Influence of respiratory muscle work on VO(2) and leg blood flow during submaximal exercise.
Influence of respiratory muscle work on VO(2) and leg blood flow during submaximal exercise.
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DOI：
10.1097/00005768-199905001-00325
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发表时间：
1999-05
影响因子：
3.3
通讯作者：
T. J. Wetter;C. Harms;W. Nelson;D. Pegelow;J. Dempsey
中科院分区：
文献类型：
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作者：
T. J. Wetter;C. Harms;W. Nelson;D. Pegelow;J. Dempsey
在最大强度运动中通常发生的呼吸功（W（B））不仅需要大量的心输出量和O（2）消耗（VO（2）），而且还引起运动肌肉中的血管收缩并损害腿部血流量（Q（leg））。我们想知道在次极量运动中正常产生的W（B）是否也会降低Q（leg）。因此，我们研究了通过热稀释法改变10名健康训练的男性自行车运动员的W（B）对Q（腿）的影响[最大VO（2）（VO（2 max））= 59 +/- 9 ml。kg（-1）。min（-1）]，在对应于VO（2 max）的50%和75%的工作率下进行循环运动。吸气肌功：1）通过比例辅助呼吸机减少40 +/- 6%，2）未操作（对照），或3）通过增加吸气阻力负荷增加61 +/- 8%。在亚极量运动中增加W（B）导致VO（2）增加;降低W（B）与较低的VO（2）相关（在VO（2 max）的50%和75%时，W（B）的变化约为100%时，Δ VO（2）分别为0.12和0.21 l/min）。当W（B）减少或增加时，腿部血管阻力（LVR）、去甲肾上腺素溢出、动脉压或Q（腿部）无显著变化。为什么LVR、去甲肾上腺素溢出和Q（腿）在最大运动时受W（B）的影响，而在次最大运动时不受其影响？我们假设在次最大作功率和通气率下，所需的正常W（B）对VO（2）和心输出量的需求不足，不需要任何心血管调节，并且太小而不能激活交感血管收缩剂的传出输出。此外，即使在次极量运动期间W（B）增加50-70%，如在通气速率和/或吸气流动阻力高于正常的条件下可能遇到的，也不会引起LVR或Q（腿部）的变化。
The work of breathing (W(b)) normally incurred during maximal exercise not only requires substantial cardiac output and O(2) consumption (VO(2)) but also causes vasoconstriction in locomotor muscles and compromises leg blood flow (Q(leg)). We wondered whether the W(b) normally incurred during submaximal exercise would also reduce Q(leg). Therefore, we investigated the effects of changing the W(b) on Q(leg) via thermodilution in 10 healthy trained male cyclists [maximal VO(2) (VO(2 max)) = 59 +/- 9 ml. kg(-1). min(-1)] during repeated bouts of cycle exercise at work rates corresponding to 50 and 75% of VO(2 max). Inspiratory muscle work was 1) reduced 40 +/- 6% via a proportional-assist ventilator, 2) not manipulated (control), or 3) increased 61 +/- 8% by addition of inspiratory resistive loads. Increasing the W(b) during submaximal exercise caused VO(2) to increase; decreasing the W(b) was associated with lower VO(2) (DeltaVO(2) = 0.12 and 0.21 l/min at 50 and 75% of VO(2 max), respectively, for approximately 100% change in W(b)). There were no significant changes in leg vascular resistance (LVR), norepinephrine spillover, arterial pressure, or Q(leg) when W(b) was reduced or increased. Why are LVR, norepinephrine spillover, and Q(leg) influenced by the W(b) at maximal but not submaximal exercise? We postulate that at submaximal work rates and ventilation rates the normal W(b) required makes insufficient demands for VO(2) and cardiac output to require any cardiovascular adjustment and is too small to activate sympathetic vasoconstrictor efferent output. Furthermore, even a 50-70% increase in W(b) during submaximal exercise, as might be encountered in conditions where ventilation rates and/or inspiratory flow resistive forces are higher than normal, also does not elicit changes in LVR or Q(leg).