Associação entre a aptidão física e as respostas cardiovasculares ao metaborreflexo muscular em pacientes com doença arterial coronariana

Abstract

The muscle metaboreflex regulates cardiovascular function during physical exercise. The increase in blood pressure mediated by the muscle metaboreflex in patients with coronary artery disease (CAD) seems to rely more on an increase in sympathetic-mediated vasoconstriction (increase in peripheral vascular resistance [PVR]) rather than on the flow-mediated mechanism (increase in stroke volume [SV] and cardiac output [CO]). Sustained PVR may lead to early fatigue during exertion in these patients. However, the mediators of this response have not yet been elucidated. Objective: To investigate the association between cardiorespiratory and muscular fitness with cardiovascular responses to muscle metaboreflex activation in patients with CAD. Methods: Patients with CAD (n = 20, 61.7±8.0 years, 28.4±3.9 kg/m2) underwent an exercise stress test and a maximal voluntary contraction (MVC) test using handgrip strength. Hemodynamic variables were assessed using photoplethysmography (Finometer) during the activation of the muscle metaboreflex through a post-exercise circulatory arrest (PECA) protocol. PECA consisted of 5 min of rest; 90 s of isometric handgrip exercise at 40% of MVC; 3 min of ischemia of the exercised arm (200 mmHg); and 3 min of recovery. Responses to muscle metaboreflex were calculated as the difference in values between the ischemia period and rest (Δ) for mean arterial pressure (MAP), SV and PVR. The association between variables was calculated using the Pearson’s correlation test and multiple linear regression. Results: The VO2max obtained by the patients was 31.96 ± 5.70 mL/kg/min and the MVC was 90.5 ± 21.1 lbs. There was a significant increase during muscle metaboreflex activation compared to rest for MAP (+14.74 ± 9.56 mmHg, P < 0.0001) and PVR (+0.13 ± 0.07 mmHg.seg/mL, P < 0.0001), but not for SV (+1.91 ± 5.54 mL, P = 0.13). MVC was directly associated with ΔSV (R = 0.53 and P = 0.01), but not with ΔMAP (R = 0.20 and P = 0.31) or ΔPVR (R = -0.13 and P = 0.65). The multiple linear regression model non-adjusted and adjusted for age and sex indicated ΔSV as a predictor of MVC (β = +1.95 and +1.37; P = 0.01 and 0.03; respectively). No associations were observed between VO2max and ΔSV (R = 0.29 and P = 0.22), ΔMAP (R = 0.14 and P = 0.54), or ΔPVR (R = 0.05 and P = 0.83) in response to muscle metaboreflex activation. Conclusion: The contribution of SV to the muscle metaboreflex response seems to be one of the moderators of muscular fitness in patients with CAD