TY - JOUR
T1 - Short-term modulation of the ventilatory response to exercise is preserved in obstructive sleep apnea
AU - Bernhardt, Vipa
AU - Mitchell, Gordon S.
AU - Lee, Won Y.
AU - Babb, Tony G.
N1 - Funding Information:
The authors thank J. Todd Bassett, Raksa B. Moran, and Rubria Marines-Price for assistance with data collection and analysis, as well as Christina Dulock for helping with recruiting patients at UT Southwestern Clinical Center for Sleep and Breathing Disorders. This work was funded by King Charitable Foundation Trust , Texas Health Presbyterian Hospital, and NIH Grant R01 HL096782 .
Publisher Copyright:
© 2016 Elsevier B.V.
PY - 2017/2/1
Y1 - 2017/2/1
N2 - 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 PCO2 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/m2, AHI: 25 ± 24 events/h [range 6–73], mean ± SD) and 8 obese adults without OSA (age: 38 ± 10 yr, BMI: 37 ± 6 kg/m2, 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˙E), oxygen consumption V˙O2), carbon dioxide production (V˙CO2), and end-tidal PCO2 (PETCO2). The exercise ventilatory response was defined as the slope of the V˙E-V˙CO2 relationship (ΔV˙E/ΔV˙CO2). Results In control (i.e. no added dead space), the exercise ventilatory response was not significantly different between non-OSA and OSA groups (ΔV˙E/ΔV˙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, ΔV˙E/ΔV˙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.
AB - 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 PCO2 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/m2, AHI: 25 ± 24 events/h [range 6–73], mean ± SD) and 8 obese adults without OSA (age: 38 ± 10 yr, BMI: 37 ± 6 kg/m2, 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˙E), oxygen consumption V˙O2), carbon dioxide production (V˙CO2), and end-tidal PCO2 (PETCO2). The exercise ventilatory response was defined as the slope of the V˙E-V˙CO2 relationship (ΔV˙E/ΔV˙CO2). Results In control (i.e. no added dead space), the exercise ventilatory response was not significantly different between non-OSA and OSA groups (ΔV˙E/ΔV˙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, ΔV˙E/ΔV˙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.
KW - Obesity
KW - Obesity hypoventilation syndrome
KW - P
KW - Sleep apnea
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U2 - 10.1016/j.resp.2016.11.003
DO - 10.1016/j.resp.2016.11.003
M3 - Article
C2 - 27840272
AN - SCOPUS:84998893234
SN - 1569-9048
VL - 236
SP - 42
EP - 50
JO - Respiratory Physiology and Neurobiology
JF - Respiratory Physiology and Neurobiology
ER -