Autonomic nervous system control of the heart

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Abstract
The purpose of this study was to assess hemodynamic responses to lower body negative pressure (LBNP) to −45 torr with selective cardiac parasympathetic (using atropine sulphate), sympathetic efferent (using metoprolol tartrate), and combined (atropine + metoprolol) blockade prior to and following 8 months of endurance exercise training in eight young men. Training resulted in significant increases of maximal oxygen uptake (27%) and blood volume (16%) and a decrease of baseline heart rate (HR, from 66 ± 4 to 57 ± 4 bpm). This training related bradycardia was exclusively determined by an enhanced vagal tone as there was no significant difference in intrinsic HR pre- to post-training and only atropine (pre: 100 ± 3 vs post: 101 ± 3 bpm), not metoprolol (pre: 56 ± 3 vs post: 49 ± 4 bpm), abolished the HR difference. The reflex tachycardia in the control experiment was significantly diminished following training. However, the increase in HR at LBNP −45 torr between pre- and post-training was similar after either atropine (+13 ± 2 vs +14 ± 1 bpm) or metoprolol (+8 ± 1 vs +8 ± 1 bpm). Reflex tachycardia was greater during atropine than metoprolol blockade and the sum of the HR increase during selective blockade (21 and 22 bpm) was greater when compared with the control (no blockade, 16 ± 2 vs 11 ± 2 bpm). There was no difference pre-to post-training in SV or Qc response to −45 torr LBNP during the control condition. However, selective β1-receptor blockade resulted in a greater decrease in SV to −45 torr LBNP post-training compared to pre-training (P < 0.05). These data indicate that the 8-month endurance exercise training program significantly increased vagal tone and its inhibitory influence on reflex cardiac responses, but did not change the intrinsic HR. Reflex tachycardia during LBNP was less with cardiac sympathetic blockade than with vagal blockade.

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