Creatine is widely recognized for its role in supporting cellular energy metabolism, particularly in tissues with high energy demand such as skeletal muscle and the brain. The scientific justification for its use in supporting mitochondrial function stems from its involvement in the creatine-phosphocreatine system, a critical energy buffering and transfer mechanism. Within cells, creatine kinase catalyzes the reversible transfer of a phosphate group from phosphocreatine to ADP, rapidly regenerating ATP—the main energy currency—especially during periods of high energy demand. This system is functionally coupled with mitochondria, where phosphocreatine is replenished using mitochondrial ATP.

Multiple studies have shown that creatine supplementation can enhance mitochondrial respiration, increase cellular ATP availability, and protect against mitochondrial dysfunction in both healthy individuals and disease models. For example, research in neurodegenerative diseases (such as Parkinson’s and Huntington’s disease) suggests that creatine may help buffer energy deficits caused by impaired mitochondrial function. Additionally, in muscle cells, creatine supplementation has been demonstrated to support endurance and recovery, further implicating its role in mitochondrial energy metabolism.

While creatine is most commonly associated with athletic performance, there is robust scientific evidence supporting its role in maintaining and supporting mitochondrial health and energy transfer. However, most evidence is indirect or from disease models, and more research is needed to determine the extent of its benefits in healthy populations specifically for mitochondrial function.