Free radicals are chemicals with unpaired electrons that are highly reactive. When present in the body they tend to react with cell components and the damage they cause can lead to disease if their reactivity is not controlled. Antioxidants are chemicals that can react with free radicals before they have a chance to cause cellular damage, and in this way antioxidants can protect from disease. Some antioxidants are synthesised in the body, whereas others are derived from the diet, mainly from plant foods. Plants are rich sources of antioxidants because plants use antioxidants extensively to protect themselves from environmental stress. Dietary antioxidant work synergistically with endogenously produced antioxidants and in this way our cellular defence to free radicals are dependent on both diet and endogenous synthesis. Some dietary antioxidants can increase the synthesis of endogenous antioxidants thought a sparing effect or through their ability to provide chemical groups for the synthesis of endogenous compounds.
An example of free radical generation in humans can be seen during muscle damage. Skeletal muscle injury, as might occur through intensive training, is treated by the body much like any other injury. The cellular damage is detected by the immune system and in response leukocytes (white blood cells) infiltrate the area and invade the damaged tissue. The result of this infiltration is an increase in the local concentrations of cytokines, powerful inflammatory chemicals that are release at sites of tissue injury. The inflammation associated with damaged muscle tissue can be felt in the form of delayed onset muscle soreness that is experienced following exercise periods and this represents a catabolic period of net proteolysis (protein breakdown). The inflammation is then followed by a period of tissue regeneration where protein synthesis is increased and new muscle tissue is generated. However, it is becoming clear that for the regeneration period to be effective, the inflammatory reaction must be allowed to proceed.
The ability of dietary antioxidants to increase cellular defenses in muscle would at first glance appear beneficial. However, boosting the antioxidant defences in muscle is thought to alter the inflammatory period following exercise and in turn this may affect the tissue remodelling and regeneration phase. For example, in one study1 researchers used N-acetylcysteine (NAC), a thiol containing dietary antioxidant to increase cellular glutathione levels within skeletal muscle. They then measured a number of biochemical markers of the inflammatory response to exercise. The results showed that the NAC at a dose of 20 mg per kg body weight reduced the post exercise inflammatory response in skeletal muscle tissue. In addition, the NAC supplementation also decreased the reduction in strength seen during the first two days post-exercise. However, this decrease in inflammation was accompanied by a decrease in biomarkers for protein synthesis, indicating that the late stage remodelling phase may have been blunted by the NAC supplement.
This study is interesting because it showed that a common thio-containing dietary supplement could alter the markers of inflammation and tissue regeneration following exercise. Dietary NAC is known to increase glutathione concentrations in skeletal muscle, and this is likely because the NAC provides cysteine that is available for glutathione synthesis. In addition, NAC may act as a cellular antioxidant itself in skeletal muscle and in this way spare cellular glutathione. Glutathione is in term required as part of the cellular reaction involving glutathione peroxidase, an enzyme that decreases oxidative stress through its participation in the removal of hydrogen peroxide. The authors suggested that NAC at the dose administered (1500 mg for a 75 kg individual) caused an attenuation of the late stage strength recovery as represented by reduced expression of some markers of tissue repair 3 to 8 days post exercise. However, if this translates into impaired physical performance and reductions in strength over time is not fully understood.
RdB
