OBJECTIVE: To determine if arteriovenous oxygen difference was lower in asymptomatic individuals with human immunodeficiency virus (HIV) infection than in sedentary but otherwise healthy controls. DESIGN: Quasi-experimental cross-sectional. SETTING: Clinical exercise laboratory. PARTICIPANTS: Fifteen subjects (10 men, 5 women) with HIV and 15 healthy gender- and activity level-matched controls (total N=30). INTERVENTION: Participants performed an incremental maximal exercise treadmill test to exhaustion. Electrocardiogram, metabolic, and noninvasive cardiac output measurements were evaluated at rest and throughout the tests. Data were analyzed by using analysis of covariance. MAIN OUTCOME MEASURES: Peak oxygen consumption (Vo(2)), cardiac output, stroke volume, and arteriovenous oxygen difference. The arteriovenous oxygen difference was determined indirectly using the Fick equation. RESULTS: Peak VO(2) was significantly lower (P<.0005) in participants with HIV (24.6+/-1.2mL.kg(-1).min(-1)) compared with controls (32.0+/-1.2mL.kg(-1).min(-1)). There were no significant intergroup differences in cardiac output or stroke volume at peak exercise. Peak arteriovenous oxygen difference was significantly lower (P<.04) in those infected with HIV (10.8+/-0.5 volume %) than in controls (12.4+/-0.5 volume %). CONCLUSION: The observed deficit in aerobic capacity in the participants with HIV appeared to be the result of a peripheral tissue oxygen extraction or utilization limitation. In addition to deconditioning, potential mechanisms for this significant attenuation may include HIV infection and inflammation, highly active antiretroviral therapy medication regimens, or a combination of these factors.
OBJECTIVE: To determine if arteriovenousoxygen difference was lower in asymptomatic individuals with human immunodeficiency virus (HIV) infection than in sedentary but otherwise healthy controls. DESIGN: Quasi-experimental cross-sectional. SETTING: Clinical exercise laboratory. PARTICIPANTS: Fifteen subjects (10 men, 5 women) with HIV and 15 healthy gender- and activity level-matched controls (total N=30). INTERVENTION: Participants performed an incremental maximal exercise treadmill test to exhaustion. Electrocardiogram, metabolic, and noninvasive cardiac output measurements were evaluated at rest and throughout the tests. Data were analyzed by using analysis of covariance. MAIN OUTCOME MEASURES: Peak oxygen consumption (Vo(2)), cardiac output, stroke volume, and arteriovenousoxygen difference. The arteriovenousoxygen difference was determined indirectly using the Fick equation. RESULTS: Peak VO(2) was significantly lower (P<.0005) in participants with HIV (24.6+/-1.2mL.kg(-1).min(-1)) compared with controls (32.0+/-1.2mL.kg(-1).min(-1)). There were no significant intergroup differences in cardiac output or stroke volume at peak exercise. Peak arteriovenousoxygen difference was significantly lower (P<.04) in those infected with HIV (10.8+/-0.5 volume %) than in controls (12.4+/-0.5 volume %). CONCLUSION: The observed deficit in aerobic capacity in the participants with HIV appeared to be the result of a peripheral tissue oxygen extraction or utilization limitation. In addition to deconditioning, potential mechanisms for this significant attenuation may include HIV infection and inflammation, highly active antiretroviral therapy medication regimens, or a combination of these factors.
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