Whole-body resting and exercise-induced lipolysis in sarcopenic [corrected] patients with COPD.
Impaired beta-adrenoceptor-mediated lipolysis has been reported in sarcopenic [corrected] chronic obstructive pulmonary disease (COPD) patients. This could play a role in the shift in body composition towards decreased fat-free mass (FFM) and relative maintenance of fat mass (FM). Lipolysis could be affected by chronic treatment with beta(2)-agonists or disease-related factors. Therefore, whole-body resting and exercise-induced lipolysis were investigated in sarcopenic [corrected] COPD patients with moderate disease severity. Seven sarcopenic [corrected] COPD patients (mean+/-sem forced expiratory volume in one second (FEV(1)) 53+/-5% of the predicted value; body mass index (BMI) 27.5+/-0.9 kg x m(-2)) and seven controls matched for age, sex and BMI were studied. In addition, six underweight COPD patients (FEV(1) 51+/-5% pred; BMI 20.6+/-0.7 kg x m(-2)) matched for disease severity were recruited. Lipolysis and plasma levels of catecholamines were assessed during infusion of [(2)H(5)]glycerol at rest and during submaximal cycling exercise. The proportional FM was comparable between sarcopenic [corrected] patients and controls, whereas the FFM index was significantly reduced in patients. At rest, the rate of appearance (R(a)) of glycerol (4.1+/-0.6 and 3.3+/-0.2 micromol x kg FFM(-1) x min(-1), respectively) did not differ significantly. In underweight patients, glycerol R(a) (4.3+/-0.5 micromol x kg FFM(-1) x min(-1)) was also comparable. End-of-exercise lipolytic rates did not differ significantly between groups. Glycerol R(a) was not related to FM. Resting adrenalin levels were significantly increased in underweight COPD patients and were related to resting lipolysis. Sarcopenia [corrected] in chronic obstructive pulmonary disease patients with moderate disease severity is not characterised by an abnormal lipolytic rate. Altered regulation of muscle protein turnover seems to be the trigger in the body compositional shift observed in these patients.
Franssen
F M E
FM
Dept of Respiratory Medicine, NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht University Hospital, Maastricht, The Netherlands. f.franssen@pul.unimaas.nl
Sauerwein
H P
HP
Rutten
E P A
EP
Wouters
E F M
EF
Schols
A M W J
AM
D000273:Adipose Tissue; D000318:Adrenergic beta-Agonists / Q000627:therapeutic use; D000368:Aged; D001823:Body Composition; D015992:Body Mass Index; D002100:Cachexia / Q000175:diagnosis / Q000503:physiopathology; D002395:Catecholamines / Q000378:metabolism; D015444:Exercise; D006801:Humans; D008066:Lipolysis; D008297:Male; D008875:Middle Aged; D029424:Pulmonary Disease, Chronic Obstructive / Q000503:physiopathology* / Q000628:therapy*; D011943:Receptors, Adrenergic, beta / Q000378:metabolism; D015431:Weight Loss
D000318:Adrenergic beta-Agonists; D002395:Catecholamines; D011943:Receptors, Adrenergic, beta