Human Cardiovascular Physiology Laboratory, Department of Health and Exercise Science, Colorado State University, Fort Collins, CO, USA.
Medical Center of the Rockies Foundation, University of Colorado Health, Loveland, CO, USA.
J Physiol. 2020 Jul;598(13):2621-2636. doi: 10.1113/JP279682. Epub 2020 May 17.
During exercise, blood flow to working skeletal muscle increases in parallel with contractile activity such that oxygen delivery is sufficient to meet metabolic demand. K released from active skeletal muscle fibres could facilitate vasodilatation in proportion to the degree of muscle fibre recruitment. Once released, K stimulates inwardly rectifying K (K ) channels on the vasculature to elicit an increase in blood flow. In the present study, we demonstrate that K channels mediate the rapid vasodilatory response to an increase in exercise intensity. We also show that K channels augment vasodilatation during exercise which demands greater muscle fibre recruitment independent of the total amount of work performed. These results suggest that K plays a key role in coupling the magnitude of vasodilatation to the degree of contractile activity. Ultimately, the findings from this study help us understand the signalling mechanisms that regulate muscle blood flow in humans.
Blood flow to active skeletal muscle is augmented with greater muscle fibre recruitment. We tested whether activation of inwardly rectifying potassium (K ) channels underlies vasodilatation with elevated muscle fibre recruitment when work rate is increased (Protocol 1) or held constant (Protocol 2). We assessed forearm vascular conductance (FVC) during rhythmic handgrip exercise under control conditions and during local inhibition of K channels (intra-arterial BaCl ). In Protocol 1, healthy volunteers performed mild handgrip exercise for 3 min, then transitioned to moderate intensity for 30 s. BaCl eliminated vasodilatation during the first contraction at the moderate workload (ΔFVC, BaCl : -1 ± 17 vs. control: 30 ± 28 ml min 100 mmHg ; n = 9; P = 0.004) and attenuated the 30 s area under the curve by 56 ± 14% (n = 9; P < 0.0001). In Protocol 2, participants performed two exercise bouts in which muscle fibre recruitment was manipulated while total contractile work was held constant via reciprocal changes in contraction frequency: (1) low fibre recruitment, with contractions at 12.5% maximal voluntary contraction once every 4 s and (2) high fibre recruitment, with contractions at 25% maximal voluntary contraction once every 8 s. Under control conditions, steady-state FVC was augmented in high vs. low fibre recruitment (211 ± 90 vs. 166 ± 73 ml min ⋅100 mmHg ; n = 10; P = 0.0006), whereas BaCl abolished the difference between high and low fibre recruitment (134 ± 59 vs. 134 ± 63 ml min 100 mmHg ; n = 10; P = 0.85). These findings demonstrate that K channel activation is a key mechanism linking local vasodilatation with muscle fibre recruitment during exercise.
在运动过程中，向工作骨骼肌的血流增加与收缩活动平行，以确保氧输送足以满足代谢需求。来自活跃的骨骼肌纤维的 K 可以促进血管舒张，舒张程度与肌肉纤维募集的程度成正比。一旦释放，K 就会刺激血管内的内向整流钾 (K) 通道，从而增加血流量。在本研究中，我们证明 K 通道介导了运动强度增加时的快速血管舒张反应。我们还表明，K 通道在运动期间增强了血管舒张，而运动期间需要更大程度的肌肉纤维募集，而与完成的总工作量无关。这些结果表明 K 在将血管舒张的幅度与收缩活动的程度相匹配方面起着关键作用。最终，这项研究的结果帮助我们了解了调节人类肌肉血流量的信号机制。
向活跃的骨骼肌的血流量随着肌肉纤维募集的增加而增加。我们测试了在工作率增加（方案 1）或保持不变（方案 2）时，内向整流钾 (K) 通道的激活是否是在肌肉纤维募集增加时血管舒张的基础。我们在手握运动过程中评估了前臂血管传导率 (FVC) 在对照条件下和局部抑制 K 通道时（动脉内 BaCl）。在方案 1 中，健康志愿者进行轻度手握运动 3 分钟，然后过渡到中等强度 30 秒。BaCl 在中等工作量的第一次收缩时消除了血管舒张（ΔFVC，BaCl：-1 ± 17 与对照：30 ± 28 ml min ⁇ 100 mmHg；n = 9；P = 0.004），并使 30 秒的曲线下面积减少了 56 ± 14%（n = 9；P < 0.0001）。在方案 2 中，参与者进行了两次运动回合，通过收缩频率的相互变化来操纵肌肉纤维募集，同时保持总收缩工作量不变：（1）低纤维募集，以 12.5%最大自主收缩的收缩频率为 4 秒一次，（2）高纤维募集，以 25%最大自主收缩的收缩频率为 8 秒一次。在对照条件下，高纤维募集时的稳态 FVC 高于低纤维募集（211 ± 90 与 166 ± 73 ml min ⁇ 100 mmHg；n = 10；P = 0.0006），而 BaCl 消除了高纤维募集和低纤维募集之间的差异（134 ± 59 与 134 ± 63 ml min ⁇ 100 mmHg；n = 10；P = 0.85）。这些发现表明，K 通道激活是将运动期间局部血管舒张与肌肉纤维募集联系起来的关键机制。
