| Summary |
Skeletal muscle capillary proliferation is known to occur in response to an overload hypertrophy stimulus. Nitric oxide is necessary for muscle capillary proliferation in an aerobic exercise model; however, nitric oxide's role in capillary proliferation in overloaded skeletal muscle is unknown. Thus, the aim of this investigation was to determine to effect of Nw-nitro-L-arginine methyl ester L-NAME (a nitric oxide synthase inhibitor) administration on capillary angiogenesis in overloaded, hypertrophying rat skeletal muscle. Adult female Sprague Dawley rats (200-225g) were weight matched into either a control group (n=8) or L-NAME group (n=10). Twenty-one days of functional overload of the plantaris muscle in the left leg was produced by unilateral surgical ablation of the synergistic gastrocnemius muscle, while the right leg of each animal underwent a sham operation. A dosage of 20.9±0.3 mg/kg BW/day of L-NAME was administered to the L-NAME group two days prior to surgery and continuing throughout the loading period. After the loading period, plantaris muscles were harvested, analyzed for wet weight and total protein content, and subjected to immunohistochemical staining for capillarity and fiber size in 10pm cross-sections. Although plantaris mass, protein content, fiber cross-sectional area, and fiber perimeter were all lower in the L-NAME group, all of these variables increased to an equal relative extent with overload in both groups. In contrast, increases in capillary contacts per fiber and capillaries per fiber due to overload were observed only in the control group. L-NAME administration prevented the increase in capillarity due to the overload stimulus in rat plantaris muscles, indicating that nitric oxide is important for the angiogenic response observed in overloaded, hypertrophying skeletal muscle. |
