Chronic exercise induces adaptations that increase the functional capacity of the cardiovascular system. Aside from ventricular growth, these adaptations include a shift in the MHC isoenzyme pattern to enhance ventricular contractility. It is unclear whether adaptations by the contractile elements are an early event and specific to exercise, or whether they progress as a function of cardiac growth. Examining early adaptations to training is also important because it is during this period when the greatest imbalance between increased demand and functional capacity exists, and it is likely that the mechanisms responsible for propagating changes in the myocardial phenotype are most active.
To determine whether changes in left ventricular (LV) contractile elements are an early adaptation to chronic exercise.
Rats were randomly assigned to sedentary control or exercise training groups for 1 or 10 wk of training. After training, the LV was analyzed for protein by Western blot or mRNA by Northern and real-time QRT-PCR analysis.
Plantaris cytochrome oxidase activity was significantly (P < 0.05) increased by 1 wk (+28%) or 10 wk (+32%) of training. Training significantly increased LV myofibrillar α-MHC protein and α-MHC-mRNA after both training periods. No changes in myofibrillar β-MHC protein or β-MHC-mRNA were observed. After 1 wk of training, LV skeletal α-actin-mRNA was significantly increased, whereas no changes were found for ANF, glyceraldehyde dehydrogenase, or cytochrome oxidase IV. Gel mobility shift analysis determined that YY1 DNA binding was significantly decreased in LV extracts from trained animals, although no change in YY1-mRNA expression was observed.
Increased myofibrillar α-MHC protein and α-MHC-mRNA expression are early events in the adaptation to chronic exercise and occur before significant cardiac growth. These adaptations enhance myocardial contractility and permit increases in maximal cardiac output during heavy exercise.
Department of Physiology, New York Medical College, Valhalla, NY
Address for correspondence: John G. Edwards, Ph.D., Department of Physiology, New York Medical College, Valhalla, New York, 10595; E-mail: firstname.lastname@example.org.
Submitted for publication December 2005.
Accepted for publication July 2006.