stress for 60 min. The test consisted of placing the subjects' lower legs into a 42 degrees C water bath while they sat in otherwise constant environmental conditions (ambient temperature 25 degrees C and 45% relative humidity). Rectal (T-re) and skin temperatures, local sweating rates (m(sw): on the chest, back, forearm and thigh) and the frequency of sweating expulsions (f(sw): as an indicator of central sudomotor activity) were measured during the test. During the passive heating. no group differences were observed for the increase in T-re, mean skin temperature and metabolic heat production. However, mean body temperature (<(T)over bar (b)>) during heating was significantly higher for the boys (P < 0.001) because of a higher baseline T-re. The boys had lower m(sw), on the chest (P < 0.004) and thigh (P < 0.001) during the latter half of the 60-min exposure compared to the young men, although a similar m(sw) was observed between the groups during the first half of the test. The group difference of m(sw) on the back was similar to that of the chest and thigh, but the difference was not significant (P=0.10). In contrast, the boys had a greater m(sw) on the forearm throughout the heating (P < 0.03). The slope of the m(sw) vs f(sw) relationship was compared to the men (P < 0.05), and the same tendency was observed for the back (but was not significant, P = 0.10). In contrast, no difference was observed between the groups for the slope of m(sw) vs f(sw) for the forearm. Furthermore, a lower sweat output per gland was also observed on the chest, back, and thigh in the boys (P < 0.01), but not on the forrarm. No group difference was observed for the slope of the f(sw) vs T-b relationship, These results suggest that the lower m(sw) observed in the prepubertal boys were due possibly to underdeveloped peripheral mechanisms, including the sweat glands and their surrounding tissues, rather than to an underdeveloped central drive activity related to sudomotor function. Regional differences map well exist in any underdeveloped peripheral mechanism associated with maturation., SPRINGER VERLAG, Oct. 1997, EUROPEAN JOURNAL OF APPLIED PHYSIOLOGY AND OCCUPATIONAL PHYSIOLOGY, 76 (4), 340 - 345, web_of_science

    Scientific journal

  • Sweating responses to passive and active limb movements

    SHIBASAKI Manabu; Kondo N; Tominaga H; Shiojiri T; Shibasaki M; Aoki K; Takano S; Koga S; Nishiyasu T

    Oct. 1997, Journal of Thermal Biology, 22 (4/5), 351-356

  • Effects of reduced muscle temperature on the oxygen uptake kinetics at the start of exercise

    T Shiojiri; M Shibasaki; K Aoki; N Kondo; S Koga

    The purpose of this study was to examine the effects of reduced muscle temperature (T-m) on gas exchange kinetics and haemodynamics al the start of exercise. Six male subjects performed moderate cycle exercise under reduced (C) and normal (N) T-m conditions. T-m and rectal temperature were significantly reduced by immersion in cold water (by 6.6 degrees C and 1.8 degrees C, respectively). The increases in oxygen uptake (VO2) and oxygen pulse (VO2/HR) during phase 1 (abrupt increase after the start of exercise) were significantly tower under C than under N. The time constant for O-2 under C (36.0 +/- 7.7 (SD) s) was significantly greater than under N (27.5 +/- 4.4 s); however. the time constants of cardiac output under C (38.3 +/- 16.6 s) and N (33.7 +/- 18.5 s) were similar. These results suggest that the slower VO2 on-response under reduced T-m conditions is caused by decreased O-2 extraction in working muscle and/or by impairment of oxidative reactions by reduced muscle temperature., BLACKWELL SCIENCE LTD, Apr. 1997, ACTA PHYSIOLOGICA SCANDINAVICA, 159 (4), 327 - 333, web_of_science

    Scientific journal

  • The effect of change in skin temperature due to evaporative cooling on sweating response during exercise

    N Kondo; M Nakadome; KR Zhang; T Shiojiri; M Shibasaki; K Hirata; A Iwata

    The purpose of this study was to investigate whether there are any effects of skin temperature changes on sweating response in the first few minutes of mild exercise. Six healthy males performed a bicycle exercise at 100 W (50 rpm) for 30 min under an ambient temperature of 23 degrees C (40% RH). Esophageal temperature (T-es), mean skin temperature ((T) over bar(sk)), local skin temperature at the lower left scapula (T-sl), local sweating rate ((M)over dot (sw)), and cutaneous blood flow by laser-Doppler flowmetry (LDF) were measured continuously. Although T-sl decreased markedly. just after the onset of sweating, (T) over bar(sk) did not change, (M)over dot (sw) did not increase constantly in the early stag es of exercise, and there was a temporary interruption in the increase of (M)over dot (sw). This interruption in sweating was affected by the rate of change in T-sl rather than by the absolute value of T-sl, since there was a positive and significant correlation between the time of the interruption in the increase of (M)over dot (sw) and the rate of decrease in T-sl (y=6.47x+0.04; r=0.86, P<0.05). The results suggest that sweating response in the early stages of exercise may be influenced by changes in local skin temperature due to evaporative cooling., SPRINGER VERLAG, Apr. 1997, INTERNATIONAL JOURNAL OF BIOMETEOROLOGY, 40 (2), 99 - 102, web_of_science

    Scientific journal

  • Thermoregulatory responses of prepubertal boys and young men during moderate exercise

    M Shibasaki; Y Inoue; N Kondo; A Iwata

    Seven prepubertal boys (aged 10-11 years) and eleven young men (aged 21-25 years), matched for skinfold thickness and maximal oxygen uptake (over dotVO(2max)) per unit of mass, cycled at an intensity of approximately 40% over dotVO(2max) for 45 min in a warm condition (30 degrees C, 45% relative humidity). During exercise no age-related differences were observed for the increases in rectal temperature (T-re) and heart rate (HR), although the absolute T-re and HR were significantly greater for the boys because of a higher initial baseline (P < 0.05). Total body sweating rate [181 (SEM 12) vs 245 (SEM 12) g . m(-2). 45 min(-1) P < 0.002] and local sweating rates (over dotm(sw)) on chest, back, and forearm were significantly lower for the boys (P < 0.001), as was metabolic heat production [203 (SEM 9) vs 276 (SEM 9) W . m(-2); P < 0.01]. The lower over dotm(sw) in the boys was due to a lower output per activated sweat gland, even though they had a higher activated sweat gland density regardless of site. In contrast, cutaneous blood flow by laser Doppler flowmetry (LDF) in the boys was significantly greater on the chest and back, compared to the men (P < 0.003). The age-related differences in cutaneous vascular conductance (CVC) were more marked because of lower mean arterial pressure in the boys during exercise. However, forearm LDF and CVC were significantly lower for the boys (P < 0.008). No significant differences in LDF among sites were observed for the boys, whereas for the men LDF on the forearm was significantly greater than on the chest and back (P < 0.01). The boys showed lower mean skin temperatures (especially on the back and chest despite greater increments of LDF) after starting to sweat, whereas the men remained unchanged, suggesting that the heat loss on the trunk in the boys was promoted by greater increments of LDF despite lower over dotm(sw), compared to the young men. It was concluded that during moderate exercise in an air temperature at 30 degrees C, prepubertal boys could thermoregulate as efficiently as young men by greater vasodilatation on their trunk despite lower over dotm(sw). Furthermore regional differences may exist in the maturation-related modification of vasodilatation., SPRINGER VERLAG, Mar. 1997, EUROPEAN JOURNAL OF APPLIED PHYSIOLOGY AND OCCUPATIONAL PHYSIOLOGY, 75 (3), 212 - 218, web_of_science

    Scientific journal

  • Regional differences in age-related decrements of the cutaneous vascular and sweating responses to passive heating

    Y Inoue; M Shibasaki

    Ten older (aged 64-76 years) and ten younger (aged 20-24 years) healthy men were exposed to a standard heat stress [by placing the lower legs and feet in a water bath at 42 degrees C while sitting in a controlled environment (ambient temperature 35 degrees C and 45% relative humidity) for 60 min]. During passive heating, the rectal temperature of the older men was significantly greater (P <0.05) and mean skin temperature was Lower (P <0.001), compared to the younger men. Skill blood flow by laser Doppler flowmetry (LDF) was significantly lower on the chest and thigh for the older men (P <0.001), but forehead LDF did not differ between the groups. The percentages of total LDF in the older men to total LDF in the younger men for the last 30 min were 99%, 58% and 50% on the forehead, chest and thigh, respectively. The age-related differences in LDF responses mirrored cutaneous vascular conductances (CVC), since no group and time effects were observed in mean arterial blood pressure during the test. During the last 30 min the local sweat rates (m(sw)) on the back and thigh were significantly lower for the older men (P <0.02), but not on forehead, chest and forearm, although the older men had lower m(sw) during the first 30 min exposure regardless of site (P <0.03). The percentages of total LDF in the older men to total LDF in the younger men during the last 30 min were 105%, 99%, 63%, 106% and 88% on the forehead, chest, thigh, forearm, and back, respectively. During the latter half of the exposure, the older men had similar LDF, CVC and m(sw) the forehead, lower on LDF and CVC and a similar m(sw) on the chest, and lower LDF, CVC and m(sw) on the thigh, compared to the younger men. These results suggest firstly that regional differences exist in the age-related decrement of cutaneous vasodilatation as well as sweat gland function, secondly that the age-related decrement in cutaneous vascular function may precede a decrement in sweat gland function, and thirdly that the successive decrements may develop sequentially From the lower limbs to the upper body, and head., SPRINGER VERLAG, Aug. 1996, EUROPEAN JOURNAL OF APPLIED PHYSIOLOGY AND OCCUPATIONAL PHYSIOLOGY, 74 (1-2), 78 - 84, web_of_science

    Scientific journal

  • The influence of work loads on regional differences in sweating rates

    S Takano; N Kondo; M Shibasaki; K Aoki; Y Inoue; A Iwata

    The influence of work loads (20, 40 and 60% V-O2max) on regional differences in sweating rates was investigated in six healthy male students, The ratios of local sweating rate (m(sw)) on the chest and back to estimated total sweating rate (mean m(sw) of four sites examined X body surface area) at 20% work load were significantly greater than those on the forearm and forehead, whereas the ratio on the forehead at 60% work load was greater than at the other sites, The ratios on the forearm at 40 and 60% work loads were significantly greater than at 20% work load. The regional differences in sweating rates change with the increase in work load as seen by the greater variation in the ratios of m(sw) on each site at 20% work load compared with 40 and 60% work loads. The results indicate that redistribution of this sweat activity to whole body or head with the rise in work load induces favorable conditions for evaporation and controlling brain temperature., CENTER ACAD PUBL JAPAN, Apr. 1996, JAPANESE JOURNAL OF PHYSIOLOGY, 46 (2), 183 - 186, web_of_science

    Scientific journal

  • Kinetics of oxygen uptake and cardiac output at onset of arm exercise

    S Koga; T Shiojiri; M Shibasaki; Y Fukuba; Y Fukuoka; N Kondo

    Pulmonary oxygen uptake (Vover dot(O2)) kinetics at onset of exercise is reported to be slower for arm than for leg exercise. This could be attributed to reduced cardiac output (Qover dot) or reduced arteriovenous O-2 content difference or both. To test this, Vover dot(O2), mean tissue oxygen consumption (Vover dot(O2T)), and Qover dot kinetics in arm cranking were compared with corresponding values found in leg cycling. The increase in Vover dot(O2) during phase 1 (abrupt increase after onset of exercise) was less in arm than in leg exercise, suggesting that immediate Qover dot adjustments to arm exercise were less pronounced. Mean response times (MRT, the relative rates at which a steady state was attained) for Vover dot(O2), Vover dot(O2T), and Qover dot were prolonged during arm exercise. The MRT of Vover dot(O2) in arm exercise at a given blood lactate increase was higher than in leg exercise. The delayed Vover dot(O2) kinetics in arm exercise might be due to delayed Qover dot kinetics and higher anaerobic glycolysis occurring early during arm exercise., ELSEVIER SCIENCE BV, Feb. 1996, RESPIRATION PHYSIOLOGY, 103 (2), 195 - 202, web_of_science

    Scientific journal

  • THE EFFECT OF DIURNAL-VARIATION ON THE REGIONAL DIFFERENCES IN SWEATING AND SKIN BLOOD-FLOW DURING EXERCISE

    K AOKI; T SHIOJIRI; M SHIBASAKI; S TAKANO; N KONDO; A IWATA

    The aim of the present study was to examine changes in the control of heat-dissipation responses to exercise associated with the diurnal variation in core temperature from the viewpoint of the regional response patterns. We studied seven men during exercise on a cycle ergometer at 100 W for 40 min at 25 degrees C at 0630 (morning) 1630 (evening) hours on 2 separate days. Oesophageal temperature (T-oes), local skin temperature, local sweating rate (m(sw)) on the forehead, back, forearm and thigh, and skin blood flow by laser Doppler flowmeter (LDF) on the back and forearm were measured continuously. The T-oes at rest was significantly higher in the evening than in the morning, the difference averaging approximately 0.4 degrees C (P < 0.05). The T-oes thresholds for each site in m(sw) and that for back in LDF were significantly different between the two times of day (P < 0.05). The change in T-oes thresholds for sweating and vasodilatation for morning and evening were similar to T-oes at rest. Although m(sw) on the forehead was significantly higher in the morning than in the evening, m(sw) on the back was significantly higher in the evening than in the morning (P < 0.05). Total local sweating rate (m(sw,tot)) for each site during exercise was significantly higher on the forehead than on the forearm in the morning, and on the back than on the forearm in the evening, respectively (P < 0.05). The results would suggest that the diurnal variation of heat-dissipation responses to exercise is influenced not only by a central controlling mechanism but also by changes in the regional differences., SPRINGER VERLAG, Aug. 1995, EUROPEAN JOURNAL OF APPLIED PHYSIOLOGY AND OCCUPATIONAL PHYSIOLOGY, 71 (2-3), 276 - 280, web_of_science

    Scientific journal

MISC

  • 加齢に伴う体温調節機能の変化と衣服への提案

    SHIBASAKI Manabu

    Mar. 2015, 日本衣服学会, 58 (2), 60 - 70

  • 体温調節に関する研究の動向 ?子どもと高齢者?

    SHIBASAKI Manabu

    Aug. 2014, 月刊せんい, 67 (8), 475-480

  • 暑熱環境下における体温調節

    SHIBASAKI Manabu

    Jul. 2014, 体育の科学, 64 (7), 461-465

  • 発汗研究の新たなツール

    SHIBASAKI Manabu

    Apr. 2013, 発汗学, 20 (1), 21-24

  • 高齢者の発汗反応

    SHIBASAKI Manabu

    Dec. 2012, 発汗学, 19 (2), 52-55

  • 若手から見た生気象学-生理学分野から-

    SHIBASAKI Manabu

    Mar. 2012, 日本生気象学会雑誌 日本生気象学会50周年記念誌, 59-61

  • 運動時の発汗反応-皮内マイクロダイアリシスと発汗に関する研究への応用-

    SHIBASAKI Manabu

    Dec. 2009, 発汗学, 16 (2), 58-62

  • 人における運動時の熱放散反応

    SHIBASAKI Manabu

    2000, 体育・スポーツ科学, 9, 1-13

Books etc

  • 生理学

    彼末, 一之; 全国柔道整復学校協会

    南江堂, Mar. 2020, xvi, 262p, cinii_books (ISBN: 9784524240296)

  • 被服学事典

    牛膓, ヒロミ; 布施谷, 節子; 佐々井, 啓; 増子, 富美; 平田, 耕造; 石原, 久代; 藤田, 雅夫; 長山, 芳子 (, Range: 第1章1.4人体生理 1.4.3体温調節,1.4.5重力(姿勢変化)と体温調節,1.4.6運動と体温調節)

    朝倉書店, Oct. 2016, ix, 490p, 図版 [4] p, cinii_books (ISBN: 9784254620153)

  • Fluid Balance, Hydration, and Athletic Performance

    SHIBASAKI Manabu; Manabu Shibasaki; Scott L. Davis (, Range: 分担)

    CRC Press, Jan. 2016, 33-58 (ISBN: 9781482223286)

  • ニュー運動生理学 II

    宮村 実晴 (, Range: 「運動と体温」3.皮膚における体温調節 193-201頁)

    真興交易(株)医書出版部, Sep. 2014, 冊, cinii_books (ISBN: 9784880038865)

  • イラスト社会・環境と健康

    朝山正己,稲葉 裕,池田若葉,井谷 徹,北川 章,黒澤美智子,芝崎 学,城 憲秀,竹谷 淳,新川美紀,本多恭子

    東京教学社, Apr. 2011, ix, 295p, cinii_books (ISBN: 9784808260316)

  • 運動生理学のニューエビデンス

    宮村, 実晴 (, Range: 「運動と体温」2.末梢調節 329-336頁)

    真興交易(株)医書出版部, Nov. 2010, 462p, cinii_books (ISBN: 9784880038469)

  • 体温調節システムとその適応

    井上芳光; 近藤徳彦 (, Range: 第1章IV汗腺活動と皮膚血管,第2章IV体温上昇と血圧調節 37-51頁,106-116頁)

    ナップ, Nov. 2010, xiii, 304p, cinii_books (ISBN: 9784931411005)

  • カラダの百科事典

    日本生理人類学会 (, Range: 「汗って?」,420-424頁)

    丸善, Sep. 2009, xxii, 724p, cinii_books (ISBN: 9784621081723)

  • Nonthermoregulatory modification of sweating and skin blood flow Exercise, Nutrition, and Environmental Stress Vol. 4

    SHIBASAKI Manabu

    Cooper Publishing Group, 2005, 227-243頁

  • Pulmonary and muscle oxygen uptake kinetics at the onset of exercise Exercise, Nutrition, and Environmental Stress Vol. 3

    SHIBASAKI Manabu

    Cooper Publishing Group, 2003, 63-84頁

  • 運動時の体温調節システムとそれを修飾する要因

    平田, 耕造; 井上, 芳光; 近藤, 徳彦 (, Range: 汗腺と皮膚血管の調節)

    ナップ, Sep. 2002, x, 251p, cinii_books (ISBN: 9784931411319)

  • これでなっとく使えるスポーツサイエンス

    征矢, 英昭; 本山, 貢; 石井, 好二郎; 講談社サイエンティフィク (, Range: 複数)

    講談社, Jun. 2002, viii, 173p, cinii_books (ISBN: 4061531182)

  • Strategy for preventing heat illness in children and in the elderly Exercise, Nutrition, and Environmental Stress Vol. 2

    SHIBASAKI Manabu

    Cooper Publishing Group, 2002, 239-271頁

  • 新運動生理学

    宮村, 実晴 (, Range: 「運動と体温」2.皮膚血管と汗腺の活動 258-265頁)

    真興交易医書出版部, 2001, 2冊, cinii_books (ISBN: 4880036692)

  • The effect of density of activated sweat glands and sweat output per gland on the change in sweating rate The 1997 Nagano symposium on sports sciences

    SHIBASAKI Manabu

    Cooper Publishing Group, 1998

  • 人間科学計測ハンドブック

    日本生理人類学会計測研究部会 (, Range: 「発汗」201-211頁)

    技報堂出版, Oct. 1996, 631p, cinii_books (ISBN: 4765500292)

  • 体温の「なぜ?」がわかる生理学-からだで感じる・考える・理解する-

    (, Range: 54-55)

    20 Apr. 2021

  • 次世代自動車の熱マネジメント

    技術情報協会 (, Range: 76-83)

    技術情報協会, 25 Dec. 2020, 649p, cinii_books (ISBN: 9784861048197)

Teaching Experience

  • 温熱生理学演習 (Nara Women's University)

  • 温熱生理学 (Nara Women's University)

Works

  • Neural and non-neural modulators of skin blood flow and sweating in humans.

    Sep. 2006, Oct. - 2010

  • Neural and non-neural modulators of skin blood flow and sweating in humans.

    Sep. 2006, Oct. - 2010

  • 暑熱負荷時における血圧変動による皮膚血流量調節

    Jun. 2006, Jul. - 2006

  • 機械受容器反射の発汗および皮膚血流量に対する影響

    Sep. 2003, Oct. - 2003

  • Effect of mechanoreflex on sweating and skin blood flow during recovery of dynamic exercise

    Sep. 2003, Oct. - 2003

  • 暑熱環境下運動中の発汗および皮膚血流量に対するセントラルコマンドの影響

    May 2002, Jul. - 2002

  • Effect of central command on sweating and skin blood flow during isometric handgrip exercise in the heat stressed human

    May 2002, Jul. - 2002

  • 暑熱暴露時における皮膚血管反応に対するコリン作動性神経から放出されるアセチルコリンの影響

    Aug. 2000, Sep. - 2000

  • Modulation of cutaneous vasodilation during heat stress due to acetylcholine released from cholinergic nerves

    Aug. 2000, Sep. - 2000

  • 掌握運動中の発汗反応における代謝受容器反射の影響

    Aug. 1999, Sep. - 1999

  • Effect of metaboreflex on sweating during isometric handgrip exercise

    Aug. 1999, Sep. - 1999



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