Dept. of Pulmonary Physiology, Sir Charles Gairdner Hospital, Hospital Ave., Nedlands, Western Australia 6009, Australia.
J Appl Physiol (1985). 2009 Nov;107(5):1397-405. doi: 10.1152/japplphysiol.91465.2008. Epub 2009 Aug 20.
Hyperpnea with exercise or hypercapnia causes phasic contraction of abdominal muscles, potentially lengthening the diaphragm at end expiration and unloading it during inspiration. Muscle efficiency in vitro varies with load, fiber length, and precontraction stretch. To examine whether these properties of muscle contractility determine diaphragm efficiency (Eff(di)) in vivo, we measured Eff(di) in six healthy adults breathing air and during progressive hypercapnia at three levels of end-tidal Pco(2) with mean values of 48 (SD 2), 55 (SD 2), and 61 (SD 1) Torr. Eff(di) was estimated as the ratio of diaphragm power (Wdi) [the product of mean inspiratory transdiaphragmatic pressure, diaphragm volume change (DeltaVdi) measured fluoroscopically, and 1/inspiratory duration (Ti(-1))] to activation [root mean square values of inspiratory diaphragm electromyogram (RMS(di)) measured from esophageal electrodes]. At maximum hypercapnea relative to breathing air, 1) gastric pressure and diaphragm length at end expiration (Pg(ee) and Ldi(ee), respectively) increased 1.4 (SD 0.2) and 1.13 (SD 0.08) times, (P < 0.01 for both); 2) inspiratory change (Delta) in Pg decreased from 4.5 (SD 2.2) to -7.7 (SD 3.8) cmH(2)O (P < 0.001); 3) DeltaVdi.Ti(-1), Wdi, RMS(di), and Eff(di) increased 2.7 (SD 0.6), 4.9 (SD 1.8), 2.6 (SD 0.9), and 1.8 (SD 0.3) times, respectively (P < 0.01 for all); and 4) net and inspiratory Wdi were not different (P = 0.4). Eff(di) was predicted from Ldi(ee) (P < 0.001), Pg(ee) (P < 0.001), DeltaPg.Ti(-1) (P = 0.03), and DeltaPg (P = 0.04) (r(2) = 0.52) (multivariate regression analysis). We conclude that, with hypercapnic hyperpnea, 1) approximately 47% of the maximum increase of Wdi was attributable to increased Eff(di); 2) Eff(di) increased due to preinspiratory lengthening and inspiratory unloading of the diaphragm, consistent with muscle behavior in vitro; 3) passive recoil of the diaphragm did not contribute to inspiratory Wdi or Eff(di); and 4) phasic abdominal muscle activity with hyperpnea reduces diaphragm energy consumption.
运动或高碳酸血症引起的过度通气会导致腹部肌肉阶段性收缩，这可能会在呼气末期延长横膈膜，并在吸气时减轻其负担。体外肌肉效率随负荷、纤维长度和预收缩伸展而变化。为了研究肌肉收缩能力的这些特性是否决定了体内横膈膜的效率（Eff(di)），我们在 6 名健康成年人呼吸空气和在三个不同的终末 Pco2 水平（平均值分别为 48（SD 2）、55（SD 2）和 61（SD 1）托）下进行递增性高碳酸血症时，测量了 Eff(di)。Eff(di) 被估计为横膈膜功率（Wdi）[平均吸气跨膈压、荧光透视测量的膈膜体积变化（DeltaVdi）和吸气持续时间（Ti(-1)）的乘积]与激活（从食管电极测量的吸气膈神经肌电图的均方根值（RMS(di)）]的比值。在与呼吸空气相比的最大高碳酸血症时，1）胃压和呼气末期的膈膜长度（分别为 Pg(ee)和 Ldi(ee)）分别增加了 1.4（SD 0.2）和 1.13（SD 0.08）倍（两者均 P < 0.01）；2）吸气时的变化（Delta）在 Pg 中从 4.5（SD 2.2）降低到-7.7（SD 3.8）cmH2O（P < 0.001）；3）DeltaVdi.Ti(-1)、Wdi、RMS(di)和 Eff(di)分别增加了 2.7（SD 0.6）、4.9（SD 1.8）、2.6（SD 0.9）和 1.8（SD 0.3）倍（所有 P < 0.01）；4）净和吸气 Wdi 没有差异（P = 0.4）。Eff(di) 可以从 Ldi(ee)（P < 0.001）、Pg(ee)（P < 0.001）、DeltaPg.Ti(-1)（P = 0.03）和 DeltaPg（P = 0.04）（r(2) = 0.52）（多元回归分析）中预测（r(2) = 0.52）。我们得出结论，在高碳酸血症性过度通气时，1）Wdi 的最大增加约 47%归因于 Eff(di)的增加；2）Eff(di)的增加是由于膈膜的预吸气伸展和吸气卸载引起的，与体外肌肉行为一致；3）膈膜的被动回弹并没有增加吸气 Wdi 或 Eff(di)；4）过度通气时的腹部肌肉阶段性活动可降低膈膜的能量消耗。
