| Skeletal muscle mitochondrial function and exercise capacity in HIV-infected patients with lipodystrophy and elevated p-lactate levels. | |
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MedLine Citation:
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PMID: 11953463 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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OBJECTIVE: To investigate the skeletal muscle mitochondrial function in HIV-infected patients with lipodystrophy 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 (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. CONCLUSION: 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. |
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Authors:
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Birgit T Røge; José A L Calbet; Kirsten Møller; Henrik Ullum; Helle W Hendel; Jan Gerstoft; Bente K Pedersen |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: AIDS (London, England) Volume: 16 ISSN: 0269-9370 ISO Abbreviation: AIDS Publication Date: 2002 May |
Date Detail:
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Created Date: 2002-04-15 Completed Date: 2002-08-15 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 8710219 Medline TA: AIDS Country: England |
Other Details:
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Languages: eng Pagination: 973-82 Citation Subset: IM; X |
Affiliation:
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Department of Infectious Diseases, Rigshospitalet, University Hospital of Copenhagen, Blegdamsvej 9, DK-2100 Copenhagen, Denmark. roege@rh.dk |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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3-Hydroxyacyl CoA Dehydrogenases
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analysis Acidosis, Lactic / etiology, prevention & control Adult Aged Anti-HIV Agents / adverse effects, pharmacology Antiretroviral Therapy, Highly Active / adverse effects Biopsy Body Composition Citrate (si)-Synthase / analysis Exercise Test Exercise Tolerance* Female Glycogen / analysis HIV Infections / blood, drug therapy, metabolism* Humans Lactates / blood* Lipodystrophy / chemically induced, metabolism* Male Middle Aged Mitochondria, Muscle / drug effects, physiology* Muscle, Skeletal / enzymology, metabolism, pathology Nucleotides / analysis Oxygen Consumption Pyruvates / blood Reverse Transcriptase Inhibitors / adverse effects, pharmacology |
| Chemical | |
Reg. No./Substance:
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0/Anti-HIV Agents; 0/Lactates; 0/Nucleotides; 0/Pyruvates; 0/Reverse Transcriptase Inhibitors; 9005-79-2/Glycogen; EC 1.1.1.35/3-Hydroxyacyl CoA Dehydrogenases; EC 2.3.3.1/Citrate (si)-Synthase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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