Laghi F, D'Alfonso N, Tobin M J
Division of Pulmonary and Critical Care Medicine, Edward Hines, Jr. Veterans Affairs Hospital, Hines, Illinois 60141, USA.
J Appl Physiol (1985). 1995 Aug;79(2):539-46. doi: 10.1152/jappl.1995.79.2.539.
The rate of recovery from diaphragmatic fatigue beyond 1 h is unknown. To investigate this question, we studied 12 healthy subjects and measured transdiaphragmatic twitch pressure (Pditw) using magnetic stimulation of the phrenic nerves. Measurements were obtained at baseline and after a fatigue protocol consisting of inspiratory resistive loading in which the subjects generated 60% of maximal transdiaphragmatic pressure until task failure. At baseline, Pditw was 38.9 +/- 1.1 (SE) cmH2O and fell to 25.1 +/- 0.6 cmH2O 10 min after the conclusion of the fatigue protocol (P < 0.01). Pditw increased to 27.6 +/- 0.9, 31.6 +/- 1.1, and 32.7 +/- 1.2 cmH2O 1, 8 and 24 h, respectively, after the conclusion of the fatigue protocol; the 24-h value was significantly lower than baseline (P < 0.01). The nadir in Pditw after the protocol was delayed by 10 min. In separate experiments, we showed that this delay was probably due to the development of twitch potentiation as a result of forceful diaphragmatic contractions during the fatigue protocol. In conclusion, induction of diaphragmatic fatigue with this experimental protocol produced a marked decrease in diaphragmatic contractility that persisted for at least 24 h.
膈肌疲劳超过1小时后的恢复速率尚不清楚。为了研究这个问题，我们对12名健康受试者进行了研究，并通过膈神经磁刺激测量跨膈抽搐压力（Pditw）。在基线时以及在疲劳方案后进行测量，该疲劳方案包括吸气阻力负荷，即受试者产生最大跨膈压力的60%，直至任务失败。在基线时，Pditw为38.9±1.1（标准误）cmH₂O，在疲劳方案结束后10分钟降至25.1±0.6 cmH₂O（P<0.01）。在疲劳方案结束后1、8和24小时，Pditw分别升至27.6±0.9、31.6±1.1和32.7±1.2 cmH₂O；24小时的值显著低于基线（P<0.01）。方案后Pditw的最低点延迟了10分钟。在单独的实验中，我们表明这种延迟可能是由于在疲劳方案期间膈肌强力收缩导致抽搐增强的发展。总之，用该实验方案诱导膈肌疲劳会导致膈肌收缩力显著下降，且这种下降至少持续24小时。
