1,3,7-Trimethylpurine-2,6-dione is the chemical name for caffeine. There is substantial scientific evidence supporting caffeine's effects on mitochondrial function, particularly within the context of energy metabolism and exercise performance. Caffeine is known to act as a central nervous system stimulant, but it also influences cellular metabolism by increasing cyclic AMP (cAMP) through inhibition of phosphodiesterase. This elevation in cAMP enhances lipolysis, the breakdown of fats into free fatty acids, which can then be oxidized in mitochondria to produce ATP, the primary energy currency of the cell.

Several studies have demonstrated that caffeine intake can increase mitochondrial biogenesis and function, especially in skeletal muscle. For example, research has shown that caffeine activates AMP-activated protein kinase (AMPK), a key energy sensor in cells, which in turn stimulates the production of new mitochondria and enhances their efficiency. This is particularly relevant during endurance exercise, where mitochondrial capacity is critical for sustained energy production.

Additionally, caffeine has been shown to reduce perceived exertion and improve endurance, effects partially attributed to its enhancement of mitochondrial energy output. However, while caffeine supports mitochondrial function, its use as a specific "mitochondrial support supplement" outside of athletic or metabolic contexts is less established.

Overall, the evidence for caffeine’s support of mitochondrial energy metabolism is strong, especially in the context of physical activity and metabolic stimulation.