Low anaerobic threshold and increased skeletal muscle lactate production in subjects with Huntington's disease.

ABSTRACT: Mitochondrial defects that affect cellular energy metabolism have long been implicated in the etiology of Huntington's disease (HD). Indeed, several studies have found defects in the mitochondrial functions of the central nervous system and peripheral tissues of HD patients. In this study, we investigated the in vivo oxidative metabolism of exercising muscle in HD patients. Ventilatory and cardiometabolic parameters and plasma lactate concentrations were monitored during incremental cardiopulmonary exercise in twenty-five HD subjects and twenty-five healthy subjects. The total exercise capacity was normal in HD subjects but notably the HD patients and presymptomatic mutation carriers had a lower anaerobic threshold than the control subjects. The low anaerobic threshold of HD patients was a

SUBMITTER: Ciammola A 

PROVIDER: S-EPMC3081141 | biostudies-literature | 2011 Jan

REPOSITORIES: biostudies-literature