|Title:||Skeletal muscle mitochondrial function and exercise capacity in HIV-infected patients with lipodystrophy and elevated p-lactate levels||Authors:||Røge, Birgit T.
Calbet, José A.L.
Hendel, Helle W.
Pedersen, Bente K.
|UNESCO Clasification:||241106 Fisiología del ejercicio||Keywords:||Exercise
mitochondrial toxicity, et al
|Issue Date:||2002||Publisher:||0269-9370||Journal:||AIDS||Abstract:||Objective To investigate the skeletal muscle mitochondrial function in HIV-infected patients with lipdystrophy or elevated p-lactate levels. Design Eight HIV patients treated with highly active antiretroviral therapy, with lipodystrophy or elevated p-lactate, and eight healthy controls were exposed to incremental exercise until exhaustion. Methods Blood samples and gas analysis were performed at rest, during exercise and in recovery. Oxygen consumption, workload and blood lactate were assessed. Before and immediately after exercise muscle biopsies were obtained, in which citrate synthase (CS), hydroxyacyl-coenzyme A dehydrogenase (HD), glycogen and nucleotides were measured. Results Maximal workload was significantly lower in patients compared with controls [171 Watt (88–206) versus 235 Watt (118–294) P = 0.05]. A trend towards lower maximal oxygen consumption (VO2max) was detected in patients [2136 ml/min (1221–2598) versus 2985 ml/min (1506–3959) P = 0.11]. Patients had significantly elevated levels of blood lactate at rest [1.55 mmol/l (1–2.5) versus 0.8 mmo/l (0.37–1.1) P < 0.01), but no significant difference in maximal blood-lactate values was found. The decline in blood lactate in the recovery period was similar between groups. There was no significant difference in CS, HD, glycogen or nucleotides. Conclusion The significantly lower working capacity and the trend towards reduced VO2max in patients could be caused by mitochondrial dysfunction, but may also be caused by impaired physical fitness. The similar levels of nucleotides, CS, HD, and glycogen and the normal increase in blood lactate during exercise indicates a normal oxidative phosphorylation. No evidence of serious damage to skeletal muscle mitochondrial function was found.||URI:||http://hdl.handle.net/10553/50982||ISSN:||0269-9370||DOI:||10.1097/00002030-200205030-00003||Source:||AIDS[ISSN 0269-9370],v. 16, p. 973-982|
|Appears in Collections:||Artículos|
checked on Jan 29, 2023
WEB OF SCIENCETM
checked on Oct 2, 2022
checked on Sep 3, 2022
Items in accedaCRIS are protected by copyright, with all rights reserved, unless otherwise indicated.