Active Voice: Sympathetic Activity in Patients with Obstructive Sleep Apnea

By Linda Massako Ueno-Pardi, Ph.D.

Viewpoints presented in SMB commentaries reflect opinions of the authors and do not necessarily reflect positions or policies of ACSM.

Linda Massako Ueno-Pardi, Ph.D., was trained as a physiologist and researcher at the School of Arts, Science, and Humanities of University of São Paulo in Brazil. Her research focuses on neurovascular modulation, sleep, cognition, and exercise training in health and disease.

This commentary presents Dr. Ueno-Pardi’s views on the topic of a research article she and her colleagues authored together. Their article appeared in the July 2017 issue of
Medicine & Science in Sports & Exercise® (MSSE).

Obstructive sleep apnea (OSA) is characterized by partial (hypopnea) and/or total obstructions (apnea) of the upper airway at night. In contrast to healthy individuals who have a decrease in muscle sympathetic nerve activity (MSNA) during sleep, patients with OSA experience repetitive apneas and hypopneas that result in decreased airflow to the lungs, hypoxia, reoxygenation and surges in sympathetic activation. Together, these factors may play a role in alterations in cardiovascular system regulation that, over time, may contribute to increased risk of hypertension and cardiovascular morbidity.

In our published study, reported in the July 2017 issue of MSSE, we compared neurovascular control during metaboreflex activation in patients with moderate to severe OSA with a matched control group. The metaboreflex is measured during post-isometric handgrip muscle ischemia that induced a reflex increase in systemic arterial pressure, heart rate and sympathetic outflow to maintain adequate perfusion of exercising muscle. Post-isometric handgrip muscle ischemia causes the metabolites produced during exercise to become trapped in the forearm, stimulating the chemically sensitive muscle afferents of the exercise pressor reflex, eliminating the input from mechanically sensitive afferents and central command.

Our findings provide evidence that OSA patients, who are normotensive at rest, experience MSNA overactivation during moderate intensity (30 percent of maximum force for 3 minutes) static handgrip exercise, when compared with individuals without OSA. During post-handgrip muscle ischemia, when the muscle metaboreflex was isolated, MSNA remained significantly elevated in relation to baseline in the control group. In contrast, muscle metaboreflex activation elicited a decrease in MSNA to baseline values in the OSA group.

The metaboreflex response of MSNA was associated with markers of intermittent hypoxia and severity of nocturnal hypoxemia in middle-aged, sedentary patients with OSA. Notably, these were subjects without other comorbidities and no use of medications. Thus, patients with OSA experience MSNA overactivation during moderate static exercise and decreased muscle metaboreflex control of MSNA.