The blockade of central nitric oxide (NO) signaling modifies the thermoregulatory and metabolic adjustments that occur during exercise, thereby impairing physical performance. However, the brain areas involved in this response remain unknown. Nitrergic neurons are present in the hypothalamic areas that are activated during exercise and participate in autonomic and neuroendocrine responses, such as, the hypothalamic paraventricular nucleus (PVN) and the supraoptic nucleus (SON). To investigate whether brain NO signaling affects thermoregulation during exercise through the activation of hypothalamic neurons, rats underwent acute submaximal treadmill exercise (18 mmin(-1), 5% inclination) until fatigue received an intracerebroventricular injection of 1.43 μmol Nω-nitro-l-arginine metil ester (L-NAME), a nitric oxide synthase inhibitor, or saline (SAL). Skin tail temperature (Tsk) and internal body temperature (Ti) were continuously recorded and c-Fos expression was determined in the PVN and the SON. L-NAME treatment reduced physical performance by 48%, which was positively correlated with tail vasodilation capacity, which was reduced by 28%, and negatively correlated with heat storage rate (HSR), which was increased by 38%. Physical exercise until fatigue increased the number of c-Fos-immunoreactive (ir) neurons in the PVN and the SON. L-NAME-treatment significantly reduced the exercise-induced c-Fos expression in the PVN, whereas it had no effect in the SON. Interestingly, the number of c-Fos-ir neurons in the PVN was closely correlated with physical performance and inversely associated with HSR. Thus, the inhibition of central NO attenuates neuronal activation induced by exercise in the PVN, impairs the autonomic regulation of heat dissipation, and anticipates the fatigue. Brain NO seems to play a role in exercise performance through the regulation of neuronal activation in the PVN, but not in the SON, although the SON neurons are also activated by running exercise. Moreover, this role in performance mediated by neuronal activation in the PVN can be related with the improvement of thermoregulatory adjustments that occur during exercise.

The effects of physical training on hypothalamic activation after exercise and their relationship with heat dissipation were investigated. Following 8 weeks of physical training, trained (TR, n = 9) and untrained (UN, n = 8) Wistar rats were submitted to a regimen of incremental running until fatigue while body and tail temperatures were recorded. After exercise, hypothalamic c-Fos immunohistochemistry analysis was performed. The workload, body-heating rate, heat storage and body temperature threshold for cutaneous vasodilation were calculated. Physical training increased the number of c-Fos immunoreactive neurons in the paraventricular, medial preoptic and median preoptic nucleus by 112%, 90% and 65% (P < 0.01) after exercise, respectively. In these hypothalamic regions, increased neuronal activation was directly associated with the increased workload performed by TR animals (P < 0.01). Moreover, a reduction of 0.6°C in the body temperature threshold for cutaneous vasodilation was shown by TR animals (P < 0.01). This reduction was possibly responsible for the lower body-heating rate (0.019 ± 0.002°C/min, TR vs 0.030 ± 0.005°C/min, UN, P < 0.05) and the decreased ratio between heat storage and the workload performed by TR animals (18.18 ± 1.65 cal/kg, TR vs 31.38 ± 5.35 cal/kg, UN, P < 0.05). The data indicate that physical training enhances hypothalamic neuronal activation during exercise. This enhancement is the central adaptation relating to better physical performance, characterized by a lower ratio of heat stored to workload performed, due to improved heat dissipation.

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The purpose of this study was to examine whether the neuronal recruitment induced by exercise in autonomic nuclei is dependent of thermoregulatory phase and/or physical performance. Rats that were subjected to submaximal running exercise stopped in 3 different times: REST (control group), NADIR (the minimum heat dissipation phase), 20MIN (the stabilization phase of both body temperature ‐ Tb ‐ and tail skin temperature ‐ Tsk), and FATIGUE (Tb and Tsk reach their highest values​).The brains were removed and processed for determination of c‐Fos expression in the medial, median, and ventromedial preoptic areas (mPOA, mnPOA, and vmPOA, respectively), and paraventricular and supraoptic nucleus of hypothalamus (PVN and SON, respectively). Physical exercise induced an increase of c‐Fos expression in all brain areas. The c‐Fos expression in the vmPOA was similar for all exercising groups, while for mPOA, mnPOA, and PVN, it was gradually increased as the exercise and hyperthermic response are prolonged. Only after 20 min of exercise an increase in SON c‐Fos expression was verified. The neuronal recruitment within the mPOA, mnPOA, PVN, and SON was directly correlated to both physical performance and heat storage. The thermoregulatory brain areas are recruited even at small Tb changes, while the SON is recruited only when Tb reaches its higher values, possibly inducing changes on fluid balance. The recruitment rate in these areas is also influenced by duration of stress stimulus, either by increasing running time, as the prolonged hyperthermic response arising of exercise. Cnpq, Capes, and Fapemig.