Nitric oxide pathway is an important modulator of heat loss in rats during exercise

Abstract

To assess the role of nitric oxide (NO) in central thermoregulatory mechanisms during exercise, 1.43 μmol (2 μL) of N ω-nitro- l-arginine methyl ester ( l-NAME, n = 6), a NO synthase inhibitor, or 2 μL of 0.15 M NaCl (SAL, n = 6) was injected into the lateral cerebral ventricle of male Wistar rats immediately before the animals started running (18 m min −1, 5% inclination). Core ( T b) and skin tail ( T tail) temperatures were measured. Body heating rate (BHR), threshold T b for tail vasodilation (TTbV), and workload ( W) were calculated. During the first 11 min of exercise, there was a greater increase in T b in the l-NAME group than in the SAL group (BRH = 0.17 ± 0.02 °C min −1, l-NAME, versus 0.09 ± 0.01 °C min −1, SAL, p < 0.05). Following the first 11 min until ∼40 min of exercise, T b levels remained stable in both groups, but levels remained higher in the l-NAME group than in the SAL group (39.16 ± 0.04 °C, l-NAME, versus 38.33 ± 0.02 °C, SAL, p < 0.01). However, exercise went on to induce an additional rise in T b in the SAL group prior to fatigue. These results suggest that the reduced W observed in l-NAME-treated rats (10.8 ± 2.0 kg m, l-NAME, versus 25.0 ± 2.1 kg m, SAL, p < 0.01) was related to the increased BHR in l-NAME-treated animals observed during the first 11 min of exercise ( r = 0.74, p < 0.01) due to the change in TTbV (39.12 ± 0.24 °C, l-NAME, versus 38.27 ± 0.10 °C, SAL, p < 0.05). Finally, our data suggest that the central nitric oxide pathway modulates mechanisms of heat dissipation during exercise through an inhibitory mechanism.