Effect of chronic heart failure in older rats on respiratory muscle and hindlimb blood flow during submaximal exercise

Exercise performance in chronic heart failure is severely impaired, due in part to a peripherally mediated limitation. In addition to impaired maximal exercise capacity, the O2 uptake (O2) response during submaximal exercise may be affected, with a greater reliance on anaerobiosis leading to early fatigue. However, the response of O2 kinetics to submaximal exercise in chronic heart failure has not been studied extensively; in particular, the relationship between oxygen utilization and the peripheral response to exercise has not been studied. The present investigation examined the time-constant (τ, corresponding to 63% of the total response fitted from exercise onset) of the O2 kinetics on-response to submaximal exercise and its relationship to maximal peripheral blood flow in patients with chronic heart failure, and compared responses with those in healthy sedentary subjects. Subjects were 10 patients with chronic heart failure (NYHA class II/III). The mean age was 50±12 years, with a mean resting left ventricular ejection fraction of 25±9%. Controls were 10 age-matched healthy subjects. O2(max) was first determined for all subjects. Repeated transitions from rest to exercise were performed on a cycle ergometer while measuring breath-by-breath responses of O2 at a fixed work rate of 50% of O2(max) (heart failure patients and healthy controls) and at a work rate equivalent to the average in heart failure patients (65 W; healthy controls only). On a separate occasion, post-maximal ischaemic exercise calf blood flow was measured (strain-gauge plethysmography).Whereas heart failure subjects displayed a significantly prolonged O2 kinetics response at a similar absolute workload (i.e. 65 W), as indicated by a longer τ value (42 s, compared with 22 s in controls; P< 0.01), there was no difference in τ at a similar relative work rate [50% of O2(max)]. In addition, heart failure subjects demonstrated a lower maximal calf blood flow (P< 0.05) than control subjects. These results indicate that patients with heart failure have a prolonged O2 kinetics on-response compared with healthy subjects at a similar absolute work rate (i.e. 65 W), but not at a similar relative work rate [50% of O2(max)]. Thus, despite a reduced maximal calf blood flow response associated with heart failure, it does not appear that this contributes to an impairment of the submaximal exercise response beyond that explained by a reduced maximal exercise capacity [O2(max)].

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The effects of inspiratory intrathoracic pressure production on the cardiovascular response to submaximal exercise in health and chronic heart failure

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00211.2006 ◽

2007 ◽

Vol 292 (1) ◽

pp. H580-H592 ◽

Cited By ~ 33

Author(s):

Jordan D. Miller ◽

Curtis A. Smith ◽

Sarah J. Hemauer ◽

Jerome A. Dempsey

Keyword(s):

Heart Failure ◽

Blood Flow ◽

Cardiac Output ◽

Steady State ◽

Chronic Heart Failure ◽

Flow Distribution ◽

Submaximal Exercise ◽

Positive Pressure ◽

Blood Flow Distribution ◽

Limb Blood Flow

We sought to determine whether the normal inspiratory intrathoracic pressures (PITP) produced during exercise contribute to the blunted cardiac output and locomotor limb blood flow responses observed in chronic heart failure (CHF). Five chronically instrumented dogs exercised on a treadmill at 2.5 mile/h at 5% grade while healthy or after the induction of tachycardia-induced CHF. We observed several key differences in the cardiovascular responses to changes in the inspiratory PITP excursion between health and CHF; namely, 1) removing ∼70% of the normally produced inspiratory PITP excursion during exercise (with 15 cmH2O inspiratory positive pressure ventilation) significantly reduced stroke volume (SV) in healthy animals by 5 ± 2% ( P < 0.05) but significantly increased SV and cardiac output (QTOT) in animals with CHF by 5 ± 1% ( P < 0.05); 2) doubling the magnitude of the inspiratory PITP excursion had no effect on SV or QTOT in healthy animals but significantly reduced steady-state QTOT and SV in animals with CHF by −4 ± 3% and −10 ± 3%, respectively; 3) removing the majority of the normally produced inspiratory PITP excursion had no effect on blood flow distribution in healthy animals but increased hindlimb blood flow (9 ± 3%, P < 0.05) out of proportion to the increases in QTOT; and 4) the only similarity between healthy and CHF animals was that increasing the inspiratory PITP excursion significantly reduced steady-state locomotor limb blood flow by 5 ± 2% and 6 ± 3%, respectively ( P < 0.05 for both). We conclude that 1) the normally produced inspiratory PITP excursions are required for a maximal SV response to submaximal exercise in healthy animals but detrimental to the SV and QTOT responses to submaximal exercise in CHF, 2) the respiratory muscle ergoreflex tonically restrains locomotor limb blood flow during submaximal exercise in CHF, and 3) excessive inspiratory muscle work further compromises cardiac function and blood flow distribution in both health and CHF.

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

Journal of Applied Physiology ◽

10.1152/japplphysiol.00862.2005 ◽

2006 ◽

Vol 101 (1) ◽

pp. 213-227 ◽

Cited By ~ 29

Author(s):

Jordan D. Miller ◽

Sarah J. Hemauer ◽

Curtis A. Smith ◽

Michael K. Stickland ◽

Jerome A. Dempsey

Keyword(s):

Heart Failure ◽

Blood Flow ◽

Cardiac Output ◽

Chronic Heart Failure ◽

Cardiac Pacing ◽

Intrathoracic Pressure ◽

Submaximal Exercise ◽

Resistive Load ◽

Expiratory Flow Limitation ◽

Vascular Conductance

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.

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3604 Physical training reduces peripheral monocyte-related inflammatory markers and improves peripheral blood flow in patients with chronic heart failure

European Heart Journal ◽

10.1016/s0195-668x(03)96194-x ◽

2003 ◽

Vol 24 (5) ◽

pp. 701

Author(s):

S ADAMOPOULOS

Keyword(s):

Heart Failure ◽

Blood Flow ◽

Chronic Heart Failure ◽

Physical Training ◽

Peripheral Blood ◽

Inflammatory Markers ◽

Peripheral Blood Flow ◽

Peripheral Monocyte

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The relation of respiratory muscle strength to disease severity and abnormal ventilation during exercise in chronic heart failure patients

Research in Cardiovascular Medicine ◽

10.5812/cardiovascmed.28944 ◽

2015 ◽

Vol 4 (4) ◽

pp. 6 ◽

Cited By ~ 8

Author(s):

Yusuke Kasahara ◽

KazuhiroP Izawa ◽

Satoshi Watanabe ◽

Naohiko Osada ◽

Kazuto Omiya

Keyword(s):

Heart Failure ◽

Chronic Heart Failure ◽

Muscle Strength ◽

Disease Severity ◽

Respiratory Muscle ◽

Respiratory Muscle Strength ◽

Heart Failure Patients

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Metabolic abnormality of calf skeletal muscle is improved by localised muscle training without changes in blood flow in chronic heart failure

Heart ◽

10.1136/hrt.78.5.437 ◽

1997 ◽

Vol 78 (5) ◽

pp. 437-443 ◽

Cited By ~ 25

Author(s):

M. Ohtsubo ◽

K. Yonezawa ◽

H. Nishijima ◽

K. Okita ◽

A. Hanada ◽

...

Keyword(s):

Heart Failure ◽

Skeletal Muscle ◽

Blood Flow ◽

Chronic Heart Failure ◽

Metabolic Abnormality ◽

Muscle Training

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Exercise Capacity, Skeletal Muscle Strength and Blood Flow following Exercise Rehabilitation in Chronic Heart Failure

Clinical Science ◽

10.1042/cs088018p ◽

1995 ◽

Vol 88 (s32) ◽

pp. 18P-18P

Author(s):

TP Chua ◽

S McKinlay ◽

M Volterrani ◽

J Toman ◽

AJS Coats

Keyword(s):

Heart Failure ◽

Skeletal Muscle ◽

Blood Flow ◽

Chronic Heart Failure ◽

Muscle Strength ◽

Exercise Capacity ◽

Exercise Rehabilitation ◽

Skeletal Muscle Strength

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Effects of chronic heart failure on skeletal muscle capillary hemodynamics at rest and during contractions

Journal of Applied Physiology ◽

10.1152/japplphysiol.00308.2003 ◽

2003 ◽

Vol 95 (3) ◽

pp. 1055-1062 ◽

Cited By ~ 88

Author(s):

Troy E. Richardson ◽

Casey A. Kindig ◽

Timothy I. Musch ◽

David C. Poole

Keyword(s):

Heart Failure ◽

Skeletal Muscle ◽

Blood Flow ◽

Chronic Heart Failure ◽

Muscle Function ◽

Muscle Blood Flow ◽

Rat Skeletal Muscle ◽

Exercise Onset ◽

Final Response ◽

Microscopy Techniques

Chronic heart failure (CHF) reduces muscle blood flow at rest and during exercise and impairs muscle function. Using intravital microscopy techniques, we tested the hypothesis that the speed and amplitude of the capillary red blood cell (RBC) velocity ( VRBC) and flux (FRBC) response to contractions would be reduced in CHF compared with control (C) spinotrapezius muscle. The proportion of capillaries supporting continuous RBC flow was less ( P < 0.05) in CHF (0.66 ± 0.04) compared with C (0.84 ± 0.01) muscle at rest and was not significantly altered with contractions. At rest, VRBC (C, 270 ± 62; CHF, 179 ± 14 μm/s) and FRBC (C, 22.4 ± 5.5 vs. CHF, 15.2 ± 1.2 RBCs/s) were reduced (both P < 0.05) in CHF vs. C muscle. Contractions significantly (both P < 0.05) elevated VRBC (C, 428 ± 47 vs. CHF, 222 ± 15 μm/s) and FRBC (C, 44.3 ± 5.5 vs. CHF, 24.0 ± 1.2 RBCs/s) in C and CHF muscle; however, both remained significantly lower in CHF than C. The time to 50% of the final response was slowed (both P < 0.05) in CHF compared with C for both VRBC (C, 8 ± 4; CHF, 56 ± 11 s) and FRBC (C, 11 ± 3; CHF, 65 ± 11 s). Capillary hematocrit increased with contractions in C and CHF muscle but was not different ( P > 0.05) between CHF and C. Thus CHF impairs diffusive and conductive O2 delivery across the rest-to-contractions transition in rat skeletal muscle, which may help explain the slowed O2 uptake on-kinetics manifested in CHF patients at exercise onset.

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