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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. 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. [ABSTRACT FROM AUTHOR]

We evaluated the effects of the menstrual cycle and physical training on heat loss (sweating and cutaneous vasodilation) responses during moderate exercise in a temperate environment. Ten untrained (group U) and seven endurance-trained (group T) women (maximal [O.sub.2] uptake of 36.7 [+ or -] 1.1 vs. 49.4 [+ or -] 1.7 ml x [kg.sup.-1] x [min.sup.-1], respectively: P < 0.05) performed a cycling exercise at 50% maximal [O.sub.2] uptake for 30 min during both the midfollicular and midluteal menstrual phase in a temperate environment (ambient temperature of 25[degrees]C, relative humidity of 45%). In group U, plasma levels of estrone, estradiol, and progesterone at rest and esophageal temperature ([T.sub.es]) during exercise were significantly higher during the midluteal than during the midfollicular phase (P < 0.05). Sweating rate and cutaneous blood flow (measured via laser-Doppler flowmetry) on the chest, back, forearm, and thigh were lower during the midluteal than during the midfollicular phase during exercise. [T.sub.es] threshold for heat loss responses was significantly higher and sensitivity of the heat loss responses was significantly lower in the midluteal than in the midfollicular phase, regardless of body site. These effects of the menstrual cycle in group U were not observed in group T. The sweating rate and cutaneous blood flow were significantly higher in group T than in group U, regardless of menstrual phase or body site. [T.sub.es] threshold for heat loss responses was significantly lower and sensitivity of heat loss responses was significantly greater in group T than in group U in the midluteal phase: however, sensitivity of the sweating response was significantly greater in the midfollicular phase. These results suggest that heat loss responses in group U were inhibited in the midluteal phase compared with in the midfollicular phase. Menstrual cycle had no remarkable effects in group T. Physical training improved heat loss responses, which was more marked in the midluteal than in the midfollicular phase. thermoregulation; estradiol; progesterone; long-term endurance training; heat acclimatization

To investigate quantitatively how sweating and cutaneous blood flow responses at the onset of dynamic exercise are affected by increasing exercise intensity in mildly heated humans, 18 healthy male subjects performed cycle exercise at 30, 50, and 70% of maximal [O.sub.2] uptake (V[O.sub.2] max) for 60 s in a warm environment. The study was conducted in a climatic chamber with a regulated ambient temperature of 35[degrees]C and relative humidity of 50%. The subjects rested in the semisupine position in the chamber for 60 min, and then sweating rate (SR) and skin blood flow were measured during cycle exercise at three different intensities. Changes in the heart rate, rating of perceived exertion, and mean arterial blood pressure were proportional to increasing exercise intensity, whereas esophageal and mean skin temperatures were essentially constant throughout the experiment. The SR on the chest, forearm, and thigh, but not on the palm, increased significantly with increasing exercise intensity (P < 0.05). The mean SR of the chest, forearm, and thigh increased 0.05 mg*[cm.sup.-2]*[min.sup.-1] with an increase in exercise intensity equivalent to 10% V[O.sub.2] max. On the other hand, the cutaneous vascular conductance (CVC) on the chest, forearm, and palm decreased significantly with increasing exercise intensity (P < 0.05). The mean CVC of the chest and forearm decreased 5.5% and the CVC on the palm decreased 8.0% with an increase in exercise intensity equivalent to 10% V[O.sub.2] max. In addition, the reduction in CVC was greater on the palm than on the chest and forearm at all exercise intensities (P < 0.01). We conclude that nonthermal sweating and cutaneous blood flow responses are exercise intensity dependent but directionally opposite at the onset of dynamic exercise in mildly heated humans. Furthermore, cutaneous blood flow responses to increased exercise intensity are greater in glabrous (palm) than in nonglabrous (chest and forearm) skin. thermal factors; nonthermal factors; glabrous skin; nonglabrous skin; feedforward manner

New Findings: What is the central question to this study?Do the sweat glands' maximum ion reabsorption rates increase following heat acclimation in healthy older individuals and is this associated with elevated aldosterone concentrations?What is the main finding and its importance?Sweat gland maximum ion reabsorption rates improved heterogeneously across body sites, which occurred without any changes in aldosterone concentration following a controlled hyperthermic heat acclimation protocol in healthy older individuals. We examined whether the eccrine sweat glands' ion reabsorption rates improved following heat acclimation (HA) in older individuals. Ten healthy older adults (>65 years) completed a controlled hyperthermic (+0.9°C rectal temperature, Tre) HA protocol for nine non‐consecutive days. Participants completed a passive heat stress test (lower leg 42°C water submersion) pre‐HA and post‐HA to assess physiological regulation of sweat gland ion reabsorption at the chest, forearm and thigh. The maximum ion reabsorption rate was defined as the inflection point in the slope of the relation between galvanic skin conductance and sweat rate (SR). We explored the responses again after a 7‐day decay. During passive heating, the Tb thresholds for sweat onset on the chest and forearm were lowered after HA (P < 0.05). However, sweat sensitivity (i.e. the slope), the SR at a given Tre and gross sweat loss did not improve after HA (P > 0.05). Any changes observed were lost during the decay. Pilocarpine‐induced sudomotor responses to iontophoresis did not change after HA (P ≥ 0.801). Maximum ion reabsorption rate was only enhanced at the chest (P = 0.001) despite unaltered aldosterone concentration after HA. The data suggest that this adaptation is lost after 7 days' decay. The HA protocol employed in the present study induced partial adaptive sudomotor responses. Eccrine sweat gland ion reabsorption rates improved heterogeneously across the skin sites. It is likely that aldosterone secretion did not alter the chest sweat ion reabsorption rates observed in the older adults. [ABSTRACT FROM AUTHOR]