Influence of exercise intensity and duration on functional and biochemical perturbations in the human heart.

Abstract

Strenuous endurance exercise induces transient functional and biochemical cardiac perturbations that persist for 24-48h. The magnitude and time-course of exercise-induced reductions in ventricular function and increases in cardiac injury markers are influenced by the intensity and duration of exercise. In a human experimental model, exercise-induced reductions in ventricular strain and increases in cardiac troponin are greater, and persist for longer, when exercise is performed within the heavy- compared to moderate-intensity exercise domain, despite matching for total mechanical work. The results of the present study help us better understand the dose-response relationship between endurance exercise and acute cardiac stress/injury, a finding that has implications for the prescription of day-to-day endurance exercise regimes. Strenuous endurance exercise induces transient cardiac perturbations with ambiguous health outcomes. The present study investigated the magnitude and time-course of exercise-induced functional and biochemical cardiac perturbations by manipulating the exercise intensity-duration matrix. Echocardiograph-derived left (LV) and right (RV) ventricular global longitudinal strain (GLS), and serum high-sensitivity cardiac troponin (hs-cTnI) concentration, were examined in 10 males (age: 27±4years; V̇O2, peak : 4.0±0.8lmin(-1) ) before, throughout (50%, 75% and 100%), and during recovery (1, 3, 6 and 24h) from two exercise trials. The two exercise trials consisted of 90 and 120min of heavy- and moderate-intensity cycling, respectively, with total mechanical work matched. LVGLS decreased (P<0.01) during the 90min trial only, with reductions peaking at 1h post (pre: -19.9±0.6%; 1h post: -18.5±0.7%) and persisting for >24h into recovery. RVGLS decreased (P<0.05) during both exercise trials with reductions in the 90min trial peaking at 1h post (pre: -27.5±0.7%; 1h post: -25.1±0.8%) and persisting for >24h into recovery. Serum hs-cTnI increased (P<0.01) during both exercise trials, with concentrations peaking at 3h post but only exceeding cardio-healthy reference limits (14ngl(-1) ) in the 90min trial (pre: 4.2±2.4ngl(-1) ; 3h post: 25.1±7.9ngl(-1) ). Exercise-induced reductions in ventricular strain and increases in cardiac injury markers persist for 24h following exercise that is typical of day-to-day endurance exercise training; however, the magnitude and time-course of this response can be altered by manipulating the intensity-duration matrix.