Eastwood P R, Hillman D R, Finucane K E
Department of Pulmonary Physiology, Sir Charles Gairdner Hospital, Nedlands, Australia.
J Appl Physiol (1985). 1994 Jan;76(1):185-95. doi: 10.1152/jappl.1994.76.1.185.
To examine respiratory muscle recruitment pattern during inspiratory loading and role of fatigue in limiting endurance, we studied seven normal subjects on 17 +/- 6 days during breathing against progressive inspiratory threshold load. Threshold pressure (Pth) was progressively increased 14 +/- 5 cmH2O every 2 min until voluntary cessation (task failure). Subjects could adopt any breathing pattern. Tidal volume (VT), chest wall motion, end-tidal PCO2, and arterial O2 saturation were measured. At moderate loads [50-75% of maximum Pth (Pthmax)], inspiratory time (TI) decreased and VT/TI and expiratory time increased, increasing time for recovery of muscles between inspirations. At high loads (> 75% Pthmax), VT/TI decreased, which, with progressive decrease in end-expiratory lung volume (EELV) throughout, increased potential for inspiratory force development. Progressive hypoxia and hypercapnia occurred at higher work loads. Immediately after task failure all subjects could recover at high loads and still reachieve initial Pthmax on reimposition of progressive loading. Respiratory pressures were measured in subgroup of three subjects: transdiaphragmatic pressure response to 0.1-ms bilateral supramaximal phrenic nerve stimulation at end expiration initially increased with increasing load/decreasing EELV, consistent with increasing mechanical advantage of diaphragm, but decreased at highest loads, suggesting diaphragm fatigue. Full recovery had not occurred at 30 min after task failure. We demonstrated that progressive threshold loading is associated with systematic changes in breathing pattern that act to optimize muscle strength and increase endurance. Task failure occurred when these compensatory mechanisms were maximal. Inspiratory muscles appeared relatively resistant to fatigue, which was late but persistent.
为了研究吸气负荷期间呼吸肌的募集模式以及疲劳在限制耐力方面的作用，我们对7名正常受试者在17±6天内进行了研究，让他们在对抗逐渐增加的吸气阈值负荷的情况下呼吸。每2分钟将阈值压力（Pth）逐渐增加14±5 cmH₂O，直至自主停止（任务失败）。受试者可以采用任何呼吸模式。测量潮气量（VT）、胸壁运动、呼气末PCO₂和动脉血氧饱和度。在中等负荷[最大Pth（Pthmax）的50 - 75%]时，吸气时间（TI）缩短，VT/TI和呼气时间增加，增加了吸气之间肌肉恢复的时间。在高负荷（>75% Pthmax）时，VT/TI降低，这与整个呼气末肺容积（EELV）的逐渐减少一起，增加了吸气力发展的潜力。在较高工作负荷下出现了逐渐加重的低氧血症和高碳酸血症。任务失败后，所有受试者立即能够在高负荷下恢复，并且在重新施加逐渐增加的负荷时仍能再次达到初始Pthmax。在三名受试者的亚组中测量了呼吸压力：在呼气末对0.1毫秒双侧超强膈神经刺激的跨膈压反应最初随着负荷增加/ EELV降低而增加，这与膈肌机械优势增加一致，但在最高负荷时降低，提示膈肌疲劳。任务失败后30分钟尚未完全恢复。我们证明，逐渐增加的阈值负荷与呼吸模式的系统性变化有关，这些变化有助于优化肌肉力量并增加耐力。当这些代偿机制达到最大时发生任务失败。吸气肌似乎对疲劳相对有抵抗力，疲劳出现较晚但持续存在。
