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The effects of obesity and surgically-induced weight loss on exercise ventilation: influence of central adiposity and serum leptinHerrick, Jeffrey 14 July 2009 (has links)
Truncal adiposity impairs ventilation in obese adults by altering normal ventilatory mechanics. Leptin, an inflammatory adipocytokine, is elevated in obesity and has been shown to alter ventilatory responses to exercise. Leptin’s bioavailability appears to be regulated by its soluble receptor (LRe), which is reduced in obesity. Roux-en-Y gastric bypass surgery (RYGBS) is a weight loss intervention that reduces total fat mass and improves several obesity related co-morbidities including pulmonary dysfunction. The purpose of this study was to first evaluate the differences between ventilatory responses to carbon dioxide (VE/VCO2 slope) during progressive treadmill walking in morbidly obese and normal weight females. Second, we will analyze the relationships between the VE/VCO2 slope, truncal adiposity, serum leptin, and LRe. Lastly, we want to evaluate the changes in the ventilatory responses to exercise (VE/VCO2 slope), truncal adiposity, serum leptin, and LRe 3 months following Roux-en Y gastric bypass surgery. Thirteen obese (OB 37.7 ±11.4 years, 42.0 ± 4.8 kg/m2) and 12 normal weight females (NW 36.1 ±8.0 years, 22.8 ± 1.2 kg/m2) participated in this study. Blood samples for measure of fasting serum leptin and soluble leptin receptor were obtained prior to exercise. Cardiopulmonary variables were measured throughout exercise. Regional adiposity was determined through dual energy x-ray absorptiometry. Truncal adiposity was significantly greater in the obese group than the normal weight group. Serum leptin was greater in the obese group while LRe was lower than the normal weight group. The VE/VCO2 slopes were lower in obese group when compared to the normal weight group. There were no significant group differences in maximal ventilation, tidal volume or respiratory rate. Stepwise regression determined that truncal adiposity accounted for 31.5% of variance in VE/VCO2 slope (R= 0.561, R2 =0.315, p = 0.004). At 3 months post-surgery we observed significant reductions in the obese group in total percentages of fat, truncal adiposity, serum leptin. The soluble leptin receptor was not changed at any measured time point following RYGBS. There were no changes in 3 months post-surgery VE/VCO2 slopes in the obese group. Truncal adiposity, serum leptin and LRe were associated with reduced ventilatory responses to weight bearing exercise (VE/VCO2 slope) in obese females when compared to normal weight females. There were no differences between obese and normal weight females in maximal minute ventilation, tidal volume or respiratory rate. This result suggests that differences in VE/VCO2 slopes may not be entirely from maximal pulmonary capacity. Rather, the differences in VE/VCO2 slope may be attributed to truncal adiposity and its positive relationship with leptin. Elevated leptin in the obese group may indicate a state of central leptin resistance which has been shown to reduce the ventilatory responses to exercise. At 3 months post RYGBS significant reductions in total percent fat, serum leptin, truncal adiposity and BMI were observed. However, despite improvement in fat mass and serum leptin there were no changes in the VE/VCO2 slope and LRe at 3 months post RYGBS. Therefore, it is possible that the improvements in body composition and leptin following RYGBS were not sufficient to increase ventilation responses to weight bearing exercise in obese females.
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