title: Effects of high-intensity intermittent swimming on glucose transport in rat epitrochlearis muscle.
abstract: Recently (K. Kawanaka, I. Tabata, and M. Higuchi. J. Appl. Physiol. 83: 429-433, 1997), we demonstrated that glucose transport activity after repeated 10-s-long in vitro tetani in rat epitrochlearis (Epi) muscle was negatively correlated with the postcontraction muscle glycogen concentration. Therefore, we examined whether high-intensity intermittent swimming, which depletes muscle glycogen to a lower level than that observed after ten 10-s-long in vitro tetani, elicits higher glucose transport than that observed after ten 10-s-long in vitro tetani, which has been regarded as the exercise-induced maximal stimulus for glucose transport. In male rats, 2-deoxy-D-glucose transport rate in Epi muscle after eight bouts of high-intensity intermittent swimming with a weight equal to 18% of body mass (exercise duration: 20 s, rest duration between exercise bouts: 40 s) was higher than that observed after the ten 10-s-long tetani (2.25 +/- 0.08 vs. 1.02 +/- 0.16 micromol . ml intracellular water-1 . 20 min-1). Muscle glycogen concentration in Epi after eight bouts of high-intensity intermittent swimming was significantly lower than that observed after ten 10-s-long in vitro tetani (7.6 +/- 0.5 vs. 14.8 +/- 1.4 micromol glucose/g muscle). These observations show that the high-intensity intermittent swimming increases glucose transport in rat Epi to a much higher level than that induced by ten 10-s-long in vitro tetani, which has been regarded as the exercise-related maximal stimulus for glucose transport. Furthermore, this finding suggests that the lower muscle glycogen level after high-intensity intermittent swimming than after in vitro tetani may play a role, because there was a significant negative correlation between glucose transport and muscle glycogen concentration in Epi after high-intensity swimming and in vitro tetani.
authors.affiliation: Division of Health Promotion, National Institute of Health and Nutrition, Toyama 1-23-1, Shinjuku City, Tokyo 162-8636, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Kawanaka
authors.forename: I
authors.initials: I
authors.lastname: Tabata
authors.forename: A
authors.initials: A
authors.lastname: Tanaka
authors.forename: M
authors.initials: M
authors.lastname: Higuchi
mesh_terms: D000818:Animals; D003847:Deoxyglucose / Q000378:metabolism; D004558:Electric Stimulation; D005947:Glucose / Q000378:metabolism*; D006003:Glycogen / Q000378:metabolism; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007328:Insulin / Q000494:pharmacology; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D018482:Muscle, Skeletal / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013550:Swimming / Q000502:physiology*
chemical_list: D007004:Hypoglycemic Agents; D007328:Insulin; D006003:Glycogen; D003847:Deoxyglucose; D005947:Glucose