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

Abstract

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 (VO(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 O(2) 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.

Impaired central hemodynamic response and exaggerated vasoconstriction during muscle metaboreflex activation in heart failure patients

“…Am J Physiol Heart Circ Physiol 292: H2988 -H2996, 2007. First published February 16,2007; doi: 10.1152/ajpheart.00008.2007.-The muscle metaboreflex is enhanced in chronic heart failure (CHF) patients, and this fact has been associated with the early fatigue shown by these patients in response to exercise. In animal studies of CHF, it was found that the limited capacity to enhance ventricular performance is responsible for a functional shift from a cardiac output to a systemic vascular resistance (SVR) increase in the mechanism by which the cardiovascular system raises blood pressure in response to the metaboreflex.…”

Comportamento do ergorreflexo na insuficiência cardíaca

“…With that, the autonomic balance is maintained through the complex interaction between the arterial baroreflex, central and peripheral chemoreflex, ergoreflex and pulmonary stretch reflex 10 . During the exercise, the central hemodynamics and the ventilatory responses are under the control of the autonomic nervous system, which depends on the interaction between the receptors of the brain's motor cortex and the peripheral afferences (baroreceptors, mechano and metaboreceptors) 11 . This system regulates the cardiac output, the vascular conductance and the ventilation, in an attempt to supply the adequate oxygenated blood flow to eliminate muscle metabolic byproducts.…”

“…The baroreceptors work with the control of muscle vasodilation and of heart rate through the sympathetic activation to maintain the blood pressure (BP) and counterbalance any disequilibrium between vascular resistance and cardiac output. On the other hand, the muscle receptors activate the nervous afferences, which, in turn, induce sympathetic-cardiovascular adjustments mediated in response to the mechanical and metabolic conditions of the working muscle 8,11 . There is evidence that the autonomic disequilibrium contributes to the pathogenesis and progression of heart failure.…”

“…Initially, the disequilibrium leads to the increase in BP, ventilation, renal vascular resistance and peripheral vascular resistance. Consequently, one reaches the increase in heart rate and this disequilibrium might be responsible for the disease progression 11 . A summary of the autonomic alterations found in HF, as well as their interactions can be seen in Figure 1.…”

Efeitos do intervalo de recuperação entre as séries sobre a pressão arterial após exercícios resistidos

“…Additionally, there may be a reduction in vascular resistance influenced by an accumulation of metabolites produced in muscle contraction, which, according to MacDonald et al 36 , is one of the factors accounting for vasodilatation and subsequent decrease in peripheral vascular resistance. This may occur so that BP is regulated in a way that permits an adequate circulation for metabolite buffering and supply of the required nutrients 37,38 . This could explain the postexercise decrease in DBP found in the present study, because the protocol with the lowest RI promoted longer PEH.…”