Association between angiotensin-converting enzyme gene polymorphisms and exercise performance in patients with COPD.
OBJECTIVE
Recent studies have shown that polymorphisms of the angiotensin-converting enzyme (ACE) gene are closely associated with pulmonary disorders. The ACE gene is involved in the regulation of inflammatory reactions to lung injury, respiratory drive, erythropoiesis and tissue oxygenation. The hypothesis for this study was that the ACE gene may be associated with the ventilatory response to exercise and the aerobic work efficiency of skeletal muscle in patients with COPD.


METHODS
Sixty-one Chinese Han COPD patients and 57 healthy control subjects performed incremental cardiopulmonary exercise testing on a cycle ergometer. ACE genotypes were determined using PCR amplification.


RESULTS
Resting lung function and blood gas index were not significantly different among the three ACE genotype COPD groups. Similarly, there were no significant differences in AT, maximal O(2) uptake, maximal O(2) pulse, maximal dyspnoea index, ventilatory response (DeltaVE/DeltaVCO(2)), O(2) cost of ventilation (VO(2)/W/VE), end-tidal partial pressure of carbon dioxide at maximal exercise and maximal SaO(2) among the three ACE genotype COPD patients. Maximal work load and aerobic work efficiency were higher in the COPD group with the II genotype than in those with the ID or DD genotype. There were no significant differences in resting lung function and cardiopulmonary exercise testing parameters among the three ACE genotype control groups.


CONCLUSIONS
The ACE gene may be involved in the regulation of skeletal muscle aerobic work efficiency, but is not associated with the ventilatory responses to exercise in COPD patients.
Zhang
Xiaolei
X
Beijing Institute of Respiratory Medicine, Beijing Chaoyang Hospital, Beijing, China.
Wang
Chen
C
Dai
Huaping
H
Lin
Yingxiang
Y
Zhang
Jun
J
D000368:Aged; D044466:Asian People / Q000235:genetics; D016022:Case-Control Studies; D005080:Exercise Test; D017079:Exercise Tolerance / Q000235:genetics* / Q000502:physiology*; D005260:Female; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000503:physiopathology; D010101:Oxygen Consumption / Q000502:physiology; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic / Q000235:genetics*; D029424:Pulmonary Disease, Chronic Obstructive / Q000208:ethnology / Q000503:physiopathology*; D012123:Pulmonary Ventilation / Q000502:physiology
D007703:Peptidyl-Dipeptidase A