Abstract
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 (Effdi) in vivo, we measured Effdiin six healthy adults breathing air and during progressive hypercapnia at three levels of end-tidal Pco2with mean values of 48 (SD 2), 55 (SD 2), and 61 (SD 1) Torr. Effdiwas estimated as the ratio of diaphragm power (W˙di) [the product of mean inspiratory transdiaphragmatic pressure, diaphragm volume change (ΔVdi) measured fluoroscopically, and 1/inspiratory duration (Ti−1)] to activation [root mean square values of inspiratory diaphragm electromyogram (RMSdi) measured from esophageal electrodes]. At maximum hypercapnea relative to breathing air, 1) gastric pressure and diaphragm length at end expiration (Pgeeand Ldiee, respectively) increased 1.4 (SD 0.2) and 1.13 (SD 0.08) times, ( P < 0.01 for both); 2) inspiratory change (Δ) in Pg decreased from 4.5 (SD 2.2) to −7.7 (SD 3.8) cmH2O ( P < 0.001); 3) ΔVdi·Ti−1, W˙di, RMSdi, and Effdiincreased 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 W˙di were not different ( P = 0.4). Effdiwas predicted from Ldiee( P < 0.001), Pgee( P < 0.001), ΔPg·Ti−1( P = 0.03), and ΔPg ( P = 0.04) ( r2= 0.52) (multivariate regression analysis). We conclude that, with hypercapnic hyperpnea, 1) ∼47% of the maximum increase of W˙di was attributable to increased Effdi; 2) Effdiincreased 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 W˙di or Effdi; and 4) phasic abdominal muscle activity with hyperpnea reduces diaphragm energy consumption.