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ABSTRACT: It is now accepted that exercise training is a safe and effective therapeutic intervention to improve clinical status, functional capacity, and quality of life in people with chronic heart failure (CHF). Nevertheless, this therapeutic modality remains underprescribed and underutilized. Both aerobic and resistance training improve exercise capacity and may partially reverse some of the cardiac, vascular, and skeletal muscle abnormalities in individuals with CHF. Aerobic training has more beneficial effects on aerobic power (peak oxygen consumption) and cardiac structure and function than resistance exercise training, while the latter is more effective for increasing muscle strength and endurance and promoting favorable arterial remodeling. Combined aerobic and resistance training is the preferred exercise intervention to reverse or attenuate the loss of muscle mass and improve exercise and functional capacity, muscle strength, and quality of life in individuals with CHF. The challenge now is to translate these research findings into clinical practice.
Current Heart Failure Reports 12/2011; 9(1):57-64.
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ABSTRACT: Chronic heart failure (CHF) is a complex syndrome characterised by progressive decline in left ventricular function, low exercise tolerance and raised mortality and morbidity. Regular exercise participation has been shown to be a safe and effective treatment modality in the majority of CHF patients, partially reversing some of the maladaptations evident in myocardial and skeletal muscle function, and resulting in improvements in physical fitness and quality of life, and perhaps reduced mortality. The volume and intensity of exercise that is recommended depends on the syndrome severity, however in most patients it should consist of a combination of low-to-moderate intensity aerobic (endurance) exercise on most days of the week and individually prescribed low-to-moderate intensity resistance (strength) training at least twice per week. Additionally, all patients should be closely monitored prior to and during exercise for contraindications by an appropriately trained health professional. The purpose of this statement is to inform and guide exercise practitioners and health professionals in the safe and effective prescription and supervision of exercise for patients with CHF.
Journal of science and medicine in sport / Sports Medicine Australia. 03/2010; 13(3):288-94.
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British journal of sports medicine 08/2007; 41(7):407-8. · 2.55 Impact Factor
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ABSTRACT: Alkalosis enhances human exercise performance, and reduces K+ loss in contracting rat muscle. We investigated alkalosis effects on K+ regulation, ionic regulation and fatigue during intense exercise in nine untrained volunteers. Concentric finger flexions were conducted at 75% peak work rate (3 W) until fatigue, under alkalosis (Alk, NaHCO3, 0.3 g kg(-1)) and control (Con, CaCO3) conditions, 1 month apart in a randomised, double-blind, crossover design. Deep antecubital venous (v) and radial arterial (a) blood was drawn at rest, during exercise and recovery, to determine arterio-venous differences for electrolytes, fluid shifts, acid-base and gas exchange. Finger flexion exercise barely perturbed arterial plasma ions and acid-base status, but induced marked arterio-venous changes. Alk elevated [HCO3-] and PCO2, and lowered [H+] (P < 0.05). Time to fatigue increased substantially during Alk (25 +/- 8%, P < 0.05), whilst both [K+]a and [K+]v were reduced (P < 0.01) and [K+]a-v during exercise tended to be greater (P= 0.056, n= 8). Muscle K+ efflux at fatigue was greater in Alk (21.2+/- 7.6 micromol min(-1), 32 +/- 7%, P < 0.05, n= 6), but peak K+ uptake rate was elevated during recovery (15 +/- 7%, P < 0.05) suggesting increased muscle Na+,K+-ATPase activity. Alk induced greater [Na+]a, [Cl-]v, muscle Cl- influx and muscle lactate concentration ([Lac-]) efflux during exercise and recovery (P < 0.05). The lower circulating [K+] and greater muscle K+ uptake, Na+ delivery and Cl- uptake with Alk, are all consistent with preservation of membrane excitability during exercise. This suggests that lesser exercise-induced membrane depolarization may be an important mechanism underlying enhanced exercise performance with Alk. Thus Alk was associated with improved regulation of K+, Na+, Cl- and Lac-.
The Journal of Physiology 01/2006; 570(Pt 1):185-205. · 4.72 Impact Factor
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ABSTRACT: Resistance exercise training was applied to patients with chronic heart failure (CHF) on the basis that it may partly reverse deficiencies in skeletal muscle strength and endurance, aerobic power (VO(2peak)), heart rate variability (HRV), and forearm blood flow (FBF) that are all putative factors in the syndrome.
Thirty-nine CHF patients (New York Heart Association Functional Class=2.3+/-0.5; left ventricular ejection fraction 28%+/-7%; age 65+/-11 years; 33:6 male:female) underwent 2 identical series of tests, 1 week apart, for strength and endurance of the knee and elbow extensors and flexors, VO(2peak), HRV, FBF at rest, and FBF activated by forearm exercise or limb ischemia. Patients were then randomized to 3 months of resistance training (EX, n=19), consisting of mainly isokinetic (hydraulic) ergometry, interspersed with rest intervals, or continuance with usual care (CON, n=20), after which they underwent repeat endpoint testing. Combining all 4 movement patterns, strength increased for EX by 21+/-30% (mean+/-SD, P<.01) after training, whereas endurance improved 21+/-21% (P<.01). Corresponding data for CON remained almost unchanged (strength P<.005, endurance P<.003 EX versus CON). VO(2peak) improved in EX by 11+/-15% (P<.01), whereas it decreased by 10+/-18% (P<.05) in CON (P<.001 EX versus CON). The ratio of low-frequency to high-frequency spectral power fell after resistance training in EX by 44+/-53% (P<.01), but was unchanged in CON (P<.05 EX versus CON). FBF increased at rest by 20+/-32% (P<.01), and when stimulated by submaximal exercise (24+/-32%, P<.01) or limb ischemia (26+/-45%, P<.01) in EX, but not in CON (P<.01 EX versus CON).
Moderate-intensity resistance exercise training in CHF patients produced favorable changes to skeletal muscle strength and endurance, VO(2peak), FBF, and HRV.
Journal of Cardiac Failure 03/2004; 10(1):21-30. · 3.66 Impact Factor
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ABSTRACT: This study investigated whether fatiguing dynamic exercise depresses maximal in vitro Na(+)-K(+)-ATPase activity and whether any depression is attenuated with chronic training. Eight untrained (UT), eight resistance-trained (RT), and eight endurance-trained (ET) subjects performed a quadriceps fatigue test, comprising 50 maximal isokinetic contractions (180 degrees /s, 0.5 Hz). Muscle biopsies (vastus lateralis) were taken before and immediately after exercise and were analyzed for maximal in vitro Na(+)-K(+)-ATPase (K(+)-stimulated 3-O-methylfluoroscein phosphatase) activity. Resting samples were analyzed for [(3)H]ouabain binding site content, which was 16.6 and 18.3% higher (P < 0.05) in ET than RT and UT, respectively (UT 311 +/- 41, RT 302 +/- 52, ET 357 +/- 29 pmol/g wet wt). 3-O-methylfluoroscein phosphatase activity was depressed at fatigue by -13.8 +/- 4.1% (P < 0.05), with no differences between groups (UT -13 +/- 4, RT -9 +/- 6, ET -22 +/- 6%). During incremental exercise, ET had a lower ratio of rise in plasma K(+) concentration to work than UT (P < 0.05) and tended (P = 0.09) to be lower than RT (UT 18.5 +/- 2.3, RT 16.2 +/- 2.2, ET 11.8 +/- 0.4 nmol. l(-1). J(-1)). In conclusion, maximal in vitro Na(+)-K(+)-ATPase activity was depressed with fatigue, regardless of training state, suggesting that this may be an important determinant of fatigue.
Journal of Applied Physiology 11/2002; 93(5):1650-9. · 3.75 Impact Factor
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ABSTRACT: PURPOSE: The objective of this study was to assess the reliability of testing skeletal muscle strength and peak aerobic power in a clinical population of patients with chronic heart failure (CHF).
METHODS: Thirty-three patients with CHF (New York Heart Association (NYHA) Functional Class 2.3 ± 0.5; left ventricular ejection fraction 27% ± 7%; age 65 ± 9 years; 28:5 male-female ratio) underwent two identical series of tests (T1 and T2), 1 week apart, for strength and endurance of the muscle groups responsible for knee extension/flexion and elbow extension/flexion. The patients also underwent two graded exercise tests on a bicycle ergometer to measure peak oxygen consumption (VO2peak). Three months later, 18 of the patients underwent a third test (T3) for each of the measures. Means were compared using MANOVA with repeated measures for strength and endurance, and ANOVA with repeated measures for VO2peak.
RESULTS: Combining data for all four movement patterns, the expression of strength increased from T1 to T2 by 12% ± 25% (P < .001; intraclass correlation coefficient [ICC] = 0.89). Correspondingly, endurance increased by 13% ± 23% (P = .004; ICC = 0.87). Peak oxygen consumption was not significantly different (16.2 ± 0.8 and 16.1 ± 0.8 mL·kg-1·min-1 for T1 and T2, respectively;P = .686; ICC = 0.91). There were no significant differences between T2 and T3 for strength (2% ± 17%;P = .736; ICC = 0.92) or muscle endurance (-1% ± 15%;P = .812; ICC = 0.96), but VO2peak decreased from 16.7 ± 1.2 to 14.9 ± 0.9 mL·kg-1·min-1 (-10% ± 18%;P = .021; ICC = 0.89).
CONCLUSIONS: These data suggest that in a population of patients with CHF, a familiarization trial for skeletal muscle strength testing is necessary. Although familiarization is not required for assessing oxygen consumption as a single measurement, VO2peak declined markedly in the 3-month period for which these patients were followed. Internal consistency within patients was high for the second and third strength trials and the first and second tests of VO2peak.
Journal of cardiopulmonary rehabilitation and prevention 06/2002; 22(4):282-289. · 1.69 Impact Factor
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ABSTRACT: The objective of this study was to assess the reliability of testing skeletal muscle strength and peak aerobic power in a clinical population of patients with chronic heart failure (CHF).
Thirty-three patients with CHF (New York Heart Association (NYHA) Functional Class 2.3 +/- 0.5; left ventricular ejection fraction 27% +/- 7%; age 65 +/- 9 years; 28:5 male-female ratio) underwent two identical series of tests (T1 and T2), 1 week apart, for strength and endurance of the muscle groups responsible for knee extension/flexion and elbow extension/flexion. The patients also underwent two graded exercise tests on a bicycle ergometer to measure peak oxygen consumption (VO(2peak)). Three months later, 18 of the patients underwent a third test (T3) for each of the measures. Means were compared using MANOVA with repeated measures for strength and endurance, and ANOVA with repeated measures for VO(2peak).
Combining data for all four movement patterns, the expression of strength increased from T1 to T2 by 12% +/- 25% (P <.001; intraclass correlation coefficient [ICC] = 0.89). Correspondingly, endurance increased by 13% +/- 23% (P =.004; ICC = 0.87). Peak oxygen consumption was not significantly different (16.2 +/- 0.8 and 16.1 +/- 0.8 mL.kg(-1).min(-1) for T1 and T2, respectively; P =.686; ICC = 0.91). There were no significant differences between T2 and T3 for strength (2% +/- 17%; P =.736; ICC = 0.92) or muscle endurance (-1% +/- 15%; P =.812; ICC = 0.96), but VO(2peak) decreased from 16.7 +/- 1.2 to 14.9 +/- 0.9 mL.kg(-1).min(-1) (-10% +/- 18%; P =.021; ICC = 0.89).
These data suggest that in a population of patients with CHF, a familiarization trial for skeletal muscle strength testing is necessary. Although familiarization is not required for assessing oxygen consumption as a single measurement, VO(2peak) declined markedly in the 3-month period for which these patients were followed. Internal consistency within patients was high for the second and third strength trials and the first and second tests of VO(2peak).
Journal of Cardiopulmonary Rehabilitation 22(4):282-9.
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ABSTRACT: Background. We aimed to determine the role of skeletal muscle mitochondrial ATP production rate (MAPR) in relation to exercise tolerance following resistance training in CHF.
Methods and Results. Thirteen CHF patients (NYHA functional class 2.3 ± 0.5; LVEF 26 ± 8%; age 70 ± 8 years) underwent testing for VO2peak, and resting vastus lateralis muscle biopsy. Patients were then randomly allocated to 11 weeks of RT, (n = 7) or continuance of usual care (C, n = 6) following which testing was repeated. Muscle samples were analysed for MAPR, metabolic enzyme activity and capillary density.
VO2peak and MAPR in the presence of the pyruvate and malate (P+M) substrate combination, representing carbohydrate metabolism, increased in RT (p<0.05) and decreased in C (p<0.05) with a significant difference between groups (VO2peak p = 0.005; MAPR p = 0.03). There was a strong correlation between the change in MAPR and the change in VO2peak over the study (r = 0.875; p < 0.0001), the change in MAPR accounting for 70% of the change in VO2peak.
Conclusions. These findings suggest that mitochondrial ATP production is a major determinant of aerobic capacity in CHF patients and can be favourably altered by muscle trengthening exercise.
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[show abstract]
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ABSTRACT: Alkalosis enhances human exercise performance, and reduces K+ loss in contracting rat muscle. We investigated alkalosis effects on K+ regulation, ionic regulation and fatigue during intense exercise in nine untrained volunteers. Concentric finger flexions were conducted at 75% peak work rate (3 W) until fatigue, under alkalosis (Alk, NaHCO3, 0.3 g kg–1) and control (Con, CaCO3) conditions, 1 month apart in a randomised, double-blind, crossover design. Deep antecubital venous (v) and radial arterial (a) blood was drawn at rest, during exercise and recovery, to determine arterio-venous differences for electrolytes, fluid shifts, acid–base and gas exchange. Finger flexion exercise barely perturbed arterial plasma ions and acid–base status, but induced marked arterio-venous changes. Alk elevated [HCO3–] and PCO2, and lowered [H+] (P < 0.05). Time to fatigue increased substantially during Alk (25 ± 8%, P < 0.05), whilst both [K+]a and [K+]v were reduced (P < 0.01) and [K+]a-v during exercise tended to be greater (P= 0.056, n= 8). Muscle K+ efflux at fatigue was greater in Alk (21.2 ± 7.6 µmol min–1, 32 ± 7%, P < 0.05, n= 6), but peak K+ uptake rate was elevated during recovery (15 ± 7%, P < 0.05) suggesting increased muscle Na+,K+-ATPase activity. Alk induced greater [Na+]a, [Cl–]v, muscle Cl– influx and muscle lactate concentration ([Lac–]) efflux during exercise and recovery (P < 0.05). The lower circulating [K+] and greater muscle K+ uptake, Na+ delivery and Cl– uptake with Alk, are all consistent with preservation of membrane excitability during exercise. This suggests that lesser exercise-induced membrane depolarization may be an important mechanism underlying enhanced exercise performance with Alk. Thus Alk was associated with improved regulation of K+, Na+, Cl– and Lac–.
