Abstract

At rest, heart rate is maintained at approximately 60-100 beats per minute by innervation of the parasympathetic nervous system [1]. Elevated parasympathetic activity via constant stimulation of the Vagus nerve will yield a significant decline in heart rate, known clinically as bradycardia [2,3]. The right branch of the Vagus nerve inhibits the SA node, or the cardiac pacemaker, while the left branch of the Vagus nerve inhibits the AV node [2]. While performing exercise, the heart will conduct the same functions as it would at rest, but at a much more accelerated rate. Given that the cardiovascular system is a closed system, there exists only a set volume of blood in pulmonic and systemic circulation of approximately 5 Liters in the reference person [1]. To accommodate increased metabolic activity, cardiac output, defined as the product of heart rate and stroke volume, must be increased to match the metabolic demands of the activity i.e. the finite quantity of blood must be circulated at a much greater rate than it would be at rest [1,2]. Heart rate increases observed upon initiation of physical activity are attributed to a withdrawal of vagal tone, or a reduction in parasympathetic influence over the myocardium [1]. Once the heart rate reaches approximately 100 beats per minute, or the base sinus rhythm set by the sinoatrial node, sympathetic activation takes control and elevates heart rate up to 250 beats per minute, depending upon exercise intensity [1,2]. Heart rate can be calculated using ECG tracings by identifying the duration of the R-R interval [4].