Shin Terada

An acute bout of high-intensity intermittent swimming induces glycogen supercompensation in rat skeletal muscle

Abstract High-intensity intermittent exercise substantially increases muscle glucose transport, which is thought to be the rate-limiting step for glycogen synthesis. In the present study, we compared muscle glycogen supercompensation after high-intensity intermittent exercise with that observed after low-intensity continuous exercise in rats. Four- to five-week-old male Sprague-Dawley rats performed either low-intensity swimming (240 min of swimming exercise with a weight equivalent to 1% of their body mass; LOW) or high-intensity swimming (twenty 30-s swimming bouts with 30 s rest between bouts with a weight equivalent to 16% of their body mass; HIGH) to deplete muscle glycogen. After the glycogen-depleting exercise, rats were given a rodent chow diet plus 5% glucose solution for 6 h or 24 h. Immediately after the two types of exercise, glycogen concentration in rat epitrochlearis muscle was similarly depleted. After the 6-h and 24-h recovery periods, muscle glycogen concentrations in both the HIGH and LOW groups were restored well above the normally fed state. Furthermore, muscle glycogen accumulation in the HIGH group for the 6-h and 24-h recovery periods was not significantly different from that observed in the LOW group. The high-intensity intermittent swimming exercise also induced muscle glycogen supercompensation in well-trained rats that had performed 7 days of endurance swimming training (6 h per day). Our results indicate that high-intensity intermittent exercise as well as low-intensity continuous exercise could induce glycogen supercompensation in rat skeletal muscle.