Publications by authors named "Tatsuro Amano"

49 Publications

Comparisons of isomaltulose, sucrose, and mixture of glucose and fructose ingestions on postexercise hydration state in young men.

Eur J Nutr 2021 Jun 15. Epub 2021 Jun 15.

Advanced Research Institutes, Bourbon Corporation, Niigata, Japan.

Purpose: Isomaltulose is a low glycemic and insulinaemic carbohydrate available as a constituent in sports drink. However, it remains unclear whether postexercise rehydration achieved by isomaltulose drink ingestion alone differs as compared to other carbohydrates.

Methods: Thirteen young men performed intermittent exercise in the heat (35 °C and relative humidity 40%) to induce a state of hypohydration as defined by a 2% loss in body mass. Thereafter, participants were rehydrated by ingesting drinks equal to the volume of body mass loss with either a mixture of 3.25% glucose and 3.25% fructose, 6.5% sucrose (SUC), or 6.5% isomaltulose (ISO) within the first 30 min of a 3-h recovery. The change in plasma volume (ΔPV) from pre-exercise baseline, blood glucose, and plasma insulin concentration were assessed every 30-min.

Results: ΔPV was lower in ISO as compared to SUC until 90 min of the recovery (all P ≤ 0.038) with no difference thereafter (all P ≥ 0.391). The ΔPV were paralleled by concomitant changes in blood glucose levels that were greater in ISO as compared to other drinks after 90 min of the recovery (all P ≤ 0.035). Plasma insulin secretion, which potentially enhances renal sodium reabsorption and fluid retention, did not differ between the trials (interaction, P = 0.653). ISO induced a greater net fluid volume retention as compared to SUC (P = 0.010).

Conclusion: We showed that rehydration with an isomaltulose drink following exercise-heat stress induces comparable recovery of PV and a greater net fluid retention as compared to other drinks, albeit this response is delayed. The delayed water transport along with glucose absorption may modulate this response. This trial was registered in 25th Sep 2019 at https://www.umin.ac.jp/ as UMIN000038099. (249/250).
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http://dx.doi.org/10.1007/s00394-021-02614-zDOI Listing
June 2021

Type 2 diabetes impairs vascular responsiveness to nitric oxide, but not the venoarteriolar reflex or post-occlusive reactive hyperaemia in forearm skin.

Exp Dermatol 2021 Jun 11. Epub 2021 Jun 11.

Human and Environmental Physiology Research Unit, University of Ottawa, Ottawa, Canada.

The venoarteriolar reflex (VAR) is a local mechanism by which vasoconstriction is mediated in response to venous congestion. This response may minimize tissue overperfusion, preventing capillary damage and oedema. Post-occlusive reactive hyperaemia (PORH) is used to assess microvascular function by performing a brief local arterial occlusion resulting in a subsequent rapid transient vasodilation. In the current study, we hypothesized that type 2 diabetes (T2D) attenuates VAR and PORH responses in forearm skin in vivo. In 11 healthy older adults (Control, 58 ± 8 years) and 13 older adults with controlled T2D (62 ± 10 years), cutaneous blood flow measured by laser-Doppler flowmetry was monitored following a 3-min venous occlusion of 45 mm Hg that elicited the VAR, followed by a 3-min recovery period and then a 5-min arterial occlusion of 240 mm Hg that induced PORH. Finally, sodium nitroprusside, a nitric oxide donor, was administered to induce maximum vasodilation. VAR and PORH variables were similar between groups. By contrast, maximal cutaneous blood flow induced by sodium nitroprusside was lower in the T2D group. Taken together, our observations indicate that T2D impairs vascular smooth muscle responsiveness to nitric oxide, but not VAR and PORH in forearm skin.
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http://dx.doi.org/10.1111/exd.14408DOI Listing
June 2021

Effects of Isomaltulose Ingestion on Thermoregulatory Responses during Exercise in a Hot Environment.

Int J Environ Res Public Health 2021 05 27;18(11). Epub 2021 May 27.

Laboratory for Exercise and Environmental Physiology, Faculty of Education, Niigata University, 8050, Igarashi-Ninocho, Nishiku, Niigata 950-2181, Japan.

Isomaltulose is a low glycemic and insulinemic carbohydrate available as a constituent of sports drinks. However, it remains unclear whether thermoregulatory responses (sweating and cutaneous vasodilation) after isomaltulose drink ingestion differ from those of sucrose and water during exercise in a hot environment. Ten young healthy males consumed 10% sucrose, 10% isomaltulose, or water drinks. Thirty-five minutes after ingestion, they cycled for fifteen minutes at 75% peak oxygen uptake in a hot environment (30 °C, 40% relative humidity). Sucrose ingestion induced greater blood glucose concentration and insulin secretion at the pre-exercise state, compared with isomaltulose and/or water trials, with no differences during exercise in blood glucose. Change in plasma volume did not differ between the three trials throughout the experiment, but both sucrose and isomaltulose ingestions similarly increased plasma osmolality, as compared with water (main beverage effect, = 0.040)-a key response that potentially delays the onset of heat loss responses. However, core temperature thresholds and slopes for heat loss responses were not different between the trials during exercise. These results suggest that ingestion of isomaltulose beverages induces low glycemic and insulinemic states before exercise but does not alter thermoregulatory responses during exercise in a hot environment, compared with sucrose or water.
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http://dx.doi.org/10.3390/ijerph18115760DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8198363PMC
May 2021

The effect of seasonal acclimatization on whole-body heat loss response during exercise in a hot humid environment with different air velocity.

J Appl Physiol (1985) 2021 05 27. Epub 2021 May 27.

Laboratory for Applied Human Physiology, Graduate School of Human Development and Environment, Kobe University, Kobe, Japan.

Seasonal acclimatization from winter to summer is known to enhance thermoeffector responses in hot-dry environments during exercise whilst its impact on sweat evaporation and core temperature (T) responses in hot-humid environments remains unknown. We therefore sought to determine whether seasonal acclimatization is able to modulate whole-body sweat rate (WBSR), evaporated sweat rate, sweating efficiency and thermoregulatory function during cycling exercise in a hot-humid environment (32∘C, 75% RH). We also determined whether the increase in air-velocity, could enhance evaporated sweat rate and sweating efficiency before and after seasonal acclimatization. Twelve males cycled for 1-hour at 40% VOmax in winter (pre-acclimatization) and repeated the trial again in summer (after-acclimatization). For the last 20-min of cycling at a steady-state of T, air-velocity increased from 0.2 (0.04) m/s to 1.1 (0.02) m/s by using an electric fan located in front of the participant. Seasonal acclimatization enhanced WBSR, unevaporated sweat rate, local sweat rate and mean skin temperature compared to pre-acclimatization state (all P<0.05) whilst sweating efficiency was lower (P<0.01) until the 55-min of exercise. T and evaporated sweat rate were unaltered by acclimatization status (all P>0.70). In conclusion, seasonal acclimatization enhances thermoeffector responses but does not attenuate T during exercise in a hot-humid environment. Furthermore, increasing air-velocity enhances evaporated sweat rate and sweating efficiency irrespective of acclimated state.
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http://dx.doi.org/10.1152/japplphysiol.00837.2020DOI Listing
May 2021

Effects of sex and menstrual cycle on sweating during isometric handgrip exercise and postexercise forearm occlusion.

Exp Physiol 2021 Jul 19;106(7):1508-1523. Epub 2021 May 19.

Laboratory for Exercise and Environmental Physiology, Faculty of Education, Niigata University, Niigata, Japan.

New Findings: What is the central question of this study? Do sex and menstrual cycle modulate sweating during isometric handgrip exercise and muscle metaboreceptor stimulation? What is the main finding and its importance? Sex modulates sweating during isometric handgrip exercise, as indicated by the lower sweat output per gland in women than in men, but not during muscle metaboreceptor stimulation. Sweat output per gland during isometric handgrip exercise and muscle metaboreceptor stimulation were lower in the mid-luteal phase than in the early follicular phase in women. Cholinergic sweat gland sensitivity might explain, in part, the individual variation of the response. Our results provide new insights regarding sex- and menstrual cycle-related modulation of the sweating response.

Abstract: We investigated whether sex and menstrual cycle could modulate sweating during isometric handgrip (IH) exercise and muscle metaboreceptor stimulation. Twelve young, healthy women in the early follicular (EF) and mid-luteal (ML) phases and 14 men underwent two experimental sessions consisting of a 1.5 min IH exercise at 25 and 50% of maximal voluntary contraction (MVC) in a hot environment (35°C, relative humidity 50%) followed by 2 min forearm occlusion to stimulate muscle metaboreceptors. Sweat rates, the number of activated sweat glands and the sweat output per gland (SGO) on the forearm and chest were assessed. Pilocarpine-induced sweating was also assessed via transdermal iontophoresis to compare the responses with those of IH exercise and muscle metaboreceptor stimulation, based on correlation analysis. Sweat rates on the forearm and chest during IH exercise and muscle metaboreceptor stimulation did not differ between men and women in either menstrual cycle phase (all P ≥ 0.144). However, women in both phases showed lower SGO on the forearm and/or chest compared with men during IH exercise at 50% of MVC, with no differences in muscle metaboreceptor stimulation. Women in the ML phase had a lower forearm sweat rate during IH exercise at 50% of MVC (P = 0.015) and SGO during exercise and muscle metaboreceptor stimulation (main effect, both P ≤ 0.003) compared with those in the EF phase. Overall, sweat rate and SGO during IH exercise and muscle metaboreceptor stimulation were correlated with pilocarpine-induced responses (all P ≤ 0.064, r ≥ 0.303). We showed that sex and menstrual cycle modulate sudomotor activity during IH exercise and/or muscle metaboreceptor stimulation. Cholinergic sweat gland sensitivity might explain, in part, the individual variation of the response.
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http://dx.doi.org/10.1113/EP089464DOI Listing
July 2021

Effects of short-term heat acclimation on whole-body heat exchange and local nitric oxide synthase- and cyclooxygenase-dependent heat loss responses in exercising older men.

Exp Physiol 2021 Feb 28;106(2):450-462. Epub 2020 Dec 28.

Human and Environmental Physiology Research Unit, School of Human Kinetics, University of Ottawa, Ottawa, Ontario, Canada.

New Findings: What is the central question of this study? Does short-term heat acclimation enhance whole-body evaporative heat loss and augment nitric oxide synthase (NOS)-dependent cutaneous vasodilatation and NOS- and cyclooxygenase (COX)-dependent sweating, in exercising older men? What is the main finding and its importance? Our preliminary data (n = 8) demonstrated that short-term heat acclimation improved whole-body evaporative heat loss, but it did not influence the effects of NOS and/or COX inhibition on cutaneous vasodilatation or sweating in older men during an exercise-heat stress. These outcomes might imply that although short-term heat acclimation enhances heat dissipation in older men, it does not modulate NOS- and COX-dependent control of cutaneous vasodilatation or sweating on the forearm.

Abstract: Ageing is associated with decrements in whole-body heat loss (evaporative + dry heat exchange), which might stem from alterations in nitric oxide synthase (NOS)- and cyclooxygenase (COX)-dependent cutaneous vasodilatation and sweating. We evaluated whether short-term heat acclimation would (i) enhance whole-body heat loss primarily by increasing evaporative heat loss, and (ii) augment NOS-dependent cutaneous vasodilatation and NOS- and COX-dependent sweating, in exercising older men. Eight older men [mean (SD) age, 59 (8) years] completed a calorimetry and microdialysis trial before and after 7 days of exercise-heat acclimation. For the calorimetry trials, whole-body evaporative and dry heat exchange were assessed using direct calorimetry during 30 min bouts of cycling at light, moderate and vigorous metabolic heat productions (150, 200 and 250 W/m , respectively) in dry heat (40°C, 20% relative humidity). For the microdialysis trials, local cutaneous vascular conductance and sweat rate were assessed during 60 min exercise in the heat (35°C, 20% relative humidity) at four dorsal forearm skin sites treated with lactated Ringer solution (control), NOS inhibitor, COX inhibitor or combined NOS and COX inhibitors, via microdialysis. Evaporative heat loss during moderate (P = 0.036) and vigorous (P = 0.021) exercise increased after acclimation. Inhibition of NOS alone reduced cutaneous vascular conductance to a similar extent before and after acclimation (P < 0.040), whereas separate and combined NOS and COX inhibition had no significant effects on sweating relative to the control site (P = 0.745). Our preliminary results might suggest that short-term heat acclimation improves evaporative heat loss, but does not significantly modulate the contributions of NOS or COX to cutaneous vasodilatation or sweating on the forearm in older men during an exercise-heat stress.
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http://dx.doi.org/10.1113/EP089025DOI Listing
February 2021

TRPV4 channel blockade does not modulate skin vasodilation and sweating during hyperthermia or cutaneous postocclusive reactive and thermal hyperemia.

Am J Physiol Regul Integr Comp Physiol 2021 04 21;320(4):R563-R573. Epub 2020 Oct 21.

Faculty of Health and Sport Sciences, University of Tsukuba, Tsukuba, Japan.

Transient receptor potential vanilloid 4 (TRPV4) channels exist on vascular endothelial cells and eccrine sweat gland secretory cells in human skin. Here, we assessed whether TRPV4 channels contribute to cutaneous vasodilation and sweating during whole body passive heat stress () and to cutaneous vasodilation during postocclusive reactive hyperemia and local thermal hyperemia (). Intradermal microdialysis was employed to locally deliver pharmacological agents to forearm skin sites, where cutaneous vascular conductance (CVC) and sweat rate were assessed. In (12 young adults), CVC and sweat rate were increased by passive whole body heating, resulting in a body core temperature elevation of 1.2 ± 0.1°C. The elevated CVC and sweat rate assessed at sites treated with TRPV4 channel antagonist (either 200 µM HC-067047 or 125 µM GSK2193874) were not different from the vehicle control site (5% dimethyl sulfoxide). After whole body heating, the TRPV4 channel agonist (100 µM GSK1016790A) was administered to each skin site, eliciting elevations in CVC. Relative to control, this response was partly attenuated by both TRPV4 channel antagonists, confirming drug efficacy. In (10 young adults), CVC was increased following a 5-min arterial occlusion and during local heating from 33 to 42°C. These responses did not differ between the control and the TRPV4 channel antagonist sites (200 µM HC-067047). We show that TRPV4 channels are not required for regulating cutaneous vasodilation or sweating during a whole body passive heat stress. Furthermore, they are not required for regulating cutaneous vasodilation during postocclusive reactive hyperemia and local thermal hyperemia.
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http://dx.doi.org/10.1152/ajpregu.00123.2020DOI Listing
April 2021

Caffeine Exacerbates Hyperventilation and Reductions in Cerebral Blood Flow in Physically Fit Men Exercising in the Heat.

Med Sci Sports Exerc 2021 04;53(4):845-852

Faculty of Health and Sport Sciences, University of Tsukuba, Tsukuba, JAPAN.

Introduction: Caffeine is an exercise performance enhancer widely used by individuals engaged in training or competition under heat-stressed conditions. Caffeine ingestion during exercise in the heat is believed to be safe because it does not greatly affect body temperature responses, heart rate, or body fluid status. However, it remains unknown whether caffeine affects hyperthermia-induced hyperventilation or reductions in the cerebral blood flow index. We tested the hypothesis that under conditions inducing severe hyperthermia, caffeine exacerbates hyperthermia-induced hyperventilation and reduces the cerebral blood flow index during exercise.

Methods: Using a randomized, single-blind, crossover design, 12 physically active healthy young men (23 ± 2 yr) consumed a moderate dose of caffeine (5 mg·kg-1) or placebo in the heat (37°C). Approximately 60 min after the ingestion, they cycled for ~45 min at a workload equal to ~55% of their predetermined peak oxygen uptake (moderate intensity) until their core temperature increased to 2.0°C above its preexercise baseline level.

Results: In both trials, ventilation increased and the cerebral blood flow index assessed by middle cerebral artery mean blood velocity decreased as core temperature rose during exercise (P < 0.05), indicating that hyperthermia-induced hyperventilation and lowering of the cerebral blood flow occurred. When core temperature was elevated by 1.5°C or more (P < 0.05), ventilation was higher and the cerebral blood flow was lower throughout the caffeine trial than the placebo trial (P < 0.05).

Conclusions: A moderate dose of caffeine exacerbates hyperthermia-induced hyperventilation and reductions in the cerebral blood flow index during exercise in the heat with severe hyperthermia.
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http://dx.doi.org/10.1249/MSS.0000000000002537DOI Listing
April 2021

The relative contribution of α- and β-adrenergic sweating during heat exposure and the influence of sex and training status.

Exp Dermatol 2020 12 21;29(12):1216-1224. Epub 2020 Oct 21.

Laboratory for Applied Human Physiology, Graduate School of Human Development and Environment, Kobe University, Kobe, Japan.

While human eccrine sweat glands respond to adrenergic agonists, there remains a paucity of information on the factors modulating this response. Thus, we assessed the relative contribution of α- and β-adrenergic sweating during a heat exposure and as a function of individual factors of sex and training status. α- and β-adrenergic sweating was assessed in forty-eight healthy young men (n = 35) and women (n = 13) including endurance-trained (n = 12) and untrained men (n = 12) under non-heat exposure (temperate, 25°C; n = 17) and heat exposure (hot, 35°C; n = 48) conditions using transdermal iontophoresis of phenylephrine (α-adrenergic agonist) and salbutamol (β-adrenergic agonist) on the ventral forearm, respectively. Adrenergic sweating was also measured after iontophoretic administration of atropine (muscarinic receptor antagonist) or saline (control) to evaluate how changes in muscarinic receptor activity modulate the adrenergic response to a heat exposure (n = 12). α- and β-adrenergic sweating was augmented in hot compared with temperate conditions (both P ≤ .014), albeit the relative increase was greater in β (~5.4-fold)- as compared to α (~1.5-fold)-adrenergic-mediated sweating response. However, both α- and β-adrenergic sweating was abolished by atropinization (P = .001). Endurance-trained men showed an augmentation in α- (P = .043) but not β (P = .960)-adrenergic sweating as compared to untrained men. Finally, a greater α- and β-adrenergic sweating response (both P ≤ .001) was measured in habitually active men than in women. We show that heat exposure augments α-and β-adrenergic sweating differently via mechanisms associated with altered muscarinic receptor activity. Sex and training status modulate this response.
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http://dx.doi.org/10.1111/exd.14208DOI Listing
December 2020

The sweat glands' maximum ion reabsorption rates following heat acclimation in healthy older adults.

Exp Physiol 2021 Jan 13;106(1):302-315. Epub 2020 Oct 13.

Laboratory for Applied Human Physiology, Graduate School of Human Development and Environment, Kobe University, Kobe, Japan.

New Findings: What is the central question to this study? Do the sweat glands' maximum ion reabsorption rates increase following heat acclimation in healthy older individuals and is this associated with elevated aldosterone concentrations? What is the main finding and its importance? Sweat gland maximum ion reabsorption rates improved heterogeneously across body sites, which occurred without any changes in aldosterone concentration following a controlled hyperthermic heat acclimation protocol in healthy older individuals.

Abstract: We examined whether the eccrine sweat glands' ion reabsorption rates improved following heat acclimation (HA) in older individuals. Ten healthy older adults (>65 years) completed a controlled hyperthermic (+0.9°C rectal temperature, T ) HA protocol for nine non-consecutive days. Participants completed a passive heat stress test (lower leg 42°C water submersion) pre-HA and post-HA to assess physiological regulation of sweat gland ion reabsorption at the chest, forearm and thigh. The maximum ion reabsorption rate was defined as the inflection point in the slope of the relation between galvanic skin conductance and sweat rate (SR). We explored the responses again after a 7-day decay. During passive heating, the T thresholds for sweat onset on the chest and forearm were lowered after HA (P < 0.05). However, sweat sensitivity (i.e. the slope), the SR at a given T and gross sweat loss did not improve after HA (P > 0.05). Any changes observed were lost during the decay. Pilocarpine-induced sudomotor responses to iontophoresis did not change after HA (P ≥ 0.801). Maximum ion reabsorption rate was only enhanced at the chest (P = 0.001) despite unaltered aldosterone concentration after HA. The data suggest that this adaptation is lost after 7 days' decay. The HA protocol employed in the present study induced partial adaptive sudomotor responses. Eccrine sweat gland ion reabsorption rates improved heterogeneously across the skin sites. It is likely that aldosterone secretion did not alter the chest sweat ion reabsorption rates observed in the older adults.
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http://dx.doi.org/10.1113/EP088486DOI Listing
January 2021

Effects of L-type voltage-gated Ca channel blockade on cholinergic and thermal sweating in habitually trained and untrained men.

Am J Physiol Regul Integr Comp Physiol 2020 11 23;319(5):R584-R591. Epub 2020 Sep 23.

Laboratory for Applied Human Physiology, Graduate School of Human Development and Environment, Kobe University, Kobe, Japan.

We evaluated the hypothesis that the activation of L-type voltage-gated Ca channels contributes to exercise training-induced augmentation in cholinergic sweating. On separate days, 10 habitually trained and 10 untrained men participated in two experimental protocols. Prior to each protocol, we administered 1% verapamil (Verapamil, L-type voltage-gated Ca channel blocker) and saline (Control) at forearm skin sites on both arms via transdermal iontophoresis. In , we administered low (0.001%) and high (1%) doses of pilocarpine at both the verapamil-treated and verapamil-untreated forearm sites. In , participants were passively heated by immersing their limbs in hot water (43°C) until rectal temperature increased by 1.0°C above baseline resting levels. Sweat rate at all forearm sites was continuously measured throughout both protocols. Pilocarpine-induced sweating in Control was higher in trained than in untrained men for both the concentrations of pilocarpine (both ≤ 0.001). Pilocarpine-induced sweating at the low-dose site was attenuated at the Verapamil versus the Control site in both the groups (both ≤ 0.004), albeit the reduction was greater in trained as compared with in untrained men ( = 0.005). The verapamil-mediated reduction in sweating remained intact at the high-dose pilocarpine site in the untrained men ( = 0.004) but not the trained men ( = 0.180). Sweating did not differ between Control and Verapamil sites with increases in rectal temperature in both groups (interaction, = 0.571). We show that activation of L-type voltage-gated Ca channels modulates sweat production in habitually trained men induced by a low dose of pilocarpine. However, no effect on sweating was observed during passive heating in either group.
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http://dx.doi.org/10.1152/ajpregu.00167.2020DOI Listing
November 2020

Ageing augments β-adrenergic cutaneous vasodilatation differently in men and women, with no effect on β-adrenergic sweating.

Exp Physiol 2020 10 1;105(10):1720-1729. Epub 2020 Sep 1.

Human and Environmental Physiology Research Unit, University of Ottawa, Ottawa, Ontario, Canada.

New Findings: What is the central question of this study? β-Adrenergic receptor activation modulates cutaneous vasodilatation and sweating in young adults. In this study, we assessed whether age-related differences in β-adrenergic regulation of these responses exist and whether they differ between men and women. What is the main finding and its importance? We showed that ageing augmented β-adrenergic cutaneous vasodilatation, although the pattern of response differed between men and women. Ageing had no effect on β-adrenergic sweating in men or women. Our findings advance our understanding of age-related changes in the regulation of cutaneous vasodilatation and sweating and provide new directions for research on the significance of enhanced β-adrenergic cutaneous vasodilatation in older adults.

Abstract: β-Adrenergic receptor agonists, such as isoprenaline, can induce cutaneous vasodilatation and sweating in young adults. Given that cutaneous vasodilatation and sweating responses to whole-body heating and to pharmacological agonists, such as acetylcholine, ATP and nicotine, can differ in older adults, we assessed whether ageing also modulates β-adrenergic cutaneous vasodilatation and sweating and whether responses differ between men and women. In the context of the latter, prior reports showed that the effects of ageing on cutaneous vasodilatation (evoked with ATP and nicotine) and sweating (stimulated by acetylcholine) were sex dependent. Thus, in the present study, we assessed the role of β-adrenergic receptor activation on forearm cutaneous vasodilatation and sweating in 11 young men (24 ± 4 years of age), 11 young women (23 ± 5 years of age), 11 older men (61 ± 8 years of age) and 11 older women (60 ± 8 years of age). Initially, a high dose (100 µm) of isoprenaline was administered via intradermal microdialysis for 5 min to induce maximal β-adrenergic sweating. Approximately 60 min after the washout period, three incremental doses of isoprenaline were administered (1, 10 and 100 µm, each for 25 min) to assess dose-dependent cutaneous vasodilatation. Isoprenaline-mediated cutaneous vasodilatation was greater in both older men and older women relative to their young counterparts. Augmented cutaneous vasodilatory responses were observed at 1 and 10 µm in women and at 100 µm in men. Isoprenaline-mediated sweating was unaffected by ageing, regardless of sex. We show that ageing augments β-adrenergic cutaneous vasodilatation differently in men and women, without influencing β-adrenergic sweating.
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http://dx.doi.org/10.1113/EP088583DOI Listing
October 2020

Does the iontophoretic application of bretylium tosylate modulate sweating during exercise in the heat in habitually trained and untrained men?

Exp Physiol 2020 10 18;105(10):1692-1699. Epub 2020 Aug 18.

Laboratory for Applied Human Physiology, Graduate School of Human Development and Environment, Kobe University, Kobe, Japan.

New Findings: What is the central question of this study? Does the administration of the adrenergic presynaptic release inhibitor bretylium tosylate modulate sweating during exercise in the heat, and does this response differ between habitually trained and untrained men? What is the main finding and its importance? Iontophoretic administration of bretylium tosylate attenuates sweating during exercise in the heat in habitually trained and untrained men. However, a greater reduction occurred in trained men. The findings demonstrate a role for cutaneous adrenergic nerves in the regulation of eccrine sweating during exercise in the heat and highlight a need to advance our understanding of neural control of human eccrine sweat gland activity.

Abstract: We recently reported an influence of cutaneous adrenergic nerves on eccrine sweat production in habitually trained men performing an incremental exercise bout in non-heat stress conditions. Based on an assumption that increasing heat stress induces cholinergic modulation of sweating, we evaluated the hypothesis that the contribution of cutaneous adrenergic nerves on sweating would be attenuated during exercise in the heat. Twenty young habitually trained and untrained men (n = 10/group) underwent three successive bouts of 15 min of light-, moderate- and vigorous-intensity cycling (equivalent to 30, 50, and 70% of peak oxygen uptake ( ) respectively), each separated by a 15 min recovery while wearing a perfusion suit perfused with warm water (43°C). Sweat rate (ventilated capsule) was measured continuously at two bilateral forearm skin sites treated with 10 mm bretylium tosylate (an inhibitor of neurotransmitter release from adrenergic nerve terminals) and saline (control) via transdermal iontophoresis. A greater sweat rate was measured during vigorous exercise only in trained as compared to untrained men (P = 0.014). In both groups, sweating was reduced at the bretylium tosylate versus control sites, albeit the magnitude of reduction was greater in the trained men (P ≤ 0.024). These results suggest that cutaneous adrenergic nerves modulate sweating during exercise performed under a whole-body heat stress, albeit a more robust response occurs in trained men. While it is accepted that a cholinergic mechanism plays a primary role in the regulation of sweating during an exercise-heat stress, our findings highlight the need for additional studies aimed at understanding the neural control of human eccrine sweating.
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http://dx.doi.org/10.1113/EP088797DOI Listing
October 2020

Does α-adrenergic receptor blockade modulate sweating during incremental exercise in young endurance-trained men?

Eur J Appl Physiol 2020 May 27;120(5):1123-1129. Epub 2020 Mar 27.

Laboratory for Applied Human Physiology, Graduate School of Human Development and Environment, Kobe University, Kobe, Japan.

Purpose: Human eccrine sweat glands respond to α-adrenergic receptor agonists. We recently reported that adrenergic mechanisms contribute to sweating in endurance-trained men during an incremental exercise to volitional fatigue. However, it remains unclear if this response is mediated by α-adrenergic receptor activation.

Methods: Twelve endurance-trained men performed an incremental cycling bout until exhaustion while wearing a water-perfused suit to clamp skin temperature at ~ 34 °C. Bilateral forearm sweat rates were measured wherein the distal area was treated with either 1% terazosin (α-adrenergic receptor antagonist) or saline solution on the opposite limb (Control) via transdermal iontophoresis. We also measured proximal bilateral forearm sweat rate in untreated sites to confirm that no between-limb differences in forearm sweat rate occurred. Once sweat rate returned to pre-exercise resting levels at ~ 20 min postexercise, 0.25% phenylephrine (α-adrenergic receptor agonist) was iontophoretically administered to skin to verify α-adrenergic receptor blockade.

Results: Sweat rates at the proximal untreated right and left forearm sites were similar during exercise (interaction, P = 0.581). Similarly, no effect of terazosin on sweat rate was measured relative to control site (interaction, P = 0.848). Postexercise administration of phenylephrine increased sweat rate at the control site (0.08 ± 0.09 mg cm min), which was suppressed by ~ 90% at the terazosin-treated site (0.01 ± 0.02 mg cm min) (P = 0.026), confirming that α-adrenergic receptor blockade was intact.

Conclusion: Our findings demonstrate that α-adrenergic receptors located at eccrine sweat glands do not contribute to eccrine sweating during incremental exercise in young endurance-trained men.
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http://dx.doi.org/10.1007/s00421-020-04351-3DOI Listing
May 2020

Effects of Casein Hydrolysate Ingestion on Thermoregulatory Responses in Healthy Adults during Exercise in Heated Conditions: A Randomized Crossover Trial.

Nutrients 2020 Mar 24;12(3). Epub 2020 Mar 24.

Laboratory for Exercise and Environmental Physiology, Faculty of Education, Niigata University, Niigata, Niigata-Pref. 950-2181, Japan.

Food ingestion has been shown to affect thermoregulation during exercise, while the impact of protein degradant consumption remains unclear. We investigated the effects of casein hydrolysate ingestion on thermoregulatory responses during exercise in the heat. In a randomized, placebo-controlled, double-blind, crossover trial, five men and five women consumed either 5 g of casein hydrolysate or placebo. Thirty minutes after ingestion, participants cycled at 60% VOmax until voluntary exhaustion wearing a hot-water (43 °C) circulation suit. Exercise time to exhaustion, body core temperature, forearm sweat rate, and forearm cutaneous vascular conductance did not differ different between the conditions. However, chest sweat rate and mean skin temperature increased upon casein hydrolysate ingestion compared with placebo during exercise. Increased chest sweat rate upon casein hydrolysate ingestion was associated with elevated sudomotor sensitivity to increasing body core temperature, but not the temperature threshold for initiating sweating. A positive correlation was found between chest sweat rate and plasma total amino acid concentration during exercise. These results suggest that casein hydrolysate ingestion enhances sweating heterogeneously by increasing peripheral sensitivity of the chest's sweating mechanism and elevating skin temperature during exercise in the heat. However, the physiological link between plasma amino acid concentration and sweat rate remains unclear.
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http://dx.doi.org/10.3390/nu12030867DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7146450PMC
March 2020

Regional influence of nitric oxide on cutaneous vasodilatation and sweating during exercise-heat stress in young men.

Exp Physiol 2020 05 20;105(5):773-782. Epub 2020 Apr 20.

Human and Environmental Physiology Research Unit, School of Human Kinetics, University of Ottawa, Ottawa, Ontario, Canada.

New Findings: What is the central question of this study? Do regional differences exist in nitric oxide synthase (NOS)-dependent cutaneous vasodilatation and sweating during exercise-heat stress in young men. What is the main finding and its importance? Exercise-induced increases in cutaneous vasodilatation and sweating were greater on the chest and upper back compared to the forearm, although the NOS contribution to cutaneous vasodilatation was similar across all regions. Conversely, there was a greater NOS-dependent rate of change in sweating on the chest compared to the forearm, with a similar trend on the back.

Abstract: While it is established that nitric oxide synthase (NOS) is an important modulator of forearm cutaneous vasodilatation and sweating during an exercise-heat stress in young men, it remains unclear if regional differences exist in this response. In 15 habitually active young men (24 ± 4 (SD) years), cutaneous vascular conductance (CVC) and local sweat rate (LSR) were assessed at three body regions. On each of the dorsal forearm, chest and upper-back (trapezius), sites were continuously perfused with either (1) lactated Ringer solution (control) or (2) 10 Mm N -nitro-l-arginine (l-NNA, NOS inhibitor), via microdialysis. Participants rested in the heat (35°C) for ∼75 min, followed by 60 min of semi-recumbent cycling performed at a fixed rate of heat production of 200 W m (equivalent to ∼42% ). During exercise, the chest and upper-back regions showed higher CVC and LSR responses relative to the forearm (all P < 0.05). Within each region, l-NNA attenuated CVC and LSR relative to control (all P < 0.05). However, the NOS contribution was not different across regions for the rate of change and plateau for CVC or for the LSR plateau (all P > 0.05). Conversely, there was a greater NOS contribution to the rate of change for LSR at the chest relative to the forearm (P < 0.05) with a similar trend for the back. In habitually active young men, NOS-dependent cutaneous vasodilatation was similar across regions while the NOS contribution to LSR was greater on the chest relative to the forearm. These findings advance our understanding of the mechanisms influencing regional variations in cutaneous vasodilatation and sweating during an exercise-heat stress.
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http://dx.doi.org/10.1113/EP088388DOI Listing
May 2020

NO-mediated activation of K channels contributes to cutaneous thermal hyperemia in young adults.

Am J Physiol Regul Integr Comp Physiol 2020 02 8;318(2):R390-R398. Epub 2020 Jan 8.

Faculty of Health and Sport Sciences, University of Tsukuba, Tsukuba, Japan.

Local skin heating to 42°C causes cutaneous thermal hyperemia largely via nitric oxide (NO) synthase (NOS)-related mechanisms. We assessed the hypothesis that ATP-sensitive K (K) channels interact with NOS to mediate cutaneous thermal hyperemia. In 13 young adults (6 women, 7 men), cutaneous vascular conductance (CVC) was measured at four intradermal microdialysis sites that were continuously perfused with ) lactated Ringer solution (control), ) 5 mM glibenclamide (K channel blocker), ) 20 mM -nitro-l-arginine methyl ester (NOS inhibitor), or ) a combination of K channel blocker and NOS inhibitor. Local skin heating to 42°C was administered at all four treatment sites to elicit cutaneous thermal hyperemia. Thirty minutes after the local heating, 1.25 mM pinacidil (K channel opener) and subsequently 25 mM sodium nitroprusside (NO donor) were administered to three of the four sites (each 25-30 min). The local heating-induced prolonged elevation in CVC was attenuated by glibenclamide (19%), but the transient initial peak was not. However, glibenclamide had no effect on the prolonged elevation in CVC in the presence of NOS inhibition. Pinacidil caused an elevation in CVC, but this response was abolished at the glibenclamide-treated skin site, demonstrating its effectiveness as a K channel blocker. The pinacidil-induced increase in CVC was unaffected by NOS inhibition, whereas the increase in CVC elicited by sodium nitroprusside was partly (15%) inhibited by glibenclamide. In summary, we showed an interactive effect of K channels and NOS for the plateau of cutaneous thermal hyperemia. This interplay may reflect a vascular smooth muscle cell K channel activation by NO.
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http://dx.doi.org/10.1152/ajpregu.00176.2019DOI Listing
February 2020

Regional contributions of nitric oxide synthase to cholinergic cutaneous vasodilatation and sweating in young men.

Exp Physiol 2020 02 19;105(2):236-243. Epub 2020 Jan 19.

Human and Environmental Physiology Research Unit, School of Human Kinetics, University of Ottawa, Ottawa, Ontario, Canada.

New Findings: What is the central question of this study? We evaluated whether regional variations exist in NO-dependent cutaneous vasodilatation and sweating during cholinergic stimulation. What is the main finding and its importance? Peak cutaneous vasodilatation and sweating were greater on the torso than the forearm. Furthermore, we found that NO was an important modulator of cholinergic cutaneous vasodilatation, but not sweating, across body regions, with a greater contribution of NO to cutaneous vasodilatation in the limb compared with the torso. These findings advance our understanding of the mechanisms influencing regional variations in cutaneous vasodilator and sweating responses to pharmacological stimulation.

Abstract: Regional variations in cutaneous vasodilatation and sweating exist across the body. Nitric oxide (NO) is an important modulator of these heat loss responses in the forearm. However, whether regional differences in NO-dependent cutaneous vasodilatation and sweating exist remain uncertain. In 14 habitually active young men (23 ± 4 years of age), cutaneous vascular conductance (CVC ) and local sweat rates were assessed at six skin sites. On each of the dorsal forearm, chest and upper back (trapezius), sites were continuously perfused with either lactated Ringer solution (control) or 10 mm N -nitro-l-arginine (l-NNA; an NO synthase inhibitor) dissolved in Ringer solution, via microdialysis. At all sites, cutaneous vasodilatation and sweating were induced by co-administration of the cholinergic agonist methacholine (1, 10, 100, 1000 and 2000 mm; 25 min per dose) followed by 50 mm sodium nitroprusside (20-25 min) to induce maximal vasodilatation. The l-NNA attenuated CVC relative to the control conditions for all regions (all P < 0.05), and NO-dependent vasodilatation was greater at the forearm compared with the back and chest (both P < 0.05). Furthermore, maximal vasodilatation was higher at the back and chest relative to the forearm (both P < 0.05). Conversely, l-NNA had negligible effects on sweating across the body (all P > 0.05). Peak local sweat rate was higher at the back relative to the forearm (P < 0.05), with a similar trend observed for the chest. In habitually active young men, NO-dependent cholinergic cutaneous vasodilatation varied across the body, and the contribution to cholinergic sweating was negligible. These findings advance our understanding of the mechanisms influencing regional variations in cutaneous vasodilatation and sweating during pharmacological stimulation.
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http://dx.doi.org/10.1113/EP088295DOI Listing
February 2020

Contribution of nitric oxide synthase to cutaneous vasodilatation and sweating in men of black-African and Caucasian descent during exercise in the heat.

Exp Physiol 2019 12 13;104(12):1762-1768. Epub 2019 Nov 13.

Human and Environmental Physiology Research Unit, School of Human Kinetics, University of Ottawa, Ottawa, ON, Canada.

New Findings: What is the central question of this study? Nitric oxide modulates cutaneous vasodilatation and sweating during exercise-induced heat stress in young men. However, it remains uncertain whether these effects are reduced in black-African descendants, who commonly demonstrate reduced nitric oxide bioavailability. Therefore, we assessed whether black-African descendants display reduced nitric oxide-dependent cutaneous vasodilatation and sweating compared with Caucasians in these conditions. What is the main finding and its importance? Nitric oxide-dependent cutaneous vasodilatation and sweating were similar between groups, indicating that reduced nitric oxide bioavailability in black-African descendants does not attenuate these heat-loss responses during an exercise-induced heat stress.

Abstract: Men of black-African descent are at an increased risk of heat-related illness relative to their Caucasian counterparts. This might be attributable, in part, to reduced cutaneous nitric oxide (NO) bioavailability in this population, which might alter local cutaneous vasodilatation and sweating. To evaluate this, we compared these heat-loss responses in young men (18-30 years of age) of black-African (n = 10) and Caucasian (n = 10) descent during rest, exercise and recovery in the heat. Participants were matched for physical characteristics and fitness, and they were all born and raised in the same temperate environment (i.e. Canada; second generation and higher). Both groups rested for 10 min and then performed 50 min of moderate-intensity exercise at 200 W m , followed by 30 min of recovery in hot, dry heat (35°C, 20% relative humidity). Local cutaneous vascular conductance (CVC ) and sweat rate (SR) were measured at two forearm skin sites treated with either lactated Ringer solution (control) or 10 mm N -nitro-l-arginine methyl ester (l-NAME, a nitric oxide (NO) synthase inhibitor). l-NAME significantly reduced CVC throughout rest, exercise and recovery in both groups (both P < 0.001). However, there were no significant main effects for the contribution of NO to CVC between groups (all P > 0.500). l-NAME significantly reduced local SR in both groups (both P < 0.050). The contribution of NO to SR was similar between groups such that l-NAME reduced SR relative to control at 40 and 50 min into exercise (both P < 0.05). We demonstrate that ethnicity per se does not influence NO-dependent cutaneous vasodilatation and sweating in healthy young men of black-African and Caucasian descent during exercise in dry heat.
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http://dx.doi.org/10.1113/EP088115DOI Listing
December 2019

Nicotinic receptors modulate skin perfusion during normothermia, and have a limited role in skin vasodilatation and sweating during hyperthermia.

Exp Physiol 2019 12 13;104(12):1808-1818. Epub 2019 Nov 13.

Faculty of Health and Sport Sciences, University of Tsukuba, Tsukuba, Japan.

New Findings: What is the central question of this study? What is the role of nicotinic receptors in the regulation of normothermic cutaneous blood flow and cutaneous vasodilatation and sweating during whole-body heating induced following resting in a non-heat-stress condition? What is the main finding and its importance? Nicotinic receptors modulated cutaneous vascular tone during rest in a non-heat-stress condition and in the early stage of heating, but they had a limited role in mediating cutaneous vasodilatation when core temperature increased >0.4°C. Further, the contribution of nicotinic receptors to sweating was negligible during whole-body heating. Our findings provide new insights into the role of nicotinic receptors in end-organ function of skin vasculature and sweat glands in humans.

Abstract: Nicotinic receptors are present in human skin including cutaneous vessels and eccrine sweat glands as well as peripheral nerves. We tested the hypothesis that nicotinic receptors do not contribute to the control of cutaneous vascular tone in the normothermic state, but are involved in mediating cutaneous vasodilatation and sweating during a whole-body passive heat stress in humans. We first performed a nicotinic receptor blocker verification protocol in six young adults (one female) wherein increases in cutaneous vascular conductance and sweating elicited by 10 mm nicotine were blocked by administration of 500 µm hexamethonium to confirm effective blockade. Thereafter, 12 young males participated in a passive heating protocol. After an instrumentation period in a non-heat-stress condition, participants rested for a 10 min baseline period. Thereafter, oesophageal temperature was increased by 1.0°C using water-perfusion suits. Cutaneous vascular conductance, sweat rate, active sweat gland density and sweat output per individual gland were assessed with and without 500 µm hexamethonium administered via intradermal microdialysis. Hexamethonium reduced cutaneous vascular conductance by 22-34% during normothermia and the early stage of heating. However, this effect was diminished as oesophageal temperature increased >0.4°C. Active sweat gland density was reduced by hexamethonium when oesophageal temperature was elevated by 0.4-0.6°C above baseline resting. However, this was paralleled by a marginal increase in sweat gland output. Consequently, sweat rate remained unchanged. We showed that nicotinic receptors modulate cutaneous perfusion during normothermia and the early stage of heating, but not when core temperature increases >0.4°C. Additionally, they play a limited role in mediating sweating during heating.
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http://dx.doi.org/10.1113/EP088072DOI Listing
December 2019

Effects of isomaltulose ingestion on postexercise hydration state and heat loss responses in young men.

Exp Physiol 2019 10 26;104(10):1494-1504. Epub 2019 Aug 26.

Bourbon Institutes of Health Nutraceuticals Science Laboratory, Bourbon Corporation, Niigata, Japan.

New Findings: What is the central question of this study? What are the effects of isomaltulose, an ingredient in carbohydrate-electrolyte beverages to maintain glycaemia and attenuate the risk of dehydration during exercise heat stress, on postexercise rehydration and physiological heat loss responses? What is the main finding and its importance? Consumption of a 6.5% isomaltulose-electrolyte beverage following exercise heat stress restored hydration following a 2 h recovery as compared to a 2% solution or water only. While the 6.5% isomaltulose-electrolytes increased plasma volume and plasma osmolality, which are known to modulate postexercise heat loss, sweating and cutaneous vascular responses did not differ between conditions. Consequently, ingestion beverages containing 6.5% isomaltulose-electrolytes enhanced postexercise rehydration without affecting heat loss responses.

Abstract: Isomaltulose is a disaccharide carbohydrate widely used during exercise to maintain glycaemia and hydration. We investigated the effects of ingesting a beverage containing isomaltulose and electrolytes on postexercise hydration state and physiological heat loss responses. In a randomized, single-blind cross-over design, 10 young healthy men were hypohydrated by performing up to three 30 min successive moderate-intensity (50% heart rate reserve) bouts of cycling, each separated by 10 min, while wearing a water-perfusion suit heated to 45°C. The protocol continued until a 2% reduction in body mass was achieved. Thereafter, participants performed a final 15 min moderate-intensity exercise bout followed by a 2 h recovery. Following cessation of exercise, participants ingested a beverage consisting of (i) water only (Water), (ii) 2% isomaltulose (CHO-2%), or (iii) 6.5% isomaltulose (CHO-6.5%) equal to the volume of 2% body mass loss within the first 30 min of the recovery. Changes in plasma volume (ΔPV) after fluid ingestion were greater for CHO-6.5% compared with CHO-2% (120 min postexercise) and Water (90 and 120 min) (all P ≤ 0.040). Plasma osmolality remained elevated with CHO-6.5% compared with consumption of the other beverages at 30 and 90 min postexercise (all P ≤ 0.050). Urine output tended to be reduced with CHO-6.5% compared to other fluid conditions (main effect, P = 0.069). Rectal and mean skin temperatures, chest sweat rate and cutaneous perfusion did not differ between conditions (all P > 0.05). In conclusion, compared with CHO-2% and Water, consuming a beverage consisting of CHO-6.5% and electrolytes during recovery under heat stress enhances PV recovery without modulating physiological heat loss responses.
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http://dx.doi.org/10.1113/EP087843DOI Listing
October 2019

Evidence for TRPV4 channel induced skin vasodilatation through NOS, COX, and KCa channel mechanisms with no effect on sweat rate in humans.

Eur J Pharmacol 2019 Sep 16;858:172462. Epub 2019 Jun 16.

Faculty of Health and Sport Sciences, University of Tsukuba, Tsukuba, Japan.

Transient receptor potential vanilloid 4 (TRPV4) channels exist in the endothelial cells of cutaneous blood vessels and the secretory cells of eccrine sweat glands. We assessed if exogenous TRPV4 channel activation elicits cutaneous vasodilatation and sweating in humans in vivo, and if so, whether this response is mediated by nitric oxide synthase (NOS)- cyclooxygenase (COX)- and/or Ca-sensitive K (KCa) channel-related mechanisms. In ten healthy young adults (24±2 years, 5 women), cutaneous vascular conductance and sweat rate were assessed at four dorsal forearm skin sites continuously treated with either: 1) lactated Ringer's solution (Control), 2) 20 mM L-NAME, a non-selective NOS inhibitor, 3) 10 mM ketorolac, a non-selective COX inhibitor, or 4) 50 mM TEA, a non-selective KCa channel blocker. A potent and selective TRPV4 channel agonist, GSK1016790 A (GSK101), was administered to each skin site in a dose-dependent manner (1, 10, 100, 1000 μM each for ≥30min) via intradermal microdialysis. Administration of 100 and 1000 μM GSK101 increased cutaneous vascular conductance from pre-infusion level at the Control site (48±12 and 57±9%max, respectively, P≤0.004). This response was markedly (53-83%) attenuated by NOS inhibition, COX inhibition, or KCa channel blockade (all P≤0.037), except KCa channel blockade had no effect during 1000 μM GSK101 administration. GSK101 did not influence sweat rate regardless of skin site. We showed that in human skin in vivo, exogenous activation of TRPV4 channels mediates cutaneous vasodilatation, but not sweating through NOS, COX, and KCa channel mechanisms.
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http://dx.doi.org/10.1016/j.ejphar.2019.172462DOI Listing
September 2019

Effect of ice slushy ingestion and cold water immersion on thermoregulatory behavior.

PLoS One 2019 27;14(2):e0212966. Epub 2019 Feb 27.

Centre for Exercise and Sports Science Research, School of Medical and Health Sciences, Edith Cowan University, Joondalup, Western Australia, Australia.

Two studies were conducted to examine the effects of ice slushy ingestion (ICE) and cold water immersion (CWI) on thermoregulatory and sweat responses during constant (study 1) and self-paced (study 2) exercise. In study 1, 11 men cycled at 40-50% of peak aerobic power for 60 min (33.2 ± 0.3°C, 45.9 ± 0.5% relative humidity, RH). In study 2, 11 men cycled for 60 min at perceived exertion (RPE) equivalent to 15 (33.9 ± 0.2°C and 42.5 ± 3.9%RH). In both studies, each trial was preceded by 30 min of CWI (~22°C), ICE or no cooling (CON). Rectal temperature (Tre), skin temperature (Tsk), thermal sensation, and sweat responses were measured. In study 1, ICE decreased Tre-Tsk gradient versus CON (p = 0.005) during first 5 min of exercise, while CWI increased Tre-Tsk gradient versus CON and ICE for up to 20 min during the exercise (p<0.05). In study 2, thermal sensation was lower in CWI versus CON and ICE for up to 35-40 min during the exercise (p<0.05). ICE reduced thermal sensation versus CON during the first 20 min of exercise (p<0.05). In study 2, CWI improved mean power output (MPO) by ~8 W, compared with CON only (p = 0.024). In both studies, CWI (p<0.001) and ICE (p = 0.019) delayed sweating by 1-5 min but did not change the body temperature sweating threshold, compared with CON (both p>0.05). Increased Tre-Tsk gradient by CWI improved MPO while ICE reduced Tre but did not confer any ergogenic effect. Both precooling treatments attenuated the thermal efferent signals until a specific body temperature threshold was reached.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0212966PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6392407PMC
November 2019

β-Adrenergic receptor blockade does not modify non-thermal sweating during static exercise and following muscle ischemia in habitually trained individuals.

Eur J Appl Physiol 2018 Dec 20;118(12):2669-2677. Epub 2018 Sep 20.

Laboratory for Applied Human Physiology, Graduate School of Human Development and Environment, Kobe University, Kobe, Japan.

Purpose: This study investigated the influence of β-adrenergic receptor blockade on sweating during bilateral static knee extension (KE) and lateral isometric handgrip (IH) exercises followed by post-exercise muscle ischemia (PEMI) in habitually trained individuals.

Method: Ten habitually trained men (maximum oxygen uptake, 57.1 ± 3.4 ml kg min) were mildly heated by increasing their skin temperature, and bilateral KE or lateral IH exercises at an intensity of 60% maximum voluntary contraction were subsequently performed for 1 min, followed by PEMI to stimulate muscle metaboreceptors for 2 min. Sweat rates were measured on the bilateral forearms (KE) or thighs (IH) transdermally administered with 1% propranolol (propranolol, a non-selective β-adrenergic receptor inhibitor) or saline (control) via iontophoresis.

Results: Relative to the pre-exercise baseline values, IH exercise (P = 0.038) followed by PEMI (P = 0.041) similarly increased sweat rates on the thighs at both control and propranolol sites (baseline, 0.05 ± 0.04 vs. 0.05 ± 0.04; IH, 0.14 ± 0.12 vs. 0.15 ± 0.14; PEMI, 0.14 ± 0.16 vs. 0.14 ± 0.16 mg cm min). KE increased sweat rates on the forearms (P = 0.001) at both control and propranolol sites similarly (baseline, 0.02 ± 0.03 vs. 0.02 ± 0.03; KE, 0.21 ± 0.19 vs. 0.20 ± 0.18), whereas PEMI did not significantly induce sweating at these sites (P = 0.260) (0.09 ± 0.12 and 0.10 ± 0.12 mg cm min, respectively).

Conclusion: These results suggest that non-thermal drives induced by static exercise and PEMI do not elicit β-adrenergic sweating in habitually trained individuals even when the non-thermal drives are originated from leg(s) under the conditions in the present study.
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http://dx.doi.org/10.1007/s00421-018-3993-xDOI Listing
December 2018

Cutaneous adrenergic nerve blockade attenuates sweating during incremental exercise in habitually trained men.

J Appl Physiol (1985) 2018 10 19;125(4):1041-1050. Epub 2018 Jul 19.

Laboratory for Applied Human Physiology, Graduate School of Human Development and Environment, Kobe University , Kobe , Japan.

It remains unknown whether cutaneous adrenergic nerves functionally contribute to sweat production during exercise. This study examined whether cutaneous adrenergic nerve blockade attenuates sweating during incremental exercise, specifically in habitually trained individuals. Accordingly, 10 habitually trained and 10 untrained males (V̇o: 56.7 ± 5.4 and 38.9 ± 6.7 ml·kg·min, respectively; P < 0.001) performed incremental semirecumbent cycling (20 W/min) until exhaustion. Sweat rates (ventilated capsule) were measured at two bilateral forearm skin sites on which either 10 mM bretylium tosylate (BT) (an inhibitor of neurotransmitter release from sympathetic adrenergic nerve terminals) or saline (Control) was transdermally administered via iontophoresis. BT treatment delayed sweating onset in both groups (∼0.66 min; P = 0.001) and suppressed the sweat rate relative to the Control treatment at ≥70% relative total exercise time in trained individuals (each 10% increment; all P ≤ 0.009) but not in untrained counterparts ( P = 0.122, interaction between relative time × treatment). Changes in total sweat production at the BT site relative to the Control site were greater in trained individuals than in untrained counterparts (area under the curve, -0.86 ± 0.67 and -0.22 ± 0.39 mg/cm, respectively; P = 0.023). In conclusion, we demonstrated that cutaneous adrenergic nerves do modulate sweating during incremental exercise, which appeared to be more apparent in habitually trained men (e.g., ≥70% maximum workload). Although our results indicated that habitual exercise training may augment neural adrenergic sweat production during incremental exercise, additional studies are required to confirm this possibility. NEW & NOTEWORTHY We demonstrated for the first time that cutaneous adrenergic nerves do modulate sweating during high-intensity exercise in humans (≥70% maximum workload). In addition, neural adrenergic sweating appeared to be greater in habitually trained individuals than in untrained counterparts, although further studies are necessary to confirm such a possibility. Nonetheless, the observations presented herein advance our understanding on human thermoregulation while providing new evidence for the neutral mediation of adrenergic sweating during exercise.
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http://dx.doi.org/10.1152/japplphysiol.00370.2018DOI Listing
October 2018

Influence of dietary nitrate supplementation on local sweating and cutaneous vascular responses during exercise in a hot environment.

Eur J Appl Physiol 2018 Aug 15;118(8):1579-1588. Epub 2018 May 15.

Laboratory for Applied Human Physiology, Graduate School of Human Development and Environment, Kobe University, 3-11 Tsurukabuto, Nada-ku, Kobe, 657-8501, Japan.

Purpose: We investigated the influence of inorganic nitrate ([Formula: see text]) supplementation on local sweating and cutaneous vascular responses during exercise in hot conditions.

Method: Eight healthy, young subjects were assigned in a randomized, double-blind, crossover design to receive [Formula: see text]-rich beetroot (BR) juice (140 mL/day, containing ~ 8 mmol of [Formula: see text]) and [Formula: see text]-depleted placebo (PL) juice (140 mL/day, containing ~ 0.003 mmol of [Formula: see text]) for 3 days. On day 3 of supplementation, subjects cycled at an intensity corresponding to 55% of [Formula: see text]O for 30 min in hot conditions (30 °C, 50% relative humidity). Chest and forearm sweat rate (SR) and skin blood flow (SkBF), were measured continuously. Cutaneous vascular conductance (CVC) was calculated by SkBF/mean arterial pressure (MAP).

Results: Prior to exercise, plasma [Formula: see text] (21 ± 6 and 581 ± 161 µM) and nitrite ([Formula: see text], 87 ± 28 and 336 ± 156 nM) concentrations were higher after BR compared to PL supplementation (P ≤ 0.011, n = 6). Oesophageal, mean skin, and mean body temperatures during exercise were not different between conditions. In addition, BR supplementation did not affect SR, SkBF, and CVC during exercise. A lower MAP was found after 30 min of exercise following BR supplementation (112 ± 6 and 103 ± 6 mmHg for PL and BR, respectively, P = 0.021).

Conclusion: These results suggest that inorganic [Formula: see text] supplementation, which increases the potential for O-independent NO production, does not affect local sweating and cutaneous vascular responses, but attenuates blood pressure in young healthy subjects exercising in a hot environment.
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http://dx.doi.org/10.1007/s00421-018-3889-9DOI Listing
August 2018

The effects of exercise and passive heating on the sweat glands ion reabsorption rates.

Physiol Rep 2018 03;6(5)

Laboratory for Applied Human Physiology, Graduate School of Human Development and Environment, Kobe University, Kobe, Japan.

The sweat glands maximum ion reabsorption rates were investigated (n = 12, 21.7 ± 3.0 years, 59.4 ± 9.8 kg, 166.9 ± 10.4 cm and 47.1 ± 7.5 mL/kg/min) during two separate endogenous protocols; cycling at 30% (LEX) and 60% VO (MEX) and one exogenous trial; passive heating (PH) (43°C water lower leg immersion) in 27°C, 50%RH. Oesophageal temperature (T ), skin temperature (T ), and forearm, chest and lower back sweat rate (SR) and galvanic skin conductance (GSC) were measured. Salivary aldosterone was measured pre-and postheating (n = 3). Using the ∆SR threshold for an increasing ∆GSC to identify maximum sweat ion reabsorption rate revealed higher reabsorption rates during MEX compared to PH (mean of all regions: 0.63 ± 0.28 vs. 0.44 ± 0.3 mg/cm /min, P < 0.05). It was not possible to identify the ion reabsorption rate during LEX for some participants. T and mean T were different between conditions but mean body temperature (T ) and local T (forearm, chest and back) were similar (P > 0.05). Aldosterone increased more during MEX (72.8 ± 36.6 pg/mL) compared to PH (39.2 ± 17.5 pg/mL) and LEX (1.8 ± 9.7 pg/mL). The back had a higher threshold than the forearm (P < 0.05) but it was similar to the chest (P > 0.05) (mean of all conditions; 0.64 ± 0.33, 0.42 ± 0.25, 0.54 ± 0.3 mg/cm /min, respectively). Although the differences between conditions may be influenced by thermal or nonthermal mechanism, our results indicate a possibility that the sweat glands maximum ion reabsorption rates may be different between exercise and passive heating without mediating skin regional differences.
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http://dx.doi.org/10.14814/phy2.13619DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5828933PMC
March 2018

Do nitric oxide synthase and cyclooxygenase contribute to sweating response during passive heating in endurance-trained athletes?

Physiol Rep 2017 Sep;5(17)

Laboratory for Applied Human Physiology Graduate School of Human Development and Environment Kobe University, Kobe, Japan.

The aim of our study was to determine if habitual endurance training can influence the relative contribution of nitric oxide synthase (NOS) and cyclooxygenase (COX) in the regulation of sweating during a passive heat stress in young adults. Ten trained athletes and nine untrained counterparts were passively heated until oral temperature (as estimated by sublingual temperature, T) increased by 1.5°C above baseline resting. Forearm sweat rate (ventilated capsule) was measured at three skin sites continuously perfused with either lactated Ringer's solution (Control), 10 mmol/L -nitro--arginine methyl ester (-NAME, non-selective NOS inhibitor), or 10 mmol/L ketorolac (Ketorolac, non-selective COX inhibitor) via intradermal microdialysis. Sweat rate was averaged for each 0.3°C increase in T Sweat rate at the -NAME site was lower than Control following a 0.9 and 1.2°C increase in T in both groups (all ≤0.05). Relative to the Control site, NOS-inhibition reduced sweating similarly between the groups (=0.51). Sweat rate at the Ketorolac site was not different from the Control at any levels of T in both groups (>0.05). Nevertheless, a greater sweat rate was measured at the end of heating in the trained as compared to the untrained individuals (≤0.05). We show that NOS contributes similarly to sweating in both trained and untrained individuals during a passive heat stress. Further, no effect of COX on sweating was measured for either group. The greater sweat production observed in endurance-trained athletes is likely mediated by factors other than NOS- and COX-dependent mechanisms.
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http://dx.doi.org/10.14814/phy2.13403DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5599863PMC
September 2017

The effect of dietary nitrate supplementation on the spatial heterogeneity of quadriceps deoxygenation during heavy-intensity cycling.

Physiol Rep 2017 Jul;5(14)

Applied Physiology Laboratory, Kobe Design University, Kobe, Hyogo, Japan

This study investigated the influence of dietary inorganic nitrate (NO) supplementation on pulmonary O uptake (V˙O) and muscle deoxyhemoglobin/myoglobin (i.e. deoxy [Hb + Mb]) kinetics during submaximal cycling exercise. In a randomized, placebo-controlled, cross-over study, eight healthy and physically active male subjects completed two step cycle tests at a work rate equivalent to 50% of the difference between the gas exchange threshold and peak V˙O over separate 4-day supplementation periods with NO-rich (BR; providing 8.4 mmol NO∙day) and NO-depleted (placebo; PLA) beetroot juice. Pulmonary V˙O was measured breath-by-breath and time-resolved near-infrared spectroscopy was utilized to quantify absolute deoxy [Hb + Mb] and total [Hb + Mb] within the , , and There were no significant differences (>0.05) in the primary deoxy [Hb + Mb] mean response time or amplitude between the PLA and BR trials at each muscle site. BR significantly increased the mean (three-site) end-exercise deoxy [Hb + Mb] (PLA: 91 ± 9 vs. BR: 95 ± 12 mol/L, <0.05), with a tendency to increase the mean (three-site) area under the curve for total [Hb + Mb] responses (PLA: 3650 ± 1188 vs. BR: 4467 ± 1315 mol/L sec, =0.08). The V˙O slow component reduction after BR supplementation (PLA: 0.27 ± 0.07 vs. BR: 0.23 ± 0.08 L min, =0.07) correlated inversely with the mean increases in deoxy [Hb + Mb] and total [Hb + Mb] across the three muscle regions ( = 0.62 and 0.66, <0.05). Dietary NO supplementation increased O diffusive conductance across locomotor muscles in association with improved V˙O dynamics during heavy-intensity cycling transitions.
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http://dx.doi.org/10.14814/phy2.13340DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5532482PMC
July 2017

Evidence for β-adrenergic modulation of sweating during incremental exercise in habitually trained males.

J Appl Physiol (1985) 2017 Jul 4;123(1):182-189. Epub 2017 May 4.

Laboratory for Applied Human Physiology, Graduate School of Human Development and Environment, Kobe University, Kobe, Japan.

The aim of the present study was to determine the β-adrenergic contribution to sweating during incremental exercise in habitually trained males. Nine habitually trained and 11 untrained males performed incremental cycling until exhaustion (20 W/min). Bilateral forearm sweat rates (ventilated capsule) were measured at two skin sites that were transdermally administered via iontophoresis with either 1% propranolol (Propranolol, a nonselective β-adrenergic receptor antagonist) or saline (Control). The sweat rate was evaluated as a function of both relative (percentage of maximum workload) and absolute exercise intensities. The sweat rate at the Propranolol site was lower than the control during exercise at 80 (0.57 ± 0.21 and 0.45 ± 0.19 mg·cm·min for Control and Propranolol, respectively) and 90% (0.74 ± 0.22 and 0.65 ± 0.17 mg·cm·min, respectively) of maximum workload in trained males (all < 0.05). By contrast, no between-site differences in sweat rates were observed in untrained counterparts (all > 0.05). At the same absolute intensity, higher sweat rates on the control site were observed in trained males relative to the untrained during exercise at 160 (0.23 ± 0.20 and 0.04 ± 0.05 mg·cm·min for trained and untrained, respectively) and 180 W (0.40 ± 0.20 and 0.13 ± 0.13 mg·cm·min, respectively) (all < 0.05), whereas this between-group difference was not observed at the Propranolol site (all > 0.05). We show that the β-adrenergic mechanism does modulate sweating during exercise at a submaximal high relative intensity in habitually trained males. The β-adrenergic mechanism may in part contribute to the greater sweat production in habitually trained males than in untrained counterparts during exercise. We demonstrated for the first time that the β-adrenergic mechanism does modulate sweating (i.e., β-adrenergic sweating) during exercise using a localized β-adrenoceptor blockade in humans in vivo. β-Adrenergic sweating was evident in habitually trained individuals during exercise at a submaximal high relative intensity (80-90% maximal work). This observation advances our understanding of human thermoregulation during exercise and of the mechanism that underlies sweat gland adaptation to habitual exercise training.
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http://dx.doi.org/10.1152/japplphysiol.00220.2017DOI Listing
July 2017
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