TY - JOUR
T1 - Expiratory threshold loading impairs cardiovascular function in health and chronic heart failure during submaximal exercise
AU - Miller, Jordan D.
AU - Hemauer, Sarah J.
AU - Smith, Curtis A.
AU - Stickland, Michael K.
AU - Dempsey, Jerome A.
PY - 2006
Y1 - 2006
N2 - 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.
AB - 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.
KW - Blood flow distribution
KW - Cardiac output
KW - Exercise
KW - Expiratory flow limitation
KW - Heart failure
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U2 - 10.1152/japplphysiol.00862.2005
DO - 10.1152/japplphysiol.00862.2005
M3 - Article
C2 - 16575025
AN - SCOPUS:33745858991
SN - 8750-7587
VL - 101
SP - 213
EP - 227
JO - Journal of Applied Physiology
JF - Journal of Applied Physiology
IS - 1
ER -