Abstract
The effect of swimming training (ST) on vagal and sympathetic cardiac effects was investigated in sedentary (S, N = 12) and trained (T, N = 12) male Wistar rats (200-220 g). ST consisted of 60-min swimming sessions 5 days/week for 8 weeks, with a 5% body weight load attached to the tail. The effect of the autonomic nervous system in generating training-induced resting bradycardia (RB) was examined indirectly after cardiac muscarinic and adrenergic receptor blockade. Cardiac hypertrophy was evaluated by cardiac weight and myocyte morphometry. Plasma catecholamine concentrations and citrate synthase activity in soleus muscle were also determined in both groups. Resting heart rate was significantly reduced in T rats (355 +/- 16 vs 330 +/- 20 bpm). RB was associated with a significantly increased cardiac vagal effect in T rats (103 +/- 25 vs 158 +/- 40 bpm), since the sympathetic cardiac effect and intrinsic heart rate were similar for the two groups. Likewise, no significant difference was observed for plasma catecholamine concentrations between S and T rats. In T rats, left ventricle weight (13%) and myocyte dimension (21%) were significantly increased, suggesting cardiac hypertrophy. Skeletal muscle citrate synthase activity was significantly increased by 52% in T rats, indicating endurance conditioning. These data suggest that RB induced by ST is mainly mediated parasympathetically and differs from other training modes, like running, that seems to mainly decrease intrinsic heart rate in rats. The increased cardiac vagal activity associated with ST is of clinical relevance, since both are related to increased life expectancy and prevention of cardiac events.
Highlights
Exercise training has been associated with several metabolic, cardiovascular and neurovegetative benefits
To study the mechanism involved in resting bradycardia after swimming training, the intrinsic heart rate (IHR) and sympathetic and parasympathetic cardiac autonomic controls were calculated
The main findings of the present investigation were that: 1) an 8-week swimmingtraining period significantly decreases resting heart rate (HR) in rats; 2) swimming training-induced bradycardia was associated with an increased cardiac vagal effect, but not with a sympathetic cardiac effect or IHR, and 3) swimming training induced cardiac hypertrophy in rats
Summary
Exercise training has been associated with several metabolic, cardiovascular and neurovegetative benefits. Resting bradycardia has been considered to be the hallmark cardiovascular effect of exercise-training adaptation in both animals [1,2] and humans [3]. Reduction in intrinsic heart rate (IHR) in exercise-trained rats [9] and exercise-trained humans [10], and more recently longer atrio-ventricular conduction time [11] have led some investigators to attribute resting bradycardia to intrinsic cardiac alteration. These contrasting results might be due to the methodology used to analyze the cardiac autonomic balance, the species studied, and probably to the different training regimens and modes applied
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