Why the study?
Does a 12-week high-intensity interval training program improve exercising central haemodynamics and skeletal muscle oxygenation in patients with chronic heart failure?
Does a 12-week high-intensity interval training program improve exercising central haemodynamics and skeletal muscle oxygenation in patients with chronic heart failure?
A 12-week high-intensity interval training program improves maximal exercise capacity and exercising haemodynamics in CHF patients, with submaximal improvements likely mediated by improved microvascular oxygen delivery-to-utilisation matching.
HIT effects on exercising hemodynamics in CHF need clarification; leaves open whether central or peripheral factors drive capacity gains.
High-intensity interval training (HIT) improves exercise capacity in patients with chronic heart failure (CHF). Moreover, HIT was associated with improved resting cardiac function. However, the extent to which these improvements actually contribute to training-induced changes in exercise capacity remains to be elucidated. Therefore, we evaluated the effects of HIT on exercising central haemodynamics and skeletal muscle oxygenation. Twenty-six CHF patients were randomised to a 12-week 4 × 4 minute HIT program at 85–95% of peak VO2 or usual care. Patients performed maximal and submaximal cardiopulmonary exercise testing with simultaneous assessment of cardiac output and skeletal muscle oxygenation by near infrared spectroscopy, using the amplitude of the tissue saturation index (TSIamp). Peak workload increased by 11% after HIT (p between group = 0.01) with a non-significant increase in peak VO2 (+7%, p between group = 0.19). Cardiac reserve increased by 37% after HIT (p within group = 0.03, p between group = 0.08); this increase was not related to improvements in peak workload. Oxygen uptake recovery kinetics after submaximal exercise were accelerated by 20% (p between group = 0.02); this improvement was related to a decrease in TSIamp (r = 0.71, p = 0.03), but not to changes in cardiac output kinetics. HIT induced improvements in maximal exercise capacity and exercising haemodynamics at peak exercise. Improvements in recovery after submaximal exercise were associated with attenuated skeletal muscle deoxygenation during submaximal exercise, but not with changes in cardiac output kinetics, suggesting that the effect of HIT on submaximal exercise capacity is mediated by improved microvascular oxygen delivery-to-utilisation matching.
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Spee et al. (2016) studied this question.
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