Greater V˙O2peak is correlated with greater skeletal muscle deoxygenation amplitude and hemoglobin concentration within individual muscles during ramp-incremental cycle exercise.

It is axiomatic that greater aerobic fitness (V˙O2peak) derives from enhanced perfusive and diffusive O2 conductances across active muscles. However, it remains unknown how these conductances might be reflected by regional differences in fractional O2 extraction (i.e., deoxy [Hb+Mb] and tissue O2 saturation [StO2]) and diffusive O2 potential (i.e., total[Hb+Mb]) among muscles spatially heterogeneous in blood flow, fiber type, and recruitment (vastus lateralis, VL; rectus femoris, RF). Using quantitative time-resolved near-infrared spectroscopy during ramp cycling in 24 young participants (V˙O2peak range: ~37.4-66.4 mL kg-1 min-1), we tested the hypotheses that (1) deoxy[Hb+Mb] and total[Hb+Mb] at V˙O2peak would be positively correlated with V˙O2peak in both VL and RF muscles; (2) the pattern of deoxygenation (the deoxy[Hb+Mb] slopes) during submaximal exercise would not differ among subjects differing in V˙O2peak Peak deoxy [Hb+Mb] and StO2 correlated with V˙O2peak for both VL (r = 0.44 and -0.51) and RF (r = 0.49 and -0.49), whereas for total[Hb+Mb] this was true only for RF (r = 0.45). Baseline deoxy[Hb+Mb] and StO2 correlated with V˙O2peak only for RF (r = -0.50 and 0.54). In addition, the deoxy[Hb+Mb] slopes were not affected by aerobic fitness. In conclusion, while the pattern of deoxygenation (the deoxy[Hb+Mb] slopes) did not differ between fitness groups the capacity to deoxygenate [Hb+Mb] (index of maximal fractional O2 extraction) correlated significantly with V˙O2peak in both RF and VL muscles. However, only in the RF did total[Hb+Mb] (index of diffusive O2 potential) relate to fitness

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

The aim of our study was to determine if habitual endurance training can influence the relative contribution of nitric oxide synthase (NOS) and cyclooxygenase (COX) in the regulation of sweating during a passive heat stress in young adults. Ten trained athletes and nine untrained counterparts were passively heated until oral temperature (as estimated by sublingual temperature, Tor) increased by 1.5°C above baseline resting. Forearm sweat rate (ventilated capsule) was measured at three skin sites continuously perfused with either lactated Ringer\u27s solution (Control), 10 mmol/L NG‐nitro‐L‐arginine methyl ester (L‐NAME, non‐selective NOS inhibitor), or 10 mmol/L ketorolac (Ketorolac, non‐selective COX inhibitor) via intradermal microdialysis. Sweat rate was averaged for each 0.3°C increase in Tor. Sweat rate at the L‐NAME site was lower than Control following a 0.9 and 1.2°C increase in Tor in both groups (all P ≤ 0.05). Relative to the Control site, NOS‐inhibition reduced sweating similarly between the groups (P = 0.51). Sweat rate at the Ketorolac site was not different from the Control at any levels of Tor in both groups (P > 0.05). Nevertheless, a greater sweat rate was measured at the end of heating in the trained as compared to the untrained individuals (P ≤ 0.05). We show that NOS contributes similarly to sweating in both trained and untrained individuals during a passive heat stress. Further, no effect of COX on sweating was measured for either group. The greater sweat production observed in endurance‐trained athletes is likely mediated by factors other than NOS‐ and COX‐dependent mechanisms

Sweat from gland to skin surface: Production, transport and skin absorption

By combining galvanic skin conductance (GSC), stratum corneum hydration (HYD) and regional surface sweat rate (RSR) measurements at the arm, thigh, back and chest, we closely monitored the passage of sweat from gland to skin surface. Through a varied exercise-rest protocol, sweating was increased slowly and decreased in 16 male and female human participants (25.3 ± 4.7 yrs, 174.6 ± 10.1 cm, 71.3 ± 12.0 kg, 53.0 ± 6.8 ml∙kg∙min-1). ∆GSC and HYD increased prior to RSR, indicating pre-secretory sweat gland activity and skin hydration. ∆GSC and HYD typically increased concomitantly during rest in a warm environment (30.1 ± 1.0°C, 30.0 ± 4.7% RH) and only at the arm did ∆GSC increase prior to an increase in HYD. HYD increased prior to RSR, before sweat was visible on the skin, but not to full saturation, contradicting earlier hypotheses. Maximal skin hydration did occur, as demonstrated by a plateau in all regions. Post exercise rest resulted in a rapid decrease in HYD and RSR but a delayed decline in ∆GSC. Evidence for reabsorption of surface sweat into the skin following a decline in sweating, as hypothesized in the literature, was not found. This suggests that skin surface sweat, after sweating is decreased, may not diffuse back into the dermis, but is only evaporated. These data, showing distinctly different responses for the three measured variables, provide useful information about the fate of sweat from gland to surface that is relevant across numerous research fields (e.g. thermoregulation, dermatology, ergonomics and material design)

Body temperature and cold sensation during and following exercise under temperate room conditions in cold‐sensitive young trained females

We evaluated cold sensation at rest and in response to exercise‐induced changes in core and skin temperatures in cold‐sensitive exercise trained females. Fifty‐eight trained young females were screened by a questionnaire, selecting cold‐sensitive (Cold‐sensitive, n = 7) and non‐cold‐sensitive (Control, n = 7) individuals. Participants rested in a room at 29.5°C for ~100 min after which ambient temperature was reduced to 23.5°C where they remained resting for 60 min. Participants then performed 30‐min of moderate intensity cycling (50% peak oxygen uptake) followed by a 60‐min recovery. Core and mean skin temperatures and cold sensation over the whole‐body and extremities (fingers and toes) were assessed throughout. Resting core temperature was lower in the Cold‐sensitive relative to Control group (36.4 ± 0.3 vs. 36.7 ± 0.2°C). Core temperature increased to similar levels at end‐exercise (~37.2°C) and gradually returned to near preexercise rest levels at the end of recovery (>36.6°C). Whole‐body cold sensation was greater in the Cold‐sensitive relative to Control group during resting at a room temperature of 23.5°C only without a difference in mean skin temperature between groups. In contrast, cold sensation of the extremities was greater in the Cold‐sensitive group prior to, during and following exercise albeit this was not paralleled by differences in mean extremity skin temperature. We show that young trained females who are sensitive to cold exhibit augmented whole‐body cold sensation during rest under temperate ambient conditions. However, this response is diminished during and following exercise. In contrast, cold sensation of extremities is augmented during resting that persists during and following exercise

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

Two studies were conducted to examine the effects of ice slushy ingestion (ICE) and cold water immersion (CWI) on thermoregulatory and sweat responses during constant (study 1) and self-paced (study 2) exercise. In study 1, 11 men cycled at 40–50% of peak aerobic power for 60 min (33.2 ± 0.3C, 45.9 ± 0.5% relative humidity, RH). In study 2, 11 men cycled for 60 min at perceived exertion (RPE) equivalent to 15 (33.9 ± 0.2C and 42.5 ± 3.9%RH). In both studies, each trial was preceded by 30 min of CWI (~22C), ICE or no cooling (CON). Rectal temperature (T re ), skin temperature (T sk ), thermal sensation, and sweat responses were measured. In study 1, ICE decreased T re- T sk gradient versus CON (p = 0.005) during first 5 min of exercise, while CWI increased T re- T sk gradient versus CON and ICE for up to 20 min during the exercise (p0.05). Increased T re -T sk gradient by CWI improved MPO while ICE reduced T re but did not confer any ergogenic effect. Both precooling treatments attenuated the thermal efferent signals until a specific body temperature threshold was reached. © 2019 Choo et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

Wearing graduated compression stockings augments cutaneous vasodilation but not sweating during exercise in the heat

The activation of cutaneous vasodilation and sweating are essential to the regulation of core temperature during exercise in the heat. We assessed the effect of graduated compression induced by wearing stockings on cutaneous vasodilation and sweating during exercise in the heat (30°C). On two separate occasions, nine young males exercised for 45 min or until core temperature reached ~1.5°C above baseline resting while wearing either (1) stockings causing graduated compression (graduate compression stockings, GCS), or (2) loose‐fitting stockings without compression (Control). Forearm vascular conductance was evaluated by forearm blood flow (venous occlusion plethysmography) divided by mean arterial pressure to estimate cutaneous vasodilation. Sweat rate was estimated using the ventilated capsule technique. Core and skin temperatures were measured continuously. Exercise duration was similar between conditions (Control: 42.2 ± 3.6 min vs. GCS: 42.2 ± 3.6 min, P = 1.00). Relative to Control, GCS increased forearm vascular conductance during the late stages (≥30 min) of exercise (e.g., at 40 min, 15.6 ± 5.6 vs. 18.0 ± 6.0 units, P = 0.01). This was paralleled by a greater sensitivity (23.1 ± 9.1 vs. 32.1 ± 15.0 units°C−1, P = 0.043) and peak level (14.1 ± 5.1 vs. 16.3 ± 5.7 units, P = 0.048) of cutaneous vasodilation as evaluated from the relationship between forearm vascular conductance with core temperature. However, the core temperature threshold at which an increase in forearm vascular conductance occurred did not differ between conditions (Control: 36.9 ± 0.2 vs. GCS: 37.0 ± 0.3°C, P = 0.13). In contrast, no effect of GCS on sweating was measured (all P > 0.05). We show that the use of GCS during exercise in the heat enhances cutaneous vasodilation and not sweating

Respiratory mechanics and cerebral blood flow during heat‐induced hyperventilation and its voluntary suppression in passively heated humans

We investigated whether heat‐induced hyperventilation can be voluntarily prevented, and, if so, how this modulates respiratory mechanics and cerebral blood flow in resting heated humans. In two separate trials, 10 healthy men were passively heated using lower body hot‐water immersion and a water‐perfused garment covering their upper body (both 41°C) until esophageal temperature (Tes) reached 39°C or volitional termination. In each trial, participants breathed normally (normal‐breathing) or voluntarily controlled minute ventilation (VE) at a level equivalent to that observed after 5 min of heating (controlled‐breathing). Respiratory gases, middle cerebral artery blood velocity (MCAV), work of breathing, and end‐expiratory and inspiratory lung volumes were measured. During normal‐breathing, VE increased as Tes rose above 38.0 ± 0.3°C, whereas controlled‐breathing diminished the increase in VE (VE at Tes = 38.6°C: 25.6 ± 5.9 and 11.9 ± 1.3 L min−1 during normal‐ and controlled‐breathing, respectively, P < 0.001). During normal‐breathing, end‐tidal CO2 pressure and MCAV decreased with rising Tes, but controlled‐breathing diminished these reductions (at Tes = 38.6°C, 24.7 ± 5.0 vs. 39.5 ± 2.8 mmHg; 44.9 ± 5.9 vs. 60.2 ± 6.3 cm sec−1, both P < 0.001). The work of breathing correlated positively with changes in VE (P < 0.001) and was lower during controlled‐ than normal‐breathing (16.1 ± 12.6 and 59.4 ± 49.5 J min−1, respectively, at heating termination, P = 0.013). End‐expiratory and inspiratory lung volumes did not differ between trials (P = 0.25 and 0.71, respectively). These results suggest that during passive heating at rest, heat‐induced hyperventilation increases the work of breathing without affecting end‐expiratory lung volume, and that voluntary control of breathing can nearly abolish this hyperventilation, thereby diminishing hypocapnia, cerebral hypoperfusion, and increased work of breathing

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

Purpose We investigated the influence of inorganic nitrate (NO−3) supplementation on local sweating and cutaneous vascular responses during exercise in hot conditions. Method Eight healthy, young subjects were assigned in a randomized, double-blind, crossover design to receive NO−3 -rich beetroot (BR) juice (140 mL/day, containing ~8 mmol of NO−3) and NO−3-depleted placebo (PL) juice (140 mL/day, containing ~0.003 mmol of NO−3) for 3 days. On day 3 of supplementation, subjects cycled at an intensity corresponding to 55% of V̇ O2max for 30 min in hot conditions (30 °C, 50% relative humidity). Chest and forearm sweat rate (SR) and skin blood flow (SkBF), were measured continuously. Cutaneous vascular conductance (CVC) was calculated by SkBF/mean arterial pressure (MAP). Results Prior to exercise, plasma NO− 3 (21±6 and 581±161 µM) and nitrite (NO− 2 , 87±28 and 336±156 nM) concentrations were higher after BR compared to PL supplementation (P≤0.011, n=6). Oesophageal, mean skin, and mean body temperatures during exercise were not different between conditions. In addition, BR supplementation did not affect SR, SkBF, and CVC during exercise. A lower MAP was found after 30 min of exercise following BR supplementation (112±6 and 103±6 mmHg for PL and BR, respectively, P=0.021). Conclusion These results suggest that inorganic NO− 3 supplementation, which increases the potential for O2-independent NO production, does not affect local sweating and cutaneous vascular responses, but attenuates blood pressure in young healthy subjects exercising in a hot environment

Effects of exercise intensity on the sweating response to a sustained static exercise

8 sujets masculins sont couchés pendant une heure dans une chambre climatique à une température de 35°C avec un taux d'humidité de 50%. Ils effectuent ensuite une série d'exercices de préhension isométrique à différents niveaux de contraction (15,30,45, 60%). Comparaison des taux de sudation selon l'intensité de contractio