The magnitude of exercise-induced hyperthermia is directly associated with the increase in intestinal permeability.

Nitrate (NO3 -) is an ergogenic nutritional supplement that is widely used to improve physical performance. However, the effectiveness of NO3 - supplementation has not been systematically investigated in individuals with different physical fitness levels. The present study analysed whether different fitness levels (non-athletes v. athletes or classification of performance levels), duration of the test used to measure performance (short v. long duration) and the test protocol (time trials v. open-ended tests v. graded-exercise tests) influence the effects of NO3 - supplementation on performance. This systematic review and meta-analysis was conducted and reported according to the guidelines outlined in the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) statement. A systematic search of electronic databases, including PubMed, Web of Science, SPORTDiscus and ProQuest, was performed in August 2017. On the basis of the search and inclusion criteria, fifty-four and fifty-three placebo-controlled studies evaluating the effects of NO3 - supplementation on performance in humans were included in the systematic review and meta-analysis, respectively. NO3 - supplementation was ergogenic in non-athletes (mean effect size (ES) 0·25; 95 % CI 0·11, 0·38), particularly in evaluations of performance using long-duration open-ended tests (ES 0·47; 95 % CI 0·23, 0·71). In contrast, NO3 - supplementation did not enhance the performance of athletes (ES 0·04; 95 % CI -0·05, 0·15). After objectively classifying the participants into different performance levels, the frequency of trials showing ergogenic effects in individuals classified at lower levels was higher than that in individuals classified at higher levels. Thus, the present study indicates that dietary NO3 - supplementation improves physical performance in non-athletes, particularly during long-duration open-ended tests.

Rats are used worldwide in experiments that aim to investigate the physiological responses induced by a physical exercise session. Changes in body temperature regulation, which may affect both the performance and the health of exercising rats, are evident among these physiological responses. Despite the universal use of rats in biomedical research involving exercise, investigators often overlook important methodological issues that hamper the accurate measurement of clear thermoregulatory responses. Moreover, much debate exists regarding whether the outcome of rat experiments can be extrapolated to human physiology, including thermal physiology. Herein, we described the impact of different exercise intensities, durations and protocols and environmental conditions on running-induced thermoregulatory changes. We focused on treadmill running because this type of exercise allows for precise control of the exercise intensity and the measurement of autonomic thermoeffectors associated with heat production and loss. Some methodological issues regarding rat experiments, such as the sites for body temperature measurements and the time of day at which experiments are performed, were also discussed. In addition, we analyzed the influence of a high body surface area-to-mass ratio and limited evaporative cooling on the exercise-induced thermoregulatory responses of running rats and then compared these responses in rats to those observed in humans. Collectively, the data presented in this review represent a reference source for investigators interested in studying exercise thermoregulation in rats. In addition, the present data indicate that the thermoregulatory responses of exercising rats can be extrapolated, with some important limitations, to human thermal physiology.

The quantitative [14C]-2-deoxyglucose autoradiographic method was utilized to assess regional cerebral metabolic rate for glucose (rCMRglc) in rat brain during withdrawal from cocaine self-administration. RCMRglc was determined in 62 regions from brains of naive rats which were placed into an empty operant chamber for 12 hr continuously, and rats trained to self-administer cocaine during 3 hr training sessions and subsequently placed into the operant chamber for 12 hr continuously with or without access to cocaine. Animals placed into the chamber without access to cocaine were examined 6 hr later, while animals allowed access to the 12 hr cocaine binge were examined either 6 or 72 hr post-cocaine. Metabolic activity was reduced during withdrawal in the nucleus accumbens, olfactory tubercle, islands of Calleja region, basolateral and central amygdaloid nuclei, medial septum, piriform and cingulate cortices, rostral caudatoputamen, entopeduncular nucleus and the adjacent lateral hypothalamus, somatosensory, auditory, and motor cortices compared to the naive state. These effects were usually more severe at 72 than at 6 hr after binge exposure, with intermediate values observed in cocaine trained animals without binge exposure. The response was negatively correlated with the amount of cocaine consumed during binge exposure in the striatum, olfactory tubercle, piriform, cingulate, somatosensory, and motor cortices. Thus, the amount of cocaine consumed can affect the extent of metabolic depression after sustained drug exposure. The pattern of regional effects suggests that mesolimbic and rostral extrapyramidal dopamine terminal regions and certain of their efferent pathways are preferentially affected during cocaine withdrawal. The reduction of basal metabolic rate observed in these brain regions during cocaine withdrawal may become more severe with time despite the apparent recovery of certain behavioral-motivational responses.

This study investigated the effects of manipulating the load components of aerobic training sessions on the physical performance of rats. To achieve this purpose, adult male Wistar rats were divided into four groups: an untrained control (CON) group and training groups with a predominant overload in intensity (INT) or duration (DUR) or alternating and similar overloads in intensity and duration (ID). Prior to, during, and after 8 weeks of the control or training protocols, the performance of the rats (evaluated by their workload) was determined during fatiguing, incremental-speed treadmill running. Two additional incremental running tests were performed prior to and at the end of the protocols to measure the peak rate of oxygen consumption (VO2peak). As expected, the rats in the trained groups exhibited increased performance, whereas the untrained rats showed stable performance throughout the 8 weeks. Notably, the performance gain exhibited by the DUR rats reached a plateau after the 4th week. This plateau was not present in the INT or ID rats, which exhibited increased performance at the end of training protocol compared with the DUR rats. None of the training protocols changed the VO2peak values; however, these values were attained at faster speeds, which indicated increased running economy. In conclusion, our findings demonstrate that the training protocols improved the physical performance of rats, likely resulting from enhanced running economy. Furthermore, compared with overload in duration, overload in the intensity of training sessions was more effective at inducing performance improvements across the 8 weeks of the study.

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.

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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.