Hemodynamics during active and passive recovery from a single bout of supramaximal exercise

The aim of this work was to study the differences in cardiovascular response during two modes of recovery [active (AR): pedalling at 40 W; and passive (PR): complete rest seated] from a single bout of supramaximal exercise. Eight male amateur soccer players underwent two supramaximal cycle-ergometer tests, each consisting of pedalling against a resistance equivalent to 150% of the maximum workload achieved in a previous incremental test, followed by randomly assigned AR or PR. Cardiodynamic variables were obtained using an impedance cardiograph. Subjects were also connected to a sphygmomanometer, for systolic and diastolic blood pressure, and to a metabolimeter for oxygen uptake ((V) over dot O-2) assessments. We measured: heart rate (HR), stroke volume (SV), cardiac output (CO), the inverse of myocardial contractility calculated as pre-ejection period/left ventricular ejection time ratio (PEP/LVET), mean blood pressure (MBP), thoracic electrical impedance (Z(0)) as an index of central blood volume, and arterio-venous oxygen difference (A-V 02 Diff.). PR caused a lower CO compared to AR [mean (SE): 7 (0.7) vs. 10.4 (0.6) l.min(-1) at the 5th min of recovery] due to lower HR [106.2 (3.6) vs. 121.8 (4.5) bpm at the 5th min of recovery], SV [67.1 (5) vs. 86.1 (4.8) ml at the 5th min of recovery], and PEP/VET values [0.44 (0.007) vs. 0.39 (0.015) at the 5th min of recovery]. No differences were found in MBP and Z(0) between PR and AR [95.1 (1.9) vs. 92.3 (2.7) mmHg and 26.2 (1.1) vs. 26.6 (1) Omega respectively at the 5th min of recovery], while A-V O-2 Diff. values were higher during AR than during PR [108.8 (4.3) vs. 75.2 (5.4) ml.l(-1) at the 5th min of recovery]. Thus, although after a single bout of supramaximal exercise SV and CO are lower during PR than during AR, these differences are not due to an impairment of cardiovascular function, but are fully explained by the lesser muscular engagement that leads to a reduction in stimuli deriving from mechanoreceptors and central commands, thus causing a faster return of myocardial contractility and HR to resting values.