Control of Heart Rate
Heart rate is normally determined by the pacemaker activity of the sinoatrial node (SA node) located in the posterior wall of the right atrium. The SA node exhibits automaticity that is determined by spontaneous changes in Ca++, Na+, and K+ conductances. This intrinsic automaticity, if left unmodified by neurohumoral factors, exhibits a spontaneous firing rate of 100-115 beats/min. This intrinsic firing rate decreases with age.
Heart rate is decreased below the intrinsic rate primarily by activation of the vagus nerve innervating the SA node. Normally, at rest, there is significant vagal tone on the SA node so that the resting heart rate is between 60 and 80 beats/min. This vagal influence can be demonstrated by administration of atropine, a muscarinic receptor antagonist, which leads to a 20-40 beats/min increase in heart rate depending upon the initial level of vagal tone.
For heart rate to increase above the intrinsic rate, there is both a withdrawal of vagal tone and an activation of sympathetic nerves innervating the SA node. This reciprocal change in sympathetic and parasympathetic activity permits heart rate to increase during exercise, for example.
Heart rate is also modified by circulating catecholamines acting via β1-adrenoceptors located on SA nodal cells. Heart rate is also modified by changes in circulating thyroxin (thyrotoxicosis causes tachycardia) and by changes in body core temperature (hyperthermia increases heart rate).
The maximal heart rate that can be achieved in an individual is estimated by
Maximal Heart Rate = 220 beats/min − age in years
Therefore a 20-year-old person will have a maximal heart rate of about 200 beats/min, and this will decrease to about 170 beats/min when the person is 50 years of age. This maximal heart rate is genetically determined and cannot be modified by exercise training or by external factors.