Improved gas exchange during exercise after weight loss in morbid obesity

Abstract

The aim of this study was to determine the effect of weight loss induced by 6 weeks very-low-calorie-diet (VLCD) and behavioural intervention on pulmonary gas exchange during exercise in non-smoking morbid obese (BMI>40 kg/m2) otherwise healthy patients. Seven obese patients underwent a maximal bicycle ergometer test with continuous analysis of expired air and arterial blood sampling before and after a mean weight loss of 18% (25.7 kg, range: 10-50 kg). Body mass index (BMI) decreased with weight loss from 46.6 (6.3) kg/m2 to 38.0 (4.7) kg/m2 (P<0.01). Oxygen consumption (VO2) at low and submaximal exercise levels decreased after weight reduction, but the change was not statistically significant. The peak oxygen consumption related to body weight (VO2/kg) increased 22% from the initial 16.2 (3.6) ml/min/kg to 19.8 (3.1) ml/min/kg (P<0.05). Decrease in VCO2 was significant at submaximal exercise level. Ventilatory equivalent for CO2 increased significantly after weight reduction (P<0.05). Standing up and light exercise resulted in a significant increase in the mean arterial oxygen tension (PaO2) (P<0.05) and a significant decrease in the mean alveolar-arterial difference P(A-a)O2 (P<0.05) when compared to supine values. The mean increase in PaO2 with weight loss was not significant. The peak P(A-a)O2 decreased significantly after weight reduction. In conclusion, weight reduction induced by VLCD and behavioural intervention without exercise therapy can improve gas exchange during exercise in morbid obesity. Increased wasted ventilation, and a tendency to alveolar hyperventilation, after weight loss may reflect a delay in the adaptation of regulation of breathing to rapid weight loss.

Compensatory Exercise Hyperventilation is Restored in the Morbidly Obese After Bariatric Surgery

“…Therefore, the literature demonstrates as a whole that the morbidly obese do not have poor pulmonary gas exchange during intense exercise. Our data presented in this study corroborate these findings [8][9][10][11] and extend to include measurements over a wide range of exercise intensities before and after 21 kg of weight loss.…”

“…Correcting for core temperature changes throughout exercise is important because increases in temperature affect blood-gas measurements [12,13]. Nonetheless, the few studies that did not temperature-correct blood-gas data suggest that the mean PaO 2 in the morbidly obese at near maximal to maximal exercise is approximately 84 to 98 mm Hg and that the AaDO 2 is 11 to 25 mm Hg [8][9][10][11]. These studies show that, on average, the morbidly obese do not have poor pulmonary gas exchange during intense exercise.…”

“…Inadequate compensatory hyperventilation is defined as PaCO 2 between 35.1 and 38.0 mm Hg, and PaCO 2 >38.0 mm Hg suggests an absence of a compensatory hyperventilatory response during intense exercise [13]. The limited data have shown that in the morbidly obese, mean PaCO 2 is ≥35 mm Hg at peak exercise, suggesting insufficient compensatory hyperventilation [8][9][10][11]. Temperature-correcting those data would increase PaCO 2 even more [12], further supporting insufficient hyperventilation during exercise in these subjects.…”

“…There are few studies that have examined arterial blood gases during exercise in the morbidly obese, and in the few that did measure arterial blood gases, they were either not temperature-corrected [8][9][10][11] or the blood gases were measured at only one exercise intensity [8,12]. Correcting for core temperature changes throughout exercise is important because increases in temperature affect blood-gas measurements [12,13].…”

Oxygen Uptake and Cardiac Performance in Obese and Normal Subjects during Exercise

“…Recent studies in pathological obesity demonstrated an improvement in gas exchange [7] as well as left-ventricular morphology and function during exercise after weight reduction [8].…”