British Journal of Nutrition

Research Article

Dietary whey protein increases liver and skeletal muscle glycogen levels in exercise-trained rats

Masashi Morifujia1a2 c1, Kensuke Sakaia1a2, Chiaki Sanbongia1a2 and Katsumi Sugiuraa2

a1 Meiji Seika Kaisha Ltd., Health and Bioscience Laboratories and

a2 Meiji Seika Kaisha Ltd., SAVAS Sports and Nutrition Laboratory, 5-3-1 Chiyoda, Sakado-shi, Saitama, 350-0289, Japan


We investigated the effect of different types of dietary protein on glycogen content in liver and skeletal muscle of exercise-trained rats. Twenty-four male Sprague-Dawley rats (approximately 100 g; n 6 per group) were divided into sedentary or exercise-trained groups with each group being fed either casein or whey protein as the source of dietary protein. Rats in the exercised groups were trained during 2 weeks using swimming exercise for 120 min/d, 6 d/week. Exercise training resulted in an increase in the skeletal muscle glycogen content. Furthermore, the whey protein group significantly increased the skeletal muscle glycogen content compared with the casein group. The increase in glycogen content in liver was significantly greater in rats fed the whey protein diet compared with those fed the casein diet. We also found that the whey protein diet increased the activity of liver glucokinase, whereas it decreased the activities of 6-phosphofructokinase and pyruvate kinase compared with the casein diet. However, hepatic total glycogen synthase activity and mRNA expression were similar with the two diets. In the skeletal muscle, whey protein decreased only 6-phosphofructokinase activity compared with casein. Total glycogen synthase activity in the skeletal muscle in the whey protein group was significantly higher than that in the casein group. The present study is the first to demonstrate that a diet based on whey protein may increase glycogen content in liver and skeletal muscle of exercise-trained rats. We also observed that whey protein regulated glycogen metabolism in these two tissues by different mechanisms.

(Received July 01 2004)

(Revised November 02 2004)

(Accepted November 19 2004)


c1 *Corresponding author: Dr Masashi Morifuji, fax +81 49 284 7598, email