Nitric oxide synthase inhibition impairs muscle regrowth following immobilization

Nitric oxide (NO) has been shown to increase skeletal muscle protein synthesis. However, the role of NO during skeletal muscle regrowth after immobilization remains unknown. The purpose of this study was to determine whether NO is required for muscle regrowth/recovery after a period of disuse by immobilization. Male Wistar rats were divided into 4 groups: recovered, 1-(2-trifluoromethyl-phenyl)-imidazole (TRIM; 10 mg·kg body mass−1·day−1), NG-nitro-L-arginine methyl ester (L-NAME; 90 mg·kg body mass−1·day−1), and control. The recovered, TRIM, L-NAME groups were submitted to a 7-d muscle recovery period (by remobilization), following a 10-d immobilization period (to induce plantaris [PLA] muscle atrophy). After the experimental period, the PLA muscle was collected for morphometrical (muscle fibers cross-sectional area [CSA]) and molecular (Phospho-mTORSer2448 protein expression) analysis. After 7 d of recovery, the recovered group displayed complete muscle regrowth (CSA, recovered: 2.216 ± 214 vs. control: 2.219 ± 280 cm2; P > 0.05). However, CSA of the L-NAME (1.911 ± 267 cm2) and TRIM (1.896 ± 219 cm2) groups were statistically (P < 0.05) lower than the recovered and control groups. Additionally, there was a 29% increase in Phos-mTORSer2448 protein expression levels in the recovered group compared to control group, and this increase was blocked in both TRIM and L-NAME groups. In conclusion, our results indicate that NO is crucial for skeletal muscle regrowth after an immobilization period, potentially via the mTOR signaling pathway.