<p>Sarcopenia is a metabolic disorder characterized by the loss of muscle mass and function related to the aging process that adversely affects mobility, independence, and the burden of disease. Some of the key mechanisms associated with the loss of muscle mass and strength in sarcopenia, which have been referenced in the literature, are mitochondrial “dysfunction” and cellular “senescence,” which both cause muscle degradation. Mitochondrial dysfunction can lead to reduced production of ATP, increased oxidative stress, and inhibition of the muscle repair process. Cellular senescence impairs tissue homeostasis via mechanisms related to cellular senescence, including telomere shortening, inflammatory factors, and accumulation of senescent cells. The focus of this review is to elaborate on the complex interactions between aging and sarcopenia. Also, non-mitochondrial related mechanisms may further increase the loss of muscle due to the aging process, including astrocyte-derived pro-inflammatory cytokines, which have been shown to promote muscle atrophy during aging. There are several approaches to mitigate these outcomes using mitochondrial-specific antioxidants, exercise to enhance mitochondrial biogenesis, or utilizing senolytic approaches, some currently being investigated. In conclusion, these outcomes represent a review to assist in managing the multifactorial process of sarcopenia. Given sarcopenia, future work should also focus on establishing suitable biomarkers for identifying at-risk patients or establishing personalized approaches to managing and preventing loss of muscle and subsequent geriatric syndromes in association with loss of muscle. Addressing cellular aging and mitochondrial dysfunction may help maintain physical function and muscle health in older adults, enhancing their overall quality of life.</p> Graphical Abstract <p></p>