Saturday, March 12, 2011

Heat shock proteins preserve muscle

I’ve written two articles for Ironman magazine about heat shock proteins (HSP). HSP are stress-induced proteins that protect cells. They do so through a variety of mechanisms, such as preventing protein misfolding, which can interfere with protein synthesis, and also by opposing the effects of excess oxidation byproducts in cells that cause cellular death. Exercise, particularly high intensity weight-training, promotes the synthesis of a few heat shock proteins, such as HSP72 and others. Now a new study involving mice suggests that another HSP, HSP10, can preserve and protect muscles as we age. In fact, the authors of the new study make the bold assertion that “age-related loss of skeletal muscle mass is not inevitable.”

It has to do with mitochondria. Mitochondria are cigar-shaped cellular organelles that are the site of both energy production and fat oxidation in cells. The mitochondria also are the site of the most intensive level of oxidation. This oxidation is an unavoidable side effect of high oxygen exposure required for the production of energy as ATP. But after a while, the mitochondria get burned out by exposure to this oxidative effect, which leads to a cascade resulting in the mitochondria killing themselves, a process called apoptosis. Since the mitochondria are the cell’s power units, when they die, the cells also die, too. Muscles are particuarly prone to mitochondrial dysfunction, and a current theory of aging suggests that loss of mitochondria in muscle is largely responsible for the loss of muscle mass and strength with aging. This implies that if we could prevent mitochondrial destruction, muscles may age far slower, and may not even atrophy or weaken with age.

The new mouse study found that HSP10 works to preserve muscle by protecting muscle against contraction-induced damage, and also by preserving muscle force through blocking the effects of oxidation on muscle proteins, which results in excess levels of protein carbonyls that eventually lead to muscle weakness. If you could block these effects, muscles will stay big and strong for life. Overexpression of HSP10 in mice did just that. The next step is to figure out how to increase the expression of HSP10 in muscle mitochondria in humans. When that happens, they may even resurrect the Master’s Mr.Olympia.

Kayani, A, et al. Overexpression of HSP10 in skeletal muscle of trangenic mice prevents the age-related fall in maximum tetanic force generation and muscle cross-sectional area.Am J Physiol Regul Integr Comp Physiol 2010;In press.

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