Prolonged decrease in cardiac volumes after maximal upright bicycle exercise

Abstract

Sequential exercise-gated cardiac blood pool scintigrams provide a noninvasive technique for evaluating the effect of therapeutic interventions on cardiac volumes and function only if both exercise periods are equivalent in the absence of an intervention. To assess whether they are indeed equivalent, 14 healthy subjects underwent gated blood pool scintigraphy during two maximal upright exercise periods separated by 60 min without changing position. Although resting cardiac output and blood pressure returned to base-line values 60 min after the first exercise period, mean resting heart rate was markedly higher (89.4 +/- 2.7 vs. 66.5 +/- 2.5 beats/min, P less than 0.001) and upright cardiac volumes lower [39.1 +/- 4.9 vs. 56.3 +/- 6.0 ml, P less than 0.001, for end-systolic volume (ESV) and 112.6 +/- 8.0 vs. 144.9 +/- 9.0 ml, P less than 0.001, for end-diastolic volume (EDV)] than before the first exercise period. These differences persisted during low levels of the subsequent exercise but not at high and maximum work loads. Cardiac volumes and heart rate 60 min after an identical exercise protocol in a second group of 22 subjects who received propranolol, 0.15 mg/kg iv, after their initial exercise, however, were the same as those preexercise. Thus higher sympathetic tone may be responsible for the persistently higher heart rate and decreased cardiac volumes after exercise, and the assumption that cardiac volumes and function are similar during two closely spaced sequential exercise studies is not always valid.

The sex-specific impact of systolic hypertension and systolic blood pressure on arterial-ventricular coupling at rest and during exercise

“…All cardiac volumes were normalized to body surface area, yielding their respective indexes: end-systolic volume index (ESVI) and stroke volume index (SVI). The coefficients of variation for the cardiac volumes in our laboratory were 8.6 and 6.4% at rest and at peak exercise, respectively (29,32).…”

Payments for Debts Associated With Exercise Can Become Higher as We Age and Limit Exercise Capacity⁎⁎Editorials published in the Journal of American College of Cardiologyreflect the views of the authors and do not necessarily represent the views of JACCor the American College of Cardiology.

“…Prolonged exposure of the older heart to catecholamines leads to excessive mitochondrial Ca 2ϩ gain (11) and continued activation of oxidative phosphorylation that might transiently persist in the absence of a continued energy demand. This markedly increases the catecholamine drive and might add to the O 2 debt particularly in older subjects, because in assuming the seated position after exercise, smaller cardiac volumes and a higher heart rate are reported and these effects are blunted by beta AR blockade (10). Cellular effects of beta AR stimulation, which include phosphorylation of numerous proteins, are reversed after exercise, in large part by activation of cholinergic receptor stimulation, which unfortunately also declines with aging (9).…”