Aging impacts microvascular oxygen pressures during recovery from contractions in rat skeletal muscle

Aging impacts microvascular oxygen pressures during recovery from contractions in rat skeletal muscle
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DOI:
10.1016/j.resp.2009.10.005
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发表时间:
2009-12-31
影响因子:
2.3
通讯作者:
Musch, Timothy I.
Musch, Timothy I.
中科院分区:
医学4区
文献类型:
--
作者:
Hirai, Daniel M.;Copp, Steven W.;Musch, Timothy I.

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在收缩过程中,衰老引起的外周循环控制的改变降低了微血管的氧分压(P-O2 MV:反映了O-2递送与O-2摄取比率的动态平衡),导致肌肉内代谢障碍的夸大和过早的疲劳。然而,在收缩过程中这种P-O2 mV的改变与延长肌肉代谢恢复的程度尚不清楚。我们验证了一种假设,即衰老引起的P-O2 mV开启动力学的加快预示着P-O2 mV关闭动力学的减慢。用6只青年(6~8月龄)和7只老年(26~28月龄)雄性Fischer 344×Brown挪威杂交F1大鼠暴露脊斜方肌。分别在静息状态、电刺激收缩时(1 Hz,7~9V,2ms脉冲宽度,180 S)和整个恢复期(180 S)用磷光猝灭的方法测量P-O2 mV的动力学曲线。老年大鼠P-O2 mV开启动力学明显减慢(平均反应时间缩短,青年:2 7.3±-3.6 S,老年:19.2+/-1.6 S;P;0.0 5),P-O2 MU离动力学明显减慢(平均反应时间延长,青年:46.5±-5.9 S,老年:84.8+/-7.9 S;P相应地,在老年肌肉中观察到了更大程度的P-O2 MV开关不对称性(MRT OFF-MRT ON)(青年:19.1±-4.5 S,老年:65.6+/-8.6 S;P<0.01)。我们的结论是,衰老引起的P-O2 mV开启动力学的加快确实预示着P-O2 mV关闭动力学的减慢,这可能会损害肌肉代谢的恢复,并可能降低随后的收缩性能。此外,老年肌肉中P-O2 MV开关不对称的程度更大,这表明在运动过渡期间微血管氧合受损和肌肉代谢反应改变之间存在机制联系。(C)2009爱思唯尔B.V.保留所有权利。
Aging-induced alterations in peripheral circulatory control during contractions reduce the microvascular partial pressure of O-2 (P-O2 mv: which reflects the dynamic balance in the O-2 delivery-to-O-2 uptake ratio), resulting in exaggerated intramuscular metabolic disturbances and premature fatigue. However, the extent to which this altered P-O2 mv during contractions is associated with prolongated muscle metabolic recovery is not known. We tested the hypothesis that the aging-induced speeding of the P-O2 mv on-kinetics would presage slowed P-O2 mv off-kinetics. The spinotrapezius muscle was exposed in six young (6-8 months) and seven old (26-28 months) male Fischer 344 x Brown Norway F1-hybrid rats. The P-O2 mv kinetic profile was measured via phosphorescence quenching at rest, during electrically stimulated contractions (1 Hz, 7-9 V. 2 ms pulse duration, 180 s), and throughout recovery (180 s). Aged rats which evidenced faster P-O2 mv on-kinetics (reduced mean response time (MRTon), young: 27.3 +/- 3.6 s, old: 19.2 +/- 1.6 s; P < 0.05) exhibited markedly slowed P-O2 mu off-kinetics (increased MRT off, young: 46.5 +/- 5.9 s, old: 84.8 +/- 7.9 s; P < 0.05). Accordingly, a greater degree of P-O2 mv on-off asymmetry (MRT off-MRT on) in the aged muscle was observed (young: 19.1 +/- 4.5 s, old: 65.6 +/- 8.6 s; P < 0.01). We conclude that aging-induced speeding of the P-O2 mv on-kinetics does indeed presage a slowed P-O2 mv off-kinetics, which likely compromises muscle metabolic recovery and may reduce subsequent contractile performance. Moreover, the greater degree of P-O2 mv on-off asymmetry in the aged muscle suggests a mechanistic link between impaired microvascular oxygenation and altered muscle metabolic responses during exercise transitions. (C) 2009 Elsevier B.V. All rights reserved.