Papel do Óxido Nítrico central na termorregulação durante o exercício físico em ratos

Abstract

To assess the role of nitric oxide (NO) in central thermoregulatory mechanisms duringexercise, 1.43 µmol (2µl) of Nù-nitro-L-arginine methyl ester (L-NAME, n=6), a NOsynthase inhibitor, or 2 µl of 0.15 M NaCl (SAL, n=6) was injected into the lateralcerebral ventricle of male Wistar rats immediately before the animals started running(18m/min, 5% inclination). Core and skin tail temperatures, as well as oxygenconsumption were measured at rest, during exercise until fatigue, and thereafter duringthe 30 minutes of recovery. Body heating rate, heat storage, threshold core temperaturefor tail vasodilation, and mechanical efficiency were calculated. There were a greaterincrease in body heating rate (0.17 ± 0.02 ºC.min-1, L-NAME vs 0.09 ± 0.01 ºC.min-1,Sal, p<0.01) and heat storage (454.6+62.8 cal, L-NAME vs 250.0+37.3 cal, Sal, p<0.05)in the L-NAME group than in the SAL group during the first 11 minutes of exercise(dynamic state). Furthermore, the L-NAME-treated animals had a greater oxygenconsumption (66.8+0.7 mLO2.kg-1.min-1, L-NAME vs. 57.1+0.3 mLO2.kg-1.min-1, Sal;p<0.05) and a lower mechanical efficiency (17.8+0.7 %, L-NAME vs 21.7+0.7 %, Sal,p<0.05) following the first 11 minutes until fatigue (steady state). In addition, there wasa significant reduction in running performance by L-NAME-treated animals comparedto SAL-treated animals. These results suggest that the reduced workload (11.82 + 1.45kgm, L-NAME vs 24.05 + 2.12 kgm, Sal, p<0.01) observed in L-NAME-treated ratswas related to the increased body heating rate in L-NAME-treated animals observedduring the first 11 minutes of exercise (r=0.74, p<0.01) due to the change in thresholdcore temperature for tail vasodilation (39.12+0.24 ºC, L-NAME vs 38.27+0.10 ºC, Sal,p<0.05). Finally, our data suggest that the central nitric oxide pathway modulatesmechanisms of heat dissipation and heat production during exercise, through aninhibitory mechanism, delaying fatigue.