Premium
Effects of muscle specific VEGF loss on muscle hypertrophy and function induced by functional overload in mice (1102.6)
Author(s) -
Huey Kimberly,
Delavar Hamid,
Breen Ellen
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1102.6
Subject(s) - endocrinology , medicine , isometric exercise , skeletal muscle , muscle hypertrophy , angiogenesis , chemistry
Functional overload (FO) stimulates muscle growth and increases strength and endurance. Vascular endothelial growth factor (VEGF) is essential for exercise‐induced angiogenesis. We hypothesized VEGF expressed by skeletal myofibers is critical for muscle growth and improvements in force production and fatigue resistance. To test this hypothesis, adult mice with conditional skeletal myofiber specific VEGF gene deletion (skmVEGF ‐/‐ ) and wild type (WT) littermates underwent functional overload (FO) of the plantaris (removal of gastrocnemius and soleus) or sham surgery. In vivo plantaris isometric force and fatigue resistance (% of maximal force after 10 contractions) were measured 7 or 14d after FO or sham surgery with a dual mode foot plate system in anesthetized skmVEGF ‐/‐ or WT mice. Mass increased ~ 35% in both 14d‐FO groups compared to sham (p<0.01). In WT mice subjected to FO, maximal isometric force was unchanged at 7d and increased at 14d (sham, 0.37±0.03; FO, 0.46±0.04 g/mg body mass, p<0.05). In skmVEGF ‐/‐ mice, FO was associated with a decrease in maximal force after 7d (sham, 0.39±0.0; FO, 0.23±0.03 g/mg body mass, p<0.05) and 14d (sham, 0.39±0.03; FO, 0.27±0.04 g/mg body mass, p<0.05). Fatigue resistance was not different between groups at 7d. After 14d of FO, fatigue resistance increased from 58±3%‐sham to 73±2%‐FO of maximal force in WT mice (p<0.05) and was unchanged in skmVEGF ‐/‐ mice. These data suggest that VEGF‐dependent functions are essential for improving muscle strength and fatigue resistance, independent of muscle growth, in response to a hypertrophic stimulus. Grant Funding Source : Supported by NIH R15AR060469