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1 Centro di Bioingegneria, Fondazione Don Gnocchi e Politecnico I-20148 Milano; 2 Dipartimento di Bioingegneria, Politecnico di Milano, I-20133 Milan; 3 Fondazione Don Gnocchi, I-50020 Pozzolatico; 4 Clinica Medica III, Università di Firenze, I-50134 Florence, Italy; 5 Westmead Hospital, NSW-2145 Sydney, Australia; 6 University of Geneva, CH-1217 Geneva, Switzerland; 7 Meakins-Christie Laboratories, Montreal Chest Institute, McGill University Health Centre, Montreal, Quebec, Canada H2X 2P4; and 8 Department of Respiratory Medicine, Institute of Tuberculosis and Lung Disease, 01-138 Warsaw, Poland
To determine
how decreasing velocity of shortening (U) of expiratory muscles affects
breathing during exercise, six normal men performed incremental
exercise with externally imposed expiratory flow limitation (EFLe) at
~1 l/s. We measured volumes of chest wall, lung- and
diaphragm-apposed rib cage (Vrc,p and Vrc,a, respectively), and abdomen
(Vab) by optoelectronic plethysmography; esophageal, gastric, and
transdiaphragmatic pressures (Pdi); and end-tidal CO2
concentration. From these, we calculated velocity of shortening and
power (
) of diaphragm, rib cage, and abdominal muscles (di, rcm,
ab, respectively). EFLe forced a decrease in Uab, which increased Pab
and which lasted well into inspiration. This imposed a load, overcome
by preinspiratory diaphragm contraction. Udi and inspiratory Urcm
increased, reducing their ability to generate pressure. Pdi, Prcm, and
ab increased, indicating an increased central drive to all
muscle groups secondary to hypercapnia, which developed in all
subjects. These results suggest a vicious cycle in which EFLe decreases
Uab, increasing Pab and exacerbating the hypercapnia, which increases
central drive increasing Pab even more, leading to further
CO2 retention, and so forth.
muscle shortening velocity; respiratory failure; hypercapnia; ventilation; diaphragm; abdominal muscles; rib cage muscles; muscle power
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