We demonstrated that patients with obstructive sleep apnea (OSA) have reduced muscle metaboreflex control of muscle sympathetic nerve activity (MSNA). In addition, exercise training increased muscle metaboreflex control in heart failure patients.
We tested the hypothesis that exercise training would increase muscle metaboreflex control of MSNA in patients with OSA.
Forty-one patients with OSA were randomized into the following two groups: 1) nontrained (OSANT, n = 21) and 2) trained (OSAT, n = 20). Muscle sympathetic nerve activity was assessed by microneurography technique, muscle blood flow (FBF) by venous occlusion plethysmography, heart rate by electrocardiography, and blood pressure with an automated oscillometric device. All physiological variables were simultaneously assessed at rest, during isometric handgrip exercise at 30% of the maximal voluntary contraction, and during posthandgrip muscle ischemia (PHMI). Muscle metaboreflex sensitivity was calculated as the difference in MSNA between PHMI and the rest period. Patients in the OSAT group underwent 72 sessions of moderate exercise training, whereas patients in the OSANT group were clinical follow-up for 6 months.
The OSANT and OSAT groups were similar in anthropometric, neurovascular, hemodynamic and sleep parameters. Exercise training reduced the baseline MSNA (34 ± 2 bursts per minute vs 25 ± 2 bursts per minute; P < 0.05) and increased the baseline FBF (2.1 ± 0.2 mL·min−1 per 100 g vs 2.4 ± 0.2 mL·min−1 per 100 g; P < 0.05). Exercise training significantly reduced MSNA levels and increased FBF responses during isometric exercise. Exercise training significantly increased MSNA responses during PHMI (Δ6.5 ± 1 vs −1.7 ± 1 bursts per minute, P < 0.01). No significant changes in FBF or hemodynamic parameters in OSANT patients were found.
Exercise training increases muscle metaboreflex sensitivity in patients with OSA. This autonomic change associated with increased muscle blood flow may contribute to the increase in exercise performance in this set of patients.
1Heart Institute (InCor) HCFMUSP, University of Sao Paulo Medical School, Sao Paulo, SP, BRAZIL;
2Experimental Physiopathology, University of Sao Paulo, Sao Paulo, SP, BRAZIL;
3School of Arts, Sciences and Humanities, University of Sao Paulo, Sao Paulo, SP, BRAZIL; and
4School of Physical Education and Sport, University of Sao Paulo, Sao Paulo, SP, BRAZIL
Address for correspondence: Renan Segalla Guerra, Dr. Eneas de Carvalho Aguiar, 44, Cerqueira Cesar, Sao Paulo, SP, CEP: 05403-904, Sao Paulo, Brazil; E-mail: email@example.com.
Submitted for publication May 2018.
Accepted for publication October 2018.