Cancer-induced cachexia is a complex syndrome marked by skeletal muscle mass loss, impacting functional independence, quality of life, and cancer treatment outcomes. While muscle wasting has traditionally been attributed to circulating factors, recent research revealing mitochondrial dysfunction preceding the onset of muscle atrophy suggests it may play a role. Understanding the muscle-specific and time-dependent nature of mitochondrial responses to cancer may offer insights for targeted therapeutic interventions to mitigate muscle weakness and wasting in cachexia. This study examines the  relationship between muscle dysfunction and mitochondrial bioenergetics in locomotor and respiratory muscles, revealing diverse responses that underscore the need for tailored approaches to treating muscle complications in cancer cachexia.