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Hypoxia during supramaximal exercise reduces aerobic metabolism with a compensatory increase in anaerobic metabolism without affecting exercise performance. A similar response is elicited by preexercise voluntary hypocapnic hyperventilation, but it remains unclear whether hypocapnic hyperventilation and hypoxia additively reduce aerobic metabolism and increase anaerobic metabolism during supramaximal exercise. To address that issue, 12 healthy subjects (8 males and 4 females) performed the 30-second Wingate anaerobic test (WAnT) after (1) spontaneous breathing in normoxia (control, ∼21% fraction of inspired O2 [FiO2]), (2) voluntary hypocapnic hyperventilation in normoxia (hypocapnia, ∼21% FiO2), (3) spontaneous breathing in hypoxia (hypoxia, ∼11% FiO2), or (4) voluntary hypocapnic hyperventilation in hypoxia (combined, ∼11% FiO2). Mean power output during the 30-second WAnT was similar among the control (561 [133] W), hypocapnia (563 [140] W), hypoxia (558 [131] W), and combined (560 [133] W) trials (P = .778). Oxygen uptake during the 30-second WAnT was lower in the hypocapnia (1523 [318] mL/min), hypoxia (1567 [300] mL/min), and combined (1203 [318] mL/min) trials than in the control (1935 [250] mL/min) trial, and the uptake in the combined trial was lower than in the hypocapnia or hypoxia trial (all P P

When one is exposed to a stressful situation in their daily life, a common response is hyperventilation. Although the physiological significance of stress-induced hyperventilation remains uncertain, this response may blunt perception of the stress-inducing stimulus. This study examined the effects of voluntary hyperventilation and resultant hypocapnia on the local skin thermal detection threshold in normothermic resting humans. Local skin thermal detection thresholds were measured in 15 young adults (three females) under three breathing conditions: 1) spontaneous breathing (Control trial), 2) voluntary hypocapnic hyperventilation (HH trial), and 3) voluntary normocapnic hyperventilation (NH trial). Local skin thermal detection thresholds were measured using thermostimulators containing a Peltier element that were attached to the forearm and forehead. The temperature of the probe was initially equilibrated to the skin temperature, then gradually increased or decreased at a constant rate (±0.1 °C/s) until the participants felt warmth or coolness. The difference between the initial skin temperature and the local skin temperature at which the participant noticed warmth/coolness was assessed as an index of the local skin warm/cool detection threshold. Local detection of warm and cool stimuli did not differ between the Control and NH trials, but it was blunted in the HH trial as compared with the Control and NH trials, except for detection of warm stimuli on the forearm. These findings suggest that hyperventilation-induced hypocapnia, not hyperventilation per se, attenuates local skin thermal perception, though changes in responses to warm stimuli may not be clearly perceived at some skin areas (e.g., forearm).

Isomaltulose is a low glycemic and insulinaemic carbohydrate increasingly used as an alternative sweetener in commercial beverages. While isomaltulose beverages can improve hydration status compared to sucrose-based beverages, it remains unclear if ingestion of an isomaltulose beverage prior to exercise in the heat may improve plasma volume (PV) and thermoregulatory responses.Twelve endurance-trained men consumed a 1L carbohydrate beverage containing either 6.5%-sucrose (SUC) or 6.5%-isomaltulose (ISO) 60 min prior to 5 successive, 15-min bouts of moderate-intensity (60% of their pre-determined maximum oxygen uptake) in the heat (32 °C, 50% relative humidity), each separated by a 5 min rest. A 6th bout was performed, wherein the participant adjusted running speed to maximize distance covered within the 15-min period. The change (Δ) in PV, heart rate (HR), body core (rectal and gastrointestinal) and skin temperatures, and whole-body sweat loss were assessed during each exercise bout.Ingestion of ISO induced a higher ΔPV at 4th bout only (P 0.001) and lower HR (P = 0.032, main effect of beverage) during exercise compared to those of SUC. Body core and skin temperatures and whole-body sweat loss did not differ between conditions (all P ≥ 0.192, interaction effect). Running distance covered in final exercise bout tended to increase (~ 5%) in ISO versus SUC (P = 0.057, d = 0.64).Relative to a sucrose-based beverage, ISO ingestion prior to exercise in the heat reduced cardiovascular strain by preserving PV and attenuating HR, albeit with no corresponding benefit on thermoregulatory function. The former response may facilitate improvements in exercise performance.

Purpose Women remain underrepresented in the exercise thermoregulation literature despite their participation in leisure-time and occupational physical activity in heat-stressful environments continuing to increase. Here, we determined the relative contribution of the primary ovarian hormones (estrogen [E2] and progesterone [P4]) alongside other morphological (e.g., body mass), physiological (e.g., sweat rates), functional (e.g., aerobic fitness) and environmental (e.g., vapor pressure) factors in explaining the individual variation in core temperature responses for trained women working at very high metabolic rates, specifically peak core temperature (Tpeak) and work output (mean power output). Methods Thirty-six trained women (32 ± 9 year, 53 ± 9 ml·kg−1·min−1), distinguished by intra-participant (early follicular and mid-luteal phases) or inter-participant (ovulatory vs. anovulatory vs. oral contraceptive pill user) differences in their endogenous E2 and P4 concentrations, completed a self-paced 30-min cycling work trial in warm–dry (2.2 ± 0.2 kPa, 34.1 ± 0.2 °C, 41.4 ± 3.4% RH) and/or warm–humid (3.4 ± 0.1 kPa, 30.2 ± 1.2 °C, 79.8 ± 3.7% RH) conditions that yielded 115 separate trials. Stepwise linear regression was used to explain the variance of the dependent variables. Results Models were able to account for 60% of the variance in Tpeak ($$\overline{R }$$ R ¯ 2: 41% core temperature at the start of work trial, $$\overline{R }$$ R ¯ 2: 15% power output, $$\overline{R }$$ R ¯ 2: 4% [E2]) and 44% of the variance in mean power output ($$\overline{R }$$ R ¯ 2: 35% peak aerobic power, $$\overline{R }$$ R ¯ 2: 9% perceived exertion). Conclusion E2 contributes a small amount toward the core temperature response in trained women, whereby starting core temperature and peak aerobic power explain the greatest variance in Tpeak and work output, respectively.

Background: The protein klotho protects cellular function during various physiological stressors, such as exercise, however it is unknown how the age-related decline in klotho production affects responses during exercise, especially in the heat. Objective: Our objective was to determine the effect of exercise in temperate and hot environmental conditions on serum klotho concentrations in young and older men. Methods: 12 young (mean ± SD: 22 ± 3 years) and 12 older (59 ± 4 years) men performed 180 minutes of moderate-intensity treadmill walking (metabolic rate: 200 W/m2) in a temperate (wetbulb globe temperature [WBGT] 16°C, achieved with 21.9°C, 35% relative humidity [RH]) and hot (WBGT 32°C, achieved with 41.4°C, 35% RH) environment. Serum klotho was assessed before and after exercise, as well as 60-min post-exercise recovery in the respective environments. Results: Absolute klotho concentrations were greater in young versus older men during all measured time points in the temperate (p = 0.032), but not the hot condition (p = 0.064). In the hot condition, the change in serum klotho from baseline was significantly higher after exercise in the heat (mean ± SEM: +251 ± 73 pg/mL) than the temperate (+75 ± 57 pg/mL) environment in both groups (p = 0.026). However, this elevation was not maintained during recovery. Conclusion: We showed that prolonged exercise in a temperate environment does not elicit a klotho response in either group. In contrast, despite lower resting klotho levels, the older men showed a similar exercise-induced increase in serum klotho response as their younger counterparts.

Hyperthermia stimulates ventilation (hyperthermia-induced hyperventilation). In exercising humans, once the core temperature reaches ~37°C, minute ventilation (VE) increases linearly with rising core temperature, and the slope of the relation between VE and core temperature reflects the sensitivity of the response. We previously reported that sodium bicarbonate ingestion reduces VE during prolonged exercise in the heat without affecting the sensitivity of hyperthermia-induced hyperventilation. Here, we hypothesized that reductions in VE associated with sodium bicarbonate ingestion reflect elevation of the core temperature threshold for hyperthermia-induced hyperventilation. Thirteen healthy young males ingested sodium bicarbonate (0.3 g/kg body weight) (NaHCO3 trial) or sodium chloride (0.208 g/kg body weight) (NaCl trial), after which they performed a cycle exercise at 50% of peak oxygen uptake in the heat (35°C and 50% relative humidity) following a pre-cooling. The pre-cooling enabled detection of an esophageal temperature ( Tes: an index of core temperature) threshold for hyperthermia-induced hyperventilation. The Tes thresholds for increases in VE were similar between the two trials (P = 0.514). The slopes relating VE to Tes also did not differ between trials (P = 0.131). However, VE was lower in the NaHCO3 than the NaCl trial in the range of Tes = 36.8-38.4°C (P < 0.007, main effect of trial). These results suggest that sodium bicarbonate ingestion does not alter the core temperature threshold or sensitivity of hyperthermia-induced hyperventilation during prolonged exercise in the heat; instead, it downshifts the exercise hyperpnea.

What is the central question of this study? Do transmembrane member 16A (TMEM16A) blockers modulate the activation of heat loss responses of sweating and cutaneous vasodilatation? What are the main finding and its importance? Relative to the vehicle control site, TMEM16A blockers T16Ainh-A01 and benzbromarone had no effect on sweat rate or cutaneous vascular conductance during whole-body heating inducing a 1.1 ± 0.1°C increase in core temperature above baseline resting levels. These results suggest that TMEM16A blockers T16Ainh-A01 and benzbromarone do not modulate the regulation of sweating and cutaneous vasodilatation during whole-body heat stress.Animal and in vitro studies suggest that transmembrane member 16A (TMEM16A), a Ca

What is the central question of this study? Does acute intradermal administration of the antioxidant ascorbate augment local forearm cutaneous vasodilatation and sweating via nitric oxide synthase (NOS)-dependent mechanisms during exercise-heat stress in older adults with uncomplicated controlled hypertension? What is the main finding and its importance? Relative to the control site, ascorbate had no effect on forearm cutaneous vascular conductance (CVC) and sweat rate, although CVC was reduced with NOS inhibition in older adults with hypertension. Acute local administration of ascorbate to forearm skin does not modulate heat loss responses during exercise-heat stress in older adults with hypertension.Nitric oxide synthase (NOS) contributes to the heat loss responses of cutaneous vasodilatation and sweating during exercise. However, the contribution of NOS may be attenuated in individuals with uncomplicated, controlled hypertension due to elevated oxidative stress, which can reduce NO bioavailability. We evaluated the hypothesis that the acute local intradermal administration of the antioxidant ascorbate would enhance cutaneous vasodilatation and sweating via NOS-dependent mechanisms during an exercise-heat stress in adults with hypertension. Habitually active adults who were normotensive (n = 14, 7 females, 62 ± 4 years) or had uncomplicated, controlled hypertension (n = 13, 6 females, 62 ± 5 years) performed 30 min of moderate-intensity (50% of their pre-determined peak oxygen uptake) semi-recumbent cycling in the heat (35°C, 20% relative humidity). Cutaneous vascular conductance (CVC) and sweat rate were assessed at four forearm skin sites continuously perfused with (1) lactated Ringer solution (Control), (2) 10 mM antioxidant ascorbate, (3) 10 mM N

The objective of this study was 1) to examine pooled effects of hypertension on nitric oxide (NO)-dependent vasodilation during local heating across multiple nonglabrous skin regions, and 2) explore regional differences. Responses were compared between 14 participants with uncomplicated hypertension controlled with medication (7 females, 61 ± 6 yr) and 14 age-matched nonhypertensive controls (6 females; 60 ± 5 yr). Cutaneous vascular conductance, normalized to maximum vasodilation (%CVCmax), was assessed at the upper chest, abdomen, dorsal forearm, thigh, and lateral calf during local heating. Across all regions, local skin temperatures were simultaneously increased from 33°C to 42°C (1°C·10 s−1) and held until a stable heating plateau was achieved (∼40 min), followed by continuous infusion of 20 mM of NG-nitro-l-arginine methyl ester (l-NAME; ∼40 min) at all sites until a stable l-NAME plateau was achieved. The difference between heating and l-NAME plateaus was defined as the NO-contribution. Statistical equivalence for each heating phase was determined based on equivalence bounds of ±10%CVCmax for between-group differences. Pooled (all-regions) %CVCmax responses were equivalent for baseline (two one-sided t tests; P < 0.001), heating plateau ( P = 0.002), l-NAME plateau ( P = 0.028), and NO-contribution ( P = 0.003). For individual regions, responses were equivalent at baseline for the abdomen, thigh, and calf, the heating plateau for the thigh, and the l-NAME plateau for the calf (all P < 0.05). Conversely, the calf heating plateau was lower in the hypertension group ( t test; P < 0.05). Local heat-induced cutaneous vasodilation was statistically equivalent between individuals with uncomplicated, controlled hypertension, and nonhypertensive age-matched adults when pooled across multiple skin sites. Conversely, individual between-region comparisons were generally too variable to permit definitive conclusions.

Transient receptor potential ankyrin 1 (TRPA1) channel activation induces cutaneous vasodilation in humans in vivo. However, the mechanisms underlying this response remains equivocal. We hypothesized that nitric oxide synthase (NOS) and Ca2+ activated K+ (KCa) channels contribute to the TRPA1 channel-induced cutaneous vasodilation with no involvement of cyclooxygenase (COX). Cutaneous vascular conductance (CVC) in 9 healthy young adults was assessed at 4 dorsal forearm skin sites treated by intradermal microdialysis with (1) 1.985% dimethyl sulfoxide + 0.015% lactated Ringer solution with propylene glycol (vehicle control), (2) 10 mM l-NAME, a nonselective NOS inhibitor, (3) 10 mM ketorolac, a nonselective COX inhibitor, or (4) 50 mM tetraethylammonium, a nonselective KCa channel blocker. Cinnamaldehyde, a TRPA1 channel activator, was administered to each skin site in a dose-dependent manner (2.9%, 8.8%, 26%, and 80%, each lasting ≥30 minutes). Administration of ≥8.8% cinnamaldehyde increased CVC from baseline at the vehicle control site by as much as 27.4% (95% confidence interval of 5.3; P0.001). NOS inhibitor attenuated the cinnamaldehyde-induced increases in CVC at the 8.8%, 26%, and 80% concentrations relative to the vehicle control site (all P ≤ 0.05). In contrast, both the COX inhibitor and KCa channel blockers did not attenuate the cinnamaldehyde induced-increases in CVC relative to the vehicle control site for all concentrations (all P ≥ 0.130). We conclude that in human skin in vivo, NOS plays a role in modulating the regulation of cutaneous vasodilation in response to TRPA1 channel activation with no detectable contributions of COX and KCa channels.

Hyperthermia causes hyperventilation and concomitant hypocapnia and cerebral hypoperfusion. The cerebral hypoperfusion may underlie central fatigue. We demonstrate that sodium bicarbonate ingestion reduces heat-induced hyperventilation and attenuates hypocapnia-related cerebral hypoperfusion during prolonged exercise in the heat. In addition, we show that sodium bicarbonate ingestion reduces ratings of perceived exertion during the exercise. This study provides new insight into the development of an effective strategy for preventing central fatigue during exercise in the heat.

Cutaneous thermal hyperemia during local skin heating to 39°C, which is highly dependent on nitric oxide synthase (NOS), is frequently used to assess endothelium-dependent cutaneous vasodilation. We showed that Na+-K+-ATPase mediates the regulation of cutaneous thermal hyperemia partly via NOS-dependent mechanisms although a component of the Na+-K+-ATPase modulation of cutaneous thermal hyperemia is NOS independent. Thus, as with NOS, Na+-K+-ATPase may be important in the regulation of cutaneous endothelial vascular function.

Purpose: We investigated whether varying the number of repetitions of high-intensity exercise during work-matched warm-ups modulates physiological responses (heart rate, metabolic responses, and core temperature), perceptions (ratings of perceived exertion, effort of breathing), readiness for exercise, and short-term exercise performance. Methods: Ten physically active young males performed a 30-s Wingate anaerobic test (WAnT) following a warm-up consisting of submaximal constant-workload cycling at 60% maximal oxygen uptake with no high-intensity cycling (constant-workload warm-up) or with 1, 4, or 7 repetitions of 10 s of high-intensity cycling at 110% maximal oxygen uptake. All warm-ups were matched for duration (10 min) and total work. Results: Warm-ups with seven repetitions of high-intensity cycling resulted in higher ratings of perceived whole-body exertion and effort of breathing than the constant-workload warm-up. Warm-up with four repetitions of high-intensity cycling produced greater readiness for a 30-s WAnT (7.33 ± 0.73 AU) than the constant-workload warm-up (6.33 ± 0.98 AU) (P = .022). Physiological responses did not differ among the four warm-up conditions, though peak heart rate was slightly higher (~5 beats/min) during warm-up with four or seven repetitions of high-intensity cycling than during the constant-workload warm-up. Peak, mean, and minimum power output during the 30-s WAnT did not differ among the four warm-up conditions. Conclusions: These results suggest that the effects of warm-ups with intermittent high-intensity exercise on physiological responses and short-term high-intensity exercise performance do not greatly differ from a warm-up with a work-matched submaximal constant-workload. However, they appear to modulate perceptions and readiness as a function of the number of repetitions of the high-intensity exercise.

Whether whole body heat loss and thermoregulatory function (local sweat rate and skin blood flow) are different between summer and autumn and between autumn and winter seasons during exercise with different air flow in humid heat remain unknown. We therefore tested the hypotheses that whole body sweat rate (WBSR), evaporated sweat rate, and thermoregulatory function during cycling exercise in autumn would be higher than in winter but would be lower than in summer under hot-humid environment (32 C, 75% RH). We also tested the hypothesis that the increase of air velocity would enhance evaporated sweat rate and sweating efficiency across winter, summer, and autumn seasons. Eight males cycled for 1 h at 40% V̇o2max in winter, summer, and autumn seasons. Using an electric fan, air velocity increased from 0.2 m/s to 1.1 m/s during the final 20 min of cycling. The autumn season resulted in a lower WBSR, unevaporated sweat rate, and a higher sweating efficiency compared with summer (all P ≤ 0.05) but WBSR and unevaporated sweat rate in autumn were higher than in winter and thus sweating efficiency was lower when compared with winter only at the air velocity of 0.2 m/s (All P ≤ 0.05). Furthermore, evaporated sweat rate and core temperature ( Tcore) were not different among winter, summer, and autumn seasons (All P > 0.19). In conclusion, changes in WBSR across different seasons do not alter Tcore during exercise in a hot humid environment. Furthermore, increasing air velocity enhances evaporated sweat rate and sweating efficiency across all seasons.

To investigate the nitric oxide synthase (NOS) and reactive oxygen species (ROS) contributions of the cutaneous vasodilator response to transient receptor potential ankyrin-1 channel (TRPA1) activation in young and older adults.In sixteen young (20 ± 2 years, 8 females) and sixteen older adults (61 ± 5 years, 8 females), cutaneous vascular conductance normalized to maximum vasodilation (%CVC%CVCThe NOS-dependent cutaneous vasodilator response to TRPA1 activation is maintained in older adults, with no detectable contribution of ascorbate-sensitive ROS in either age group.

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. 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. 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). 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)

The current study investigated whether ambient heat augments the inflammatory and postexercise hepcidin response in women and if menstrual phase and/or self-pacing modulate these physiological effects. Eight trained females (age: 37 ± 7 yr; V̇o2max: 46 ± 7 mL·kg−1·min−1; peak power output: 4.5 ± 0.8 W·kg−1) underwent 20 min of fixed-intensity cycling (100 W and 125 W) followed by a 30-min work trial (∼75% V̇o2max) in a moderate (MOD: 20 ± 1°C, 53 ± 8% relative humidity) and warm-humid (WARM: 32 ± 0°C, 75 ± 3% relative humidity) environment in both their early follicular (days 5 ± 2) and midluteal (days 21 ± 3) phases. Mean power output was 5 ± 4 W higher in MOD than in WARM ( P = 0.02) such that the difference in core temperature rise was limited between environments (−0.29 ± 0.18°C in MOD, P < 0.01). IL-6 and hepcidin both increased postexercise (198% and 38%, respectively); however, neither was affected by ambient temperature or menstrual phase (all P > 0.15). Multiple regression analysis demonstrated that the IL-6 response to exercise was explained by leukocyte and platelet count ( r2 = 0.72, P < 0.01), and the hepcidin response to exercise was explained by serum iron and ferritin ( r2 = 0.62, P < 0.01). During exercise, participants almost matched their fluid loss (0.48 ± 0.18 kg·h−1) with water intake (0.35 ± 0.15 L·h−1) such that changes in body mass (−0.3 ± 0.3%) and serum osmolality (0.5 ± 2.0 osmol·kgH2O−1) were minimal or negligible, indicating a behavioral fluid-regulatory response. These results indicate that trained, iron-sufficient women suffer no detriment to their iron regulation in response to exercise with acute ambient heat stress or between menstrual phases on account of a performance-physiological trade-off.

An animal study demonstrated that 6-(Methylsulfinyl)hexyl isothiocyanate (6-MSITC), a major bioactive compound in Japanese pungent spice wasabi, has an action of inhibiting the activation of calpain-1 (a protease). Increases in calpain activity can cause continual strength loss after eccentric exercise. It remains to be determined in humans whether 6-MSITC intake would modulate calpain and/or muscle damage responses after eccentric exercise. We performed a randomized, double-blind, crossover design study wherein eight healthy young males were randomly assigned to ingest 9 mg/day of 6-MSITC or placebo from 1 day before exercise to 4 days after exercise (30 maximal isokinetic eccentric contractions of the elbow flexors using an isokinetic dynamometer). Calpain-1 concentration, inflammatory and muscle damage markers (creatine kinase activity, urinary titin concentration, muscle strength, range of motion, muscle soreness and transverse relaxation time) were assessed. Plasma calpain-1 concentration after eccentric exercise was similar between the placebo- and 6-MSITC-treated conditions. All muscle damage and inflammatory markers were not affected by 6-MSITC relative to those in the placebo-treated condition. Our results suggest that 6-MSITC has no effect on plasma calpain-1 concentration and muscle damage and inflammatory markers measured after eccentric exercise.

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 ( protocol 1) and to cutaneous vasodilation during postocclusive reactive hyperemia and local thermal hyperemia ( protocol 2). Intradermal microdialysis was employed to locally deliver pharmacological agents to forearm skin sites, where cutaneous vascular conductance (CVC) and sweat rate were assessed. In protocol 1 (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 protocol 2 (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.

We aimed to evaluate whether changes in the noninvasively assessed urinary N-terminal fragment of titin (U-titin) concentration may be associated with those of serum creatine kinase (CK) activity, transverse relaxation time (T

Cao, Yinhang, Naoto Fujii, Tomomi Fujimoto, Yin-Feng Lai, Takeshi Ogawa, Tsutomu Hiroyama, Yasushi Enomoto, and Takeshi Nishiyasu. CO

Sugar-free carbonated water is consumed worldwide. The consumption of carbonated water is high in summer, when the heat loss responses of sweating and skin vasodilation are activated, and thermal perceptions (thermal sensation and comfort) and mood states are negatively modulated. However, whether ingesting carbonated water under ambient heat exposure modulates cerebral blood flow index, heat loss responses, thermal perceptions, and mood states remains to be determined. In this study, 17 healthy, habitually active, young adults (eight women) ingested 4 °C noncarbonated or carbonated water under 37 °C ambient heat-stressed resting conditions. Both drinks increased the middle cerebral artery mean blood velocity, an index of cerebral blood flow, and mean arterial pressure, with carbonated water exhibiting higher elevations than noncarbonated water (P0.05). However, the heart rate, sweat rate, and skin blood flow during and after drinking remained unchanged between the two conditions (P0.05). The thermal sensation and comfort after drinking remained unchanged between the two conditions (P0.05); but, a drink-induced reduction in sleepiness was higher, and drink-induced elevations in motivation and exhilaration were higher after ingesting carbonated water than those after ingesting noncarbonated water (P0.05). The analyses suggest that in humans under ambient heat-stressed resting conditions, ingestion of cold carbonated water increases the cerebral blood flow index, blood pressure, motivation, and exhilaration, whereas it decreases sleepiness relative to ingestion of noncarbonated cold water. However, ingestion of cold carbonated water fails to modulate thermoregulatory responses and thermal perception as opposed to noncarbonated cold water.