Short-term modulation of the ventilatory response to exercise is preserved in obstructive sleep apnea

Background: The ventilatory response to exercise can be transiently adjusted in response to environmentally (e.g., breathing apparatus) or physiologically altered conditions (e.g., respiratory disease), maintaining constant relative arterial P-CO2 regulation from rest to exercise (Mitchell and Babb, 2006); this augmentation is called short-term modulation (STM) of the exercise ventilatory response. Obesity and/or obstructive sleep apnea could affect the exercise ventilatory response and the capacity for STM due to chronically increased mechanical and/or ventilatory loads on the respiratory system, and/or recurrent (chronic) intermittent hypoxia experienced during sleep. We hypothesized that: (1) the exercise ventilatory response is augmented in obese OSA patients compared with obese non-OSA adults, and (2) the capacity for STM with added dead space is diminished in obese OSA patients. Methods: Nine obese adults with OSA (age: 39 +/- 6 yr, BMI: 40 +/- 5 kg/m(2), AHI: 25 +/- 24 events/h [range 6-73], mean +/- SD) and 8 obese adults without OSA (age: 38 +/- 10 yr, BMI: 37 +/- 6 kg/m(2), AHI: 1 +/- 2) completed three, 20-min bouts of constant-load submaximal cycling exercise (8 min rest, 6 min at 10 and 30 W) with or without added external dead space (200 or 400 mL; 20 min rest between bouts). Steady-state measurements were made of ventilation ((V) over dot(E)), oxygen consumption (V) over dot(O2)), carbon dioxide production ((V) over dot(CO2)), and end-tidal P-CO2 (PETCO2). The exercise ventilatory response was defined as the slope of the (V) over dotE-(V) over dot(CO2) relationship (Delta(V) over dotE/Delta(V) over dot(CO2)). Results: In control (i.e. no added dead space), the exercise ventilatory response was not significantly different between non-OSA and OSA groups (Delta(V) over dotE/Delta(V) over dot(CO2) slope: 30.5 +/- 4.2 vs 30.5 +/- 3.8, p > 0.05); PETCO2 regulation from rest to exercise did not differ between groups (p > 0.05). In trials with added external dead space, Delta(V) over dotE/Delta(V) over dot(CO2) increased with increased dead space (p < 0.05) and the PETCO2 change from rest to exercise remained small (<2 mmHg) in both groups, demonstrating STM. There were no significant differences between groups. Conclusions: Contrary to our hypotheses: (1) the exercise ventilatory response is not increased in obese OSA patients compared with obese non-OSA adults, and (2) the capacity for STM with added dead space is preserved in obese OSA and non-OSA adults. (C) 2016 Elsevier B.V. All rights reserved.