Voluntary exercise induces chromatin remodelling in the heart

Abstract

Chromatin remodelling regulates skeletal muscle adaptations to exercise and the development of pathological cardiac hypertrophy by interactions between repressor element 1‐silencing transcription factor (REST), mSin3A and histone deacetylases (HDAC). It is not known if chromatin remodelling regulates exercise‐induced physiological hypertrophy in the heart. Young male mice exercised on voluntary running wheels for 7 days. Heart weight:body weight and actin protein were not different compared to sedentary controls as overt cardiac hypertrophy does not occur until at least 14 days of exercise. mSin3A was higher in trained hearts but REST was not different between groups. HDAC 3, a pro‐hypertrophic class I HDAC, was higher in exercise‐trained hearts whereas HDAC 4, an anti‐hypertrophic class IIa HDAC, was lower in exercised hearts. To determine if chromatin remodelling is initiated during acute exercise, mice underwent a single bout of treadmill running for either 15 or 30 minutes and hearts were harvested immediately following exercise. Examination of the nuclear fractions revealed that REST, mSin3A and HDAC proteins were not different between groups. These data suggest that 7 days of voluntary exercise induces cardiac chromatin remodelling but that this does not occur immediately following a single exercise bout.