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Abstract

Introduction


Exercise activates the sympathetic nervous system, increasing heart rate (HR), cardiac output and mean arterial pressure. Vagal withdrawal may also play a significant role in cardiac acceleration during exercise.1-3 Parasympathetic tone dominates the resting state4 and lowers the intrinsic HR of about 100 beats min-1 to the normal values of 70 to 80 beats min.-1 5 This phenomenon led to the hypothesis that the initial increment in HR during exercise could be due to reduced vagal tone at the onset, which increases the HR to 100 beats min.-1 Pharmacological studies have supported this hypothesis.1 Further increment in HR during exercise is brought about by sympathetic stimulation.2,4,6 Questions arise about the triggers for vagal withdrawal and sympathetic stimulation. One hypothesis is that vagal withdrawal is mediated by neural impulses from the cerebral cortex associated with the volitional component of exercise, also known as central command.2,6 Alternatively, sympathetic activation has been shown to be mediated by a reflex arising from cutaneous and muscle receptors.6,7 Thus, vagal withdrawal is assumed as being anticipatory feed forward, whereas sympathetic stimulation has been shown to be a feedback reflex.7
An important question in exercise physiology is whether the change from vagal modulation to sympathetic mediated cardiac acceleration can be detected from transients of HR response to exercise. If neural modulation changes in response to shifts from low intensity to high intensity exercise, the dynamics of HR response should represent the neural modulation of both vagus and sympathetic nerves. If vagal withdrawal is feed forward, it would result in a rapid increment in HR at the onset of exercise. Later on, reflex sympathetic stimulation would become dominant and HR would display slower dynamics owing to the reflex nature of the neuronal circuitry.
The purpose of this study was to find out if the effect of vagal withdrawal on exercise induced tachycardia in humans could be assessed using the difference in cardiac acceleration between graded steps of 50 and 100 Watts workload, respectively. This study identifies the degree of the time rate changes in heart rate in response to graded workload as a marker to differentiate the vagal withdrawal component from the sympathetic one during exercise.