Randomized trial of progressive resistance training to counteract the myopathy of chronic heart failure

2001 ◽  
Vol 90 (6) ◽  
pp. 2341-2350 ◽  
Author(s):  
Charles T. Pu ◽  
Meredith T. Johnson ◽  
Daniel E. Forman ◽  
Jeffrey M. Hausdorff ◽  
Ronenn Roubenoff ◽  
...  

Chronic heart failure (CHF) is characterized by a skeletal muscle myopathy not optimally addressed by current treatment paradigms or aerobic exercise. Sixteen older women with CHF were compared with 80 age-matched peers without CHF and randomized to progressive resistance training or control stretching exercises for 10 wk. Women with CHF had significantly lower muscle strength ( P < 0.0001) but comparable aerobic capacity to women without CHF. Exercise training was well tolerated and resulted in no changes in resting cardiac indexes in CHF patients. Strength improved by an average of 43.4 ± 8.8% in resistance trainers vs. −1.7 ± 2.8% in controls ( P = 0.001), muscle endurance by 299 ± 66% vs. 1 ± 3% ( P = 0.001), and 6-min walk distance by 49 ± 14 m (13%) vs. −3 ± 19 m (−3%) ( P = 0.03). Increases in type I fiber area (9.5 ± 16%) and citrate synthase activity (35 ± 21%) in skeletal muscle were independently predictive of improved 6-min walk distance ( r 2 = 0.78; P = 0.0024). High-intensity progressive resistance training improves impaired skeletal muscle characteristics and overall exercise performance in older women with CHF. These gains are largely explained by skeletal muscle and not resting cardiac adaptations.

1997 ◽  
Vol 29 (Supplement) ◽  
pp. 148 ◽  
Author(s):  
C. T. Pu ◽  
M. T. Johnson ◽  
D. E. Forman ◽  
L. A. Piazza ◽  
M. A. Fiatarone

2005 ◽  
Vol 94 (4) ◽  
pp. 371-375 ◽  
Author(s):  
Nathan K. LeBrasseur ◽  
Kelly C. Mizer ◽  
Jascha D. Parkington ◽  
Douglas B. Sawyer ◽  
Roger A. Fielding

1994 ◽  
Vol 26 (Supplement) ◽  
pp. S31
Author(s):  
C Morganti ◽  
M. Nelson ◽  
M. Fiatarone ◽  
B. Crawford ◽  
C. Economos ◽  
...  

Circulation ◽  
1993 ◽  
Vol 87 (5) ◽  
pp. 1729-1737 ◽  
Author(s):  
H N Sabbah ◽  
F Hansen-Smith ◽  
V G Sharov ◽  
T Kono ◽  
M Lesch ◽  
...  

2013 ◽  
Vol 16 (1) ◽  
pp. 76-81 ◽  
Author(s):  
Andrew D. Williams ◽  
Kiran D.K. Ahuja ◽  
Jodi B. Almond ◽  
Iain K. Robertson ◽  
Madeleine J. Ball

2009 ◽  
Vol 107 (4) ◽  
pp. 1138-1143 ◽  
Author(s):  
Martijn A. Bekedam ◽  
Brechje J. van Beek-Harmsen ◽  
Willem van Mechelen ◽  
Anco Boonstra ◽  
Willem J. van der Laarse

The purpose of this study was to determine the myoglobin concentration in skeletal muscle fibers of chronic heart failure (CHF) patients and to calculate the effect of myoglobin on oxygen buffering and facilitated diffusion. Myoglobin concentration, succinate dehydrogenase (SDH) activity, and cross-sectional area of individual muscle fibers from the vastus lateralis of five control and nine CHF patients were determined using calibrated histochemistry. CHF patients compared with control subjects were similar with respect to myoglobin concentration: type I fibers 0.69 ± 0.11 mM (mean ± SD), type II fibers 0.52 ± 0.07 mM in CHF vs. type I fibers 0.70 ± 0.09 mM, type II fibers 0.49 ± 0.07 mM in control, whereas SDH activity was significantly lower in CHF in both fiber types ( P < 0.01). The myoglobin concentration in type I fibers was higher than in type II fibers ( P < 0.01). Consequently, the oxygen buffering capacity, calculated from myoglobin concentration/SDH activity was increased in CHF: type I fibers 11.4 ± 2.1 s, type II fibers 13.6 ± 3.9 s in CHF vs. type I fibers 7.8 ± 0.9 s, type II fibers 7.5 ± 1.0 s in control, all P < 0.01). The calculated extracellular oxygen tension required to prevent core anoxia (Po2crit) in muscle fibers was similar when controls were compared with patients in type I fibers 10.3 ± 0.9 Torr in CHF and 11.5 ± 3.3 Torr in control, but was lower in type II fibers of patients 6.1 ± 2.8 Torr in CHF and 14.7 ± 6.2 Torr in control, P < 0.01. The lower Po2crit of type II fibers may facilitate oxygen extraction from capillaries. Reduced exercise tolerance in CHF is not due to myoglobin deficiency.


2010 ◽  
Vol 299 (6) ◽  
pp. H1755-H1761 ◽  
Author(s):  
Steven W. Copp ◽  
Daniel M. Hirai ◽  
Leonardo F. Ferreira ◽  
David C. Poole ◽  
Timothy I. Musch

Chronic heart failure (CHF) induces muscle fiber-type specific alterations in skeletal muscle O2 delivery and utilization during metabolic transitions. As a result, the recovery of microvascular Po2 (PmvO2) is prolonged in slow-twitch skeletal muscle but not fast-twitch skeletal muscle in rats with CHF. We tested the hypothesis that CHF slows PmvO2 recovery in rat skeletal muscle of a mixed fiber-type analogous to human locomotory muscles and that the degree of slowing correlates with central indexes of heart failure. Healthy control [ n = 6, left ventricular end-diastolic pressure (LVEDP): 10 ± 1 mmHg], moderate CHF ( n = 6, LVEDP: 18 ± 2 mmHg), and severe CHF ( n = 4, LVEDP: 34 ± 2 mmHg) female Sprague-Dawley rats had their right spinotrapezius muscles (41% type I, 7% type IIa, and 52% type IIb and d/x) exposed, and PmvO2 was measured via phosphorescence quenching during 180 s of recovery from 180 s of electrically induced twitch contractions (1 Hz, 4–6 V). CHF progressively slowed the mean response time (MRT; the time to reach 63% of the overall dynamic response) of PmvO2 recovery (MRToff; control: 60.2 ± 6.9, moderate CHF: 72.8 ± 6.6, and severe CHF: 109.8 ± 6.6 s, P < 0.05 for all). MRToff correlated positively with central hemodynamic (LVEDP: r = 0.76, P < 0.01) and morphological (right ventricle-to-body weight ratio: r = 0.74, P < 0.01; and lung weight-to-body weight ratio: r = 0.79, P < 0.01) indexes of heart failure. The present investigation suggests that slowed PmvO2 kinetics during recovery in CHF constitutes a mechanistic link between impaired circulatory and metabolic recovery after contractions in CHF.


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