The effect of maximal treadmill exercise on the axis and amplitude of the ventricular depolarization wave

Abstract

Forty-five normal subjects (36 control subjects, four wrestlers and five cross country runners) and 21 patients with symptoms of cardiovascular disease (11 without and 10 with significant arteriographic evidence for coronary artery disease (CAD) underwent maximal exercise treadmill tests. Twelve lead ECGs were recorded and the voltage amplitude of the ventricular depolarization wave (ΣR), the frontal plane axis (FPA) and horizontal plane axis (HPA) were measured immediately before exercise in the supine (SP) and standing positions (ST), during exercise at a heart rate of 120 bpm (120), at peak exercise (MX), and in the supine position 1 minute after the completion of exercise (1R). In normal subjects (controls and athletes) there was a decrease in ΣR (p<.003) during exercise only above heart rates of 120 bpm; there was also a significant posterior shift in horizontal plane axis (p<.001) at maximal exercise. In the patient group, there was neither a decrease nor an increase in ΣR during exercise, while HPA demonstrated a posterior shift (p<.03) at maximal exercise, as compared to all other stages. The presence or absence of ischemic ST segment depression or of significant CAD at arteriography did not influence these results. The ΣR was significantly smaller in patients when compared to normal subjects at all stages (p<.005). Compared to control subjects, wrestlers had significantly less posteriorly rotated horizontal plane axis at one minute into recovery (p=.02), but no significant difference in frontal plane axis. The cross-country runners revealed no difference in frontal plane axis or horizontal plan axis when compared to controls. The ΣR for the wrestlers was not significantly different from that of controls; however, the cross-country runners had significantly highers ΣR (p<.005) when compared to controls at all stages. Athletes involved in intense aerobic activity have increased R wave amplitude as compared with other normal subjects, but they otherwise react normally to exercise by diminishing R wave amplitude above a heart rate of 120. The R wave amplitude changes with exercise are accompanied by posterior axis shifts of the R wave in the horizontal plane in all subjects. Patients with CAD do not demonstrate an exercise-induced decrease in R wave amplitude even though they shift their R wave axis posteriorly. The presence or absence of significant coronary disease by coronary arteriography or ischemic ST segment depression did not influence the results in this small group of patients.