COMPREHENSIVE MODEL OF AUTONOMIC CONTROL OF HEART RATE DURING EXERCISE

Purpose: Exercise Physiology textbooks illustrate the autonomic control of heart rate (HR) at the beginning of dynamic exercise as an immediate and selective withdrawal of parasympathetic (PS) control of the Sino-Atrial node resulting in a rise in HR up to 100 beats per min. The appearance of norepinephrine in the blood after 100 bpm was interpreted as the time at which the sympathetic nervous system was activated. In the past ten years animal investigations indicate that increases in sympathetic outflow are involved in the increase in HR at exercise onset. Therefore, we hypothesized that re-analysis of previous investigations utilizing pharmacologic blockade of the autonomic nervous system and our carotid baroreflex modeling techniques of humans during dynamic exercise would identify the role of sympathetic activity in exercise. Methods: Comprehensive analysis of HR data presented in 8 "autonomic neural control of heart rate" research articles and book chapters in both humans and animals coupled with our own neck pressure/neck suction published data was used to generate a novel model of the autonomic control of HR during exercise. Results: Throughout the progression of exercise (HR = 100, 117, 150), neck pressure stimuli induce reflexive increases in HR (+6, 3, 1), and pharmacological blockade with glycopyrrolate induces increases in HR (+24, 21, 12). Comprehensive regression modeling of the increases in heart rate during exercise identified that sympathetic activity establishes the exercise intensity related HR and it is the PS control of the heart that expresses the baroreflex response. Conclusions: These data provide compelling evidence that cardiac sympathetic and PS activities were continuously active throughout exercise. Furthermore, there was no evidence of an abrupt shift from PS withdrawal to sympathetic activation in autonomic control of HR during exercise but rather a steady rise in HR due to increasing cardiac sympathetic tone. Contrary to there being a PS withdrawal at the onset of exercise previous work identify that during exercise onset increases in PS tone dampen the sharp rise in HR in response to the immediate increase in cardiac sympathetic activity.