Exercise training and muscle microvascular oxygenation: functional role of nitric oxide
Exercise training and muscle microvascular oxygenation: functional role of nitric oxide
复制标题
DOI：
10.1152/japplphysiol.00151.2012
复制
发表时间：
2012-08-01
影响因子：
3.3
通讯作者：
Poole, David C.
中科院分区：
文献类型：
--
作者：
Hirai, Daniel M.;Copp, Steven W.;Poole, David C.
运动训练诱导骨骼肌内的多种适应，这些适应可以改善局部O-2输送-利用匹配（即，Po（2）mv）。我们检验了一氧化氮（NO）功能增加是运动训练后从休息到收缩的肌肉Po（2）mv动力学改善的内在原因这一假设。健康的年轻Sprague-Dawley大鼠被分配到久坐（n = 18）或渐进式跑步机运动训练（n = 10; 5天/周，6-8周，最终工作量为60分钟/天，速度为35 m/min，-14%等级）组。Po（2）mv通过在静息时和在对照（Krebs-Henseleit溶液）、硝普钠（SNP，NO供体; 300 μ M）和N-G-硝基-L-精氨酸甲酯（L-NAME，非特异性NO合酶阻断; 1.5 mM）灌注条件下1 Hz抽搐收缩期间的棘肌中的磷光猝灭来测量。运动训练组大鼠的最大摄氧量（（V）/doto（2 peak））高于久坐组大鼠（分别为81 +/- 1 vs. 72 +/- 2 ml.kg（-1）.min（-1）; P < 0.05）。在对照组（久坐：8.1 +/- 0.6;训练：15.2 +/- 2.8 s）中，运动训练的大鼠在整个收缩过程中Po（2）mv下降明显较慢（tau（1）;第一个分量的时间常数）。与对照组相比，SNP在更大程度上减慢了久坐大鼠的tau（1（久坐：38.7 +/- 5.6;训练：26.8 +/- 4.1 s; P > 0.05）而L-NAME消除了久坐和训练大鼠之间tau（1）的差异（久坐：12.0 +/- 1.7;训练：11.2 +/- 1.4 s; P < 0.05）。我们的研究结果表明，耐力运动训练导致更大的肌肉微血管氧合作用在收缩开始后的代谢瞬态中（即，PO（2）mv动力学减慢）部分通过增加NO介导的功能，这可能构成训练诱导的代谢适应的重要机制。
Exercise training induces multiple adaptations within skeletal muscle that may improve local O-2 delivery-utilization matching (i.e., Po(2)mv). We tested the hypothesis that increased nitric oxide (NO) function is intrinsic to improved muscle Po(2)mv kinetics from rest to contractions after exercise training. Healthy young Sprague-Dawley rats were assigned to sedentary (n = 18) or progressive treadmill exercise training (n = 10; 5 days/wk, 6-8 wk, final workload of 60 min/day at 35 m/min, -14% grade) groups. Po(2)mv was measured via phosphorescence quenching in the spinotrapezius muscle at rest and during 1-Hz twitch contractions under control (Krebs-Henseleit solution), sodium nitroprusside (SNP, NO donor; 300 mu M), and N-G-nitro-L-arginine methyl ester (L-NAME, nonspecific NO synthase blockade; 1.5 mM) superfusion conditions. Exercise-trained rats had greater peak oxygen uptake ((V) over doto(2peak)) than their sedentary counterparts (81 +/- 1 vs. 72 +/- 2 ml.kg(-1).min(-1), respectively; P < 0.05). Exercise-trained rats had significantly slower Po(2)mv fall throughout contractions (tau(1); time constant for the first component) during control (sedentary: 8.1 +/- 0.6; trained: 15.2 +/- 2.8 s). Compared with control, SNP slowed tau(1) to a greater extent in sedentary rats (sedentary: 38.7 +/- 5.6; trained: 26.8 +/- 4.1 s; P > 0.05) whereas L-NAME abolished the differences in tau(1) between sedentary and trained rats (sedentary: 12.0 +/- 1.7; trained: 11.2 +/- 1.4 s; P < 0.05). Our results indicate that endurance exercise training leads to greater muscle microvascular oxygenation across the metabolic transient following the onset of contractions (i.e., slower Po(2)mv kinetics) partly via increased NO-mediated function, which likely constitutes an important mechanism for training-induced metabolic adaptations.