The influence of endurance training on mechanical catecholamine responsiveness, beta-adrenoceptor density and myosin isoenzyme pattern of rat ventricular myocardium

Abstract

An investigation was carried out on the effects of 4 weeks' swimming training (2 X 90 min/day) on myocardial isometric tension development and rate of tension rise, and also on the changes induced therein by in vitro application of isoproterenol. This was done in 9 isolated papillary muscles of 9-week-old male Wistar rats and the results were compared with the data of age-matched sedentary controls. Ventricular beta-adrenoceptors [( 3H]-dihydroalprenolol binding) and the isoenzyme pattern of myosin (pyrophosphate gel electrophoresis) were examined in the same individuals. Isometric tension (T) and its first derivative (dT/dt) measured at the optimum of the length-tension diagram were moderately increased by long-term swimming training. Isoproterenol (10(-5) mol/l) induced a greater absolute and relative increase of both mechanical parameters in specimens of trained animals than in age-matched controls (delta T: 3.6 +/- 1.6 vs. 1.9 +/- 0.6 X 10(-2) N/mm2, p less than 0.05. delta dT/dt: 43.4 +/- 14.0 vs. 30.4 +/- 9.5 X 10(-2) N/mm2 X s, p less than 0.05). KD decreased significantly (4.23 +/- 1.0 vs. 2.44 +/- 0.3 nM, p less than 0.02), indicating an increase in receptor affinity, whereas receptor density revealed a tendency to decrease (98.8 +/- 22.6 vs. 67.1 +/- 18.0 fmol/mg protein, p less than 0.1). In addition, there was a shift in the isoenzyme pattern of myosin towards VM-1 after swimming training. Thus, under the conditions of the present experiments, the mechanical response to isoproterenol does not correlate to beta-adrenoceptor density. It is probable that, apart from the altered sensitivity of the receptors, other membrane or post-membrane processes, are responsible for the increased mechanical responsiveness to catecholamines. Although a relationship between myosin isoenzyme pattern and mechanical responsiveness to catecholamines is apparent taking into account our results and the findings on hypertensive rats as reported in the literature, it cannot be accounted for simply by altered beta-adrenoceptor density.