High intensity exercise training in heart failure: Understanding the exercise “overdose”

Abstract

Editorial on article entitled: 'Effects of high intensity interval training on central hemodynamics and skeletal muscle oxygenation during exercise in patients with chronic heart failure' by Spee et al. 1 Exercise limitation is a well-established cardinal manifestation of the heart failure (HF) syndrome and its quantification through gas exchange analysis with objective measure of oxygen uptake (VO 2 ) provides the clinician with relevant information on pathophysiology and outcome.2,3 Exercise training is an established and effective intervention that in HF improves exercise tolerance, enhances VO 2 at peak exercise and favourably affects the course of the disease. For a long time, it has been axiomatic to interpret results of interventional trials, such as those observed with exercise training, only relying on significant changes in peak VO 2 without dissecting which organ system and pathway (central, peripheral or both) really mediate the improvement in exercise performance.This simple approach has obvious limitations because knowledge about specific mechanisms involved in the benefits of a therapeutic intervention provides the background for precision medicine and may yield to significant clinical advancements.Most recent studies, especially performed in subjects with HF and preserved ejection fraction, have definitively changed this paradigm by looking at the variety of complex mechanisms that limit the oxygen (O 2 ) transport chain from air to mithocondria 5-7 and, through this, discerning how the physical therapeutic approach may work. 8 According to the Fick principle, VO 2 depends on cardiac output (CO) times O 2 artero-venous difference (A-VO 2 diff) and reflects the product of the integrated biological response of the heart and peripheral mechanisms involved in O 2 delivery (convection), diffusion and extraction during exercise. 9Patients with HF are, by definition, limited in the O 2 convection (impaired CO and quite frequent reduction in O 2 content due to anaemia) 10 along with an impaired peripheral O 2 transport (diffusion) from blood to skeletal muscle.11 Conversely, muscle ability to extract O 2 appears quite preserved. 11,12 Due to these limitations, patients with HF show a slow VO 2 kinetics with a delayed increase of VO 2 after the onset of acute exercise and also prolonged recovery. 9 This delayed kinetics triggers a perturbation of intramuscular high energy phosphate, which exacerbates glycogenolysis, increases energetic costs and precipitates premature fatigue. The slow VO 2 kinetics decreases muscle efficiency and raises the O 2 deficit. Exercise training is likely to be the best intervention to modulate the abnormalities in VO 2 kinetics favourably through a wealth of mechanisms that may vary depending on the type of programme, patient characteristics and HF stage. 13Different exercise training types (endurance and resistance), modalities (continuous versus interval) and intensities (mild, moderate and high) protocols have been developed over time, but most of the evidence of a bene...

The ‘aerobic/resistance/inspiratory muscle training hypothesis in heart failure’

“…13 These findings were confirmed by a recent study which also showed that a HIIT benefit in submaximal exercise capacity was due to a peripheral rather than a central contribution. 14,15 Thus, raised expectations were lowered and the idea of an 'optimum' exercise programme for heart failure patients started to fade away, moving towards the concept of tailoring an exercise programme according to patient specificity. 16,17 The European Association of Preventive Cardiology Exercise Prescription in Everyday Practice and Rehabilitative Training (EXPERT) tool has been recently introduced, representing a digital training and decision support system, using algorithms including a number of variables, to enable an optimized exercise prescription for each individual.…”

“…13 These findings were confirmed by a recent study which also showed that a HIIT benefit in submaximal exercise capacity was due to a peripheral rather than a central contribution. 14,15…”