Fatiguing inspiratory muscle work causes reflex sympathetic activation in humans
Fatiguing inspiratory muscle work causes reflex sympathetic activation in humans
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DOI：
10.1111/j.1469-7793.2000.00493.x
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发表时间：
2000-12-01
影响因子：
5.5
通讯作者：
Dempsey, JA
中科院分区：
文献类型：
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作者：
St Croix, CM;Morgan, BJ;Dempsey, JA
1. 我们测试了这样的假设：工作中的呼吸肌产生的反射可以引起流向肢体骨骼肌的交感血管收缩剂增加，在 7 名健康受试者的休息状态下进行测试。2。我们使用腓神经内的神经内电极测量了肌肉交感神经活动 (MSNA)，同时受试者抵抗阻力吸气（主要通过膈肌），口压 (P-M) 等于最大压力的 60%，占空比延长 (T-I/T-Tot) 为 0.70，呼吸频率 (f(b)) 为 15 次呼吸 min(-1)，潮气量 (V-T) 相当于正常呼吸的两倍。众所周知，该方案会减少膈肌血流量并导致疲劳。3。 MSNA 在前 1-2 分钟内没有变化，但随后随着时间的推移而增加，在力竭时比对照高出 77 +/- 51% (S.D.)（平均时间，7 +/- 3 分钟）。平均动脉血压 (+12 mmHg) 和心率 (+ 27 小时分钟(-1)) 也增加。4。当在不增加阻力的情况下模拟这些试验的 V-T、f(b) 和 T-I/T-Tot 时，MSNA 和动脉血压均未升高。5。 MSNA 和动脉血压也没有因两种不产生疲劳的中枢呼吸运动输出增加而变化：(a) 高吸气流速和 f(b)，无阻力增加； (b) 对抗阻力的高吸气努力，最大 P-M 为 95%，T-I/T-Tot 为 0.35，f(b) 为 12 次呼吸 min(-1)。在这些试验中，心率增加了 5-16 次/分(-1)。6。因此，在中枢呼吸运动输出增加本身对肢体 MSNA 没有任何影响的情况下，我们将高阻力、延长工作周期呼吸期间 MSNA 的时间依赖性增加归因于膈肌在面对高力输出和血流受损时积累代谢终产物的反射。
1. We tested the hypothesis that reflexes arising from working respiratory muscle can elicit increases in sympathetic vasoconstrictor outflow to limb skeletal muscle, in seven healthy human subjects at rest.2. We measured muscle sympathetic nerve activity (MSNA) with intraneural electrodes in the peroneal nerve while the subject inspired (primarily with the diaphragm) against resistance, with mouth pressure (P-M) equal to 60% of maximal, a prolonged duty cycle (T-I/T-Tot) of 0.70, breathing frequency (f(b)) of 15 breaths min(-1) and tidal volume (V-T) equivalent to twice eupnoea. This protocol was known to reduce diaphragm blood flow and cause fatigue.3. MSNA was unchanged during the first 1-2 min but then increased over time, to 77 +/- 51% (S.D.) greater than control at exhaustion (mean time, 7 +/- 3 min). Mean arterial blood pressure (+12 mmHg) and heart rate (+ 27 heats min(-1)) also increased.4. When the V-T, f(b) and T-I/T-Tot of these trials were mimicked with no added resistance, neither MSNA nor arterial blood pressure increased.5. MSNA and arterial blood pressure also did not change in response to two types of increased central respiratory motor output that did not produce fatigue: (a) high inspiratory flow rate and f(b) without added resistance; or (b) high inspiratory effort against resistance with P-M of 95% maximal, T-I/T-Tot of 0.35 and f(b) of 12 breaths min(-1). The heart rate increased by 5-16 beats min(-1) during these trials.6. Thus, in the absence of any effect of increased central respiratory motor output per se on limb MSNA, we attributed the time-dependent increase in MSNA during high resistance, prolonged duty cycle breathing to a reflex arising from a diaphragm that was accumulating metabolic end products in the face of high force output plus compromised blood flow.