Abstract

Heart rate (HR) during exercise is controlled by cardiac sympathetic (CSNA) and vagal (CVNA) efferent nerve activity and plasma catecholamines. To determine their relative contribution to the exercise tachycardia, we examined the effects of adrenalectomy (ADX) and autonomic blockades on the HR response during treadmill exercise for 32 min in 13 conscious rats. The baseline HR was not influenced by ADX, suggesting no significant role of adrenal catecholamines on the baseline HR. Since the baseline HR was increased 61 beats/min by atropine methyl nitrate (1.5 mg/kg) and decreased 26 beats/min by atenolol (3 mg/kg), CVNA determined the baseline HR more than CSNA. ADX did not affect the immediate increase in HR at 0–12 s from the exercise onset but reduced the subsequent increase in HR at 13–30 s. These increases in HR at the early period of exercise were more blunted by atenolol than atropine. On the other hand, the peak tachycardia response of 99 ± 8 beats/min at the end of exercise, which was the same between the intact and ADX conditions, was blunted to 73% by atenolol, to 77% by atropine, and to 35% by combined atenolol and atropine, respectively. In conclusion, it is likely that the tachycardia at the beginning of dynamic exercise is predominantly determined by the cardiac autonomic nerve activity, especially by a prompt increase in CSNA, and that the hormonal mechanism due to adrenal epinephrine contributes to a further increase in HR approximately in 13 s from the onset of exercise.

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