Heart Rate Recovery and Oxygen Kinetics After Exercise in Obstructive Sleep Apnea Syndrome

Abstract

Background: Patients who suffer from obstructive sleep apnea (OSA) have a decreased exercise capacity and abnormal autonomic nervous function. However, the kinetics of early oxygen (O 2 ) and heart rate recovery (HRR) have not been described. Materials and Methods:We evaluated 21 men with moderate to severe OSA (mean age: 48 ± 11 yrs, mean apnea-hypopnea index [AHI]: 55 ± 13) and without known heart disease and 10 healthy men matched for age and body mass index (BMI; controls). Men with OSA underwent overnight polysomnography, and both groups underwent symptom-limited incremental cardiopulmonary exercise testing (CPET). We recorded the CPET parameters including peak O 2 uptake (VO 2 p), kinetics of early O 2 recovery by the first degree slope of VO 2 during the first minute (VO 2 /t slope), the time required for a 50% decline of VO 2 p during recovery (T 1/2 ), and early heart rate recovery (HRR = HR at maximal exercise − HR at 1 min of recovery), as well as the chronotropic reserve to exercise ([CR] = [peak HR − resting HR/220 − age − resting HR] × 100). Patients with OSA had a lower VO 2 p (28.7 ± 4.0 vs 34.7 ± 6.2 mL/kg/min), VO 2 /t slope (1.04 ± 0.3 vs 1.4 ± 0.17 mL/kg/min 2 ), and T 1/2 (74 ± 10 vs 56 ± 6 sec) compared to controls (all P < 0.001). In addition, both HRR and CR were lower in the OSA group (22.0 ± 7.0 vs 31.0 ± 6.0 bpm,P:0.003, and 79.0% ± 15% vs 99.0% ± 13.0%, P:0.01, respectively). Conclusions: Patients with OSA demonstrate reduced exercise capacity, delayed oxygen kinetics, and reduced HRR. These data point to abnormal oxygen delivery and/or oxidative function of the peripheral muscles and impaired autonomic nervous activity in OSA patients.

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

“…We observed a significantly lower V'O 2max in patients with OSA compared to controls. This result agrees with previous studies (Lin et al, 2004;Nanas et al, 2010). Nevertheless, other studies found no evidence of reduced V'O 2max in OSA patients (Hargens et al, 2008;Kaleth et al, 2007).…”

“…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).…”

“…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). Consequently, this may cause increased total peripheral resistance (Kline et al, 2013), lack of blood supply to muscle fibers, and finally a decrease in V'O 2max (Vanuxem et al, 1997).…”

“…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).…”

Membrane Level of Omega-3 Docosahexaenoic Acid Is Associated with Severity of Obstructive Sleep Apnea

“…1 OSA is associated with a heightened infl ammatory state, 2 with autonomic dysfunction, 3 and with increased risk for sudden cardiac death. 4 Interestingly, low blood and tissue levels of omega-3 FAs (eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA]) are also associated with a heightened infl ammatory state, 5,6 with autonomic dysfunction, [7][8][9] and with increased risk for sudden cardiac death.…”