Sinoaortic denervation prevents enhanced heat loss induced by central cholinergic stimulation during physical exercise.

The present study investigated whether the effects of central cholinergic stimulation on thermoregulation during exercise are modulated by arterial baroreceptors. Wistar rats were submitted to sinoaortic denervation (SAD) or sham denervation (SHAM) and then fitted with a chronic guide cannula into the lateral cerebral ventricle. After 2 weeks, a catheter was implanted into the ascending aorta, and a temperature sensor was implanted into the peritoneal cavity. Two days later, the rats were submitted to exercise on a treadmill at 18 m/min until fatigued. Thermoregulatory and cardiovascular responses were measured after injection of 2 µL of 10mM physostigmine (Phy) or 0.15M NaCl solution (Sal) into the cerebral ventricle. In SHAM rats, Phy injection induced a greater exercise-induced increase in blood pressure and lower increase in heart rate than Sal treatment. In the SAD group, the attenuation of heart rate in response to Phy was blocked despite an exaggerated increase in blood pressure. SHAM rats treated with Phy had a higher increase in tail skin temperature compared to Sal injection (31.9 ± 0.4 °C Phy-SHAM vs. 30.1 ± 0.6 °C Sal-SHAM, 5 min after injection; p<0.05), resulting in a lower exercise-induced increase in core temperature. In contrast, SAD blocked the Phy injection effects in thermoregulatory responses during exercise (tail temperature: 30.1 ± 1.2 °C Phy-SAD vs. 29.5 ± 1.2 °C Sal-SAD, 5 min, p = 0.65). Therefore, we conclude that the enhancement of cutaneous heat loss induced by central cholinergic stimulation during exercise is mediated primarily by arterial baroreceptors.

Thermoregulatory efficiency is increased after heat acclimation in tropical natives.

To evaluate the effects of heat acclimation on sweat rate redistribution and thermodynamic parameters, 9 tropical native volunteers were submitted to 11 days of exercise-heat exposures (40+/-0 degrees C and 45.1+/-0.2% relative humidity). Sudomotor function was evaluated by measuring total and local (forehead, chest, arm, forearm, and thigh) sweat rates, local sweat sodium concentration, and mean skin and rectal temperatures. We also calculated heat production (H), heat storage (S), heat exchange by radiation (R) and by convection (C), evaporated sweat (E(sw)), sweating efficiency (eta(sw)), skin wettedness (w(sk)), and the ratio between the heat storage and the sum of heat production and heat gains by radiation and convection (S/(H+R+C)). The heat acclimation increased the whole-body sweat rate and reduced the mean skin temperature. There were changes in the local sweat rate patterns: on the arm, forearm, and thigh it increased significantly from day 1 to day 11 (all p<0.05) and the sweat rates from the forehead and the chest showed a small nonsignificant increase (p=0.34 and 0.17, respectively). The relative increase of local sweat rates on day 11 was not different among the sites; however, when comparing the limbs (arm, forearm, and thigh) with the trunk (forehead and chest), there was a significant higher increase in the limbs (32+/-5%) in comparison to the trunk (11+/-2%, p=0.001). After the heat acclimation period we observed higher w(sk) and E(sw) and reduced S/(H+R+C), meaning greater thermoregulatory efficiency. The increase in the limb sweat rate, but not the increase in the trunk sweat rate, correlated with the increased w(sk), E(sw), and reduced S/(H+R+C) (p<0.05 to all). Altogether, it can be concluded that heat acclimation increased the limbs' sweat rates in tropical natives and that this increase led to increased loss of heat through evaporation of sweat and this higher sweat evaporation was related to higher thermoregulatory efficiency.

Muscarinic cholinoceptors in the ventromedial hypothalamic nucleus facilitate tail heat loss during physical exercise.

The aim of this study was to evaluate the participation of ventromedial hypothalamic nucleus (VMH) muscarinic cholinoceptors in heat balance and central fatigue during treadmill exercise (24 m min(-1), 5% inclination). The animals were anesthetized with pentobarbital sodium (50 mg/kg body weight i.p.) and fitted with bilateral cannulae into the VMH 1 week prior to the experiments. Tail skin (T(tail)) and core body temperatures (T(b)) were measured after the injection of 0.2 microL of 5 x 10(-9) mol methylatropine (Matr) or 0.15 M NaCl solution (Sal) into the hypothalamus. Methylatropine injection into the VMH greatly increased heat storage rate (HSR) measured until fatigue (19.7+/-4.6 cal min(-1) Matr versus 9.7+/-3.3 cal min(-1) Sal; P<0.05) and attenuated the exercise-induced tail vasodilation as seen by T(tail) (23.98+/-0.43 degrees C Matr versus 25.52+/-0.85 degrees C Sal; at 6.5 min; P<0.05), indicating inhibition of the heat loss process. The 2 min delay and the increased DeltaT(b), which triggered the heat loss mechanisms observed in Matr-treated rats, are associated with increased HSR and may be responsible for the decreased running performance of these animals (21.0+/-2.9 min Matr versus 33.5+/-3.4 min Sal; P<0.001). In fact, a close negative correlation was observed between HSR and time to fatigue (r=-0.61; P<0.01). In conclusion, VMH muscarinic cholinoceptors facilitate tail heat loss mechanisms, and a delay in this adjustment would lead to a decrease in physical exercise performance due to excess heat storage.