The presence of oxygen is a fundamental component of cellular metabolism. However, sudden or chronic over-consumption of oxygen causes the production of free radicals (unpaired electrons) called “reactive oxygen species” (ROS). The production of these is a result of:
1) Μitochondrial origin where free radicals escape purifying enzymes
2) Production within the capillary endothelium where there is a hypoxic image created during intense exercise.
The development of free radicals and oxidative stress during exercise is an important factor for optimal performance, recovery and health. Aerobic energy metabolism (or oxidative phosphorylation) is a critical metabolic pathway within cells for energy production. At rest, these processes work slowly, while during periods of intense exercise, these metabolic processes increase up to 100 times.
Inside the mitochondria, electron transport is responsible for a series of redox reactions that result in ATP recomposition. In this system, O2 is reduced [by mitochondrial enzyme complex] and as the flow increases there is a possibility of free radical accumulation. It is estimated that 2-5% of the oxygen passing through the electron transport system into the mitochondria results in peroxide derivatives (the best known from free radicals, produced during the natural oxidative phosphorylation pathway).
Peroxide is easily broken down by antioxidant enzymes and is converted mainly to hydrogen peroxide which is largely disassembled into water as a by-product.
The hydroxyl radical [the most active] causes DNA to fragment, but the enzyme system antioxidant protection [peroxide dismutase and glutathione peroxidase] under normal resting conditions removes these free radicals, except in more extreme conditions such as:
1)Inadequate intake of foods containing antioxidants
2) excessive intake of pro-oxidants
3) exposure to harmful chemicals or ultraviolet radiation
4) injury / exercise [particularly eccentric]
Endogenous antioxidant systems are not able to effectively remove excess ROS production and thus oxidative stress.
Free radicals have been found to react with macromolecules (lipids, proteins, DNA) within the cell but one of the most common targets is polyunsaturated fatty acids in cell membranes that undergo oxidation (lipid peroxidation), which is quantified by malondialdehyde (MDA) which in various forms of exercise we have significant increases.
GLUTATHIONΕ [studied antioxidant] is synthesized endogenously in all cells, sometimes in relatively high concentrations, due to its great role in the fight against lipid peroxidation that occurs during oxidative stress, especially during intense exercise.
The intervention of glutathione to minimize or reduce free radicals is evident from changes in post-exercise state. In exercise the circulating levels of reduced glutathione decrease while the levels of oxidized glutathione increase.
N-acetyl-cysteine (NAC) residue of acetylated cysteine (redox thiol) has been shown to be crucial in optimizing reduced glutathione for cell protection against oxidative stress. NAC supplementation promotes a more favorable cellular environment for higher results.
N-acetyl-cysteine in experimental animals had no effect on non-tired muscle, but had a significant increase in the strength of activated muscle. NAC resulted in improved performance in the fatigue process and was effective in weakening or minimizing muscle fatigue, in strengthening of the overall redox state within the cell by better maintaining intracellular glutathione levels as well as preventing apoptosis in strenuous exercise.
N-acetyl-cysteine is an effective free radical scavenger.
SOURCE: The team of the Konstantinion Research Center