Left ventricular function during sudden strenuous exercise.

Author:

Foster C,Anholm J D,Hellman C K,Carpenter J,Pollock M L,Schmidt D H

Abstract

Strenuous exercise without warm-up has been shown to produce ischemia-like electrocardiographic (ECG) abnormalities in 60-70% of healthy subjects. These abnormalities appeared to be related to the development of an unfavorable myocardial supply/demand balance and, in chronically instrumented dogs, to transient decreases in coronary blood flow. A mechanism involving subendocardial ischemia has been proposed to explain the response to sudden strenuous exercise (SSE). To determine whether the response to SSE included the development of changes in myocardial pump performance typical of ischemia, left ventricular (LV) function at rest, during graded exercise and during SSE was evaluated in nine young (26.6 +/- 3.4 years), well-trained male volunteers using first-pass radionuclide angiography. During graded exercise, the LV ejection fraction increased from 66.9 +/- 9.4% at rest to 73.0 +/- 7.1% during peak exercise, and the LV ejection rate increased from 3.36 +/- 0.67 sec-1 at rest to 6.58 +/- 1.10 sec-1 during peak exercise. Segmental wall motion was normal in all studies. During SSE, the LV ejection fraction decreased in very subject, from an average 72.2 +/- 8.6% at rst to 57.3 +/- 8.1% during exercise. The LV ejection rate remained relatively constant (3.98 +/- 0.92 sec-1 at rest vs 4.33 +/- 0.74 sec-1 during SSE). No segmental wall motion abnormalities were observed during SSE; however, LV wall motion appeared to be diffusely hypokinetic during SSE. In contrast to previous reports, few ECG abnormalities were observed during SSE. These results support the hypothesis that subendocardial ischemia is an important mechanism in the response to SSE. However, the lack of ECG changes and segmental wall motion abnormalities and the relatively high absolute value of the LV ejection fraction suggest that if subendocardial ischemia occurs during SSE, it is attributable to physiologic rather than pathologic mechanisms.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine

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