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This Article Full Text Full Text (PDF) All Versions of this Article: 107/5/1397    most recent 91465.2008v2 91465.2008v1 Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Finucane, K. E. Articles by Singh, B. PubMed PubMed Citation Articles by Finucane, K. E. Articles by Singh, B.

Human diaphragm efficiency estimated as power output relative to activation increases with hypercapnic hyperpnea

Department of Pulmonary Physiology, Sir Charles Gairdner Hospital, Nedlands; and West Australian Sleep Disorders Research Institute, Queen Elizabeth II Medical Centre, Perth, Western Australia, Australia

Submitted 10 November 2008 ; accepted in final form 13 August 2009

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 PCO₂ 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 (di) [the product of mean inspiratory transdiaphragmatic pressure, diaphragm volume change (Vdi) 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 () in Pg decreased from 4.5 (SD 2.2) to –7.7 (SD 3.8) cmH₂O (P < 0.001); 3) Vdi·TI^–1, di, 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 di were not different (P = 0.4). Eff_di was predicted from Ldi_ee (P < 0.001), Pg_ee (P < 0.001), Pg·TI^–1 (P = 0.03), and Pg (P = 0.04) (r² = 0.52) (multivariate regression analysis). We conclude that, with hypercapnic hyperpnea, 1) 47% of the maximum increase of di 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 di or Eff_di; and 4) phasic abdominal muscle activity with hyperpnea reduces diaphragm energy consumption.

diaphragm flow, pressure and electrical activity; ventilatory loads