Interactive effects of exercise intensity and recovery posture on postexercise hypotension.

Postexercise reduction in blood pressure, termed postexercise 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 V̇o2max test on a cycle ergometer and five 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 1 h of recovery in each of the 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 [standing: -33 (11) vs. -21 (8) mmHg; seated: -34 (32) vs. -17 (37) mmHg, P < 0.01], diastolic [standing: -18 (7) vs. -8 (5) mmHg; seated: -10 (10) vs. -1 (4) mmHg, P < 0.01], and mean arterial pressures [-13 (8) vs. -2 (4) mmHg, P < 0.01], whereas in the supine recovery posture, the reduction in diastolic [-9 (9) vs. -4 (3) mmHg, P = 0.08) and mean arterial pressures [-7 (5) vs. -3 (4) mmHg, P = 0.06] was not consistently affected by prior exercise intensity. PEH is more pronounced during recovery from exercise performed above CP versus below GET. However, the effect of exercise intensity on PEH is largely abolished when recovery is performed in the supine posture.NEW & NOTEWORTHY The magnitude of postexercise hypotension is greater following the intensity above the critical power in a standing position.

Caffeine intake enhances peak oxygen uptake and performance during high-intensity cycling exercise in moderate hypoxia.

PURPOSE: We investigated whether caffeine consumption can enhance peak oxygen uptake ([Formula: see text]) by increasing peak ventilation during an incremental cycling test, and subsequently enhance time to exhaustion (TTE) during high-intensity cycling exercise in moderate normobaric hypoxia. METHODS: We conducted a double-blind, placebo cross-over design study. Sixteen recreational male endurance athletes (age: 20 ± 2 years, [Formula: see text]: 55.6 ± 3.6 ml/kg/min, peak power output: 318 ± 40 W) underwent an incremental cycling test and a TTE test at 80% [Formula: see text] (derived from the placebo trial) in moderate normobaric hypoxia (fraction of inspired O2: 15.3 ± 0.2% corresponding to a simulated altitude of ~ 2500 m) after consuming either a moderate dose of caffeine (6 mg/kg) or a placebo. RESULTS: Caffeine consumption resulted in a higher peak ventilation [159 ± 21 vs. 150 ± 26 L/min; P < 0.05; effect size (ES) = 0.31]. [Formula: see text] (3.58 ± 0.44 vs. 3.47 ± 0.47 L/min; P < 0.01; ES = 0.44) and peak power output (308 ± 44 vs. 302 ± 44 W; P = 0.02, ES = 0.14) were higher following caffeine consumption than during the placebo trial. During the TTE test, caffeine consumption enhanced minute ventilation (P = 0.02; ES = 0.28) and extended the TTE (426 ± 74 vs. 358 ± 75 s; P < 0.01, ES = 0.91) compared to the placebo trial. There was a positive correlation between the percent increase of [Formula: see text] following caffeine consumption and the percent increase in TTE (r = 0.49, P < 0.05). CONCLUSION: Moderate caffeine consumption stimulates breathing and aerobic metabolism, resulting in improved performance during incremental and high-intensity endurance exercises in moderate normobaric hypoxia.

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).

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.

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.

Indoor thermal comfort research using human participants: Guidelines and a checklist for experimental design.

Thermal comfort dictates our alliesthesia and behavioural responses in indoor environments with the primary aim of maintaining the thermal homeostasis of our human body. The recent advances in neurophysiology research have suggested that thermal comfort is a physiological response that is regulated by the deviations of both skin and core temperatures. Therefore, when conducting thermal comfort using indoor occupants in an indoor environment, proper experimental design and standardisation should be followed. However, there is no published source that provides an educational guideline on how to properly implement the thermal comfort experiment in an indoor environment using indoor occupants (normal occupational activities and during sleep in a home-based setting). Therefore, the primary purpose of this work is to illustrate how to conduct indoor thermal comfort related experiments using human trials in both normal occupational activities and during sleep in a home-based setting. Furthermore, we hope that the information presented in this article will result in better experimental design when conducting the experiment on thermal comfort using indoor occupants (occupational and home-based environments). Due to this reason, special emphasis will be focused on the experimental design, selection of participants and experimental standardisation. The key summary of this article is that thermal comfort related to indoor occupants in an indoor environment should perform priori sample analysis and follow the proper experimental design and standardisation as outlined in this article.

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.

TRPA1 Channel Activation With Cinnamaldehyde Induces Cutaneous Vasodilation Through NOS, but Not COX and KCa Channel, Mechanisms in Humans.

ABSTRACT: 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; P < 0.001). 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.

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.

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.

Menstrual phase and ambient temperature do not influence iron regulation in the acute exercise period.

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.

Looking ahead of 2021 Tokyo Summer Olympic Games: How Does Humid Heat Affect Endurance Performance? Insight into physiological mechanism and heat-related illness prevention strategies.

The combination of high humidity and ambient temperature of the 2021 Tokyo Summer Olympic Game will undoubtfully result in greater physiological strains and thereby downregulates the endurance performance of athletes. Although many research studies have highlighted that the thermoregulatory strain is greater when the environment is hot and humid, no review articles have addressed the thermoregulatory and performance differences between dry and humid heat and such lack of consensuses in this area will lead to increase the risk of heat-related injuries as well as suboptimal preparation. Furthermore, specific strategies to counteract this stressful environment has not been outlined in the current literature. Therefore, the purposes of this review are: 1) to provide a clear evidence that humid heat is more stressful than dry heat for both male and female athletes and therefore the preparation for the Tokyo Summer Olympic should be environmental specific instead of a one size fits all approach; 2) to highlight why female athletes may be facing a disadvantage when performing a prolonged endurance event under high humidity environment and 3) to highlight the potential interventional strategies to reduce thermal strain in hot-humid environment. The summaries of this review are: both male and female should be aware of the environmental condition in Tokyo as humid heat is more stressful than dry heat; Short-term heat acclimation may not elicit proper thermoregulatory adaptations in hot-humid environment; cold water immersion with proper hydration and some potential per-cooling modalities may be beneficial for both male and female athletes in hot-humid environment.

Differences in dry-bulb temperature do not influence moderate-duration exercise performance in warm environments when vapor pressure is equivalent.

PURPOSE: Recent studies have determined that ambient humidity plays a more important role in aerobic performance than dry-bulb temperature does in warm environments; however, no studies have kept humidity constant and independently manipulated temperature. Therefore, the purpose of this study was to determine the contribution of dry-bulb temperature, when vapor pressure was matched, on the thermoregulatory, perceptual and performance responses to a 30-min cycling work trial. METHODS: Fourteen trained male cyclists (age: 32 ± 12 year; height: 178 ± 6 cm; mass: 76 ± 9 kg; [Formula: see text]: 59 ± 9 mL kg-1 min-1; body surface area: 1.93 ± 0.12 m2; peak power output: 393 ± 53 W) volunteered, and underwent 1 exercise bout in moderate heat (MOD: 34.9 ± 0.2 °C, 50.1 ± 1.1% relative humidity) and 1 in mild heat (MILD: 29.2 ± 0.2 °C, 69.4 ± 0.9% relative humidity) matched for vapor pressure (2.8 ± 0.1 kPa), with trials counterbalanced. RESULTS: Despite a higher weighted mean skin temperature during MOD (36.3 ± 0.5 vs. 34.5 ± 0.6 °C, p < 0.01), none of rectal temperature (38.0 ± 0.3 vs. 37.9 ± 0.4 °C, p = 0.30), local sweat rate (1.0 ± 0.3 vs. 0.9 ± 0.4 mg cm-2 min-1, p = 0.28), cutaneous blood flow (283 ± 116 vs. 287 ± 105 PU, p = 0.90), mean power output (206 ± 37 vs. 205 ± 41 W, p = 0.87) or total work completed (371 ± 64 vs. 369 ± 70 kJ, p = 0.77) showed any difference between environments during the work trial. However, all perceptual measures (perceived exertion, thermal discomfort, thermal sensation, skin wettedness, pleasantness, all p < 0.05) were affected detrimentally during MOD compared to MILD. CONCLUSION: In a warm and compensable environment, dry-bulb temperature did not influence high-intensity cycling performance when vapor pressure was maintained, whilst the perceptual responses were affected.

On exercise thermoregulation in females: interaction of endogenous and exogenous ovarian hormones.

KEY POINTS: One in two female athletes chronically take a combined, monophasic oral contraceptive pill (OCP). Previous thermoregulatory investigations proposed that an endogenous rhythm of the menstrual cycle still occurs with OCP usage. Forthcoming large international sporting events will expose female athletes to hot environments differing in their thermal profile, yet few data exist on how trained women will respond from both a thermoregulatory and performance stand-point. In the present study, we have demonstrated that a small endogenous rhythm of the menstrual cycle still affects Tcore and also that chronic OCP use attenuates the sweating response, whereas behavioural thermoregulation is maintained. Furthermore, humid heat affects both performance and thermoregulatory responses to a greater extent than OCP usage and the menstrual cycle does. ABSTRACT: We studied thermoregulatory responses of ten well-trained ( V̇O2max , 57 ± 7 mL min-1  kg-1 ) women taking a combined, monophasic oral contraceptive pill (OCP) (≥12 months) during exercise in dry and humid heat, across their active OCP cycle. They completed four trials, each of resting and cycling at fixed intensities (125 and 150 W), aiming to assess autonomic regulation, and then a self-paced intensity (30-min work trial) to assess behavioural regulation. Trials were conducted in quasi-follicular (qF) and quasi-luteal (qL) phases in dry (DRY) and humid (HUM) heat matched for wet bulb globe temperature (WBGT) (27°C). During rest and exercise at 125 W, rectal temperature was 0.15°C higher in qL than qF (P = 0.05) independent of environment (P = 0.17). The onset threshold and thermosensitivity of local sweat rate and forearm blood flow relative to mean body temperature was unaffected by the OCP cycle (both P > 0.30). Exercise performance did not differ between quasi-phases (qF: 268 ± 31 kJ, qL: 263 ± 26 kJ, P = 0.31) but was 5 ± 7% higher during DRY than during HUM (273 ± 29 kJ, 258 ± 28 kJ; P = 0.03). Compared to matched eumenorrhoeic athletes, chronic OCP use impaired the sweating onset threshold and thermosensitivity (both P < 0.01). In well-trained, OCP-using women exercising in the heat: (i) a performance-thermoregulatory trade-off occurred that required behavioural adjustment; (ii) humidity impaired performance as a result of reduced evaporative power despite matched WBGT; and (iii) the sudomotor but not behavioural thermoregulatory responses were impaired compared to matched eumenorrhoeic athletes.

Influence of menstrual phase and arid vs. humid heat stress on autonomic and behavioural thermoregulation during exercise in trained but unacclimated women.

KEY POINTS: Despite an attenuated fluctuation in ovarian hormone concentrations in well-trained women, one in two of such women believe their menstrual cycle negatively impacts training and performance. Forthcoming large international events will expose female athletes to hot environments, and studies evaluating aerobic exercise performance in such environments across the menstrual cycle are sparse, with mixed findings. We have identified that autonomic heat loss responses at rest and during fixed-intensity exercise in well-trained women are not affected by menstrual cycle phase, but differ between dry and humid heat. Furthermore, exercise performance is not different across the menstrual cycle, yet is lower in humid heat, in conjunction with reduced evaporative cooling. Menstrual cycle phase does not appear to affect exercise performance in the heat in well-trained women, but humidity impairs performance, probably due to reduced evaporative power. ABSTRACT: We studied thermoregulatory responses of ten well-trained [V̇O2 max , 57 (7) ml min-1  kg-1 ] eumenorrheic women exercising in dry and humid heat, across their menstrual cycle. They completed four trials, each of resting and cycling at fixed intensities (125 and 150 W), to assess autonomic regulation, then self-paced intensity (30 min work trial), to assess behavioural regulation. Trials were in early-follicular (EF) and mid-luteal (ML) phases in dry (DRY) and humid (HUM) heat matched for wet bulb globe temperature (WBGT, 27°C). During rest and fixed-intensity exercise, rectal temperature was ∼0.2°C higher in ML than EF (P < 0.01) independent of environment (P = 0.66). Mean skin temperature did not differ between menstrual phases (P ≥ 0.13) but was higher in DRY than HUM (P < 0.01). Local sweat rate and/or forearm blood flow differed as a function of menstrual phase and environment (interaction: P ≤ 0.01). Exercise performance did not differ between phases [EF: 257 (37), ML: 255 (43) kJ, P = 0.62], but was 7 (9)% higher in DRY than HUM [263 (39), 248 (40) kJ; P < 0.01] in conjunction with equivalent autonomic regulation and thermal strain but higher evaporative cooling [16 (6) W m2 ; P < 0.01]. In well-trained women exercising in the heat: (1) menstrual phase did not affect performance, (2) humidity impaired performance due to reduced evaporative cooling despite matched WBGT and (3) behavioural responses nullified thermodynamic and autonomic differences associated with menstrual phase and dry vs. humid heat.

Effect of hyperthermia on simulated muscle activation in female when crossing obstacle.

It is well known that hyperthermia greatly impairs neuromuscular function and dynamic balance. However, whether a greater level of hyperthermia could potentially alter the lower limb simulated muscle activation when crossing an obstacle in female participants remains unknown. Therefore we examined the effect of a systematic increase in oral temperature on lower limb simulated muscle activation when crossing an obstacle in female participants. Eighteen female participants were recruited where they underwent a control trial (Con) and two progressive passive heating trials with Δ 1°C and Δ 2°C increase of oral temperature (Toral) using a 45°C water bath. In each trial, we assessed lower limb simulated muscle activation when crossing an obstacle height of 10%, 20%, and 30% of the participant's leg length and toe-off, toe-above-obstacle and heel-strike events were identified and analyzed. In all events, the lower limb simulated muscle activation were greater in Δ2°C than Δ1°C and Con when both leading and trailing limbs crossed the obstacle height of 20% and 30% leg length (all p < 0.001). However, the lower limb simulated muscle activation were not different between Δ1°C and Con across all obstacle heights (p > 0.05). This study concluded that a greater level of hyperthermia resulted in a greater lower limb simulated muscle activation to ensure safety and stability when females cross an obstacle height of 20% leg length or higher.

Whole-body passive heating at moderate hyperthermic state impairs static and dynamic balance in healthy females.

BACKGROUND: Whether static and dynamic balances can be impaired with increasing core temperature in female participants remains unknown. PURPOSE: We tested the hypothesis that static and dynamic balances can be further impaired with systematic increases of core temperature by Δ1 °C and Δ 2 °C using whole-body passive heating. METHOD: Eighteen female participants underwent a control trial (Con) and two progressive passive heating trials with Δ 1 °C and Δ 2 °C increase of oral temperature (TOral) using 45 °C water bath. In each trial, we assessed static balance with both eye open and closed and assessed dynamic balance using obstacle crossing at 10 %, 20 % and 30 % of the participant's leg length. RESULTS: Static balance was not different between Con and Δ1 °C but was different between Δ1 °C and Δ 2 °C in an eye closed condition. Furthermore, Δ 2 °C greatly impaired both static and dynamic balances when compared to Con. The joint angles and toe clearance increased while leading heel-obstacle distance decreased during crossing obstacles at the height of 20 % and 30 % leg length with leading limbs in the Δ2 °C compared to Δ 1 °C and Con (All P < 0.05). However, no differences in joint kinematics and toe clearance with trailing limbs were observed (All P > 0.05). CONCLUSION: In female participants, static and dynamic balances only became impaired when TOral increased 2 °C from baseline.

Effect of caffeine ingestion on time trial performance in cyclists: a systematic review and meta-analysis.

BACKGROUND: Caffeine, widely recognized as an ergogenic aid, has undergone extensive research, demonstrating its effectiveness to enhance endurance performance. However, there remains a significant gap in systematically evaluating its effects on time trial (TT) performance in cyclists. PURPOSE: This meta-analysis aimed to determine the efficacy of caffeine ingestion to increase cycling TT performance in cyclists and to evaluate the optimal dosage range for maximum effect. METHODS: A search of four databases was completed on 1 December 2023. The selected studies comprised crossover, placebo-controlled investigations into the effects of caffeine ingestion on cycling TT performance. Completion time (Time) and mean power output (MPO) were used as performance measures for TT. Meta-analyses were performed using a random-effects model to assess the standardized mean differences (SMD) in individual studies. RESULTS: Fifteen studies met the inclusion criteria for the meta-analyses. Subgroup analysis showed that moderate doses of caffeine intake (4-6 mg/kg) significantly improved cycling performance (SMD Time = -0.55, 95% confidence interval (CI) = -0.84 ~ -0.26, p < 0.01, I2 = 35%; SMD MPO = 0.44, 95% CI = 0.09 ~ 0.79, p < 0.05, I2 = 39%), while the effects of low doses (1-3 mg/kg) of caffeine were not significant (SMD Time = -0.34, 95% CI = -0.84 ~ 0.17, p = 0.19, I2 = 0%; SMD MPO = 0.31, 95% CI = -0.02 ~ 0.65, p = 0.07, I2 = 0%). CONCLUSION: A moderate dosage (4-6 mg/kg) of caffeine, identified as the optimal dose range, can significantly improve the time trial performance of cyclists, while a low dose (1-3 mg/kg) does not yield improvement. In addition, the improvements in completion time and mean power output resulting from a moderate dose of caffeine are essentially the same in cycling time trails.

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.