With advances in intensive cares, the prognosis for critically ill patients requiring intensive cares has improved. However, discharged patients often induce ICU acquired weakness (ICU-AW) as a sequela. Especially in the elderly, ICU-AW has become a problem that the frailty is exacerbated and the patients are required long-term cares. So far, it is unknown the pathophysiology of ICU-AW, and effective preventive and therapeutics have not been established. Here we established a mouse model of ICU-AW, in which unilateral lower limb fixation was performed on mice with acute respiratory distress syndrome (ARDS) by intratracheal administration of bleomycin. Mice were divided into 4 groups: the non-lower limb fixation + non-ARDS, the lower limb fixation + non-ARDS, the non-lower limb fixation + ARDS, and the lower limb fixation + ARDS. The body weight and survival rates were the worst in the lower limb fixation + ARDS group. The lower limb fixation + ARDS group showed the impairment of respiratory function and the lung pathology, along with increased expression of pulmonary inflammatory cytokines. In addition, muscular atrophy was induced by fixation of the lower limbs, and increased expression of muscular atrophy-related genes was observed. In addition, the lower limb fixation + ARDS group had more severe weight loss than the other groups and died earlier. In the lung, the respiratory function was significantly worse in the lower limb fixation + ARDS group than in the non-lower limb fixation + ARDS group. Muscle atrophy was higher in the lower limb fixed + ARDS group than in the non-fixed + ARDS group. Pathway analysis based on gene expression analysis in muscle revealed that the Apelin signaling pathway was suppressed in the lower limb fixed + ARDS group compared to the non-fixed + ARDS group. These results suggest that in ICU-AW, muscular atrophy and ARDS influence each other's pathological conditions, and the Apelin signaling pathway may be involved in this process.