A Comparison of Two Exercise Training Programs on Cardiac Responsiveness to β-Stimulation in Obesity

Abstract

We demonstrated previously that exercise training did not restore normal cardiac beta-adrenergic responsiveness in obese rabbits. This study tested the hypothesis that an increased training volume was required to attenuate obesity-related reductions in isolated heart responsiveness to isoproterenol. Female New Zealand White rabbits were divided into lean control, lean exercise-trained, obese control, and obese exercise-trained groups. For the exercise-trained groups, total treadmill work over 12 weeks was increased 27% when compared with lean and obese animals trained with lower total training volume. After 12 weeks, Langendorff isolated hearts were used to study developed pressure, +dP/dt(max), and -dP/dt(max) responses to isoproterenol (10(-9) - 3 x 10(-7) M). Concentration-response data were fit to a sigmoidal function using a four-parameter logistic equation. Controls were compared with animals trained under the low- and high-training volume programs using one-way analysis of variance and Tukey's post-hoc test; separate analyses were conducted for lean and obese rabbits. In both lean and obese groups trained under the high-training volume program, EC50 values for +dP/day(tmax) and -dP/dt(max) were higher compared with same-weight controls and animals trained under the low-training volume program, indicating that contractility and relaxation responsiveness to isoproterenol was reduced by the higher training volume. Therefore, these data indicate that increased training volume failed to attenuate obesity-related decrements in isolated heart responsiveness to beta-adrenergic stimulation and caused reduced sensitivity to isoproterenol in both lean and obese animals.

Intense exercise training induces adaptation in expression and responsiveness of cardiac β-adrenoceptors in diabetic rats

“…As for obese rabbits [19], we hypothesized that intense exercise training in diabetic rats might decrease myocardial responsiveness to β-adrenergic stimulation. Consistent with an earlier study [3], we found that diabetes induces a rightward shift in the isoproterenol dose-response relationships without altering the magnitude of the peak responses.…”

“…Intense exercise training during diabetes decreases cardiac β2-adrenoceptors expression. Thus, based on these data and others in different experimental models (healthy rats, obese rabbits...), we hypothesized that exercise training may affect differently all of the above mentioned factors depending on the load [ 18 , 19 ]. The present study was conducted to investigate the effect of 8 weeks of intense exercise training on both cardiac function and β-adrenergic system in diabetic rat hearts.…”

Progression of cardiovascular and endocrine dysfunction in a rabbit model of obesity

“…Numerous reports have documented studies in which feeding rabbits a high-fat diet, for periods ranging from 2-12 weeks, results in increased adiposity, associated with a 10-20% increase in mean arterial pressure (MAP) and a 10-35% increase in HR. 2,[6][7][8][9][10][11][12][13][14][15][16] Telemetric recordings in the fat-fed rabbit have shown that elevations in MAP and HR occur quickly, within days of commencing fat feeding, even before major changes in body weight occur. 9,17 Furthermore, increases in MAP and HR are progressive, within a 3-week time frame, but then seem to plateau.…”

Exercise training improves cardiac function and attenuates arrhythmia in CPVT mice

“…Because sympathetic activity is a major determinant of arrhythmia susceptibility, investigators have examined the effect of exercise training on the ␤-ARs using radioligand binding or protein level measurements. These measurements could not demonstrate a change in ␤-receptor expression following exercise training (3,12,16,37). While differences between the studies could result from protocol duration and intensity, none of these studies found a change in the ␤-receptor affinity.…”

“…Because the training protocol was adjusted according to the running speed of KO mice, the exercise intensity (at most 15 m/min) was rather mild for normal animals. Apparently, exercise adaptation was less pronounced in healthy animals due to inadequate training volume (3,15).…”