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Articles in PresS, published online ahead of print February 1, 2002
J Appl Physiol, 10.1152/jap.01222.2000
Submitted on December 19, 2000
Accepted on December 11, 2001
1 Dipartimento di Bioingegneria, Politecnico, Milano, Italy; Centro di Bioingegneria, Fond. Don Gnocchi, Milano, Italy
2 Fond. Don Gnocchi, Pozzolatico, Italy
3 Westmead Hospital, Sydney, Australia
4 University of Geneva, Geneva, Switzerland
5 Meakins Christie Laboratories, McGill University Health Centre, Montreal, Canada
6 Clinica Medica III, Universita delgli studi, Firenze, Italy
7 Fond. Don Gnocchi, Pozzolatico, Italy; Clinica Medica III, Universita delgli studi, Firenze, Italy
8 REspiratory Medicine, Institute of Tubercolosis and Lung Disease, Warsaw, Poland
* To whom correspondence should be addressed. E-mail: aliverti{at}mail.cbi.polimi.it.
To determine how decreasing velocity of shortening (U) of expiratory muscles affects breathing during exercise, 6 normal men performed incremental exercise with externally imposed expiratory flow-limitation (EFLe) at ~1LPS. We measured volumes of chest wall (Vcw) lung- and diaphragm-apposed rib cage (Vrc,p and Vrc,a resp.) and abdomen (Vab) by optoelectronic plethysmography, esophageal gastric and transdiaphragmatic pressures(Pes, Pga,Pdi), and end-tidal [CO2]. From these we calculated U, and power(W') of diaphragm, rib cage and abdominal muscles (di, rcm, abm). EFLe forced a decrease in Uabm which increased Pabm and which lasted well into inspiration. This imposed a load, overcome by pre-inspiratory di contraction. Udi and Urcm,i increased. reducing their ability to generate P. Pdi, Prcm, and W'abm 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 EFL decreases Uabm, increasing Pabm, exacerbating the hypercapnia, which increases central drive increasing Pabm even more, leading to further CO2 retention and so forth.
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