Abstract

Recently, we have reported that plasma L-ascorbic acid (AA, reduced form of vitamin C) concentrations in community-dwelling elderly women were related well to their muscle strength and physical performance (Saito, K. et al., 2012, J. Gerontol. A Biol. Sci. Med. Sci.). To clarify the physiological functions of AA in skeletal muscle, we investigated the effect of AA deficiency in skeletal muscle using senescence marker protein-30 (SMP30)/gluconolactonase (GNL)-knockout (KO) mice that lacks AA biosynthesis ability just like a human being. SMP30/GNL-KO female mice at age of 8 weeks were divided into two groups: AA-deficient group (AA-) given tap water and AA-sufficient group (AA+) given 1.5 g/L AA water. At 16-week of experimental period (age of 24 weeks), AA was not detected at all in skeletal muscles of AA-deficient mice. The gastrocnemius, soleus, plantaris, and tibialis anterior muscle weight of AA-deficient mice were significantly lower than those of AA-sufficient mice, but EDL muscle weight showed no difference. In soleus muscle, the area of muscle fibers and the percentage of type I fiber (slow-twitch fiber) were decreased in AA-deficient mice when compared to AA-sufficient mice. In contrast, the percentage of type IIa fiber (fast-twitch fiber) was increased in AA-deficient mice. These results strongly suggested that vitamin C deficiency in skeletal muscle leads to muscle atrophy and switches muscle fiber types from slow to fast.

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