Hemodynamic and neurohumoral responses to dynamic exercise: normal subjects versus patients with heart disease

Abstract

Exercise testing has assumed a position of growing importance in the assessment of patients with chronic congestive heart failure. The hemodynamic and neurohumoral adjustments that occur during dynamic exercise are very complex, but are basically designed to ensure that oxygen delivery is commensurate with oxygen demand. These responses are clearly altered in the presence of certain types of heart disease. Patients with chronic congestive heart failure have an attenuated heart rate and blood pressure response throughout exercise, but this is most clearly evident when the data are expressed as a percent of peak oxygen consumption (VO2) rather than as a function of absolute VO2. Likewise, the sympathetic response to exercise is altered in patients with heart failure. Plasma norepinephrine is normally augmented as a function of VO2 during exercise, but this augmentation occurs during the later stages (beyond 50% of peak VO2). Patients with congestive heart failure show a greater than normal augmentation of plasma norepinephrine during exercise when the data are expressed in terms of absolute VO2. However, when the data are expressed as a percent of peak VO2, there appears to be a relative attenuation of the sympathetic response to exercise. Current information suggests that increased plasma norepinephrine and renin activity during exercise in patients with heart failure are not directly related to a decrement in nutritive blood flow to skeletal muscles. The mechanisms responsible for exercise intolerance in patients with heart failure are not known, but do not seem directly related to a decrement in cardiac output or an increase in left ventricular filling pressure.(ABSTRACT TRUNCATED AT 250 WORDS)