Mechanical stimuli increase skeletal muscle growth in an mTOR- and p70S6K-dependent manner. It has been proposed that costameric proteins at Z bands may sense and transfer tension to these initiators of protein translation, but few candidates have been identified. The purpose of this study was to determine if a role exists for the α7 integrin in the activation of hypertrophic signaling and growth following eccentric exercise training. Five wk old, wild type (WT) and α7BX2 integrin transgenic (α7Tg) mice were randomly assigned to one of two groups: 1) sedentary (SED) or 2) exercise training (EX). Exercise training consisted of downhill running 3 sessions/wk for 4 wk (-20°, 17 m/min, 30 min). Downhill running was used to induce physiological mechanical strain. Twenty-four hr following the final training session, maximal isometric hindlimb plantarflexor force was measured. Gastrocnemius-soleus complexes were collected for further analysis of signaling changes, which included AKT, mTOR and p70S6K, and muscle growth. Despite increased p70S6K activity in WT/EX, no significant changes in CSA or force were observed in WT/EX compared to WT/SED. AKT, mTOR and p70S6K activation was higher, and whole muscle hypertrophy, relative muscle weight, myofibrillar protein, and force were significantly elevated in α7Tg/EX compared to α7Tg/SED. A marked increase in average myofiber CSA was observed in α7Tg/EX compared to all groups. Our findings demonstrate that the α7β1 integrin sensitizes skeletal muscle to mechanical strain and subsequent growth. Thus, the α7β1 integrin may represent a novel molecular therapy for the treatment of disuse muscle atrophy.
- eccentric exercise
- Copyright © 2011, Journal of Applied Physiology