The dynamics of physical exercise-induced increases in thalamic and abdominal temperatures are modified by central cholinergic stimulation.

Evidence has shown that brain and abdominal (T abd) temperatures are regulated by distinct physiological mechanisms. Thus, the present study examined whether central cholinergic stimulation would change the dynamics of exercise-induced increases in T abd and thalamic temperature (T thal), an index of brain temperature. Adult male Wistar rats were used in all of the experiments. Two guide cannulae were implanted in the rats, one in the thalamus and the other in the right lateral cerebral ventricle, to measure T thal and to centrally inject a cholinergic agonist, respectively. Then, a temperature sensor was implanted in the abdominal cavity. On the day of the experiments, the rats received an intracerebroventricular injection of 2 µL of 10(-2)M physostigmine (Phy) or a vehicle solution (Veh) and were subjected to treadmill running until volitional fatigue occurred. T thal was measured using a thermistor connected to a multimeter, and T abd was recorded by telemetry. Phy injection delayed the exercise-induced increases in T thal (37.6 ± 0.2°C Phy vs 38.7 ± 0.1°C Veh at the 10th min of exercise) and in T abd. Despite the delayed hyperthermia, Phy did not change the rats' physical performance. In addition, the more rapid exercise-induced increase in T thal relative to Tabd in the rats treated with Veh was abolished by Phy. Collectively, our data indicate that central cholinergic stimulation affects the dynamics of exercise-induced increases in T thal and T abd. These results also provide evidence of the involvement of cholinoceptors in the modulation of brain heat loss during physical exercise.

Hypothalamic temperature of rats subjected to treadmill running in a cold environment.

Different strategies for cooling the body prior to or during physical exercise have been shown to improve prolonged performance. Because of ethical and methodological issues, no studies conducted in humans have evaluated the changes in brain temperature promoted by cooling strategies. Therefore, our first aim sought to measure the hypothalamic temperature (Thyp) of rats subjected to treadmill running in a cold environment. Moreover, evidence suggests that Thyp and abdominal temperature (Tabd) are regulated by different physiological mechanisms. Thus, this study also investigated the dynamics of exercise-induced changes in Thyp and Tabd at two ambient temperatures: 25°C (temperate environment) and 12°C (cold). Adult male Wistar rats were used in these experiments. The rats were implanted with a guide cannula in the hypothalamus and a temperature sensor in the abdominal cavity. After recovery from this surgery, the rats were familiarized with running on a treadmill and were then subjected to the two experimental trials: constant-speed running (20 m/min) at 12°C and 25°C. Both Thyp and Tabd increased during exercise at 25°C. In contrast, Thyp and Tabd remained unchanged during fatiguing exercise at 12°C. The temperature differential (i.e., Thyp - Tabd) increased during the initial min of running at 25°C and thereafter decreased toward pre-exercise values. Interestingly, external cooling prevented this early increase in the temperature differential from the 2nd to the 8th min of running. In addition, the time until volitional fatigue was higher during the constant exercise at 12°C compared with 25°C. Together, our results indicate that Thyp and Tabd are regulated by different mechanisms in running rats and that external cooling affected the relationship between both temperature indexes observed during exercise without environmental thermal stress. Our data also suggest that attenuated hypothalamic hyperthermia may contribute to improved performance in cold environments.

Chronic sympathectomy of the caudal artery delays cutaneous heat loss during passive heating.

The present study aimed to investigate the chronic effects of caudal artery sympathectomy on thermoregulatory adjustments induced by passive heating. Male Wistar rats were subjected to two surgical procedures: caudal artery denervation (CAD) or sham surgery (Sham-CAD) and intraperitoneal implantation of a temperature sensor. On the day of the experiments, the animals were exposed to an ambient temperature of 36°C for 60min or allowed to rest under thermoneutral conditions (26°C). During the experiments, the tail skin temperature (T(skin)) and the core body temperature (T(core)) were measured. Under thermoneutral conditions, although sympathetic denervation did not change the average values of T(core) and T(skin), CAD rats exhibited decreased T(skin) variability compared with Sham-CAD rats (0.020±0.005°C vs. 0.031±0.005°C; P=0.024). During heat exposure, no differences were observed in the T(core) between the groups. In contrast, although peak T(skin) values were not affected by chronic sympathectomy of the caudal artery, CAD animals showed a delayed increase in T(skin); the time until the stabilization of T(skin) was three-fold longer in CAD rats than in Sham-CAD rats (15.3±2.5min vs. 4.9±0.6min; P=0.001). In conclusion, chronic sympathectomy of the caudal artery delays cutaneous heat loss during passive heating and decreases T(skin) variability under thermoneutral conditions. Taken together, our results indicate that the sympathetic innervation of cutaneous vessels is essential for the precise regulation of tail heat loss.

Six weeks of aerobic training improves VO2max and MLSS but does not improve the time to fatigue at the MLSS.

The purpose of this study was to investigate the effects of a 6-week aerobic training period on the time to fatigue (t lim) during exercise performed at the maximal lactate steady state (MLSS). Thirteen untrained male subjects (TG; age 22.5 ± 2.4 years, body mass 72.9 ± 6.7 kg and VO2max 44.9 ± 4.8 mL kg(-1) min(-1)) performed a cycle ergometer test until fatigue at the MLSS power output before and after 6 weeks of aerobic training. A group of eight control subjects (CG; age 25.1 ± 2.4 years, body mass 70.1 ± 9.8 kg and VO2max 45.2 ± 4.1 mL kg(-1) min(-1)) also performed the two tests but did not train during the 6-week period. There were no differences between the groups with respect to the VO2max or MLSS power output (MLSSw) before the treatment period. The VO2max and the MLSSw of the TG increased by 11.2 ± 7.2 % (pre-treatment = 44.9 ± 4.8 vs. post-treatment = 49.8 ± 4.5 mL kg(-1) min(-1)) and 14.7 ± 8.9 % (pre-treatment = 150 ± 27 vs. post-treatment = 171 ± 26 W), respectively, after 6 weeks of training. The results of the CG were unchanged. There were no differences in t lim between the groups or within groups before and after training. Six weeks of aerobic training increases MLSSw and VO2max, but it does not alter the t lim at the MLSS.

Muscarinic receptors within the ventromedial hypothalamic nuclei modulate metabolic rate during physical exercise.

The involvement of muscarinic cholinoceptors within the ventromedial hypothalamic nuclei (VMH) on the exercise-induced increase in oxygen consumption (VO(2)) was investigated. Rats were fitted with bilateral cannulae into the VMH for local delivery of drugs. On the day of the experiments, the animals were submitted to running exercise (20 m/min; 5% grade) until the point of fatigue. VO(2) was continuously measured after bilateral injections of either 0.2 µL of 5 × 10(-9)mol methylatropine or 0.15M NaCl solution into the VMH. Control experiments were conducted in freely moving rats on the treadmill. Muscarinic blockade within the VMH reduced time to fatigue by 32% and enhanced the increase in VO(2) from the 8th until the 17th min of exercise when compared to the control trial. In fact, time to fatigue was negatively correlated to the rate of increase in VO(2) (r(2)=0.747; P<0.001). However, bilateral injections of methylatropine in freely moving rats did not change VO(2) in comparison to saline injections. In conclusion, muscarinic cholinoceptors within the VMH are activated during exercise to modulate the increase in metabolic rate. Furthermore, blocking muscarinic transmission leads to a faster increase in VO(2) that is associated with the early interruption of exercise.

Possible biphasic sweating response during short-term heat acclimation protocol for tropical natives.

The aim of the present study was to evaluate the sweat loss response during short-term heat acclimation in tropical natives. Six healthy young male subjects, inhabitants of a tropical region, were heat acclimated by means of nine days of one-hour heat-exercise treatments (40+/-0 degrees C and 32+/-1% relative humidity; 50% (.)VO(2peak) on a cycle ergometer). On days 1 to 9 of heat acclimation whole-body sweat loss was calculated by body weight variation corrected for body surface area. On days 1 and 9 rectal temperature (T(re)) and heart rate (HR) were measured continuously, and rating of perceived exertion (RPE) every 4 minutes. Heat acclimation was confirmed by reduced HR (day 1 rest: 77+/-5 b.min(-1); day 9 rest: 68+/-3 b.min(-1); day 1 final exercise: 161+/-15 b.min(-1); day 9 final exercise: 145+/-11 b.min(-1), p<0.05), RPE (13 vs. 11, p<0.05) and T(re) (day 1 rest: 37.2+/-0.2 degrees C; day 9 rest: 37.0+/-0.2 degrees C; day 1 final exercise: 38.2+/-0.2 degrees C; day 9 final exercise: 37.9+/-0.1 degrees C, p<0.05). The main finding was that whole-body sweat loss increased in days 5 and 7 (9.49+/-1.84 and 9.56+/-1.86 g.m(-2).min(-1), respectively) compared to day 1 (8.31+/-1.31 g.m(-2).min(-1), p<0.05) and was not different in day 9 (8.48+/-1.02 g.m(-2).min(-1)) compared to day 1 (p>0.05) of the protocol. These findings are consistent with the heat acclimation induced adaptations and suggest a biphasic sweat response (an increase in the sweat rate in the middle of the protocol followed by return to initial values by the end of it) during short-term heat acclimation in tropical natives.