Interactive effects of exercise intensity and recovery posture on post-exercise hypotension.

Post-exercise reduction in blood pressure, termed post-exercise hypotension (PEH), is relevant for both acute and chronic health reasons and potentially for peripheral cardiovascular adaptations. We investigated the interactive effects of exercise intensity and recovery postures (seated, supine, and standing) on PEH. Thirteen normotensive men underwent a VO2max test on a cycle ergometer and 5 exhaustive constant load trials to determine critical power (CP) and the gas exchange threshold (GET). Subsequently, work-matched exercise trials were performed at two discrete exercise intensities (10% > CP and 10% < GET), with one hour of recovery in each of three postures. For both exercise intensities, standing posture resulted in a more substantial PEH (all P < 0.01). For both standing and seated recovery postures, the higher exercise intensity led to larger reductions in systolic, diastolic and mean arterial pressures (all P < 0.01), whereas in the supine recovery posture, the reduction in diastolic and mean arterial pressures was unaffected by prior exercise intensity (both P > 0.05). PEH is more pronounced during recovery from exercise performed above critical power versus below GET. However, the effect of exercise intensity on PEH is largely abolished when recovery is performed in the supine posture.

GH and IGF-1 in skin interstitial fluid and blood are associated with heat loss responses in exercising young adults.

PURPOSE: Sweat glands and cutaneous vessels possess growth hormone (GH) and insulin-like growth factor 1 (IGF-1) receptors. Here, we assessed if exercise increases GH and IGF-1 in skin interstitial fluid, and whether baseline and exercise-induced increases in GH and IGF-1 concentrations in skin interstitial fluid/blood are associated with heat loss responses of sweating and cutaneous vasodilation. METHODS: Sixteen young adults (7 women) performed a 50-min moderate-intensity exercise bout (50% VO2peak) during which skin dialysate and blood samples were collected. In a sub-study (n = 7, 4 women), we administered varying concentrations of GH (0.025-4000 ng/mL) and IGF-1 (0.000256-100 µg/mL) into skin interstitial fluid via intradermal microdialysis. Sweat rate (ventilated capsule) and cutaneous vascular conductance (CVC) were measured continuously for both studies. RESULTS: Exercise increased sweating and CVC (both P < 0.001), paralleled by increases of serum GH and skin dialysate GH and IGF-1 (all P ≤ 0.041) without changes in serum IGF-1. Sweating was positively correlated with baseline dialysate and serum GH levels, as well as exercise-induced increases in serum GH and IGF-1 (all P ≤ 0.044). Increases in CVC were not correlated with any GH and IGF-1 variables. Exogenous administration of GH and IGF-1 did not modulate resting sweat rate and CVC. CONCLUSION: (1) Exercise increases GH and IGF-1 levels in the skin interstitial fluid, (2) exercise-induced sweating is associated with baseline GH in skin interstitial fluid and blood, as well as exercise-induced increases in blood GH and IGF-1, and (3) cutaneous vasodilation during exercise is not associated with GH and IGF-1 in skin interstitial fluid and blood.

Comparing thermoregulatory responses between short and long moderate intensity intermittent exercise protocols with the same duty cycle.

To date, the thermoregulatory response between continuous and intermittent exercises has been investigated whilst limited studies are available to examine the thermoregulatory responses between different modes of intermittent exercises. We sought to determine the effect of two patterns of short duration intermittent exercises (180:180 (3-min) and 30:30 s (30-s) work: rest) on thermoregulatory responses in a temperate environment (25 °C, 50% RH, vapor pressure: 1.6 kPa) with low airflow (0.2 m/s). Twelve male participants (Age:24.0(5.0) year; VO2max: 53(8) mL.kg-1.min-1; BSA:1.7(0.1) m2) cycled at 50% VO2max for 60 min in 3-min and 30-s intervals to result in the same 30-min net exercise duration. Core and skin temperatures, the percent increase of skin blood flow (forearm and chest) from baseline and local sweat rate (forearm and chest) were not different between 3-min and 30-s (all P > 0.35) from the onset of exercise to the end of the exercise. Similarly, the mean body temperature onsets of skin blood flow (forearm and chest) and local sweat rates (forearm and chest) were not different between different mode of intermittent exercises (all P > 0.1). Furthermore, thermal sensitivities of skin blood flow (forearm and chest) and local sweat rate (forearm and chest) with increasing mean body temperature were not different between different mode of intermittent exercises (all P > 0.1). We conclude that intermittent exercises with different work periods at moderate exercise intensity did not alter core temperature and thermoeffector responses in a temperate environment. (241/250).

The effects of high-intensity exercise training and detraining with and without active recovery on postexercise hypotension in young men.

Whether high-intensity exercise training and detraining combined with skeletal muscle pump (MP) could alter the magnitude of postexercise hypotension has not been investigated. We therefore sought to determine whether the combination of MP (unloaded back-pedaling) with 4 weeks of high-intensity exercise training and detraining could alter the magnitude of postexercise hypotension. Fourteen healthy men underwent 4 weeks of high-intensity exercise training (5 consecutive days per week for 15 min per session at 40% of the difference between the gas exchange threshold and maximal oxygen uptake [i.e., Δ40%]) followed by detraining for 4 weeks. Assessments were conducted at Pre-training (Pre), Post-training (Post) and after Detraining with (MP) and without MP (Con). The exercise test in the Pre, Post and the Detraining consisted of 15 min exercise at Δ40% followed by 1 h of recovery. At all time-points, the postexercise reduction in mean arterial pressure (MAP) was reduced in MP compared to Con (all p < 0.01). Four weeks of high-intensity exercise training resulted in a reduction in the magnitude of postexercise hypotension (i.e., the change in MAP from baseline was mitigated) across both trials (All p < 0.01) when compared to Pre and Detraining. Following Detraining, the reduction of MAP from baseline was reduced compared to Pre, but was not different from Post. We conclude that high-intensity exercise training combined with skeletal MP reduces the magnitude of postexercise hypotension, and this effect is partially retained for 4 weeks following the complete cessation of high-intensity exercise training.

Critical power is a key threshold determining the magnitude of post-exercise hypotension in non-hypertensive young males.

The effect of different exercise intensities on the magnitude of post-exercise hypotension has not been rigorously clarified with respect to the metabolic thresholds that partition discrete exercise intensity domains (i.e., critical power and the gas exchange threshold (GET)). We hypothesized that the magnitude of post-exercise hypotension would be greater following isocaloric exercise performed above versus below critical power. Twelve non-hypertensive men completed a ramp incremental exercise test to determine maximal oxygen uptake and the GET, followed by five exhaustive constant load trials to determine critical power and W' (work available above critical power). Subsequently, criterion trials were performed at four discrete intensities matched for total work performed (i.e., isocaloric) to determine the impact of exercise intensity on post-exercise hypotension: 10% above critical power (10% > CP), 10% below critical power (10% < CP), 10% above GET (10% > GET) and 10% below GET (10% < GET). The post-exercise decrease (i.e., the minimum post-exercise values) in mean arterial (10% > CP: -12.7 ± 8.3 vs. 10% < CP: v3.5 ± 2.9 mmHg), diastolic (10% > CP: -9.6 ± 9.8 vs. 10% < CP: -1.4 ± 5.0 mmHg) and systolic (10% > CP: -23.8 ± 7.0 vs. 10% < CP: -9.9 ± 4.3 mmHg) blood pressures were greater following exercise performed 10% > CP compared to all other trials (all P < 0.01). No effects of exercise intensity on the magnitude of post-exercise hypotension were observed during exercise performed below critical power (all P > 0.05). Critical power represents a threshold above which the magnitude of post-exercise hypotension is greatly augmented. NEW FINDINGS: What is the central questions of this study? What is the influence of exercise intensity on the magnitude of post-exercise hypotension with respect to metabolic thresholds? What is the main finding and its importance? The magnitude of post-exercise hypotension is greatly increased following exercise performed above critical power. However, below critical power, there was no clear effect of exercise intensity on the magnitude of post-exercise hypotension.

Galanin receptors modulate cutaneous vasodilation elicited by whole-body and local heating but not thermal sweating in young adults.

Galanin receptor subtypes GAL1, GAL2, and GAL3 are involved in several biological functions. We hypothesized that 1) GAL3 receptor activation contributes to sweating but limits cutaneous vasodilation induced by whole-body and local heating without a contribution of GAL2; and 2) GAL1 receptor activation attenuates both sweating and cutaneous vasodilation during whole-body heating. Young adults underwent whole-body (n = 12, 6 females) and local (n = 10, 4 females) heating. Forearm sweat rate (ventilated capsule) and cutaneous vascular conductance (CVC; ratio of laser-Doppler blood flow to mean arterial pressure) were assessed during whole-body heating (water-perfusion suit circulated with warm (35 °C) water), while CVC was also assessed by local forearm heating (from 33 °C to 39 °C and elevated to 42 °C thereafter; each level of heating maintained for ∼30 min). Sweat rate and CVC were evaluated at four intradermal microdialysis forearm sites treated with either 1) 5% dimethyl sulfoxide (control), 2) M40, a non-selective GAL1 and GAL2 receptor antagonist, 3) M871 to selectively antagonize GAL2 receptor, or 4) SNAP398299 to selectively antagonize GAL3 receptor. Sweating was not modulated by any GAL receptor antagonist (P > 0.169), whereas only M40 reduced CVC (P ≤ 0.003) relative to control during whole-body heating. Relative to control, SNAP398299 augmented the initial and sustained increase in CVC during local heating to 39 °C, and the transient increase at 42 °C (P ≤ 0.028). We confirmed that while none of the galanin receptors modulate sweating during whole-body heating, GAL1 receptors mediate cutaneous vasodilation. Further, GAL3 receptors blunt cutaneous vasodilation during local heating.

Serum, interstitial and sweat ATP in humans exposed to heat stress: Insights into roles of ATP in the heat loss responses.

Hyperthermia increases intravascular adenosine triphosphate (ATP) and is associated with greater hyperthermia-induced cutaneous vasodilation. Hyperthermia may also increase skin interstitial fluid ATP thereby activating cutaneous vascular smooth muscle cells and sweat glands. We evaluated the hypothesis that whole-body heating would increase skin interstitial fluid ATP, and this response would be associated with an increase in cutaneous vasodilation and sweating. Nineteen (8 females) young adults underwent whole-body heating using a water-perfusion suit to increase core temperature by ~1°C during which time cutaneous vascular conductance (CVC, ratio of laser-Doppler blood flow to mean arterial pressure) and sweat rate (ventilated capsule technique) were measured at four forearm skin sites to minimize between-site variations. Dialysate from the skin sites were collected via intradermal microdialysis. Heating increased serum ATP, CVC, and sweat rate (all p ≤ 0.031). However, heating did not modulate dialysate ATP (median, baseline vs. end-heating: 2.38 vs. 2.70 nmol/ml) (p = 0.068), though the effect size was moderate (Cohen's d = 0.566). While the heating-induced increase in CVC was not correlated with changes in serum ATP (r = 0.439, p = 0.060), we observed a negative correlation (rs = -0.555, p = 0.017) between dialysate ATP and CVC. We did not observe a significant correlation between the heating-induced sweating and serum, dialysate, or sweat ATP (rs = 0.091 to -0.322, all p ≥ 0.222). Altogether, we showed that passive heating increases ATP in blood and possibly skin interstitial fluid, with the latter potentially blunting cutaneous vasodilation. However, ATP does not appear to modulate sweating.

In vivo assessments of microneedle arrays and iontophoresis of pilocarpine in human palmar sweating.

Emotional stress-induced sweating in glabrous skin of the palm and sole, which can be excessive in some individuals (hyperhidrosis), can negatively impact quality of life. Understanding the mechanisms underlying this response can lead to potential treatments. Transdermal iontophoresis is a method to administer ionized sudorific agents to sweat glands within the dermis. However, due to the reduced permeability of pharmacological agents in thicker skin such as the palms, this technique has been shown to be less effective when applied in thicker skin. Thus, we assessed the effectiveness of pre-treating palmar skin with microneedles to create micropores on the stratum corneum of the palm to enhance the iontophoretic delivery of pilocarpine to modulate sweat production. On three separate sessions, we applied microneedles (0.78 cm2, 190 needles with a length of 875 µm) to palm and forearm skin sites. Upon removal of the microneedles, we assessed the number of perforations colored by gentian violet in the forearm only (Protocol 1, n = 20), skin barrier function indexed by transepidermal water loss (TEWL) (Protocol 2, n = 21), and sweating induced by the iontophoretic application of 1% pilocarpine (Protocol 3, n = 43). Briefly, we measured 1) ∼172 dyed spots on forearm skin, 2) an increase of ∼300% and âˆ¼ 900% in TEWL on palm and forearm skin, respectively; and 3) a 2-fold increase in sweating on the palm only following the application of the microneedles. Notably, the microneedle array failed to enhance pilocarpine delivery at either the palm or forearm skin sites. We showed the application of a microneedle array enhanced skin permeability and sweat production on the palm without a concomitant increase in pilocarpine delivery. Therefore, this methodology could be employed to advance our understanding of the causes and treatments of medical conditions such as hyperhidrosis.

Induction and decay of seasonal acclimatization on whole body heat loss responses during exercise in a hot humid environment with different air velocities.

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.

Do E2 and P4 contribute to the explained variance in core temperature response for trained women during exertional heat stress when metabolic rates are very high?

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 ([Formula: see text]2: 41% core temperature at the start of work trial, [Formula: see text]2: 15% power output, [Formula: see text]2: 4% [E2]) and 44% of the variance in mean power output ([Formula: see text]2: 35% peak aerobic power, [Formula: see text]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.

TMEM16A blockers T16Ainh-A01 and benzbromarone do not modulate the regulation of sweating and cutaneous vasodilatation in humans in vivo.

NEW FINDINGS: 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. ABSTRACT: Animal and in vitro studies suggest that transmembrane member 16A (TMEM16A), a Ca2+ -activated Cl- channel, contributes to regulating eccrine sweating. However, direct evidence supporting this possibility in humans is lacking. We assessed the hypothesis that TMEM16A blockers attenuate sweating during whole-body heating in humans. Additionally, we assessed the associated changes in the heat loss response of cutaneous vasodilatation to determine if a functional role of TMEM16A may exist. Twelve young (24 ± 2 years) adults (six females) underwent whole-body heating using a water-perfused suit to raise core temperature 1.1 ± 0.1°C above baseline. Sweat rate and cutaneous vascular conductance (normalized to maximal conductance via administration of sodium nitroprusside) were evaluated continuously at four forearm skin sites treated continuously by intradermal microdialysis with (1) lactated Ringer's solution (control), (2) 5% dimethyl sulfoxide (DMSO) serving as a vehicle control, or (3) TMEM16A blockers 1 mM T16Ainh-A01 or 2 mM benzbromarone dissolved in 5% DMSO solution. All drugs were administered continuously via intradermal microdialysis. Whole-body heating increased core temperature progressively and this was paralleled by an increase in sweat rate and cutaneous vascular conductance at all skin sites. However, sweat rate (all P > 0.318) and cutaneous vascular conductance (all P ≥ 0.073) did not differ between the vehicle control site relative to the TMEM16A blocker-treated sites. Collectively, our findings indicate that TMEM16A blockers T16Ainh-A01 and benzbromarone do not modulate the regulation of sweating and cutaneous vasodilatation during whole-body heating in young adults in vivo.

Effects of tetraethylammonium-sensitive K+ channel blockade on cholinergic and thermal sweating in endurance-trained and untrained men.

NEW FINDINGS: What is the central question of this study? Does inhibition of K+ channels modulate the exercise-training-induced augmentation in cholinergic and thermal sweating? What is the main finding and its importance? Iontophoretic administration of tetraethylammonium, a K+ channel blocker, blunted sweating induced by a low dose (0.001%) of the cholinergic agent pilocarpine, but not heat-induced sweating. However, no differences in the cholinergic sweating were observed between young endurance-trained and untrained men. Thus, while K+ channels play a role in the regulation of eccrine sweating, they do not contribute to the increase in sweating commonly observed in endurance-trained adults. Our findings provide important new insights into the mechanisms underlying the regulation of sweating by endurance conditioning. ABSTRACT: We evaluated the hypothesis that the activation of K+ channels mediates the exercise-training-induced augmentation of cholinergic and thermal sweating. On separate days, 11 endurance-trained and 10 untrained men participated in two experimental protocols. Prior to each protocol, we administered 2% tetraethylammonium (TEA, K+ channels blocker) and saline (Control) at forearm skin sites on both arms via transdermal iontophoresis. In protocol 1, low (0.001%) and high (1%) doses of pilocarpine were administered at the TEA-treated and Control sites over a 60-min period. In protocol 2, participants were passively heated by immersing their lower limbs in hot water (43°C) until core (rectal) temperature (Tc ) increased by 0.8°C above resting levels. Administration of TEA attenuated cholinergic sweating (P = 0.001) during the initial 20 min after the treatment of low dose of pilocarpine only whilst the response was similar between the groups (P = 0.163). Cholinergic and thermal sweating were higher in the trained relative to the untrained men (all P ≤ 0.033). Thermal sweating reached ∼90% of the response at a Tc elevation of 0.8°C during the initial 20 min of passive heating, which corresponds to the period wherein TEA attenuated cholinergic sweating in protocol 1. However, sweating did not differ between the Control and TEA sites in either group (P = 0.704). We showed that activation of K+ channels does not appear to mediate the elevated sweating response induced by a low dose of pilocarpine in trained men. We also demonstrated that K+ channels do not contribute to sweating during heat stress in either group.

Influence of exercise intensity and regional differences in the sudomotor recruitment pattern in exercising prepubertal boys and young men.

We investigated the influence of exercise intensities and regional differences in the sudomotor recruitment pattern in boys. Six prepubertal boys (age 11 ± 1 yr) cycled at light, moderate, and high exercise intensity (35%, 50%, and 65% VO2max) for 30 min in a temperate condition (28 °C, 40% relative humidity). Local sweat rate (ventilated capsule) and number of activated sweat glands (starch-iodine technique) at five body sites were assessed and sweat gland output was calculated. Responses in boys were compared with those in nine young men (23 ± 1 yr) tested under identical conditions. The forehead, chest, back, and forearm, but not thigh, sweat rate increased from light to moderate and at high intensities in boys (all p ≤ 0.005) but not from moderate to high (all p ≥ 0.071). The sweat rate on the forehead was relatively higher (p ≤ 0.045) and thigh was lower (p ≤ 0.050) than other sites in boys at moderate and high intensities. Exercise intensity-dependent sweating was associated with activating more sweat glands but not increasing glandular output in boys. The sweat rate in boys was attenuated versus men heterogeneously across body sites concurrent to low glandular outputs (all p ≤ 0.027). We conclude that exercise intensity modulates the sweat rate in boys by changing the number of activated sweat glands heterogeneously among skin sites. Age-related differences in the sudomotor pattern are evident at higher exercise intensities. Development of glandular output per gland occurring from boys to young men may play a key role in modulating sweat rate with respect to exercise intensity and regional differences.

Na+-K+-ATPase plays a major role in mediating cutaneous thermal hyperemia achieved by local skin heating to 39°C.

Na+-K+-ATPase is integrally involved in mediating cutaneous vasodilation during an exercise-heat stress, which includes an interactive role with nitric oxide synthase (NOS). Here, we assessed if Na+-K+-ATPase also contributes to cutaneous thermal hyperemia induced by local skin heating, which is commonly used to assess cutaneous endothelium-dependent vasodilation. Furthermore, we assessed the extent to which NOS contributes to this response. Cutaneous vascular conductance (CVC) was measured continuously at four forearm skin sites in 11 young adults (4 women). After baseline measurement, local skin temperature was increased from 33°C to 39°C to induce cutaneous thermal hyperemia. Once a plateau in CVC was achieved, each skin site was continuously perfused via intradermal microdialysis with either: 1) lactated Ringer solution (control), 2) 6 mM ouabain, a Na+-K+-ATPase inhibitor, 3) 20 mM l-NAME, a NOS inhibitor, or 4) a combination of both. Relative to the control site, CVC during the plateau phase of cutaneous thermal hyperemia (∼50% max) was reduced by the lone inhibition of Na+-K+-ATPase (-19 ± 8% max, P = 0.038) and NOS (-32 ± 4% max, P < 0.001), as well as the combined inhibition of both (-37 ± 9% max, P < 0.001). The magnitude of reduction was similar between NOS inhibition alone and combined inhibition (P = 1.000). The administration of both Na+-K+-ATPase and NOS inhibitors fully abolished the plateau of CVC with values returning to preheating baseline values (P = 0.439). We show that Na+-K+-ATPase contributes to cutaneous thermal hyperemia during local skin heating to 39°C, and this response is partially mediated by NOS.NEW & NOTEWORTHY 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.

Measurement error of self-paced exercise performance in athletic women is not affected by ovulatory status or ambient environment.

Measurement error(s) of exercise tests for women are severely lacking in the literature. The purpose of this investigation was to 1) determine whether ovulatory status or ambient environment were moderating variables when completing a 30-min self-paced work trial and 2) provide test-retest norms specific to athletic women. A retrospective analysis of three heat stress studies was completed using 33 female participants (31 ± 9 yr, 54 ± 10 mL·min-1·kg-1) that yielded 130 separate trials. Participants were classified as ovulatory (n = 19), anovulatory (n = 4), and oral contraceptive pill users (n = 10). Participants completed trials ∼2 wk apart in their (quasi-) early follicular and midluteal phases in two of moderate (1.3 ± 0.1 kPa, 20.5 ± 0.5°C, 18 trials), warm-dry (2.2 ± 0.2 kPa, 34.1 ± 0.2°C, 46 trials), or warm-humid (3.4 ± 0.1 kPa, 30.2 ± 1.1°C, 66 trials) environments. We quantified reliability using limits of agreement, intraclass correlation coefficient (ICC), standard error of measurement (SEM), and coefficient of variation (CV). Test-retest reliability was high, clinically valid (ICC = 0.90, P < 0.01), and acceptable with a mean CV of 4.7%, SEM of 3.8 kJ (2.1 W), and reliable bias of -2.1 kJ (-1.2 W). The various ovulatory status and contrasting ambient conditions had no appreciable effect on reliability. These results indicate that athletic women can perform 30-min self-paced work trials ∼2 wk apart with an acceptable and low variability irrespective of their hormonal status or heat-stressful environments.NEW & NOTEWORTHY This study highlights that aerobically trained women perform 30-min self-paced work trials ∼2 wk apart with acceptably low variability and their hormonal/ovulatory status and the introduction of greater ambient heat and humidity do not moderate this measurement error.

Eccrine sweat glands' maximum ion reabsorption rates during passive heating in older adults (50-84 years).

PURPOSE: We examined whether eccrine sweat glands ion reabsorption rate declined with age in 35 adults aged 50-84 years. Aerobic fitness (VO2max) and salivary aldosterone were measured to see if they modulated ion reabsorption rates. METHODS: During a passive heating protocol (lower leg 42 °C water submersion) the maximum ion reabsorption rates from the chest, forearm and thigh were measured, alongside other thermophysiological responses. The maximum ion reabsorption rate was defined as the inflection point in the slope of the relation between galvanic skin conductance and sweat rate. RESULTS: The maximum ion reabsorption rate at the forearm, chest and thigh (0.29 ± 0.16, 0.33 ± 0.15, 0.18 ± 0.16 mg/cm2/min, respectively) were weakly correlated with age (r ≤ - 0.232, P ≥ 0.05) and salivary aldosterone concentrations (r ≤ - 0.180, P ≥ 0.179). A moderate positive correlation was observed between maximum ion reabsorption rate at the thigh and VO2max (r = 0.384, P = 0.015). Salivary aldosterone concentration moderately declined with age (r = - 0.342, P = 0.021). Whole body sweat rate and pilocarpine-induced sudomotor responses to iontophoresis increased with VO2max (r ≥ 0.323, P ≤ 0.027) but only moderate (r = - 0.326, P = 0.032) or no relations (r ≤ - 0.113, P ≥ 0.256) were observed with age. CONCLUSION: The eccrine sweat glands' maximum ion reabsorption rate is not affected by age, spanning 50-84 years. Aldosterone concentration in an aged cohort does not appear to modulate the ion reabsorption rate. We provide further support for maintaining cardiorespiratory fitness to attenuate any decline in sudomotor function.

Dissociation between exercise intensity thresholds: mechanistic insights from supine exercise.

This study tested the hypothesis that the respiratory compensation point (RCP) and breakpoint in deoxygenated [heme] [deoxy[heme]BP, assessed via near-infrared spectroscopy (NIRS)] during ramp incremental exercise would occur at the same metabolic rate in the upright (U) and supine (S) body positions. Eleven healthy men completed ramp incremental exercise tests in U and S. Gas exchange was measured breath-by-breath and time-resolved-NIRS was used to measure deoxy[heme] in the vastus lateralis (VL) and rectus femoris (RF). RCP (S: 2.56 ± 0.39, U: 2.86 ± 0.40 L·min-1, P = 0.02) differed from deoxy[heme]BP in the VL in U (3.10 ± 0.44 L·min-1, P = 0.002), but was not different in S in the VL (2.70 ± 0.50 L·min-1, P = 0.15). RCP was not different from the deoxy[heme]BP in the RF for either position (S: 2.34 ± 0.48 L·min-1, U: 2.76 ± 0.53 L·min-1, P > 0.05). However, the deoxy[heme]BP differed between muscles in both positions (P < 0.05), and changes in deoxy[heme]BP did not relate to ΔRCP between positions (VL: r = 0.55, P = 0.080, RF: r = 0.26, P = 0.44). The deoxy[heme]BP was consistently preceded by a breakpoint in total[heme], and was, in turn, itself preceded by a breakpoint in muscle surface electromyography (EMG). RCP and the deoxy[heme]BP can be dissociated across muscles and different body positions and, therefore, do not represent the same underlying physiological phenomenon. The deoxy[heme]BP may, however, be mechanistically related to breakpoints in total[heme] and muscle activity.

Effects of low-intensity exercise on local skin and whole-body thermal sensation in hypothermic young males.

Thermal sensation, a key component of behavioral thermoregulation, is modulated by the changes in both skin and core temperatures. Although cutaneous thermal sensation to local cold is blunted during exercise as compared to rest in normothermic humans, it remains to be determined whether this holds true during core cooling. Furthermore, when local skin thermal sensation is diminished during exercise, it remains unclear whether whole-body thermal sensation is also attenuated. We therefore tested whether low-intensity exercise (VO2: ~1300 ml min-1) attenuates local skin and/or whole-body thermal sensation in hypothermic young males. Eleven healthy young males (24 ± 2 years) were cooled through cold water immersion (18 °C) up to their lower abdomen while resting (rest trial) and during low-intensity cycling (30-60 W, 30 rpm) (exercise trial). Body temperature, cardiorespiratory variables, and whole-body (9-point scale: 0, unbearably cold; 4, neutral; 8, unbearably hot) and local skin thermal sensation were measured at baseline on land and before the esophageal temperature (Tes) began to decrease (defined as -0.0 Tes) and after 0.5 and 1.0 °C decrements in Tes from baseline during the immersion period. Local skin thermal sensation was measured using a thermostimulator with Peltier element that was attached to the chest. The temperature of the probe was initially equilibrated to the chest skin temperature, then gradually decreased at a constant rate (0.1 °C s -1) until the participants felt coolness. The difference between the initial skin temperature and the local skin temperature that felt cool was assessed as an index of local skin thermal sensation. Throughout the immersions, esophageal and mean skin temperatures did not differ between the rest and exercise trials. Local skin thermal sensation also did not differ between the two trials or at any core temperature level. By contrast, the whole-body thermal sensation score was higher (participants felt less cold) in the exercise than in the rest trial at esophageal temperature of -1.0 °C (1.25 ± 0.46 vs. 0.63 ± 0.35 units, P = 0.035). These results suggest that local skin thermal sensation during low-intensity exercise is not affected by a decrease in core temperature. However, whole-body thermal sensation mediated by a decrease in core temperature (-1.0 °C) is blunted by low-intensity exercise during cold water immersion.

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

Seasonal acclimatization from winter to summer is known to enhance thermoeffector responses in hot-dry environments during exercise whereas its impact on sweat evaporation and core temperature (Tcore) 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 h at 40% V̇o2max in winter (preacclimatization) and repeated the trial again in summer (after acclimatization). For the last 20 min of cycling at a steady-state of Tcore, 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 with preacclimatization state (all P < 0.05) whereas sweating efficiency was lower (P < 0.01) until 55 min of exercise. Tcore and evaporated sweat rate were unaltered by acclimatization status (all P > 0.70). In conclusion, seasonal acclimatization enhances thermoeffector responses but does not attenuate Tcore during exercise in a hot-humid environment. Furthermore, increasing air velocity enhances evaporated sweat rate and sweating efficiency irrespective of acclimated state. NEW & NOTEWORTHY Seasonal acclimatization to humid heat enhances eccrine sweat gland function and thus results in a higher local and whole body sweat rate but does not attenuate Tcore during exercise in a hot-humid environment. Sweating efficiency is lower after seasonal acclimatization to humid heat compared with preacclimatization with and without the increase of air velocity. However, having a lower sweating efficiency does not mitigate the Tcore response during exercise in a hot-humid environment.