BACKGROUND: The purpose of this experiment was to examine the effects of both exercise and beta-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 (i.p.) 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% VO2max. 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 beta-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.
BACKGROUND: The purpose of this experiment was to examine the effects of both exercise and beta-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 (i.p.) 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% VO2max. 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 beta-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.