Reduction of stroke volume during exercise in man following ascent to 3,100 m altitude.

Abstract

The cardiac output response to submaximal supine leg exercise was determined in 8 normal subjects, 1st at sea level and again after 10 days at 3100 m. Using the direct Fick method for O2, cardiac output was measured at rest and during 4 work loads requiring O2 uptakes of 600-1600 ml/min at both altitudes. At rest and at each level of exercise, cardiac output was less at 3100 m, by as much as 2 1/min. Reduced cardiac output was chiefly due to decrease in stroke volume. Though blood volume was less at high altitude, acute plasma volume expansion in 2 subjects failed to restore stroke volume to sea-level values. The reduction of stroke volume was apparently not a result of altered blood pH, pulmonary hypertension and right ventricular overload, depletion of myocardial nore-pinephrine stores, diminished sympathetic nervous activity, or reduction in blood volume and ventricular filling pressures. Myocardial function was probably depressed by hypoxia secondary to lowered coronary arterial O2 tension, reduced coronary blood flow, or both.