The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 13 No.
6 • December 2010
Help For the Sedentary:
Prevent Muscle Disuse Atrophy
A new paper reports on the ability of quercetin or N-acetylcysteine to prevent disuse muscle atrophy in tail-suspended mice. The problem with this study was the nonphysiological method of treatment administration: the quercetin or N-acetylcysteine or flavone (a natural flavone without antioxidant effects) were administered by injection into the gastrocnemius muscle of one leg of the seven week old male C57BL/6 mice subjected to the tail suspension procedure. Hence, the results are properly stated (as the authors did): “quercetin has the potential to suppress the atrophy of skeletal muscle when concentrated in the target tissue.” However, we would expect similar results from taking oral quercetin along with other antioxidant supplements, which could deliver considerable quantities of antioxidants to the muscles.
As the authors explain, oxidative stress is believed to be a major cause of muscle disuse atrophy. The authors themselves carried out another experiment in which they found that intragastric supplementation, which should work like oral supplementation, of the amino acid cysteine prevented unloading-induced ubiquitination in association with redox regulation in rat skeletal muscle. Moreover, in experiments “using cultured myotubes, 1 [quercetin] suppressed the expression of atrogin and MuRF-1 [muscle disuse atrophy associated signaling molecules] and the MEK/ERK signaling, a well-known mitogen-activated protein kinase (MAPK) pathway to mediate oxidative stress.”
Interestingly, although both quercetin and N-acetylcysteine individually suppressed the decrease of muscle weight to whole body weight ratio, quercetin significantly suppressed the induction of atrogin-1 and MuRF-1, while N-acetylcysteine suppressed the induction of atrogin-1, but not the induction of MuRF-1. The non-antioxidant flavone had no effect on muscle-weight loss or the expression of ubiquitin ligases.
Both quercetin and N-acetylcysteine prevented the increase in TBARS (a measure of lipid peroxidation, which is increased under conditions of oxidative stress) that occurred in the gastrocnemius muscle of the tail-suspended mice that received no quercetin or N-acetylcysteine.
These results suggest to us that adequate supplementation with quercetin and other antioxidants can reduce or suppress the muscle loss that would otherwise occur under conditions of lack of exercise (disuse atrophy). Exercise has many other beneficial effects besides helping maintain muscle mass, but the latter is probably its most important effect as loss of muscle has such a major impact on physical capabilities at any age. Hence, it is very helpful to be able to prevent or attenuate that loss, at least as far as it comes from disuse atrophy, with antioxidant supplements.
- Mukai et al. Quercetin prevents unloading-derived disused muscle atrophy by attenuating the induction of ubiquitin ligases in tail-suspension mice. J Nat Prod 73:1708-10 (2010).
- Ikemoto et al. Cysteine supplementation prevents unweighting-induced ubiquitination in association with redox regulation in rat skeletal muscle. Biol Chem 383:715-21 (2002).