Altered ventilatory responses to exercise testing in young adult men with obstructive sleep apnea

Abstract

The VO(2) response to exercise did not differ between groups. The V(E), V(E)/VCO(2), V(E)/VO(2) were higher (p< 0.05, 0.002, and p<0.02, respectively) in the OSA group across all workloads. The V(E)/VCO(2) slope was greater in the OSA group (p<0.05). The V(E)/VCO(2) slope and AHI were significantly correlated (r=0.56, p<0.03). Thus, young, overweight men with OSA exhibit increased ventilatory responses to exercise when compared to overweight controls. This may reflect alterations in chemoreflex sensitivity, and contribute to increased sympathetic drive and HTN risk.

Cardiovascular Performance Following Continuous Positive Airway Pressure in Patients with Severe Obstructive Sleep Apnea

“…This finding is in agreement with a previous study (Hargens et al, 2009). However, other studies reported similar V'E/V'CO 2 and V'E/V'O 2 at maximal exercise compared to OSA patients (Innocenti Bruni, Gigliotti, & Scano, 2012;Kline et al, 2013;Lin et al, 2004).…”

“…Mechanisms responsible for reduced V'O 2max in OSA patients remain unclear. One potential contributing factor is hypoxia-induced oxidative stress, which leads to mitochondrial damage (Ryan et al, 2005) and/or decreases in number of type I fibers and mitochondria (Nanas et al, 2010), ultimately resulting in deficit in oxidative capacity (Hargens et al, 2009). In OSA patients, an increased sympathetic drive from arousal during sleep may induce increased catecholamine release during vigorous exercise (Nanas et al, 2010).…”

“…The higher V'E/V'CO 2 and V'E/ V 'O 2 during maximal exercise might be due to sympathetic activity-induced increase ventilation drive (Kaleth et al, 2007) and mitochondrial dysfunction (Nanas et al, 2010;Ryan et al, 2005). The latter then promotes anaerobic metabolism (Hargens et al, 2009), leading to stimulating ventilation via carotid body chemoreceptors and ventilation.…”

“…These abnormal CPET responses are reduced cardiorespiratory fitness (V'O 2 ), exaggerated systolic (SBP) and/or diastolic blood pressure (DBP), chronotropic impairment (e.g. high HR reserve), impaired ventilatory equivalents for oxygen (V'E/V'O 2 ), impaired ventilatory equivalents for carbon dioxide (V'E/V'CO 2 ) at submaximal and maximal workloads, and blunt heart rate recovery (HRR) at peak exercise (Aron, Zedalis, Gregg, Gwazdauskas, & Herbert, 2009;Grote, Hedner, & Peter, 2004;Hargens et al, 2009;Nanas et al, 2010;Vanhecke et al, 2008). However, a few studies have reported similar V'O 2peak , HR reserve, SBP, and DBP at peak exercise between OSA patients and controls (Alonso-Fernandez et al, 2006;Hargens et al, 2008;Kaleth et al, 2007).…”

Effect of Nasal Continuous Positive Airway Pressure Therapy on the Functional Respiratory Parameters and Cardiopulmonary Exercise Test in Obstructive Sleep Apnea Syndrome

“…Cardiopulmonary exercise testing (CPET) is used to differentiate the etiology of exercise limitation as follows: cardiac, pulmonary, or resulting from muscle dysfunction [15][16][17][18][19]. Previous studies evaluating exercise limitation in OSA have shown improvements in cardiac dysfunction and CPET performance after 8 weeks of nasal CPAP (nCPAP) treatment [20].…”