Skeletal muscle interstitial Po2 kinetics during recovery from contractions.
Skeletal muscle interstitial Po2 kinetics during recovery from contractions.
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收缩恢复期间骨骼肌间质 Po2 动力学。
DOI：
10.1152/japplphysiol.00297.2019
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发表时间：
2019
期刊：
影响因子：
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通讯作者：
Poole,DavidC
中科院分区：
文献类型：
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作者：
Hirai,DanielM;Craig,JesseC;Colburn,TrentonD;Eshima,Hiroaki;Kano,Yutaka;Musch,TimothyI;Poole,DavidC
间隙中的氧分压（Po 2 is）通过扩散驱动O2进入肌细胞，从而支持氧化磷酸化。虽然对代谢恢复和执行重复任务的能力至关重要，但骨骼肌Po 2在收缩恢复期间的时间过程仍然未知。我们检验了这一假设，即Po 2将恢复到静息值，并显示出相当大的开-关不对称性（开-关动力学快，关-关动力学慢），反映了不对称的毛细血管血流动力学。还对微血管Po 2（Po 2 mv）进行了评价，以检验恢复期间将维持显著跨毛细血管梯度（Δ Po 2 = Po 2 mv− Po 2 is）的假设。在次最大抽搐收缩期间和之后，通过暴露的大鼠脊髓背角肌中的磷光猝灭测定Po 2 mv和Po 2 is（以mmHg表示）（n= 12）。收缩末期Po_2（11.1 ± 5.1）呈指数上升（P< 0.05），收缩末期恢复值（17.9 ± 7.9）与静息时的Po_2（18.5 ± 8.1）无显著性差异（P> 0.05）。氧分压关闭动力学慢于氧分压开启动力学（平均反应时间：53.1 ± 38.3s对18.5 ± 7.3s;P< 0.05）。收缩末期跨毛细血管Δ Po 2为16.6 ± 7.4，恢复期为18.8 ± 9.6（P> 0.05）。与我们的假设相一致，肌肉Po 2恢复到静息值，与毛细血管血流动力学的开-关不对称性相一致的开-关动力学相比，具有较慢的关动力学。在恢复过程中维持一个相当大的跨毛细血管Δ Po 2支持微血管-微血管界面提供了相当大的阻力O2运输。根据菲克定律（V ~（？）o_2 = Do_2 × Δ Po_2），恢复过程中O_2通量（V ~（？）o_2）的调节必须通过有效扩散能力的相应变化来实现（Do 2;主要是毛细血管红细胞的血流动力学和分布）面对不变的Δ Po 2。新&值得注意毛细血管血-肌细胞O2通量（V今o2）由有效弥散量决定（Do 2;主要是红细胞血流动力学和分布）和微血管间质Po 2梯度（Δ Po 2 = Po 2 mv− Po 2 is）。我们发现，PO 2 isdemonstrates开关不对称性与PO 2 mv和红细胞动力学代谢转换过程中一致。在收缩恢复过程中保留了大量的跨毛细血管Δ Po 2，表明微血管-微血管界面对O2扩散有相当大的阻力。这表明，根据Fick定律，在恢复期间，有效Do 2与Vto 2同步下降。
The oxygen partial pressure in the interstitial space (Po2 is) drives O2into the myocyte via diffusion, thus supporting oxidative phosphorylation. Although crucial for metabolic recovery and the capacity to perform repetitive tasks, the time course of skeletal muscle Po2 isduring recovery from contractions remains unknown. We tested the hypothesis that Po2 iswould recover to resting values and display considerable on-off asymmetry (fast on-, slow off-kinetics), reflective of asymmetric capillary hemodynamics. Microvascular Po2(Po2 mv) was also evaluated to test the hypothesis that a significant transcapillary gradient (ΔPo2= Po2 mv− Po2 is) would be sustained during recovery. Po2 mvand Po2 is(expressed in mmHg) were determined via phosphorescence quenching in the exposed rat spinotrapezius muscle during and after submaximal twitch contractions (n= 12). Po2 isrose exponentially (P< 0.05) from end-contraction (11.1 ± 5.1), such that the end-recovery value (17.9 ± 7.9) was not different from resting Po2 is(18.5 ± 8.1;P> 0.05). Po2 isoff-kinetics were slower than on-kinetics (mean response time: 53.1 ± 38.3 versus 18.5 ± 7.3 s;P< 0.05). A significant transcapillary ΔPo2observed at end-contraction (16.6 ± 7.4) was maintained throughout recovery (end-recovery: 18.8 ± 9.6;P> 0.05). Consistent with our hypotheses, muscle Po2 isrecovered to resting values with slower off-kinetics compared with the on-transient in line with the on-off asymmetry for capillary hemodynamics. Maintenance of a substantial transcapillary ΔPo2during recovery supports that the microvascular-interstitium interface provides considerable resistance to O2transport. As dictated by Fick’s law (V̇o2= Do2× ΔPo2), modulation of O2flux (V̇o2) during recovery must be achieved via corresponding changes in effective diffusing capacity (Do2; mainly capillary red blood cell hemodynamics and distribution) in the face of unaltered ΔPo2.NEW & NOTEWORTHYCapillary blood-myocyte O2flux (V̇o2) is determined by effective diffusing capacity (Do2; mainly erythrocyte hemodynamics and distribution) and microvascular-interstitial Po2gradients (ΔPo2= Po2 mv− Po2 is). We show that Po2 isdemonstrates on-off asymmetry consistent with Po2 mvand erythrocyte kinetics during metabolic transitions. A substantial transcapillary ΔPo2was preserved during recovery from contractions, indicative of considerable resistance to O2diffusion at the microvascular-interstitium interface. This reveals that effective Do2declines in step with V̇o2during recovery, as per Fick’s law.