Four weeks of wrist-flexor exercise training improved skeletal muscle oxidative capacity in controls but not in heart failure patients (mean difference in adaptation 0.69 min-1; 95% CI 0.43-0.96).
Observational (n=39)
Does 4 weeks of wrist-flexor exercise training improve skeletal muscle oxidative capacity in patients with systolic heart failure compared to controls?
Patients with systolic heart failure have reduced baseline skeletal muscle oxidative capacity and fail to show oxidative adaptations to endurance exercise compared to healthy controls.
Effect estimate: Mean difference 0.69 (95% CI 0.43, 0.96)
Absolute Event Rate: -0.04% vs 0.66%
p-value: p=<0.001
Systolic heart failure (HF) is associated with exercise intolerance that has been attributed, in part, to skeletal muscle dysfunction. The purpose of this study was to compare skeletal muscle oxidative capacity and training-induced changes in oxidative capacity in participants with and without HF. Participants with HF (n = 16, 65 ± 6.6 years) were compared with control participants without HF (n = 23, 61 ± 5.0 years). A subset of participants (HF: n = 7, controls: n = 5) performed 4 weeks of wrist-flexor exercise training. Skeletal muscle oxidative capacity was determined from the recovery kinetics of muscle oxygen consumption measured by near-infrared spectroscopy (NIRS) following a brief bout of wrist-flexor exercise. Oxidative capacity, prior to exercise training, was significantly lower in the HF participants in both the dominant (1.31 ± 0.30 min(-1) vs. 1.59 ± 0.25 min(-1), P = 0.002; HF and control groups, respectively) and nondominant arms (1.29 ± 0.24 min(-1) vs. 1.46 ± 0.23 min(-1), P = 0.04; HF and control groups, respectively). Following 4 weeks of endurance training, there was a significant difference in the training response between HF and controls, as the difference in oxidative training adaptations was 0.69 ± 0.12 min(-1) (P < 0.001, 95% CI 0.43, 0.96). The wrist-flexor training induced a ~50% improvement in oxidative capacity in participants without HF (mean difference from baseline = 0.66 ± 0.09 min(-1), P < 0.001, 95% CI 0.33, 0.98), whereas participants with HF showed no improvement in oxidative capacity (mean difference from baseline = -0.04 ± 0.08 min(-1), P = 0.66, 95% CI -0.24, 0.31), suggesting impairments in mitochondrial biogenesis. In conclusion, participants with HF had reduced oxidative capacity and impaired oxidative adaptations to endurance exercise compared to controls.
Southern et al. (Wed,) conducted a observational in Systolic heart failure (n=39). Wrist-flexor exercise training vs. Control participants without heart failure was evaluated on Training-induced changes in skeletal muscle oxidative capacity (Mean difference 0.69, 95% CI 0.43, 0.96, p=<0.001). Four weeks of wrist-flexor exercise training improved skeletal muscle oxidative capacity in controls but not in heart failure patients (mean difference in adaptation 0.69 min-1; 95% CI 0.43-0.96).