Does a 20- to 30-min period of rhythmic exercise lead to prolonged inhibition of vagally mediated bradycardia evoked by baroreceptor stimulation in normal human subjects?
Rhythmic exercise causes a prolonged attenuation of cardiac vagal action and baroreflex slowing of the heart, potentially mediated by neuropeptide Y release.
In normal human subjects, we tested whether a 20- to 30-min period of rhythmic exercise, intended to provoke strong activation of the sympathetic nerves, would lead to prolonged inhibition of vagally mediated bradycardia evoked reflexly by stimulation of the baroreceptors by neck suction. Negative pressure within the neck cuff (-40 to -80 mmHg) reflexly evoked a reproducible increase in pulse interval. Following exercise, this increase in pulse interval was reduced from 444 +/- 104 ms to 76 +/- 57 ms (mean +/- SEM). Recovery time was 42 +/- 9 min. These findings demonstrate a prolonged attenuation of cardiac vagal action following rhythmic exercise in normal human subjects. It is known that neuropeptide Y (NPY) is released from cardiovascular sympathetic nerves, that it attenuates cardiac vagal action and that plasma levels of NPY are elevated for a prolonged period after exercise. Therefore, it is proposed that NPY, released from sympathetic nerves during exercise, attenuates reflexly evoked cardiac vagal action for a prolonged period after exercise ends.
Ulman et al. (Thu,) studied this question.
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