Elbehairy AF; Geneidy NM; Elhoshy MS; Elsanhoury D; Elfeky MK; Abd-Elhameed A; Horsley A; O’Donnell DE;
Abd-Elwahab NH; Mahmoud MI;
Chest [Chest] 2022 Sep 29.
Date of Electronic Publication: 2022 Sep 29.
Background: Reduced exercise capacity has been previously reported in patients with obstructive sleep apnea hypopnea syndrome (OSAHS); though the underlying mechanisms are unclear.
Research Question: What are the underlying mechanisms of reduced exercise capacity in untreated patients with OSAHS? Is there a role for systemic or pulmonary vascular abnormalities?
Study Design and Methods: This is a cross-sectional observational study in which 14 patients with moderate-severe OSAHS and 10 control subjects (matched for age, body mass index (BMI), smoking history and FEV 1 ) underwent spirometry, incremental cycle cardiopulmonary exercise test (CPET) with arterial line, resting echocardiogram and assessment of arterial stiffness (pulse wave velocity (PWV) and augmentation index (AIx)).
Results: Patients (age:50±11 years, BMI: 30.5±2.7kg/m 2 , smoking: 2.4±4.0 pack-years, FEV 1 /FVC: 0.78±0.04%, FEV 1 :85±14 %predicted; mean±SD) had apnea hypopnea index of 43±19/hour. At rest, PWV, AIx, and mean pulmonary artery pressure (mPAP) were higher in patients vs. control subjects, P<.05. During CPET, patients had lower peak work rate (WR) and oxygen uptake; and greater dyspnea ratings compared with control subjects, all P<.05. Minute ventilation (V E ), ventilation/CO 2 output (V E /VCO 2 ), and dead space/tidal volume (V D /V T ) were greater in patients vs. control subjects during exercise (all P<.05). Reduction in V D /V T from rest to peak exercise was greater in control subjects compared with patients (0.24±0.08 vs. 0.04±0.14, P=.001). Dyspnea intensity at the highest equivalent WR correlated with corresponding values of V E /VCO 2 (r=0.65, P=.002), and dead space ventilation (r=0.70, P=.001). Age, PWV and mPAP explained ∼70% of the variance in peak WR, while predictors of dyspnea during CPET were rest-to-peak change in V D /V T and PWV (Rsqr=0.50, P<.001).
Interpretation: Patients with OSAHS had evidence of pulmonary gas exchange abnormalities during exercise (in the form of increased dead space) and resting systemic vascular dysfunction which may explain reduced exercise capacity and increased exertional dyspnea intensity.