IMPAIRMENT OF MUSCLE ENERGY-METABOLISM IN PATIENTS WITH SLEEP-APNEA SYNDROME

Impairment of muscle energy metabolism has been demonstrated in normal subjects with chronic hypoxaemia (altitude chronic respiratory failur e). The purpose of this study was to verify the hypothesis that a comp arable condition could develop in patients with sleep apnoea syndrome (SAS), considering that they are exposed to prolonged and repeated hyp oxaemia periods. Muscle metabolism was assessed in II patients with SA S performing a maximal effort on cycloergometer. In comparison with no rmal subjects, SAS patients reached lower maximal loads [144+/-7 vs. 1 82+/-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 th an 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 re covery 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 bl ood 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 blo od lactate concentration suggests an impairment of glycolytic metaboli sm, while decrease in the rate of lactate elimination indicates a defe ct in oxidative metabolism. Since no respiratory pathology apart from SAS was found in this group of patients, it seems legitimate to link t he genesis of these impairments to repeated bouts of nocturnal hypoxae mia.