Central NO‐signaling is important to PVN activation, improving heat dissipation and exercise performance

Abstract

To investigate whether central NO‐signaling is involved in activation of PVN induced by treadmill running, L‐NAME (n=9) or SALINE (n=9) were injected into the lateral cerebral ventricule of Wistar rats immediately before running until fatigue (18m.min, 5% inclination). Intraperitoneal temperature and tail temperature were measured during exercise. Animals were subjected to transcardiac perfusion 90 minutes after the end of the exercise session. Brains were removed for c‐Fos immunohistochemical analysis. Heat storage rate (HSR) and maximal variation of tail temperature (MVTt) were calculated. Running exercise increased 656% c‐Fos expression in the PVN (p<0.001). Rats injected with L‐NAME showed a reduction of 53% in c‐Fos expression in the PVN (p<0.01), and a reduction of 42% in running performance (p<0.01), with lower MVTt (3.2 ± 0.4 L‐NAME vs. 4.4 ± 0.3 ºC SAL, p<0.05), and consequentely, higher HSR (15.2 ± 2.2 L‐NAME vs. 10.7 ± 2.0 cal/min SAL, p<0.01) when compared with SAL‐group. c‐Fos expression was directly associated with running performance (r=0.917, p<0.01), with MVTt in the SAL‐group (r=0.978, p<0.05), and inversely associated with HSR (r=0.739, p<0.05). Central inhibition of brain nitrergic system decreases the exercise‐induced c‐Fos expression in the PVN, leading to decreased heat dissipation capacity, which in turn, increased HSR, and decreased physical performance. CNPq, Capes and Fapemig.