Effects of Hsp27 overexpression and phosphorylation state on muscle hypertrophy and function induced by functional overload in mice

Abstract

Functional overload (FO, removal of major synergists) induces muscle growth and increased strength and fatigue resistance. With FO, Hsp25 (rodent form of Hsp27) expression and phosphorylation is significantly increased in hypertrophying muscle suggesting its role in muscle adaptation to loading stressors. Since phosphorylation can modify stress‐related Hsp25 functions, we tested the hypothesis that overexpression of human Hsp27 (TG) or a nonphosphorylatable Hsp27 mutant (MUT) will respectively increase and decrease FO‐induced muscle growth and function vs. wild type (WT) mice. Plantaris (Plt) isometric force and fatigue were measured in vivo 14 or 30 d after FO or sham surgery. Plt mass increased ~ 2 fold with FO in all groups, but was lower in MUT than WT at 14d (p<0.05). Plt maximal isometric force was 30% lower in MUT than WT at 30d (p<0.05) and tended to be lower in TG than WT at 14 and 30d. Fatigue resistance was lower in MUT than WT at 14 and 30d (16 and 32% respectively) and 20% lower in TG than WT with Sham only (p<0.05). Results suggest that elevated Hsp27 levels do not alter muscle adaptation to FO; however, preventing Hsp27 phosphorylation attenuates adaptations in force and fatigability compared to WT with 14 or 30d of FO. This suggests Hsp27 phosphorylation dependent functions (e.g. reducing apoptosis) may be involved in processes that increase muscle strength and fatigue resistance. Funded by NIH R15AR060469