How Antioxidants Interfere With Glucose Metabolism
When we exercise (or when we eat, or when we perform many metabolic tasks) we generate free radicals. This is normal. However, free radicals can harm healthy cells; they can damage DNA and cause fats in our body to oxidize, or "go rancid" as cooking oils do. DNA damage and oxidized fats are factors in the development of cancer and atherosclerosis (and so heart disease). It is this negative aspect of free radicals, their power to oxidize, that gave rise to supplemental anti-oxidants. Antioxidants prevent oxidation by neutralizing free radicals (by donating electrons, or "reducing" them).
Since production of free radicals is a natural occurrence, you'd think we've evolved mechanisms to mitigate their damage. We have. Free radicals [which usually include an oxygen molecule and are known collectively as Reactive Oxygen Species (ROS)], act as signals telling cells to make more of our own, in-house (endogenous) antioxidants - like the powerful enzymes superoxide dismutase and glutathione peroxidase.
But before they're neutralized ...
- Free radicals partake in a positive feedback loop giving us more energy. Muscles need oxygen and glucose to work. When we increase the work of our muscles, e.g. when we exercise, we increase the muscle's need for glucose and oxygen. Byproducts of muscle work are ROS ... ROS act as signals to produce more mitochondria. Mitochondria are energy-producing factories inside cells that use the glucose and oxygen the muscles take up. More mitochondria lead to --> more glucose uptake, lead to --> more energy.
- Free radicals spur the expression of genes that increase sensitivity to insulin - Done through stimulation of PPARs and other compounds. (The thiazolidiediones, a class into which the diabetes drugs Avandia and Actos fall, also stimulate PPARs.)
- Free radicals stimulate the release of the hormone adiponectin. Adiponectin is produced by our fat cells and has been shown to increase insulin sensitivity. Low levels of it correlate with increased diabetes risk.
This first one is getting a lot of attention:
Antioxidants Prevent Health-Promoting Effects Of Physical Exercise In Humans, PNAS, May 2009.
"Exercise increased parameters of insulin sensitivity only in the absence of antioxidants in both previously untrained and pretrained individuals."These authors went so far as to say:
"If transient increases in oxidative stress are capable of counteracting insulin resistance in humans, it is possible that preventing the formation of ROS by, for example, antioxidants might actually increase, rather than decrease, the risk of type 2 diabetes."
"Published findings tentatively suggest that fruits and vegetables may exert health-promoting effects despite their antioxidant content and possibly due to other bio-active compounds." (Emphasis theirs.)
This one I blogged about at: Vitamin C Supplementation And Exercise Don't Mix.:
Oral Administration Of Vitamin C Decreases Muscle Mitochondrial Biogenesis And Hampers Training-Induced Adaptations In Endurance Performance, AJCN, January 2008.
"Vitamin C supplementation decreases training efficiency because it prevents some cellular adaptations to exercise. [...] The common practice of taking vitamin C supplements during training (for both health-related and performance-related physical fitness) should be seriously questioned."
How Much Is Too Much?
The DRI for vitamin C is 75 mg for women, 90 mg for men. (Both of the above studies used 1000 mg.)
The DRI for vitamin E is 15 mg, about 22 IU. (The first study used 400 IU.)
DRIs or RDAs typically contain a buffer. An estimated average requirement is multiplied by a factor to account for individual variation - to, well, play it safe.
There are about 63 mg vitamin C in a small orange.
There are about 51 mg vitamin C in a half cup of cooked broccoli.
There are about 7 mg (11 IU) vitamin E in 1 ounce of almonds.