Impairment of muscle energy metabolism in patients with sleep apnoea syndrome.

Impairment of muscle energy metabolism has been demonstrated in normal subjects with chronic hypoxaemia (altitude chronic respiratory failure). The purpose of this study was to verify the hypothesis that a comparable condition could develop in patients with sleep apnoea syndrome (SAS), considering that they are exposed to prolonged and repeated hypoxaemia periods. Muscle metabolism was assessed in II patients with SAS performing a maximal effort on cycloergometer. In comparison with normal subjects, SAS patients reached lower maximal loads [144+/-7 vs. 182+/-10 W (P<0.005)] and lower peak oxygen uptakes [26.4+/-1.2 vs. 33.2+/-1.4 ml kg(-1) min(-1) (P<0.005)]. Abnormal metabolic features were found: maximal blood lactate concentration was significantly lower than in normal subjects [0.034+/-0.004 vs. 0.044+/-0.002 mmol l(-1) W-1 (P<0.05)]; and lactate elimination rate, calculated during a 30-min recovery period, was reduced [0.127+/-0.017 vs. 0.175+/-0.014 mmol l(-1) min(-1) (P<0.025)]. The extent of these anomalies correlated with the severity of SAS. The patients also showed higher maximal diastolic blood pressures than normal subjects [104+/-5 vs. 92+/-4 mm Hg (P<0.05)]. These results can be interpreted as indications of an impairment of muscle energy metabolism in patients with SAS. Decrease in maximum blood lactate concentration suggests an impairment of glycolytic metabolism, while decrease in the rate of lactate elimination indicates a defect in oxidative metabolism. Since no respiratory pathology apart from SAS was found in this group of patients, it seems legitimate to link the genesis of these impairments to repeated bouts of nocturnal hypoxaemia.