Abstract
Authoritative sources [1, 2] and reviews [3, 4] have established that individually tailored exercise training is well tolerated and produces positive adaptations in chronic heart failure (CHF) patients, whereas, on the contrary, exercise restriction may cause deconditioning, magnify the underlying pathophysiology and hasten disease progression. Exercise training benefits have been reported in skeletal muscles, respiratory and cardiovascular systems and in their physiological responses to exercise. Although both central cardiac and peripheral adaptations may improve exercise capacity and functional status in CHF, there is a consensus that the exercise training-induced reversal of skeletal muscle abnormalities is pivotal in symptom improvement [5, 6].
Neuromuscular electrical stimulation (NMES) produces skeletal muscular contractions throughout the percutaneous stimulation of peripheral nerves, and in the clinical setting, constitutes an attractive option for maintaining muscle mass and strength to prevent muscle atrophy as a result of prolonged periods of immobilization; NMES can shorten the rehabilitation period [7]. But as transcutaneous electrical stimulation activates pain afferents as well as muscle fibres, one of the major difficulties posed by NMES is to trigger strong contractions with as little discomfort as possible. Beside patients' tolerance of electrical stimulation and electrode placement, pulse parameters, intensity, duration, frequency of repetition, and shape, should be carefully considered [8]. The time of the pulse should be short enough to avoid either the membrane accommodation phenomenon or discomfort, but long enough to elicit efficient contractile activity. The most proficient frequency of repetitive stimulation, producing maximal force, appears to range from 50 to 120 Hz, but low-frequency stimulation with long-term training can also increase muscle cross-sectional area and muscle strength and improve resistance to fatigue [9]. The mechanisms underlying the specific effects of NMES appear to be rather complex, partly because of disparity in training protocols, electrical stimulation and testing procedures to assess efficacy [8]. An increase in muscle strength is caused not only by intracellular modifications, involving metabolic changes towards a more aerobic-oxidative energy supply and fast-to-slow transitions in myosin heavy chain isoform expression [10], but also neural adaptation, including improved motor unit synchronization, the potentiation of reflex activity and the cross-transfer phenomenon [11].
In small CHF cohorts, NMES has been shown to promote beneficial changes in muscle performance and bulk [9], counteract detrimental skeletal muscle abnormalities [12], improve exercise capacity [12, 13] and quality of life, and decrease morbidity [14]. In the current issue of the journal, Deley et al. [15] report that NMES produces similar improvements in exercise capacity to those observed with conventional exercise training in 24 patients with moderate–severe CHF. Patients were randomly allocated to 5 weeks conventional training (including aerobic exercise on bicycle, treadmill and arm cycling, at a target heart rate of 60–70% of peak heart rate obtained during baseline cardiopulmonary exercise testing) or to 5 weeks of NMES training of both quadriceps and calf muscles, with low-frequency 10 Hz biphasic current and a 200 ms pulse duration. Both training interventions yielded a significant improvement in exercise capacity parameters, peak and ventilatory anaerobic threshold oxygen consumption (VO2), distance walked in 6min and time elapsed to walk 200 m, and maximal lower limb strength. Moreover, VO2 kinetic both during exercise (VO2 vs. workload) and during recovery (time required for a 50% decay from peak VO2) were significantly influenced by NMES [15]. Given the almost identical functional improvement after both intervention modalities, the authors concluded that NMES appears to be a ‘great alternative’ to conventional rehabilitation in CHF patients.
Two major considerations seem necessary. First, in contractions triggered by NMES, muscle fibres of the motor units are activated by an electric current, applied extracellularly to the nerve endings. Larger cells with low axonal input resistance are more excitable, whereas smaller motor units are not activated because of their higher axonal input resistance. The sequence appears to be reversed during submaximal voluntary exercise, as motor units are recruited in order from smaller fatigue resistant (type I) units to larger fast fatiguable (type II) units. Moreover, submaximal voluntary training elicits greater strength and endurance because smaller motor units, which present the greatest adaptation to exercise, are recruited and trained.
Second, the key components of a training programme are duration, intensity and frequency of exercise sessions, and the sum of these inputs represents the training impulse that enhances functional capacity. In CHF, the notion of a direct relationship between the amount of work performed and subsequent performance enhancement runs up against the limits of safety and tolerance, which are particularly relevant in more compromised patients. Studies on conventional exercise training have constantly enrolled patients with moderate CHF (NYHA II–III) and preserved exercise capacity, in whom high-intensity exercise training has succeeded in improving skeletal muscle function with no detrimental consequences on cardiac function [1, 2]. Patients with advanced heart failure (NYHA IV) or recent haemodynamic instability have usually been proscribed [4]. Nevertheless, in these patients deconditioning, malnutrition, inflammatory cytokine toxicity and long-standing disease determine a loss of total body fat and muscle wasting, leading, in its most severe form, to cardiac cachexia [16]. Because sustained skeletal muscle abnormalities may be a key component of the sensation of dyspnoea and fatigue, [17] breaking this vicious circle is imperative, and an alternative method of muscle training is highly desirable. NMES may be considered as a therapy to bridge the gap: by alleviating symptoms, reducing fatigue and improving functional capacity, it may facilitate the participation of severe CHF patients in conventional exercise training. NMES training can shorten the transition phase from immobilization to low-intensity exercise conventional training.
In conclusion, it is well known that conventional exercise training improves exercise capacity and cardiovascular fitness, attenuates cardiovascular risk, exerts a favourable modulation of autonomic and vascular endothelial function, increases patient surveillance, promotes self-education and healthcare, and reduces morbidity and dependency. Therefore exercise training is a highly cost-effective resource in the management of CHF. Intuitively and potentially, NMES is an attractive concept, and it may be suitable for those CHF patients who are unable to perform conventional exercise training. The complementary role of NMES challenges us to re-evaluate the role of non-moving training, and may open a new chapter in physical therapy in CHF.