In conclusion, we demonstrated that MV with endotoxemia can augment mitochondrial dysfunction, determined based on transcription regulation, mitochondrial dynamics, biogenesis, mitochondrial autophagy (mitophagy), and the ultrastructural and functional impairment of the diaphragm through HIF-1α signaling pathways by using our established animal model, which accords closely with real clinical situations. This evidence concerns the gene HIF1A and serum lipopolysaccharide activity.