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 whilst 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-hour at 40% VO2max in winter (pre-acclimatization) and repeated the trial again in summer (after-acclimatization). For the last 20-min of cycling at a steady-state of 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 to pre-acclimatization state (all P<0.05) whilst sweating efficiency was lower (P<0.01) until the 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.

Blunted sweating does not alter the rise in core temperature in people with multiple sclerosis exercising in the heat

Purpose: To determine whether thermoregulatory capacity is altered by MS during exercise in the heat. Methods: Sixteen MS (EDSS: 2.9±0.9; 47±8 y; 77.6±14.0 kg) and 14 healthy (CON) control participants (43±11 y; 78.6±17.0 kg) cycled at a heat production of 4 W.kg-1 for 60 minutes at 30˚C, 30%RH (WARM). A subset of 8 MS (EDSS: 2.6±0.5; 44±8 y; 82.3±18.2 kg) and 8 CON (44±12 y; 81.2±21.1 kg) also exercised at 35°C, 30%RH (HOT). Rectal (Tre), mean skin (Tsk) temperature, and local sweat rate on the upper-back (LSRback) and forearm (LSRarm), were measured. Results: All CON, yet only 9 of 16, and 7 of 8 MS participants completed 60 min of exercise in WARM and HOT trials, respectively. All MS participants unable to complete exercise stopped with ∆Tre between 0.2-0.5˚C. The time to reach a ∆Tre of 0.2˚C was similar (MS:28±15 min, CON: 32±18 min; P=0.51). For MS participants completing 60-min of exercise in WARM, ∆Tre (P=0.13), ∆Tsk (P=0.45), LSRback (P=0.69) and LSRarm (P=0.54) were similar to CON, but ΔTb (MS:0.16±0.13˚C, CON:0.07±0.06˚C; P=0.02) and onset time (MS:16±10 min, CON:8±5 min; P=0.02) for sweating were greater. Similarly, in HOT, ∆Tre (P=0.52), ∆Tsk (P=0.06), LSRback (P=0.59) and LSRarm (P=0.08) were similar, but ΔTb (MS: 0.19±0.16˚C, CON: 0.06±0.04˚C; P=0.04) and onset time (MS:13±7 min, CON:6±3 min; P=0.02) for sweating were greater with MS. Conclusion: Even at 35˚C, a delayed sweating onset didn't alter heat loss to sufficiently affect exercise-induced rises in core temperature. Heat intolerance with MS does not seem attributable to thermoregulatory impairments.

Combined effect of facial sweating and mounting a night vision device on helmet stability

A night vision device (NVD) equipped on a ballistic helmet violates the locational stability of a helmet, and sweating remaining inside a helmet can also reduce helmet stability. This study aimed to investigate the combined effect of sweating and mounting a NVD on helmet stability. Nine healthy males participated in the experiments which consisted of military simulated tasks and 20 min walking. Subjective evaluations containing helmet stability and comfort along with physiological measurements such as microclimate inside a helmet and sweating rate were obtained. Local sweat rate on the forehead was predicted by sweat rate on the upper back and forearm. The results showed that (1) mounting a NVD did not significantly influence on helmet stability per se before onset of sweating, however, (2) when it is combined with sweating, helmet stability reduced 50% during shooting in a prone position (P < 0.05). (3) There was a significant correlation with helmet overall comfort and helmet stability (r = 0.762, P < 0.05), and between helmet stability and helmet pressure (ρ = 0.701, P < 0.05). The present study demonstrated that mounting additional devices on the helmet violates helmet stability when accompanied by sweating, even when optimized fit provided and that just tightening bands cannot be an absolute solution. This study emphasized the importance of helmet stability as a variable for evaluating helmet comfort.

Two isothermal challenges yield comparable physiological and subjective responses

Purpose Ventilated vests are developed to reduce thermal stress by enhancing convective and evaporative cooling from skin tissue underneath the vest. The purpose of this study is to investigate whether thermal stress is equal when a ventilated vest is worn compared to a no-vest situation with similar dry thermal resistance. Methods Nine healthy males walked on a treadmill (7 km h−1) for 45 min in a desert climate (34 °C, 20% relative humidity) with and without ventilated vest. Gastrointestinal temperature (Tgi), heart rate (HR), and skin temperature (Tsk) were continuously monitored. Local sweat rate (LSR) was assessed two times on six skin locations. Subjective ratings were assessed every 10 min. Results Final Tgi (37.6 ± 0.1 °C for vest and 37.6 ± 0.1 °C for no-vest), HR (133 ± 7 bpm and 133 ± 9 bpm) and mean Tsk (34.8 ± 0.7 °C and 34.9 ± 0.6 °C) were not different between conditions (p ≥ 0.163). Scapula skin temperature (Tscapula) under the vest tended to be lower (baseline to final: ΔTscapula = 0.35 ± 0.37 °C) than without vest (ΔTscapula = 0.74 ± 0.62 °C, p = 0.096). LSR at locations outside the vest did not differ with and without vest (p ≥ 0.271). Likewise, subjective responses did not differ between conditions (χ2 ≥ 0.143). Conclusions We conclude that two systems with similar dry thermal resistance and, therefore, similar required evaporation, resulted in similar thermal stress during paced walking in a hot-dry environment. Local ventilation did not alter the sweating response on locations outside the vest.

Role of nitric oxide synthase in human sweat gland output

The contribution of nitric oxide synthase (NOS) to the process of cholinergic-mediated human eccrine sweat production is unclear. Using a novel model for cholinergic-mediated sweating in humans, I demonstrate that blocking the NOS system led to a reduction in local sweat rate (LSR). This reduction in LSR was maintained in the presence of K+ channel blockade with tetraethylammonium.

Temperature of water ingested before exercise alters the onset of physiological heat loss responses

This study sought to determine whether the temperature of water ingested before exercise alters the onset threshold and subsequent thermosensitivity of local vasomotor and sudomotor responses after exercise begins. Twenty men [24 (SD 4) yr of age, 75.8 (SD 8.1) kg body mass, 52.3 (SD 7.7) ml·min−1·kg−1peak O2consumption (V̇o2peak)] ingested 1.5°C, 37°C, or 50°C water (3.2 ml/kg), rested for 5 min, and then cycled at 50% V̇o2peakfor 15 min at 23.0 (SD 0.9) °C and 32 (SD 10) % relative humidity. Mean body temperature (Tb), local sweat rate (LSR), and skin blood flow (SBF) were measured. In a subset of eight men [25 (SD 5) yr of age, 78.6 (SD 8.3) kg body mass, 48.9 (SD 11.1) ml·min−1·kg−1V̇o2peak], blood pressure was measured and cutaneous vascular conductance (CVC) was determined. The change in Tbwas greater at the onset of LSR measurement with ingestion of 1.5°C than 50°C water [ΔTb= 0.19 (SD 0.15) vs. 0.11 (SD 0.12) °C, P = 0.04], but not 37°C water [ΔTb= 0.14 (SD 0.14) °C, P = 0.23], but did not differ between trials for SBF measurement [ΔTb= 0.18 (SD 0.15) °C, 0.11 (SD 0.13) °C, and 0.09 (SD 0.09) °C with 1.5°C, 37°C, and 50°C water, respectively, P = 0.07]. Conversely, the thermosensitivity of LSR and SBF was not different [LSR = 1.11 (SD 0.75), 1.11 (SD 0.75), and 1.34 (SD 1.11) mg·min−1·cm−2·°C−1with 1.5°C, 37°C, and 50°C ingested water, respectively ( P = 0.46); SBF = 717 (SD 882), 517 (SD 606), and 857 (SD 904) %baseline arbitrary units (AU)/°C with 1.5°C, 37°C, and 50°C ingested water, respectively ( P = 0.95)]. After 15 min of exercise, LSR and SBF were greater with ingestion of 50°C than 1.5°C water [LSR = 0.40 (SD 0.17) vs. 0.31 (SD 0.19) mg·min−1·cm−2( P = 0.02); SBF = 407 (SD 149) vs. 279 (SD 117) %baseline AU ( P < 0.001)], but not 37°C water [LSR = 0.50 (SD 0.22) mg·min−1·cm−2; SBF = 324 (SD 169) %baseline AU]. CVC was statistically unaffected [275 (SD 81), 340 (SD 114), and 384 (SD 160) %baseline CVC with 1.5°C, 37°C, and 50°C ingested water, respectively, P = 0.30]. Collectively, these results support the concept that visceral thermoreceptors modify the central drive for thermoeffector responses.

Fluid replacement modulates oxidative stress- but not nitric oxide-mediated cutaneous vasodilation and sweating during prolonged exercise in the heat

The roles of nitric oxide synthase (NOS), reactive oxygen species (ROS), and angiotensin II type 1 receptor (AT1R) activation in regulating cutaneous vasodilation and sweating during prolonged (≥60 min) exercise are currently unclear. Moreover, it remains to be determined whether fluid replacement (FR) modulates the above thermoeffector responses. To investigate, 11 young men completed 90 min of continuous moderate intensity (46% V̇o2peak) cycling performed at a fixed rate of metabolic heat production of 600 W (No FR condition). On a separate day, participants completed a second session of the same protocol while receiving FR to offset sweat losses (FR condition). Cutaneous vascular conductance (CVC) and local sweat rate (LSR) were measured at four intradermal microdialysis forearm sites perfused with: 1) lactated Ringer (Control); 2) 10 mM NG-nitro-l-arginine methyl ester (l-NAME, NOS inhibition); 3) 10 mM ascorbate (nonselective antioxidant); or 4) 4.34 nM losartan (AT1R inhibition). Relative to Control (71% CVCmax at both time points), CVC with ascorbate (80% and 83% CVCmax) was elevated at 60 and 90 min of exercise during FR (both P < 0.02) but not at any time during No FR (all P > 0.31). In both conditions, CVC was reduced at end exercise with l-NAME (60% CVCmax; both P < 0.02) but was not different relative to Control at the losartan site (76% CVCmax; both P > 0.19). LSR did not differ between sites in either condition (all P > 0.10). We conclude that NOS regulates cutaneous vasodilation, but not sweating, irrespective of FR, and that ROS influence cutaneous vasodilation during prolonged exercise with FR.