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J Appl Physiol (March 30, 2006). doi:10.1152/japplphysiol.00862.2005
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Submitted on July 17, 2005
Accepted on March 10, 2006

Expiratory threshold loading impairs cardiovascular function in health and chronic heart failure during submaximal exercise

Jordan D Miller1*, Sarah J Hemauer1, Curtis A. Smith1, Michael Stickland1, and Jerome A. Dempsey1

1 Population Health Sciences, University of Wisconsin-Madison, Madison, Wisconsin, United States

* To whom correspondence should be addressed. E-mail: jordan-miller{at}uiowa.edu.

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 cm H2O, the application of 5, 10, or 15 cm H2O 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 seconds) 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) due 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 cm H2O expiratory threshold loading. The highest level of expiratory loading significantly reduced hindlimb blood flow by -5 ± 2% due to significant reductions in vascular conductance (-7 ± 2%). After the induction of CHF by 6 weeks of rapid cardiac pacing at 210 beats per minute, the expiratory PITP excursions during non-loaded breathing were not significantly changed (8 ± 2 cm H2O), and the application of 5, 10, and 15 cm H2O 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 cm H2O 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.




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