Evidence that brain L‐arginine availability modulates heat loss during physical exercise in rats

We investigated the effects of increased brain L‐arginine (precursor of nitric oxide synthesis) availability on thermoregulatory adjustments and physical performance in rats during exercise (18 m.min ‐1 and 5% inclination) until fatigue. Under anesthesia with ketamine and xylazine, male Wistar rats received implants of a guide cannula into the right lateral cerebral ventricle and of a temperature probe into the peritoneal cavity. On the day of the experiments, core (T b ) and tail skin temperatures were measured while the rats were running after injection of 2 μL of either NaCl 0.15 M (Sal, n = 11) or L‐arginine solution (L‐arg: 0.82 M, n = 6; 1.65 M, n = 6, and 3.30 M, n = 5) into the cerebral ventricle. Heat storage rate and threshold T b for tail vasodilation (TT b V) were calculated. L‐arg injection induced a dose‐dependent reduction in the TT b V and heat storage rate (3.23 ± 0.84 cal.min −1 , L‐arg 3.30 M; 6.46 ± 1.12 cal.min −1 , L‐arg 1.65 M; 8.59 ± 0.95 cal.min −1 , L‐arg 0.82 M; 9.54 ± 0.94 cal.min −1 , Sal; p<0.05). Although the lower T b at fatigue point, treatment with L‐arg failed to change exercise performance (25.7 ± 3.5 min, L‐arg 3.30 M; 25.7 ± 2.4 min, L‐arg 1.65 M; 26.4 ± 2.9 min, L‐arg 0.82 M; 26.9 ± 1.7 min, Sal). These results indicate that brain nitric oxide transmission modulates heat loss during exercise, probably by reducing sympathetic vasoconstrictor tonus to skin vessels. Supported by: CNPq, FAPEMIG e CAPES.