The average CO in a resting man is 5.0 L/min (70 mL x 72 BPM) (Ganong, 2003). Cardiac output is controlled by many factors, primarily by the sympathetic and parasympathetic nervous system. During exercise, the sympathetic nervous system is activated. As a result, there is an increase in heart rate due to the increased sympathetic stimulation and decreased vagal stimulation to the sinoatrial node (SA node), which is the pacemaker of the heart (increased chronotropic contractility). There is also an increase in the force of contraction by the cardiac myocytes (increased inotropic contractility). From the results, it can be seen that following exercise, the heart rate (BPM) increases significantly. The mean control value was approximately 79 beats per minute and after exercise this value rose to approximately 148 beats per minute. The changes in the ECG readings were also depictive of the increase in heart rate and cardiac contractility. The mean R-T interval, which represents the peak of ventricular depolarization/contraction up to ventricular repolarization/ relaxation, shortened from 0.102 at rest to 0.106 sec during exercise. The mean value of diastole duration, which represents the period of relaxation, during which the heart fills with blood (Guyton & Hall, 2000) also shortened to 0.518 to 0.268 sec. The P-Q interval, which represents atrial depolarization to the start of ventricular repolarization (Fauci, et.al, 2008), increased which should is not the expected outcome since this too should be shortened due to the increase in heart rate. The ECG also shows that the P wave is deeper during exercise, this is because the atrium produced a more powerful contraction in order to meet the demand for oxygen. This is also true for the QRS wave which also provides more powerful contractions of the ventricles.
During exercise, there is more blood going to the active or contracting muscles. The heart and skeletal muscles are predominantly under local control whereas the splanchnic, renal and other sub-circulations are predominantly under systemic control. Since exercise causes an increased sympathetic response, the blood vessels of the splanchnic, renal and other sub-circulations constrict which causes the blood to be shunted to the exercising active skeletal and cardiac muscles. Local control of the active skeletal and cardiac muscles is also responsible for the increased blood flow because of the vasodilation due to the increased metabolic activity (release of metabolites such as Mg++, Ca++, ADP and PCO2). The premise of the cardiovascular system is that more blood is given to the organs or areas that are metabolically active. At rest, the skeletal muscles only receive 21% of the cardiac output. At peak, the exercising muscle receives 85% of the cardiac output (Berne, et.al, 2004). The milking out of blood from the skeletal muscle veins during contraction (muscle pump) and the constriction of venous capacitance vessels as a result of the sympathetic response causes the increase in stroke volume which subsequently, increases the cardiac output.
In healthy young individuals breathing at a normal rate, the heart rate varies with the phases of respiration; it accelerates during inspiration and decelerates during expiration (Ganong, 2003). This was seen in the results as the mean value of BMP during inspiration was greater (88.74) than during expiration (67.109). This is termed as sinus arrhythmia, which is considered