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

John A. Paraskos, Helenus Gratema, W. Scott Walker, Linda A. Pape, Joseph S Alpert

Research output: Contribution to journalArticle

8 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)161-166
Number of pages6
JournalJournal of Electrocardiology
Volume16
Issue number2
DOIs
StatePublished - 1983
Externally publishedYes

Fingerprint

Exercise
Coronary Artery Disease
Heart Rate
Supine Position
Exercise Test
Athletes
Angiography
Posture
Coronary Disease
Electrocardiography
Cardiovascular Diseases

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

The effect of maximal treadmill exercise on the axis and amplitude of the ventricular depolarization wave. / Paraskos, John A.; Gratema, Helenus; Walker, W. Scott; Pape, Linda A.; Alpert, Joseph S.

In: Journal of Electrocardiology, Vol. 16, No. 2, 1983, p. 161-166.

Research output: Contribution to journalArticle

Paraskos, John A. ; Gratema, Helenus ; Walker, W. Scott ; Pape, Linda A. ; Alpert, Joseph S. / The effect of maximal treadmill exercise on the axis and amplitude of the ventricular depolarization wave. In: Journal of Electrocardiology. 1983 ; Vol. 16, No. 2. pp. 161-166.
@article{ae961d3dca854a768490cf84a404cc3c,
title = "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.",
author = "Paraskos, {John A.} and Helenus Gratema and Walker, {W. Scott} and Pape, {Linda A.} and Alpert, {Joseph S}",
year = "1983",
doi = "10.1016/S0022-0736(83)80020-X",
language = "English (US)",
volume = "16",
pages = "161--166",
journal = "Journal of Electrocardiology",
issn = "0022-0736",
publisher = "Churchill Livingstone",
number = "2",

}

TY - JOUR

T1 - The effect of maximal treadmill exercise on the axis and amplitude of the ventricular depolarization wave

AU - Paraskos, John A.

AU - Gratema, Helenus

AU - Walker, W. Scott

AU - Pape, Linda A.

AU - Alpert, Joseph S

PY - 1983

Y1 - 1983

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0020546560&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0020546560&partnerID=8YFLogxK

U2 - 10.1016/S0022-0736(83)80020-X

DO - 10.1016/S0022-0736(83)80020-X

M3 - Article

C2 - 6854185

AN - SCOPUS:0020546560

VL - 16

SP - 161

EP - 166

JO - Journal of Electrocardiology

JF - Journal of Electrocardiology

SN - 0022-0736

IS - 2

ER -