Determinants of body core temperatures at fatigue in rats subjected to incremental-speed exercise: The prominent roles of ambient temperature, distance traveled, initial core temperature, and measurement site.

Understanding the factors that underlie the physical exercise-induced increase in body core temperature (TCORE) is essential to developing strategies to counteract hyperthermic fatigue and reduce the risk of exertional heatstroke. This study analyzed the contribution of six factors to TCORE attained at fatigue in Wistar rats (n = 218) subjected to incremental-speed treadmill running: ambient temperature (TAMB), distance traveled, initial TCORE, body mass, measurement site, and heat loss index (HLI). First, we ran hierarchical multiple linear regression analyses with data from different studies conducted in our laboratory (n = 353 recordings). We observed that TAMB, distance traveled, initial TCORE, and measurement site were the variables with predictive power. Next, regression analyses were conducted with data for each of the following TCORE indices: abdominal (TABD), brain cortex (TBRAIN), or colonic (TCOL) temperature. Our findings indicated that TAMB, distance traveled (i.e., an exercise performance-related variable), initial TCORE, and HLI predicted the three TCORE indices at fatigue. Most intriguingly, HLI was inversely related to TABD and TBRAIN but positively associated with TCOL. Lastly, we compared the temperature values at fatigue among these TCORE indices, and the following descendent order was noticed - TCOL, TABD, and TBRAIN - irrespective of TAMB where experiments were conducted. In conclusion, TCORE in rats exercised to fatigue depends primarily on environmental conditions, performance, pre-exercise TCORE, and measurement site. Moreover, the influence of cutaneous heat loss on TCOL is qualitatively different from the influence on TABD and TBRAIN, and the temperature values at fatigue are not homogenous within the body core.

Physical exercise-induced thermoregulatory responses in trained rats: Effects of manipulating the duration and intensity of aerobic training sessions.

This study investigated the effects of increasing the intensity and/or duration of aerobic training sessions on thermoregulatory responses in rats subjected to exercises in temperate and warm environments. Thirty-two adult male Wistar rats were divided into four groups: a control (CON) group and three groups that were subjected to an 8-week aerobic training, during which the physical overload was achieved by predominantly increasing the exercise intensity (INT), duration (DUR) or by increasing both in an alternate manner (ID). During the last week of training, the rats received an abdominal sensor implant to measure their core body temperature (TCORE) by telemetry. After the training protocol, the 32 rats were subjected to incremental speed-exercises in temperate (23 °C) and warm (32 °C) environments. The rats had their TCORE recorded while running on a treadmill, and the ratio between the increase in TCORE and distance traveled was calculated to estimate thermoregulatory efficiency. All training protocols increased the rats' thermoregulatory efficiency during the incremental-speed exercise at 23 °C; i.e., trained rats attained faster running speeds but unchanged TCORE at fatigue compared to CON rats. However, none of the load components of training sessions - intensity or duration - was more effective than the other in improving this efficiency. At 32 °C, the aerobic training protocols did not influence the exercise-induced thermoregulatory responses. Our data indicate that different progressions in aerobic training performed at temperate conditions improved thermoregulatory efficiency during incremental exercise in the same environment; this training-induced adaptation was not clearly observed when running in warmer conditions.

Combined exercise training improves specific domains of cognitive functions and metabolic markers in middle-aged and older adults with type 2 diabetes mellitus.

AIM: To investigate the effects of 8-weeks of CT on specific domains of cognitive function, metabolic and cardiovascular parameters of subjects with Type 2 Diabetes Mellitus (T2DM). METHODS: 31 sedentary T2DM adults and older divided into CT (3x/week, during 8-week, n = 16) or Control group (CONT, n = 15). Before and after the intervention, a cognitive task battery, blood samples, and functional tests were assessed. RESULTS: CT improved inhibitory control (d = 0.89), working memory (d = 0.88), cognitive flexibility (d = 0.67) and attention/concentration (d = 0.64) in T2DM subjects. However, memory, verbal fluency, and processing speed (d < 0.1, p > 0.05 for all) were not changed. The CT-induced improvements on global cognitive z-score (r = -0.51; p < 0.001) were inversely correlated to cognitive screening scores. Moreover, CT improved functional performance (p < 0.05) and reduced insulin levels (p = 0.04). Although there was no statistical significance, there were a clinically relevant reduction of peripheral insulin sensitivity (d = 0.51, p = 0.09), resistin levels (d = 0.53, p = 0.08), diastolic (d = 0.63, p = 0.09) and mean blood pressure (d = 0.50, p = 0.09). Conversely, no changes were observed for glucose, fructosamine and blood lipids (d < 0.2 for all). CONCLUSION: CT partially reversed the negative effects of T2DM on specific cognitive domains possibly by amelioration of metabolic regulation. Moreover, lower cognitive scores may modulate the responsivity of cognitive function to CT.

Central losartan administration increases cardiac workload during aerobic exercise.

To assess the effects of central administration of losartan, an antagonist of angiotensin II AT1 receptors, on cardiovascular function during aerobic exercise, heart rate, systolic and diastolic arterial pressures and rate pressure product of Wistar rats were measured as cardiac workload indexes. The animals ran on a treadmill until fatigue after an intracerebroventricular injection of losartan or saline. Pulsatile arterial pressure was recorded by a catheter implanted into the ascending aorta, from which were derived cardiovascular parameters to estimate the cardiac workload. Total exercise time and exercise workload were determined as performance indexes. The rats showed a more intense increase in heart rate after 8 min of exercise and sustained until fatigue (P < .05). Furthermore, the rats injected with losartan had a higher increase of both systolic and diastolic arterial pressures as well as rate pressure product from approximately 6 min of exercise until fatigued (P < .05). In addition, a 22% reduction in exercise time was found in losartan-rats (P < .01). This ergolytic effect induced by losartan was strongly inversely correlated with rate-pressure product during aerobic exercise (r = 0.78, P ≤ .01). The data shows that central administration of losartan augments the cardiac workload during aerobic exercise, which courses in parallel with the reduced exercise performance.

Pre-exercise exposure to the treadmill setup changes the cardiovascular and thermoregulatory responses induced by subsequent treadmill running in rats.

Different methodological approaches have been used to conduct experiments with rats subjected to treadmill running. Some experimenters have exposed rats to the treadmill setup before initiating exercise to minimize the influences of handling and being placed in an anxiety-inducing environment on the physiological responses to subsequent running. Other experimenters have subjected rats to exercise immediately after placing them on the treadmill. Thus, the present study aimed to evaluate the effects of pre-exercise exposure to the treadmill on physical performance and cardiovascular and thermoregulatory responses during subsequent exercise. Male Wistar rats were subjected to fatiguing incremental-speed exercise at 24°C immediately after being placed on the treadmill or after being exposed to the treadmill for 70 min following removal from their home cages. Core body temperature (TCORE), tail-skin temperature (TSKIN), heart rate (HR) and mean arterial pressure (MAP) were recorded throughout the experiments. Rats exposed to the treadmill started exercise with higher TCORE, lower HR and MAP, and unaltered TSKIN. This exposure did not influence performance, but it markedly affected the exercise-induced increases in the four physiological parameters evaluated; for example, the TSKIN increased earlier and at a higher TCORE. Moreover, previous treadmill exposure notably allowed expected exercise-induced changes in cardiovascular parameters to be observed. Collectively, these data indicate that pre-exercise exposure to the treadmill induces important effects on physiological responses during subsequent treadmill running. The present data are particularly relevant for researchers planning experiments involving physical exercise and the recording of physiological parameters in rats.

Central cholinergic activation induces greater thermoregulatory and cardiovascular responses in spontaneously hypertensive than in normotensive rats.

There is evidence that central cholinergic stimulation increases heat dissipation in normotensive rats besides causing changes on the cardiovascular system via modulation of baroreceptors activity. However, the contribution of the central cholinergic system on thermoregulatory responses and its relationship with cardiovascular adjustments in spontaneously hypertensive rats (SHRs), an animal model of reduced baroreceptor sensitivity and thermoregulatory deficit, has not been completely clarified. Therefore, the aim of this study was to verify the involvement of the central cholinergic system in cardiovascular and thermoregulatory adjustments in SHRs. Male Wistar rats (n = 17) and SHRs (n = 17) were implanted with an intracerebroventricular cannula for injections of 2 µL of physostigmine (phy) or saline solution. Tail temperature (Ttail), internal body temperature (Tint), systolic arterial pressure (SAP), heart rate (HR) and metabolic rate were registered during 60 min while the animals remained at rest after randomly receiving the injections. The variability of the SAP and the HR was estimated by the fast Fourier transform. Phy treatment began a succession of cardiovascular and thermoregulatory responses that resulted in increased SAP, reduced HR and increased Ttail in both Wistar and SHRs groups. The magnitude of these effects seems to be more intense in SHRs, since the improvement of heat dissipation reflected in Tint. Taken together, these results provide evidence that hypertensive rats present greater cardiovascular and thermoregulatory responses than normotensive rats after central cholinergic stimulation.

Auditory stimulation by exposure to melodic music increases dopamine and serotonin activities in rat forebrain areas linked to reward and motor control.

Listening to melodic music is regarded as a non-pharmacological intervention that ameliorates various disease symptoms, likely by changing the activity of brain monoaminergic systems. Here, we investigated the effects of exposure to melodic music on the concentrations of dopamine (DA), serotonin (5-HT) and their respective metabolites in the caudate-putamen (CPu) and nucleus accumbens (NAcc), areas linked to reward and motor control. Male adult Wistar rats were randomly assigned to a control group or a group exposed to music. The music group was submitted to 8 music sessions [Mozart's sonata for two pianos (K. 488) at an average sound pressure of 65 dB]. The control rats were handled in the same way but were not exposed to music. Immediately after the last exposure or control session, the rats were euthanized, and their brains were quickly removed to analyze the concentrations of 5-HT, DA, 5-hydroxyindoleacetic acid (5-HIAA) and 3,4-dihydroxyphenylacetic acid (DOPAC) in the CPu and NAcc. Auditory stimuli affected the monoaminergic system in these two brain structures. In the CPu, auditory stimuli increased the concentrations of DA and 5-HIAA but did not change the DOPAC or 5-HT levels. In the NAcc, music markedly increased the DOPAC/DA ratio, suggesting an increase in DA turnover. Our data indicate that auditory stimuli, such as exposure to melodic music, increase DA levels and the release of 5-HT in the CPu as well as DA turnover in the NAcc, suggesting that the music had a direct impact on monoamine activity in these brain areas.

Physical Exercise-Induced Cardiovascular and Thermoregulatory Adjustments Are Impaired in Rats Subjected to Cutaneous Artery Denervation.

This study aimed to investigate the chronic effects of caudal artery denervation on morphometric parameters of the tail vascular smooth muscle and on physical exercise-induced thermoregulatory and cardiovascular adjustments in rats. Male Wistar rats were subjected to caudal artery denervation or the sham procedure. Approximately 26-28 days after these procedures, their thermoregulatory and cardiovascular parameters were evaluated at rest and during or following a fatiguing treadmill run. At the end of the experiments, the rats were euthanized, and samples of their tails were removed to evaluate morphometric parameters of the vascular smooth muscle surrounding the caudal artery. Denervated rats showed morphological adaptations, including increased arterial wall thickness and wall-to-lumen ratios. In resting rats and following the fatiguing exercise, caudal artery denervation barely affected the thermoregulatory and cardiovascular parameters evaluated. By contrast, caudal artery denervation attenuated the increase in tail skin temperature, decreased the spontaneous baroreflex sensitivity, and exacerbated the increases in mean arterial pressure in exercising rats. The increased wall-to-lumen ratio of denervated rats correlated negatively with the maximum tail skin temperature attained or cutaneous heat loss sensitivity but correlated positively with the maximum diastolic blood pressure attained during exercise. In conclusion, cutaneous denervation induces vascular remodeling characterized by morphological adaptations of the tail vascular smooth muscle. This vascular remodeling likely underlies the impaired tail heat loss and blood pressure adjustments in denervated rats subjected to physical exercise. Therefore, we have highlighted the importance of cutaneous vascular innervation integrity in thermal and cardiovascular control in stress-challenged rats. In this sense, our findings advance the understanding of thermoregulatory and cardiovascular system reactions after a sustained cutaneous vascular innervation injury, which is essential for the treatment of some diseases, such as Parkinson's disease and type 1 and type 2 diabetes mellitus.

Nitrate supplementation improves physical performance specifically in non-athletes during prolonged open-ended tests: a systematic review and meta-analysis.

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.

Effects of manipulating the duration and intensity of aerobic training sessions on the physical performance of rats.

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.

Association Between Exercise-Induced Hyperthermia and Intestinal Permeability: A Systematic Review.

BACKGROUND: Prolonged and strenuous physical exercise increases intestinal permeability, allowing luminal endotoxins to translocate through the intestinal barrier and reach the bloodstream. When recognized by the immune system, these endotoxins trigger a systemic inflammatory response that may affect physical performance and, in severe cases, induce heat stroke. However, it remains to be elucidated whether there is a relationship between the magnitude of exercise-induced hyperthermia and changes in intestinal permeability. OBJECTIVE: In this systematic review, we evaluated whether an exercise-induced increase in core body temperature (T Core) is associated with an exercise-induced increase in intestinal permeability. METHODS: The present systematic review screened the MEDLINE/PubMed and Web of Science databases in September 2016, without any date restrictions. Sixteen studies that were performed in healthy participants, presented original data, and measured both the exercise-induced changes in T Core and intestinal permeability were selected. These studies assessed intestinal permeability through the measurement of sugar levels in the urine and measurement of intestinal fatty acid binding protein or lipopolysaccharide levels in the blood. RESULTS: Exercise increased both T Core and intestinal permeability in most of the 16 studies. In addition, a positive and strong correlation was observed between the two parameters (r = 0.793; p < 0.001), and a T Core exceeding 39 °C was always associated with augmented permeability. CONCLUSION: The magnitude of exercise-induced hyperthermia is directly associated with the increase in intestinal permeability.

Changes in systolic arterial pressure variability are associated with the decreased aerobic performance of rats subjected to physical exercise in the heat.

Enhanced cardiovascular strain is one of the factors that explains degraded aerobic capacity in hot environments. The cardiovascular system is regulated by the autonomic nervous system, whose activity can be indirectly evaluated by analyzing heart rate variability (HRV) and systolic arterial pressure (SAP) variability. However, no study has addressed whether HRV or SAP variability can predict aerobic performance during a single bout of exercise. Therefore, this study aimed to investigate whether there is an association between cardiovascular variability and performance in rats subjected to treadmill running at two ambient temperatures. In addition, this study investigated whether the heat-induced changes in cardiovascular variability and reductions in performance are associated with each other. Male Wistar rats were implanted with a catheter into their carotid artery for pulsatile blood pressure recordings. After recovery from surgery, the animals were subjected to incremental-speed exercise until they were fatigued under temperate (25°C) and hot (35°C) conditions. Impaired performance and exaggerated cardiovascular responses were observed in the hot relative to the temperate environment. Significant and negative correlations between most of the SAP variability components (standard deviation, variance, very low frequency [VLF], and low frequency [LF]) at the earlier stages of exercise and total exercise time were observed in both environmental conditions. Furthermore, the heat-induced changes in the sympathetic components of SAP variability (VLF and LF) were associated with heat-induced impairments in performance. Overall, the results indicate that SAP variability at the beginning of exercise predicts the acute performance of rats. Our findings also suggest that heat impairments in aerobic performance are associated with changes in cardiovascular autonomic control.

Power spectrum analysis of cardiovascular variability during passive heating in conscious rats.

The cardiovascular system plays a direct role in the maintenance of body temperature. Whether passive heating alters cardiovascular autonomic modulation in conscious rats is still unknown. This study investigated the effects of passive heating on systolic blood pressure variability (SBPV) and heart rate variability (HRV) in conscious rats and the involvement of the renin-angiotensin system in the passive heating effects on SBPV and HRV. Fourteen male Wistar rats were randomly assigned to the control group or the losartan treatment group. A catheter was implanted in the left carotid artery to record pulsatile arterial pressure (PAP), and a telemetry sensor was implanted in the abdominal cavity to measure body temperature (Tbody). After recovering from surgery, the animals were subjected to a passive heating protocol (35°C; 30min) in resting conditions, during which Tbody, tail skin temperature and PAP were measured. The mean arterial pressure, systolic and diastolic blood pressure, heart rate, double product (i.e., the product of systolic blood pressure by heart rate), SBPV and HRV were calculated from the PAP. SBPV and HRV were analyzed in terms of both time and frequency domains. Increases in the thermoregulatory and cardiovascular parameters were observed during passive heating in both groups, and those increases were reflected in the higher time and frequency domains of the SBPV. However, passive heating was not effective in altering HRV. Passive heating altered SBPV but not HRV in conscious rats when they were treated with losartan.

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.

Thermoregulatory responses in exercising rats: methodological aspects and relevance to human physiology.

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.

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.

Exercising for food: bringing the laboratory closer to nature.

Traditionally, exercise physiology experiments have borne little resemblance to how animals express physical activity in the wild. In this experiment, 15 adult male rats were divided into three equal-sized groups: exercise contingent (CON), non-exercise contingent (NON) and sedentary (SED). The CON group was placed in a cage with a running wheel, where the acquisition of food was contingent upon the distance required to run. Every 3 days the distance required to run to maintain food intake at free feeding levels was increased by 90% in comparison to the previous 3 days. The NON group was housed identically to the CON group, but food acquisition was not dependent upon running in the wheel. Finally, the SED group was kept in small cages with no opportunity to perform exercise. A two-way ANOVA with repeated measures was used to determine significant differences in responses between the experimental phases and treatment groups, and ANCOVA was used to analyse growth and tissue mass variables with body length and body mass used separately as covariates. A post hoc Tukey's test was used to indicate significant differences. A Pearson's correlation was used to test the relationship between the distance travelled by the animal and the distance/food ratio. The level of significance was set at P<0.05 for all tests. The CON group showed the hypothesized correlation between distance required to run to obtain food and the mean distance travelled (P<0.001), during 45 days in the contingency phase. This group showed a decrease in body mass, rather than an increase as shown by NON and SED groups. The CON group had a significantly lower body temperature (P<0.05) and adiposity (P<0.05) when compared with the other two groups for the same body size. The present experimental model based on animals choosing the characteristics of their physical exercise to acquire food (i.e. distance travelled, speed and duration) clearly induced physiological effects (body characteristics and internal temperature), which are useful for investigating relevant topics in exercise physiology such as the link between exercise, food and body mass.

Physical exercise performance in temperate and warm environments is decreased by an impaired arterial baroreflex.

The present study aimed to investigate whether running performance in different environments is dependent on intact arterial baroreceptor reflexes. We also assessed the exercise-induced cardiovascular and thermoregulatory responses in animals lacking arterial baroafferent signals. To accomplish these goals, male Wistar rats were subjected to sinoaortic denervation (SAD) or sham surgery (SHAM) and had a catheter implanted into the ascending aorta to record arterial pressure and a telemetry sensor implanted in the abdominal cavity to record core temperature. After recovering from these surgeries, the animals were subjected to constant- or incremental-speed exercises performed until the voluntary interruption of effort under temperate (25° C) and warm (35° C) conditions. During the constant-speed exercises, the running time until the rats were fatigued was shorter in SAD rats in both environments. Although the core temperature was not significantly different between the groups, tail skin temperature was higher in SAD rats under temperate conditions. The denervated rats also displayed exaggerated increases in blood pressure and double product compared with the SHAM rats; in particular, in the warm environment, these exaggerated cardiovascular responses in the SAD rats persisted until they were fatigued. These SAD-mediated changes occurred in parallel with increased variability in the very low and low components of the systolic arterial pressure power spectrum. The running performance was also affected by SAD during the incremental-speed exercises, with the maximal speed attained being decreased by approximately 20% in both environments. Furthermore, at the maximal power output tolerated during the incremental exercises, the mean arterial pressure, heart rate and double product were exaggerated in the SAD relative to SHAM rats. In conclusion, the chronic absence of the arterial baroafferents accelerates exercise fatigue in temperate and warm environments. Our findings also suggest that an augmented cardiovascular strain accounted for the early interruption of exercise in the SAD rats.

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.