Abstract
Strenuous endurance exercise induces transient cardiac perturbations with ambiguous health outcomes. This 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 ± 4 yr; VO2peak: 4.0 ± 0.8 L·min−1) before, throughout (50-, 75- & 100-%), and during recovery (1-, 3-, 6- & 24-h) from two exercise trials. The two exercise trials consisted of 90 and 120 min of heavy- and moderate-intensity cycling, respectively, with total mechanical work matched. LVGLS decreased (P < 0.01) during the 90-min trial only, with reductions peaking at 1-h post (pre: −19.9 ± 0.6; 1-h post: −18.5 ± 0.7%) and persisting for >24-h into recovery. RVGLS decreased (P < 0.05) during both exercise trials with reductions in the 90-min trial peaking at 1-h post (pre: −27.5 ± 0.7%; 1-h post: −25.1 ± 0.8%) and persisting for >24-h into recovery. Serum hs-cTnI increased (P < 0.01) during both exercise trials with concentrations peaking at 3-h post, but only exceeding cardio-healthy reference limits (14 ng L−1) in the 90-min trial (pre: 4.2 ± 2.4 ng L−1; 3-h post: 25.1 ± 7.9 ng L−1). Exercise-induced reductions in ventricular strain and increases in cardiac injury markers persist for 24 h 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.
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