Coenzyme Q10
An important rate-limiting nutritional factor for ATP production. It acts as an electron carrier from complex I and II to complex III as part of the electron transport train during oxidative phosphorylation. Among its additional roles in the body, it provides antioxidant support and aids in the regeneration of vitamins C and E.
R‑Lipoic Acid (RLA)
R-Lipoic Acid is the naturally occurring and more biologically active enantiomer of lipoic acid. Lipoic acid, or thioctic acid, acts as a cofactor in many multi-enzyme complexes in the mitochondria, playing a role in chemical reactions in the Krebs cycle, regulating carbohydrate and protein metabolism, and aiding in the reduction of oxidative damage. Alpha-lipoic acid also acts as an antioxidant (dubbed the universal antioxidant because it has both hydrophilic and hydrophobic properties), and it also regenerates other antioxidants including glutathione and vitamins C and E. Reductions in alpha-lipoic acid may lead to a reduction in ATP production and increased oxidative stress.
L-carnitine
Aids in shuttling fats from the bloodstream into the mitochondria where they are converted into energy*
D-Ribose
is a building block of many elements in the cell, including nucleotides, coenzymes, nicotinamide adenine dinucleotide phosphate (NADP), nucleic acids, and ATP. Additionally, it is involved in several metabolic pathways and can bypass some rate-limiting enzymes to create ATP. Studies have found that supplementation of D-ribose may support increasing ATP synthesis and aid in recovering normal energy metabolism after stress, such as that from cellular insult and high-intensity exercise.*
Malic and succinic acids
Also known as succinate and malate, are intermediates in the Krebs cycle, with succinate oxidizing to fumarate, which converts to L-malate. The oxidation of succinate to fumarate is also the first step of the electron transport chain to convert flavin adenine dinucleotide (FAD) to 1,5-dihydro-FAD (FADH2). Mechanistic and animal studies have found that supplementing with these intermediates may enhance oxidative metabolism. Human studies demonstrated that supplementing with succinic acid may improve the lactate/pyruvate ratio and nicotinamide adenine dinucleotide plus hydrogen (NADH)/nicotinamide adenine dinucleotide (NAD+) redox state, signs of normalizing mitochondrial function in metabolically stressed conditions, such as traumatic brain injury.*
Vitamins B1, B2, B3, B5, and B12
These play key roles in glycolysis and the Krebs cycle. Deficiencies of vitamin B1 may impair aerobic metabolism by limiting pyruvate entering the Krebs cycle. Riboflavin acts as a precursor to FAD, so that deficiencies may limit the ability to oxidize fatty acids and branched amino acids. Riboflavin also aids in the glutathione redox cycle. Niacin (as a precursor to NAD and NAD phosphate) plays a key role in glycolysis and the Krebs cycle. Pantethine, synthesized from vitamin B5 (pantothenic acid), is an intermediate of co-enzyme A, and it is important to energy metabolism.
Resveratrol and curcumin
Support mitochondrial biogenesis and antioxidant status. Resveratrol modulates genes and induces enzymes involved in mitochondrial biogenesis, such as sirtuin 1 (SIRT-1) and proliferator-activated receptor gamma co-activator 1-alpha (PGC-1-α). Resveratrol also provides antioxidant support to maintain redox balance both directly and through its actions on redox genes and enzymes, such as SIRT1. Curcumin provides protection to the mitochondria, including protection from the effects of inflammation and oxidative stress. Curcumin enhances mitochondrial biogenesis, likely through its action on the PGC-1-α signaling pathway, and it improves the function of the electron transport chain complexes. Curcumin directly acts as an antioxidant, scavenging reactive oxygenated species (ROS), and indirectly acts through gene regulation by activating the nuclear factor-erythroid-2 related factor 2 (Nrf2) pathway, the major antioxidant regulator, and by restoring glutathione and superoxide dismutase (SOD) levels.
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