FMU January 2011 part 2

There's no question that aging is associated with some mitochondrial dysfunction. When we look at brain and muscle from older adults over the age of 65, we do see some point mutations. There are some deletions which start to occur. And that probably is due to a number of factors. One, just the normal process of living and eating. We generate free radicals which are in close proximity to the mitochondrial DNA. So it's not surprising that with drugs that we might take throughout a lifetime. With ionizing radiation and other hits, that we would get some damage to our mitochondrial DNA. Which may not be repaired in the normal repair process. So we sort of stochastically, if you will accumulate these problems throughout our lifespan, which in a very segmental region of the muscle. But eventually it becomes quantitative, because if we have these tiny little changes occurring scattered throughout a muscle fiber, ultimately that muscle fiber will slowly shrink. Or the heart will slowly be less functional. Or the brain will be less functional over time. And certainly our work and the work of many others does support that there is a role for mitochondrial dysfunction and likely an interactive role with oxidative stress, which contributes to the aging process of humans. Now, aging is probably. Well, we know it's multifactorial, but. But I think these are two important components of aging which are going to lead to a decrease in VO2 max. And that's why people are not top sport athletes when they're 65 in endurance sports. And VO2 generally declines, which is your maximal aerobic capacity from your mid-20s till you're 50 or 60, you're probably going to lose 30 to 40% of your VO2 max from aging associated mitochondrial dysfunction. Sa.