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Skeletal muscle dysfunction acquired during critical illness (intensive care unit (ICU)-acquired weakness, ICUAW) plays a pivotal role in clinical outcomes such as liberation from mechanical ventilation, ICU length of stay, hospital length of stay, physical function and mortality.1 ,2 ICUAW is a common complication of critical illness with a complex aetiology,3 affecting both limb muscles as well as respiratory muscles. The decline in muscle mass is approximately 2%–4% per day in the first week of ICU stay.4 ,5 Loss of limb muscle mass is more pronounced in patients with multiple organ failure,4 while a rapid decline in diaphragm muscle strength and thickness is associated with sepsis6 and low diaphragm contractile activity.5 Strategies to prevent or treat ICUAW are scarce and mostly focused on the treatment or reduction of risk factors associated with ICUAW (sepsis, hyperglycaemia, catabolism, neuromuscular blockers and corticosteroids).3 In addition, immobility and inactivity contribute considerably to muscle atrophy: ‘mechanical silencing’ has been identified as an important contributor to the loss of contractile properties.7 Therefore, reversing inactivity of the muscle should have the potential to prevent, reverse or ameliorate muscle wasting.
The focus of rehabilitation in patients who are critically ill is on the prevention and treatment of ICUAW, oftentimes specifically targeting lower limb muscle function. Early mobilisation, transferring patients from the bed to the chair, weight-bearing, walking, bed cycling and neuromuscular electrical stimulation are the most common modalities successfully applied to ameliorate limb muscle weakness and functional status.8 It is unclear as to …