title: Diaphragm efficiency estimated as power output relative to activation in chronic obstructive pulmonary disease.
abstract: Muscle efficiency increases with fiber length and decreases with load. Diaphragm efficiency (Eff(di)) in healthy humans, measured as power output (Wdi) relative to the root mean square of diaphragm electromyogram (RMS(di)), increases with hyperpnea due to phasic activity of abdominal muscles acting to increase diaphragm length at end expiration (L(di ee)) and decrease inspiratory load. In chronic obstructive pulmonary disease (COPD), hyperpnea may decrease Eff(di) if L(di ee) decreases and load increases due to airflow obstruction and dynamic hyperinflation. To examine this hypothesis, we measured Eff(di) in six COPD subjects (mean forced expiratory volume in 1 s: 54% predicted) when breathing air and at intervals during progressive hypercapnic hyperpnea. Wdi was measured as the product of mean inspiratory transdiaphragmatic pressure (ΔPdi(mean)), diaphragm tidal volume measured fluoroscopically, and 1/inspiratory duration. Results were compared with those of six healthy subjects reported previously. In COPD, L(di ee) was normal when breathing air. ΔPdi(mean) and Wdi increased normally, and RMS(di) increased disproportionately (P = 0.01) with hyperpnea, and, unlike health, inspiratory capacity (IC), L(di ee), and Eff(di) did not increase. IC and L(di ee) were constant with hyperpnea because mean expiratory flow increased as expiratory duration decreased (r(2) = 0.65), and because expiratory flow was terminated actively by the balance between expiratory and inspiratory muscle forces near end expiration, and these forces increased proportionately with hyperpnea (r(2) = 0.49). At maximum ventilation, diaphragm radius of curvature at end inspiration increased in COPD (P = 0.04) but not controls; diaphragm radius of curvature at end inspiration and ln(Eff(di)) were negatively correlated (P = 0.01). Thus in COPD with modest airflow obstruction, Eff(di) did not increase normally with hyperpnea due to a constant L(di ee) and inspiratory flattening of the diaphragm.
authors.affiliation: Department of Pulmonary Physiology and Sleep Medicine, Sir Charles Gairdner Hospital, Nedlands, WA 6009, Australia. finucane@cygnus.uwa.edu.au
authors.forename: Kevin E
authors.initials: KE
authors.lastname: Finucane
authors.forename: Bhajan
authors.initials: B
authors.lastname: Singh
mesh_terms: D000009:Abdominal Muscles / Q000503:physiopathology; D000368:Aged; D000369:Aged, 80 and over; D016022:Case-Control Studies; D003964:Diaphragm / Q000000981:diagnostic imaging / Q000503:physiopathology*; D004576:Electromyography; D045853:Exhalation; D005541:Forced Expiratory Volume; D006801:Humans; D006935:Hypercapnia / Q000503:physiopathology; D006985:Hyperventilation / Q000503:physiopathology; D001239:Inhalation; D008168:Lung / Q000503:physiopathology*; D008176:Lung Volume Measurements; D008875:Middle Aged; D008954:Models, Biological; D009119:Muscle Contraction; D053580:Muscle Strength; D011312:Pressure; D029424:Pulmonary Disease, Chronic Obstructive / Q000000981:diagnostic imaging / Q000503:physiopathology*; D012123:Pulmonary Ventilation; D011859:Radiography; D013997:Time Factors; D014109:Total Lung Capacity; D014939:Work of Breathing