Acute respiratory distress syndrome (ARDS) has emerged as a
Translational Medicine approach that improves patient outcomes, such as the duration of muscle strength and mechanical ventilation. It can help to early mobilization of critically ill patients. Despite the apparent efficacy of early mobility programs, their use in limited outside of specialized centers and clinical trials for clinical practice.
To evaluate the mechanisms underlying mobility therapy, with exercised acute lung injury (ALI) mice for 2 days after the instillation of lipopolysaccharides into their lungs. It was found that a short duration of moderate intensity exercise in ALI mice attenuated muscle ring finger 1 (MuRF1) mediated atrophy of the limb and respiratory muscles and improved limb muscle force generation. Exercise is also limited to the influx of neutrophils into the alveolar space through modulation of a coordinated systemic neutrophil chemokine response.
Granulocyte colony-stimulating factor (G-CSF) concentrations were systemically reduced by exercise in ALI mice and in vivo obstruction of the G-CSF receptor recapitulated the lung exercise phenotype in ALI mice and plasma G-CSF concentrations in humans with
acute respiratory failure (ARF) undergoing early mobility therapy showed greater decrements over time matched to control ARF patients. These data provides a mechanism whereby early mobility therapy attenuate muscle wasting and limits ongoing alveolar neutrophilia through modulation of systemic neutrophil chemokines in lung-injured mice and humans.
