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线粒体肌病高强度运动后的骨骼肌再氧合。

Skeletal muscle reoxygenation after high-intensity exercise in mitochondrial myopathy.

机构信息

Division of Respiratory Medicine, Department of Medicine, Pulmonary Function and Clinical Exercise Physiology Unit, Federal University of Sao Paulo, Paulista School of Medicine, Rua Botucatu, 740 3rd floor, Vila Clementino, Sao Paulo, Sao Paulo CEP 04023-062, Brazil.

出版信息

Eur J Appl Physiol. 2012 May;112(5):1763-71. doi: 10.1007/s00421-011-2136-4. Epub 2011 Sep 4.

DOI:10.1007/s00421-011-2136-4
PMID:21898145
Abstract

This study addressed whether O(2) delivery during recovery from high-intensity, supra-gas exchange threshold exercise would be matched to O(2) utilization at the microvascular level in patients with mitochondrial myopathy (MM). Off-exercise kinetics of (1) pulmonary O(2) uptake VO(2P) (2) an index of fractional O(2) extraction by near-infrared spectroscopy (Δ[deoxy-Hb + Mb]) in the vastus lateralis and (3) cardiac output (Q'(T)) by impedance cardiography were assessed in 12 patients with biopsy-proven MM (chronic progressive external ophthalmoplegia) and 12 age- and gender-matched controls. Kinetics of VO(2P) were significantly slower in patients than controls (τ = 53.8 ± 16.5 vs. 38.8 ± 7.6 s, respectively; p < 0.05). Q'(T), however, declined at similar rates (τ = 64.7 ± 18.8 vs. 73.0 ± 21.6 s; p > 0.05) being typically slower than [Formula: see text] in both groups. Importantly, Δ[deoxy-Hb + Mb] dynamics (MRT) were equal to, or faster than, τVO(2P) in patients and controls, respectively. In fact, there were no between-group differences in τVO(2P)MRTΔ[deoxy-Hb + Mb] (1.1 ± 0.4 vs. 1.0 ± 0.2, p > 0.05) thereby indicating similar rates of microvascular O(2) delivery. These data indicate that the slower rate of recovery of muscle metabolism after high-intensity exercise is not related to impaired microvascular O(2) delivery in patients with MM. This phenomenon, therefore, seems to reflect the intra-myocyte abnormalities that characterize this patient population.

摘要

这项研究旨在探讨在患有线粒体肌病(MM)的患者中,从高强度、超气体交换阈运动中恢复时的 O(2) 输送是否与微血管水平的 O(2) 利用相匹配。在 12 名经活检证实的 MM(慢性进行性眼外肌麻痹)患者和 12 名年龄和性别匹配的对照组中,评估了(1)肺摄取的 O(2) 量(VO(2P))(2)近红外光谱(Δ[脱氧-Hb + Mb])测定的分数 O(2) 提取指数和(3)阻抗心动图测定的心输出量(Q'(T))的运动后动力学。与对照组相比,患者的 VO(2P)动力学明显较慢(τ=53.8±16.5 对 38.8±7.6 s;p<0.05)。然而,Q'(T)的下降速度相似(τ=64.7±18.8 对 73.0±21.6 s;p>0.05),两组中 Q'(T)通常比 VO(2P)慢。重要的是,在患者和对照组中,Δ[脱氧-Hb + Mb]动力学(MRT)分别与或快于 τVO(2P)。事实上,两组之间在 τVO(2P)MRTΔ[脱氧-Hb + Mb](1.1±0.4 对 1.0±0.2)方面没有差异(p>0.05),表明微血管 O(2)输送的速度相似。这些数据表明,高强度运动后肌肉代谢恢复较慢与 MM 患者的微血管 O(2)输送受损无关。这种现象似乎反映了这种患者群体的肌细胞内异常。

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