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J Appl Physiol 101: 213-227, 2006. First published March 30, 2006; doi:10.1152/japplphysiol.00862.2005
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Expiratory threshold loading impairs cardiovascular function in health and chronic heart failure during submaximal exercise

Jordan D. Miller, Sarah J. Hemauer, Curtis A. Smith, Michael K. Stickland, and Jerome A. Dempsey

University of Wisconsin-Madison, John Rankin Laboratory of Pulmonary Medicine, Madison, Wisconsin

Submitted 17 July 2005 ; accepted in final form 10 March 2006

We determined the effects of augmented expiratory intrathoracic pressure (PITP) production on cardiac output (QTOT) and blood flow distribution in healthy dogs and dogs with chronic heart failure (CHF). From a control expiratory PITP excursion of 7 ± 2 cmH2O, the application of 5, 10, or 15 cmH2O expiratory threshold loads increased the expiratory PITP excursion by 47 ± 23, 67 ± 32, and 118 ± 18% (P < 0.05 for all). Stroke volume (SV) rapidly decreased (onset <10 s) with increases in the expiratory PITP excursion (–2.1 ± 0.5%, –2.4 ± 0.9%, and –3.6 ± 0.7%, P < 0.05), with slightly smaller reductions in QTOT (0.8 ± 0.6, 1.0 ± 1.1, and 1.8 ± 0.8%, P < 0.05) owing to small increases in heart rate. Both QTOT and SV were restored to control levels when the inspiratory PITP excursion was augmented by the addition of an inspiratory resistive load during 15 cmH2O expiratory threshold loading. The highest level of expiratory loading significantly reduced hindlimb blood flow by –5 ± 2% owing to significant reductions in vascular conductance (–7 ± 2%). After the induction of CHF by 6 wk of rapid cardiac pacing at 210 beats/min, the expiratory PITP excursions during nonloaded breathing were not significantly changed (8 ± 2 cmH2O), and the application of 5, 10, and 15 cmH2O expiratory threshold loads increased the expiratory PITP excursion by 15 ± 7, 23 ± 7, and 31 ± 7%, respectively (P < 0.05 for all). Both 10 and 15 cmH2O expiratory threshold loads significantly reduced SV (–3.5 ± 0.7 and –4.2 ± 0.7%, respectively) and QTOT (–1.7 ± 0.4 and –2.5 ± 0.4%, P < 0.05) after the induction of CHF, with the reductions in SV predominantly occurring during inspiration. However, the augmentation of the inspiratory PITP excursion now elicited further decreases in SV and QTOT. Only the highest level of expiratory loading significantly reduced hindlimb blood flow (–4 ± 2%) as a result of significant reductions in vascular conductance (–5 ± 2%). We conclude that increases in expiratory PITP production-similar to those observed during severe expiratory flow limitation-reduce cardiac output and hindlimb blood flow during submaximal exercise in health and CHF.

cardiac output; blood flow distribution; exercise; expiratory flow limitation; heart failure



Address for reprint requests and other correspondence: J. D. Miller, Univ. of Iowa, 200 Hawkins Dr., 340B Eckstein Medical Research Bldg., Iowa City, IA 52242 (e-mail: jordan-miller{at}uiowa.edu)




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