Therapeutic exercise in improving acute lung injury: a long distance to be covered

Skeletal muscle weakness is a common finding among critically ill patients, and many factors have been recognized to trigger its initiation early in the patients’ course in intensive care unit (ICU) (1). In acute respiratory distress syndrome (ARDS), a clinical condition which is characterized by acute respiratory failure, skeletal muscle weakness acquired in ICU is present in 25-50% of patients, and is independently associated with mortality and long term morbidity in survivors (2). Several clinical research studies suggest that early mobilization of critically ill patients improves clinically meaningful outcomes for the patient (3), however, without having clarified the mechanisms underlying this implementation. We read with interest the study by Files et al. (4) who through their experiments suggest a unifying mechanism underlying the beneficial effects of therapeutic exercise in mice with lung injury. In their study authors exercised ALI mice for 2 days after lipopolysaccharides (LPS) instillation. They found that a short duration of moderate intensity exercise attenuated muscle ring finger 1 (MuRF 1)-mediated atrophy of the limb and diaphragm and improved limb muscle force generation. Importantly, exercise also limited neutrophilic influx into the alveolar space through modulation of a co-ordinated systemic neutrophil chemokine response. Furthermore, in ALI mice exercise reduced granulocyte colony-stimulating factor (G-CSF), and in vivo blockade of the G-CSF receptor lead to recapitulation of the lung. Similarly, in humans with acute respiratory failure, early mobility therapy led to greater decrements over time in G-CSF plasma levels compared to control patients, confirming the relevance of G-CSF as a mediator of the improved outcomes of mobilized/exercised critically ill patients.