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Short‐Term Modulation of the Ventilatory Response to Exercise is Preserved in Obstructive Sleep Apnea
Author(s) -
Bernhardt Vipa,
Bassett J Todd,
Moran Raksa B,
MarinesPrice Rubria,
Mitchell Gordon S,
Lee Won Y,
Babb Tony G
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1261.15
Subject(s) - medicine , ventilation (architecture) , cardiology , obstructive sleep apnea , respiratory system , control of respiration , respiratory minute volume , apnea , dead space , anesthesia , physical therapy , mechanical engineering , engineering
Background The ventilatory response to exercise is temporarily augmented in response to environmentally (e.g., breathing apparatus) or physiologically altered conditions (e.g., respiratory disease), maintaining constant relative arterial PCO 2 regulation from rest to exercise; this augmentation is called short‐term modulation (STM) of the ventilatory response to exercise. Obesity and/or obstructive sleep apnea could affect the exercise ventilatory response and STM capacity due to the additional mechanical or ventilatory load on the respiratory system and/or the repetitive intermittent hypoxia during sleep. We hypothesized that: 1) the exercise ventilatory response is augmented in obese OSA patients compared with otherwise healthy obese 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/hr [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 O 2 , CO 2 , minute ventilation ( E ) and end‐tidal PCO 2 (P ET CO 2 ). The exercise ventilatory response was defined as the slope of the E ‐ CO 2 relationship (Δ E /Δ CO 2 ). Results In control (i.e. no added dead space), the exercise ventilatory response was not significantly different between non‐OSA and OSA groups (slope: 30.5 ± 4.2 and 30.5 ± 3.8, p > 0.05); P ET CO 2 did not differ from rest to exercise in either group (p > 0.05). In the trials with added external dead space, no significant differences between groups were observed. Δ E /Δ CO 2 increased with increasing dead space (p < 0.05); P ET CO 2 increased with increasing dead space and exercise intensity (interaction p < 0.05); however, the change in P ET CO 2 from rest to exercise remained small (<2 mmHg) in both groups, demonstrating STM. Conclusions Contrary to our hypotheses: 1) the exercise ventilatory response is not different between obese OSA patients and otherwise healthy obese adults, and 2) the capacity for STM with added dead space is not different between groups. Thus, the capacity for STM is preserved in OSA. Support or Funding Information King Charitable Foundation Trust, Texas Health Presbyterian Hospital, NIH Grant R01 HL096782