Ortmeyer Heidi K, Ryan Alice S, Hafer-Macko Charlene, Oursler KrisAnn K
Department of Medicine, Division of Gerontology and Geriatric Medicine, University of Maryland School of Medicine, Baltimore, Maryland Baltimore Veterans Affairs Medical Center Geriatric Research, Education, and Clinical Center, Veterans Affairs Maryland Health Care System, Baltimore, Maryland
Department of Medicine, Division of Gerontology and Geriatric Medicine, University of Maryland School of Medicine, Baltimore, Maryland Baltimore Veterans Affairs Medical Center Geriatric Research, Education, and Clinical Center, Veterans Affairs Maryland Health Care System, Baltimore, Maryland Veterans Affairs Research Service, Veterans Affairs Maryland Health Care System, Baltimore, Maryland.
Physiol Rep. 2016 May;4(9). doi: 10.14814/phy2.12794.
Skeletal muscle mitochondrial dysfunction may contribute to low aerobic capacity. We previously reported 40% lower aerobic capacity in HIV-infected men compared to noninfected age-matched men. The objective of this study was to compare skeletal muscle mitochondrial enzyme activities in HIV-infected men on antiretroviral therapy (55 ± 1 years of age, n = 10 African American men) with age-matched controls (55 ± 1 years of age, n = 8 Caucasian men), and determine their relationship with aerobic capacity. Activity assays for mitochondrial function including enzymes involved in fatty acid activation and oxidation, and oxidative phosphorylation, were performed in homogenates prepared from vastus lateralis muscle. Hydrogen peroxide (H2O2), cardiolipin, and oxidized cardiolipin were also measured. β-hydroxy acyl-CoA dehydrogenase (β-HAD) (38%) and citrate synthase (77%) activities were significantly lower, and H2O2 (1.4-fold) and oxidized cardiolipin (1.8-fold) were significantly higher in HIV-infected men. VO2peak (mL/kg FFM/min) was 33% lower in HIV-infected men and was directly related to β-HAD and citrate synthase activity and inversely related to H2O2 and oxidized cardiolipin. Older HIV-infected men have reduced oxidative enzyme activity and increased oxidative stress compared to age-matched controls. Further research is crucial to determine whether an increase in aerobic capacity by exercise training will be sufficient to restore mitochondrial function in older HIV-infected individuals.
骨骼肌线粒体功能障碍可能导致有氧运动能力低下。我们之前报道，与未感染的年龄匹配男性相比，感染HIV的男性有氧运动能力低40%。本研究的目的是比较接受抗逆转录病毒治疗的感染HIV男性（55±1岁，n = 10名非裔美国男性）与年龄匹配的对照组（55±1岁，n = 8名白种男性）的骨骼肌线粒体酶活性，并确定它们与有氧运动能力的关系。在从股外侧肌制备的匀浆中进行线粒体功能的活性测定，包括参与脂肪酸活化和氧化以及氧化磷酸化的酶。还测量了过氧化氢（H2O2）、心磷脂和氧化心磷脂。感染HIV的男性中，β-羟基酰基辅酶A脱氢酶（β-HAD）（38%）和柠檬酸合酶（77%）活性显著降低，而H2O2（1.4倍）和氧化心磷脂（1.8倍）显著升高。感染HIV的男性的最大摄氧量（VO2peak，mL/kg去脂体重/分钟）低33%，且与β-HAD和柠檬酸合酶活性直接相关，与H2O2和氧化心磷脂呈负相关。与年龄匹配的对照组相比，感染HIV的老年男性氧化酶活性降低，氧化应激增加。进一步的研究对于确定通过运动训练提高有氧运动能力是否足以恢复感染HIV的老年个体的线粒体功能至关重要。
