Effects of the exercise training on skeletal muscle oxygen consumption in heart failure patients with reduced ejection fraction.

AIMS: Skeletal muscle dysfunction is a systemic consequence of heart failure (HF) that correlates with functional capacity. However, the impairment within the skeletal muscle is not well established. We investigated the effect of exercise training on peripheral muscular performance and oxygenation in HF patients. METHODS AND RESULTS: HF patients with ejection fraction ≤40% were randomized 2:1 to exercise training or control for 12 weeks. Muscle tissue oxygen was measured noninvasively by near-infrared spectroscopy (NIRS) during rest and a symptom-limited cardiopulmonary exercise test (CPET) before and after intervention. Measurements included skeletal muscle oxygenated hemoglobin concentration, deoxygenated hemoglobin concentration, total hemoglobin concentration, VO2 peak, VE/VCO2 slope, and heart rate. Muscle sympathetic nerve activity by microneurography, and muscle blood flow by plethysmography were also assessed at rest pre and post 12 weeks. Twenty-four participants (47.5 ± 7.4 years, 58% men, 75% no ischemic) were allocated to exercise training (ET, n = 16) or control (CG, n = 8). At baseline, no differences between groups were found. Exercise improved VO2 peak, slope VE/VCO2, and heart rate. After the intervention, significant improvements at rest were seen in the ET group in muscle sympathetic nerve activity and muscle blood flow. Concomitantly, a significant decreased in Oxy-Hb (from 29.4 ± 20.4 to 15.7 ± 9.0 µmol, p = 0.01), Deoxi-Hb (from 16.3 ± 8.2 to 12.2 ± 6.0 µmol, p = 0.003) and HbT (from 45.7 ± 27.6 to 27.7 ± 13.4 µmol, p = 0.008) was detected at peak exercise after training. No changes were observed in the control group. CONCLUSION: Exercise training improves skeletal muscle function and functional capacity in HF patients with reduced ejection fraction. This improvement was associated with increased oxygenation of the peripheral muscles, increased muscle blood flow, and decreased sympathetic nerve activity.

Treinamento físico na distrofia muscular de becker associada à insuficiência cardíaca / Physical training in becker muscular dystrophy associated with heart failure / Entrenamiento físico en la distrofia muscular de becker asociada a la insuficiencia cardíaca

A distrofia muscular de Becker (DMB) integra as distrofinopatias que ocorrem devido a mutações genéticas que expressam a proteína distrofina no cromossomo X. O início dos sintomas neuromusculares normalmente precede o comprometimento da função cardíaca, podendo acontecer inversamente pela insuficiência cardíaca (IC). O treinamento físico é bem estabelecido na IC, porém, quando associada à DMB, é controverso e sem fundamento científico. Apresentamos o caso de um paciente com DMB associada à IC em fila de transplante cardíaco submetido a um programa de treinamento físico.

Becker muscular dystrophy (BMD) integrates dystrophy occurring due to genetic mutations that express the dystrophin protein in chromosome X. The onset of neuromuscular symptoms usually precedes the impairment of cardiac function, and may conversely happen by heart failure (HF). Physical training is well established in HF, however, when combined with BMD, it is controversial and without any scientific basis. This study presents the case of a patient with BMD associated with HF in cardiac transplant waiting list undergoing a physical training program.

La distrofia muscular de Becker (DMB) integra las distrofinopatías que ocurren debido a mutaciones genéticas que expresan la proteína distrofina en el cromosoma X. El inicio de los síntomas neuromusculares normalmente precede el compromiso de la función cardíaca, pudiendo acontecer inversamente por la insuficiencia cardíaca (IC). El entrenamiento físico es bien establecido en la IC, sin embargo, cuando está asociada a la DMB, es controvertido y sin fundamento científico. Presentamos el caso de un paciente con DMB asociada a la IC en fila de transplante cardíaco sometido a un programa de entrenamiento físico.

Physical training in Becker muscular dystrophy associated with heart failure.

Becker muscular dystrophy (BMD) integrates dystrophy occurring due to genetic mutations that express the dystrophin protein in chromosome X. The onset of neuromuscular symptoms usually precedes the impairment of cardiac function, and may conversely happen by heart failure (HF). Physical training is well established in HF, however, when combined with BMD, it is controversial and without any scientific basis. This study presents the case of a patient with BMD associated with HF in cardiac transplant waiting list undergoing a physical training program.

Heart rate dynamics in heart transplantation patients during a treadmill cardiopulmonary exercise test: a pilot study.

BACKGROUND: One way of defining an individual's heart effort is to calculate the maximum heart rate to be expected given their age, but the reinnervation seen in patients who have received heart transplants makes for different calculations from patients who have suffered heart failure. The purpose of this study is to evaluate heart rate dynamics (rest, peak and percentage of predicted heart rate for age) in heart transplant patients compared to optimized beta-blocked heart failure patients during a treadmill cardiopulmonary exercise test. METHODS: Twenty two (81% male, 46 +/- 12 years) sedentary heart failure patients and 15 (47% male, 44 +/- 13 years) sedentary heart transplant patients performed a treadmill cardiopulmonary exercise test between 10 am and 3 pm. Heart failure optimization was considered 50 mg/day or more of carvedilol, with a resting heart rate of between 50 and 60 bpm. RESULTS: Basal heart rate was lower in heart failure patients (58 +/- 5 bpm) compared to heart transplant patients (93 +/- 11 bpm; p < 0.0001). Similarly, the peak heart rate (percentage of the maximum predicted for age) was lower in heart failure patients (60 +/- 13%) compared to heart transplant patients (80 +/- 12; p < 0.0001). Maximum respiratory exchange ratio did not differ between the groups (1.05 +/- 0.06 in heart failure patients and 1.11 +/- 0.1 in heart transplant patients; p = 0.08). Moreover, the heart rate reserve between heart failure (49 +/- 22) and heart transplantation (46 +/- 16%) was not different (p = 0.644). CONCLUSIONS: No patient reached the maximum heart rate predicted for their age during a treadmill cardiopulmonary exercise test. The heart rate reserve was similar between groups. A heart rate increase in heart transplant patients during cardiopulmonary exercise test of more than 80% of the maximum age-adjusted value should be considered an effort near the maximum.