Exercise performance effect of central dopamine is mediated by hypothalamic neuronal activation.

Abstract

Acting centrally, dopamine has been shown to induce ergogenic effects derived from its influence on thermoregulation, motivation, reward, and motor control. Thus, to evaluate the role of the central dopaminergic system in hypothalamic neuronal activation and its relationship with exercise performance, Wistar rats were intracerebroventricularly injected with saline (SAL) or SCH-23390 (SCH, dopamine D1 receptor blocker) at rest and before timed submaximal exercise (∼13 min) or exercise until fatigue. Core body and tail temperatures were recorded throughout the exercise. Hypothalamic Fos immunoreactivity (c-Fos-ir) expression was evaluated in thermoregulatory areas such as the median preoptic nucleus (MnPO), medial preoptic nucleus (MPO), paraventricular nucleus (PVN) and supraoptic nucleus (SON). Despite unchanged thermoregulatory adjustments, central D1 receptor blockade markedly decreased the exercise time and the workload performed until fatigue. Subsequently to timed exercise, D1 blockade increased neuronal activation in the MnPO, PVN, and SON. However, c-Fos-ir expression in the MnPO, MPO, PVN, and SON was similar between treated and control animals at fatigue. The data indicate that dopamine D1 receptors modulate exercise performance by altering hypothalamic neuronal activation elicited by exercise.