Insulin resistance and adipose-derived hormones in young men with untreated obstructive sleep apnea.

PURPOSE: Obstructive sleep apnea (OSA) increases the risk for insulin resistance (IR). The mechanisms that link the two are not clear and are frequently confounded by obesity. OSA is associated with alterations in adipose-derived hormones (adipokines) that increase IR; however, previous studies have focused on middle-aged and older adults. The objective of this study was to determine if IR and alterations in adipokines exist in young men with OSA, independent of obesity. METHODS: Subjects were assigned into the following groups based on body mass index and presence of OSA: obese with OSA (OSA, n = 12), obese without OSA (NOSA, n = 18), and normal weight without OSA (CON, n = 15). Fasting blood was obtained for batch analysis of biomarkers of IR. The homeostasis model assessment (HOMA) method was used to assess IR. RESULTS: HOMA and leptin were higher in the OSA group than the CON group. There were no differences in insulin, tumor necrosis factor alpha (TNF-α), and interleukin-6 (IL-6) between the OSA and NOSA groups. Adiponectin was lower in the OSA group vs. NOSA and CON; however, when controlled for central abdominal fat (CAF), the difference was nullified. When controlled for total body adiposity, however, CAF was 24 % higher in the subjects with OSA vs. subjects without OSA. CONCLUSIONS: These findings suggest that excess CAF in young men with OSA may contribute to risk for type 2 diabetes indirectly by a degree that would otherwise not be reached through obesity, although further research is needed.

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

BACKGROUND: Obstructive sleep apnea (OSA) is a disorder characterized by repetitive obstructions of the upper airway. Individuals with OSA experience intermittent hypoxia, hypercapnia, and arousals during sleep, resulting in increased sympathetic activation. Chemoreflex activation, arising from the resultant oscillatory disturbances in blood gases from OSA, exerts control over ventilation, and may induce increases in sympathetic vasoconstriction, contributing to increased long-term risks for hypertension (HTN) and cardiovascular disease (CVD). METHODS: To evaluate whether OSA elicits exaggerated ventilatory responses to exercise in young men, 14 overweight men with OSA and 16 overweight men without OSA performed maximal ramping cycle ergometer exercise tests. Oxygen consumption (VO(2)), ventilation, (V(E)), ventilatory equivalents for oxygen (V(E)/VO(2)) and carbon dioxide (V(E)/VCO(2)), and V(E)/VCO(2) slope were measured. RESULTS: 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.

Attenuated heart rate recovery following exercise testing in overweight young men with untreated obstructive sleep apnea.

STUDY OBJECTIVE: To evaluate whether cardiovascular responses to maximal exercise testing and recovery are altered with obstructive sleep apnea (OSA) in overweight young adult men. DESIGN: Three sedentary subject groups were recruited: Overweight with OSA (OSA), overweight without OSA (No-OSA), and normal weight without OSA (Control). Presence of OSA was screened via portable diagnostic device. Body composition was measured with dual-energy X-ray absorptiometry. Subjects performed maximal ramping exercise testing (RXT) on a cycle ergometer with 5 minutes of active recovery. Exercise measurements included heart rate (HR), blood pressure (BP), respiratory exchange ratio (RER), and oxygen consumption (VO2). Recovery HR was converted to a HR difference (HR(diff)) calculation (HR(peak) - HR(each minute recovery)), and BP was converted to a recovery ratio for each minute. SETTING: The study was carried out on the campus of Virginia Tech, Department of Human Nutrition, Foods, and Exercise, Blacksburg, Virginia. PARTICIPANTS: 14 OSA, 16 No-OSA, and 14 Control volunteers. INTERVENTION: N/A. MEASUREMENTS AND RESULTS: In OSA subjects, HR recovery was significantly attenuated compared to the No-OSA and Control groups throughout recovery (P = 0.009). No differences were noted in the HR or BP response to exercise in any group. The VO2, adjusted for fat-free soft tissue mass, did not differ between groups. CONCLUSIONS: We found that OSA elicits alterations in the cardiovascular response post exercise, reflected by an attenuated HR recovery. This may indicate an imbalance in the autonomic regulation of HR. Exercise tests may provide utility in risk stratification for those at risk for OSA.