Mild Heat Stress Protects Muscle Mass During Immobilization in Rats

The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 8 No. 4 • October 2005

Mild Heat Stress Protects Muscle Mass During Immobilization in Rats

Earlier, we reported in this newsletter on a paper1 showing that repeated mild heat shock delays aging in cultured human skin fibroblasts. A new paper2 reports that mild heat stress also protects rats from the very significant loss of muscle mass that occurs when the animals are immobilized.

Rats were divided into three groups: a control group, an immobilized group, and an immobilized group that was heat-treated. The heat treatment consisted of warming the animals to 41–41.5ºC (about 106ºF) for 30 minutes on alternating days. The findings showed that the immobilization induced a significant increase in oxidative damage in the animals’ immobilized muscles, but this damage was significantly reduced by heating. This is strong evidence that mild heat stress protects against muscle-disuse atrophy. Great news for people who don’t like to exercise!

The heat-treated animals with relatively preserved muscle mass had higher heat-shock protein 72 (HSP72) levels. It has been proposed that HSP72 is necessary for maintenance of protein synthesis in the heated hind limbs of animals with hind-limb unweighting (suspension). In addition, it has been proposed that HSP72 protects proteins from degradation by proteolysis by refolding damaged proteins. In another study cited in the paper, scientists reported that a single bout of heat for 60 minutes was sufficient to detect an increase in HSP72 8 days later, with muscle atrophy reduced in the heated-suspended group by about 32%. This suggests that daily heating may not be necessary, as the increased levels of HSP72 (at least in rats, and probably in humans) remain for several days.


In another paper,3 enhanced expression of HSP72 as a result of heating in male rats attenuated oxidative stress and neointimal thickening in induced inflammatory arterial lesions, suggesting that increasing HSP72 by mild heat stress can provide protection against atherosclerosis. In a different study,4 scientists report that heat-shock-induced manganese superoxide dismutase (the mitochondrial version of superoxide dismutase) enhanced the tolerance of cultured cardiac myocytes to hypoxia-reoxygenation (ischemia-reperfusion) injury.


A separate study5 of 50 subjects (25 of these served as controls) that was controlled but not randomized found that immunological changes (such as increases in immunoglobulins and leukocytes) induced in people who used sauna baths resulted in a statistically significant reduction in common colds, as compared to controls. The average frequency of sauna bathing was 26.8 ± 5.5 during 6 months. As influenza viruses generate large amounts of reactive oxygen species,6 both directly and through induction of immune cells, a treatment, such as mild heat stress, that decreases oxidative damage may be a useful prophylactic against influenza-damage severity.


  1. Rattan. Repeated mild heat shock delays ageing in cultured human skin fibroblasts. Biochem Molec Biol Int 45(4):753-9 (1998).
  2. Selsby, Dodd. Heat treatment reduces oxidative stress and protects muscle mass during immobilization. Am J Physiol Regul Integr Comp Physiol 289:R134-9 (2005).
  3. Okada et al. Thermal treatment attenuates neointimal thickening with enhanced expression of heat shock protein 72 and suppression of oxidative stress. Circulation 109:1763-8 (2004).
  4. Nobushige, Yamashita, et al. Heat shock-induced manganese superoxide dismutase enhances the tolerance of cardiac myocytes to hypoxia-reoxygenation injury. J Mol Cell Cardiol 29:1805-13 (1997).
  5. Ernst et al. Regular sauna bathing and the incidence of common colds. Ann Med 22:225-7 (1990).
  6. Han et al. Effect of long-term dietary antioxidant supplementation on influenza virus infection. J Gerontol: Biol Sci 55A(10):B496-503 (2000).

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