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, Jerome A. Dempsey

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

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 P ITP 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 P ITP 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 P ITP 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.

Original languageEnglish (US)
Pages (from-to)213-227
Number of pages15
JournalJournal of Applied Physiology
Volume101
Issue number1
DOIs
StatePublished - 2006
Externally publishedYes

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Stroke Volume
Inosine Triphosphate
Heart Failure
Hindlimb
Health
Cardiac Output
Blood Vessels
Dogs
Respiration
Heart Rate
Pressure

Keywords

  • Blood flow distribution
  • Cardiac output
  • Exercise
  • Expiratory flow limitation
  • Heart failure

ASJC Scopus subject areas

  • Physiology
  • Endocrinology
  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation

Cite this

Expiratory threshold loading impairs cardiovascular function in health and chronic heart failure during submaximal exercise. / Miller, Jordan D; Hemauer, Sarah J.; Smith, Curtis A.; Stickland, Michael K.; Dempsey, Jerome A.

In: Journal of Applied Physiology, Vol. 101, No. 1, 2006, p. 213-227.

Research output: Contribution to journalArticle

Miller, Jordan D ; Hemauer, Sarah J. ; Smith, Curtis A. ; Stickland, Michael K. ; Dempsey, Jerome A. / Expiratory threshold loading impairs cardiovascular function in health and chronic heart failure during submaximal exercise. In: Journal of Applied Physiology. 2006 ; Vol. 101, No. 1. pp. 213-227.
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abstract = "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 P ITP 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 P ITP 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 P ITP 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.",
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KW - Blood flow distribution

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KW - Exercise

KW - Expiratory flow limitation

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