Introduction Muscle weakness is highly prevalent among the most clinical musculoskeletal (MSK) conditions worldwide. The degenerative effects of muscle atrophy can be seen with both acute and chronic MSK injuries that result in prolonged treatment or muscle immobilisation, such as fractures and ligament injuries.

Loss of strength is a major risk factor for osteoarthritis (OA), the most common MSK disease responsible for reduced function and quality of life of sufferers, affecting around 250 million adults worldwide with a prevalence correlating with the increasing age of the population. Muscle weakness is increasingly evident in non-injured healthy populations such as older adults due to sarcopenia.

This describes a loss of physical function due to the decrease in muscle mass and strength, vascular function and bone mineral density that occur with ageing. Sarcopenia appears to be underpinned by the reduced sensitivity of ageing muscle to anabolic stimuli such as resistance exercise. The consequences of progressive and injury-related loss of muscle strength can be life changing. Strength training is indispensable in clinical MSK rehabilitation, and clinicians are faced with the task of turning the growing body of research into effective clinical practice. For instance, greater quadriceps strength has been linked to a lower risk of symptomatic knee OA and reduced joint space narrowing, as well as reduced pain and positive changes in physical function.

Heavy-load resistance training has been advocated to offset age-related loss in muscle strength and mass, and strength training post-immobilisation is essential to regain the strength lost as a result of muscle disuse atrophy. Historically, heavy exercise loads of approximately 70% of an individual’s one repetition maximum (1RM) have been deemed necessary to elicit muscle hypertrophy and strength gains.

Recent research has demonstrated that low-load training to failure can stimulate muscle hypertrophy comparable in magnitude to that observed with heavy-load training after 6 and 817 weeks of training three times per week. However, strength adaptations were maximised with heavy-load training, and cross-sectional comparisons would suggest that hypertrophy strength gains observed with low-load training are not as great as those achieved with heavy-load training.

Nevertheless, from a clinical MSK rehabilitation perspective, training to muscular failure may provide one strategy to maximise hypertrophy when training using low loads in situations when using heavy loads is not feasible. Training with low loads may therefore be useful, as the early addition of muscle mass and function in rehabilitation may be beneficial for individuals who have suffered from atrophy. In recent years, research has demonstrated that augmentation of low-load resistance training with blood flow restriction (LLBFR) to the active musculature can produce significant hypertrophy and strength gains, using loads as low as 30% 1RM.

BFR training has been found to yield hypertrophy responses comparable to that observed with heavy-load resistance training; however, studies with such findings regarding muscle hypertrophy are not common among the present literature. Physiological adaptations in leg strength and vascular and pulmonary components have been reported with low-load aerobic exercise and BFR. From a mechanistic standpoint, it is hypothesised that an ischaemic and hypoxic muscular environment is generated during BFR to cause high levels of metabolic stress, alongside mechanical tension when BFR is used in tandem with exercise. Both metabolic stress and mechanical tension have been described as ‘primary hypertrophy factor’s and theorised to activate other mechanisms for the induction of muscle growth.

These proposed mechanisms include: elevated systemic hormone production, cell swelling, production of reactive oxygen species (ROS), intramuscular anabolic/anticatabolic signalling and increased fast-twitch fibre recruitment. However, at present these are mainly hypothetical and theoretical-based associations. Pragmatic and specific identification of these proposed mechanisms, including their magnitude of involvement and actual source of activation in BFR-induced hypertrophy is currently lacking and requires further exploration.

Nevertheless, these findings have important implications for individuals who cannot tolerate the mechanical stress of heavyload exercise. LL-BFR strength training may be a clinically relevant MSK rehabilitation tool as it does not require the high joint forces associated with heavy-load exercise. Interest in the use of BFR training as a clinical rehabilitation tool is mounting, given the practicality that this training mode may offer in a clinical setting.

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