2018 Volume 64 Issue Suppl.1 Pages 81-82
Cardiovascular regulation during sports and physical exercise is controlled by the autonomic nervous system, which exerts sympathoexcitation to increase arterial pressure and support muscle activity. High-intensity exercise is often associated with negative emotions, physical pain, and mental stress. These negative emotions affect the autonomic nervous system. Based on these facts, we considered that vigorous exercise with negative emotions possibly induces “over-activation” of the sympathetic nerves, with subsequent abnormal hemodynamics that may affect exercise performance. Thus, overcoming this negative state could potentially improve performance. Nonetheless, the relationship between neuronal mechanisms underlying negative mental states and cardiovascular regulation determining exercise performance remains unclear. The insular cortex (IC) and amygdala (AMY), parts of the limbic system, are thought to mediate negative effects. We hypothesized that IC and AMY are involved in negative mental states and in maintaining performance by tuning autonomic activities during exhausting exercise. To test this hypothesis, we first examined whether activation of IC and AMY depends on the intensity of treadmill exercise using c-Fos immunostaining. We divided Wistar/ST rats into 3 groups: high-intensity exercise (n=3, 40 m/min for 1 hour on the treadmill), middle-intensity exercise (n=3, 20 m/min for 30 min), or 1 hout (n=3, placed on the treadmill for 30 min). We observed a stronger c-Fos expression in the caudal part of IC (cIC) and the central nucleus of AMY (CeA) in the high-intensity exercise group than in the middle-intensity and sedentary groups. Subsequently, we examined whether exercise-related regions of IC and AMY (cIC and CeA) regulated cardiovascular responses. Interestingly, the microstimulation of cIC and CeA in urethane-anesthetized rats evoked contrasting cardiovascular responses, with decreased arterial pressure (n=6, -5.53 ± 3.43 mmHg, p<0.05) and increased arterial pressure (n=10, 11.3 ± 3.4 mmHg, p<0.01) in response to cIC and CeA stimulation, respectively. Finally, to confirm the anatomical connections between these areas and the nucleus of the solitary tract (nTS; a cardiovascular control center), we microinjected a retrograde tracer (Fluorogold) into nTS (n=12). We observed expression of Fluorogold in cIC and CeA, indicating direct connections between these regions and nTS. These observations suggest that both cIC and CeA are activated during exhausting exercise, but they may have differential roles in cardiac autonomic regulation via their projection to nTS.
