title: Skeletal muscle mitochondrial function and exercise capacity in HIV-infected patients with lipodystrophy and elevated p-lactate levels.
abstract: OBJECTIVE
  To investigate the skeletal muscle mitochondrial function in HIV-infected patients with lipodystrophy or elevated p-lactate levels.
  
  
  METHODS
  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 (VO(2max)) 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.
  
  
  CONCLUSIONS
  The significantly lower working capacity and the trend towards reduced VO(2max) 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.
authors.affiliation: Department of Infectious Diseases, Rigshospitalet, University Hospital of Copenhagen, Blegdamsvej 9, DK-2100 Copenhagen, Denmark. roege@rh.dk
authors.forename: Birgit T
authors.initials: BT
authors.lastname: Røge
authors.forename: José A L
authors.initials: JA
authors.lastname: Calbet
authors.forename: Kirsten
authors.initials: K
authors.lastname: Møller
authors.forename: Henrik
authors.initials: H
authors.lastname: Ullum
authors.forename: Helle W
authors.initials: HW
authors.lastname: Hendel
authors.forename: Jan
authors.initials: J
authors.lastname: Gerstoft
authors.forename: Bente K
authors.initials: BK
authors.lastname: Pedersen
mesh_terms: D015094:3-Hydroxyacyl CoA Dehydrogenases / Q000032:analysis; D000140:Acidosis, Lactic / Q000209:etiology / Q000517:prevention & control; D000328:Adult; D000368:Aged; D019380:Anti-HIV Agents / Q000009:adverse effects / Q000494:pharmacology; D023241:Antiretroviral Therapy, Highly Active / Q000009:adverse effects; D001706:Biopsy; D001823:Body Composition; D002950:Citrate (si)-Synthase / Q000032:analysis; D005080:Exercise Test; D017079:Exercise Tolerance; D005260:Female; D006003:Glycogen / Q000032:analysis; D015658:HIV Infections / Q000097:blood / Q000188:drug therapy / Q000378:metabolism*; D006801:Humans; D007773:Lactates / Q000097:blood*; D008060:Lipodystrophy / Q000139:chemically induced / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D008931:Mitochondria, Muscle / Q000187:drug effects / Q000502:physiology*; D018482:Muscle, Skeletal / Q000201:enzymology / Q000378:metabolism / Q000473:pathology; D009711:Nucleotides / Q000032:analysis; D010101:Oxygen Consumption; D011773:Pyruvates / Q000097:blood; D018894:Reverse Transcriptase Inhibitors / Q000009:adverse effects / Q000494:pharmacology
chemical_list: D019380:Anti-HIV Agents; D007773:Lactates; D009711:Nucleotides; D011773:Pyruvates; D018894:Reverse Transcriptase Inhibitors; D006003:Glycogen; D015094:3-Hydroxyacyl CoA Dehydrogenases; D002950:Citrate (si)-Synthase