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Reduced aerobic capacity in HIV infected patients is associated with decreased capacity for lactate oxidation during exercise
Author(s) -
Paul Simon,
Mau Tami,
Volkov Pavel,
Van Gundy Karl,
Brooks George A.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.111
Subject(s) - lactic acid , medicine , metabolism , human immunodeficiency virus (hiv) , lactate threshold , endocrinology , vo2 max , incremental exercise , chemistry , aerobic exercise , blood lactate , heart rate , biology , immunology , genetics , bacteria , blood pressure
Objective: Reduced aerobic capacity in HIV infected patients may be due to mitochondrial toxicity of antiretroviral therapy (HAART). We determined if changes in rates of lactate flux in HIV patients contributes to their debility. Methods: Lactate flux parameters were determined using isotope [3‐ 13 C]lactate at rest then 60 min of exercise, comparing HIV patients on HAART with uninfected controls. Results: The mean peak VO 2 for the HIV patients was lower than controls: 2.2 ±0.13 (n=9) vs. 2.6 ±0.15 L/min (n=9) (p=0.03). At rest the HIV subjects did not differ from the controls for rate of lactate appearance (Ra), disappearance (Rd), metabolic clearance rate (MCR) or relative oxidation of lactate (rel Rox). During exercise (45% of peak VO 2 ), there was no significant difference for Ra (48.9 ±3.2 vs. 45.6 ±4.5 mmol/kg/min), Rd (49.3 ±3.2 vs. 48.5 ±5.2 mmol/kg/min), or MCR (43.0 ±4.3 vs. 36.1 ±2.6 ml/kg/min). However, during exercise, the rel Rox was lower in the HIV subjects (58.8 ±1.8%) vs. controls (71.2 ±3.8%) p=0.007. Conclusion: HIV patients and controls had equal rates of generation and clearance of lactic acid. HIV subjects had reduced clearance of lactate generated during exercise via oxidation. This reduced clearance must be compensated for by increased clearance of lactate by non‐oxidative means, such as through hepatic metabolism. NIH R21 AI 058770 to SP and NIH R01 AR 042906 to GAB.