Department of Sport, Nutrition and Health Sciences, University of Milan, Milan, Italy.
J Am Coll Cardiol. 2011 Sep 20;58(13):1353-62. doi: 10.1016/j.jacc.2011.06.025.
This study sought to elucidate the mechanisms responsible for the benefits of small muscle mass exercise training in patients with chronic heart failure (CHF).
How central cardiorespiratory and/or peripheral skeletal muscle factors are altered with small muscle mass training in CHF is unknown.
We studied muscle structure, and oxygen (O(2)) transport and metabolism at maximal cycle (whole-body) and knee-extensor exercise (KE) (small muscle mass) in 6 healthy controls and 6 patients with CHF who then performed 8 weeks of KE training (both legs, separately) and repeated these assessments.
Pre-training cycling and KE peak leg O(2) uptake (Vo(2peak)) were 17% and ~15% lower, respectively, in the patients compared with controls. Structurally, KE training increased quadriceps muscle capillarity and mitochondrial density by ~21% and ~25%, respectively. Functionally, despite not altering maximal cardiac output, KE training increased maximal O(2) delivery (54%), arterial-venous O(2) difference (10%), and muscle O(2) diffusive conductance (D(M)O(2)) (39%) (assessed during KE), thereby increasing single-leg Vo(2peak) by 53%, to a level exceeding that of the untrained controls. Post-training, during maximal cycling, O(2) delivery (40%), arterial-venous O(2) difference (15%), and D(M)O(2) (52%) all increased, yielding an increase in Vo(2peak) of ~40%, matching the controls.
In the face of continued central limitations, clear improvements in muscle structure, peripheral convective and diffusive O(2) transport, and subsequently, O(2) utilization support the efficacy of local skeletal muscle training as a powerful approach to combat exercise intolerance in CHF.
本研究旨在阐明小肌群运动训练对慢性心力衰竭(CHF)患者有益的机制。
尚不清楚 CHF 中小肌群训练如何改变中心心肺和/或外周骨骼肌因素。
我们研究了肌肉结构,以及在 6 名健康对照者和 6 名 CHF 患者中进行最大循环(全身)和膝关节伸展运动(KE)(小肌群)时的氧气(O2)转运和代谢,然后患者进行 8 周的 KE 训练(双腿分开),并重复这些评估。
与对照组相比,患者的预训练循环和 KE 峰值腿部 O2 摄取量(Vo2peak)分别低约 17%和 15%。结构上,KE 训练分别使股四头肌毛细血管和线粒体密度增加约 21%和 25%。功能上,尽管最大心输出量没有改变,KE 训练仍增加了最大 O2 输送量(54%)、动静脉 O2 差(10%)和肌肉 O2 弥散传导率(D(M)O2)(39%)(在 KE 期间评估),从而使单腿 Vo2peak 增加约 53%,超过未训练的对照组。训练后,在最大循环期间,O2 输送量(40%)、动静脉 O2 差(15%)和 D(M)O2(52%)均增加,Vo2peak 增加约 40%,与对照组相匹配。
面对持续的中央限制,肌肉结构、外周对流和弥散 O2 转运以及随后的 O2 利用的明显改善支持局部骨骼肌训练作为对抗 CHF 运动不耐受的有效方法的功效。