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THE JOURNAL OF SPORTS MEDICINE AND PHYSICAL FITNESS
Rivista di Medicina, Traumatologia e Psicologia dello Sport
Indexed/Abstracted in: Chemical Abstracts, CINAHL, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,111
The Journal of Sports Medicine and Physical Fitness 1999 March;39(1):42-6
Exercise and beta-adrenergic regulation of rat cardiac myosin isoforms
Wade M. E., Herb R. A., Powers S. K., Criswell D.
Departments of Exercise and Sport Science and Physiology, Center for Exercise Science, University of Florida, Gainesville, Florida, USA
Background. The purpose of this experiment was to examine the effects of both exercise and β-adrenergic receptor blockade on the expression of native cardiac myosin isoforms. Specifically, this experiment tested two hypotheses: 1) treatment of sedentary rats with the beta blocker, propranolol, will promote increased ventricular V3 (slow) native myosin content with a concomitant reduction of V1 (fast) myosin isoforms; and 2) endurance exercise training will result in an increased sympathetic drive and therefore will retard the propranolol-induced shift in cardiac myosin isoform expression.
Methods. Adult, male Sprauge-Dawley rats (120 days old) were randomly divided into 4 groups: 1) exercise-sham (ES); 2) exercise-propranolol (EP); 3) sedentary-sham (SS); and 4) sedentary-propranolol (SP). Propranolol (30 mg drug/kg body wt) and sham (saline) injections (IP) were administered 30 minutes prior to daily exercise. Both ES and EP groups completed six weeks (5 day/wk) of treadmill running at approximately 65-70% V.O2max.
Results. Data analysis revealed that exercise training did not alter (p>0.05) ventricular myosin isoforms in the sham injected animals. In contrast, propranolol treatment resulted in a significant (p<0.05) increase in the slow (V3) myosin isoform and a concomitant decrease in the V1 isoform in both sedentary and exercise trained animals.
Conclusions. The observed increase in V3 myosin isoform in propranolol treated rats supports the notion that β-adrenergic stimulation is an important regulator of cardiac myosin isoform expression. However, our hypothesis that exercise training would retard the propranolol-induced shift in cardiac myosin was not supported.