著者

田中 純也 渋谷 顕一 大柿 哲朗

出版者

一般社団法人日本体力医学会

雑誌

体力科学 (ISSN:0039906X)

巻号頁・発行日

vol.54, no.2, pp.133-142, 2005 (Released:2006-12-01)

参考文献数

26

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Exercise intensity has been identified as a major determinant of the excess post-exercise oxygen consumption (EPOC). However, no studies have compared the prolonged EPOC after supramaximal intermittent exercise and supramaximal continuous exercise. Six young healthy male [age=26±3 (mean±SD) yr ; stature=175.4±5.7 cm ; body weight=66.8±6.7 kg ; maximal oxygen uptake (VO2max)=44.1±8.5 ml/kg/min] xercised on separate days on a cycle ergometer at two equated total energy expenditures (intermittent exercise : 7×30-second intervals at 150%VO2max with intervening 15-seconds rest periods ; continuous exercise : 5 min at 105%VO2max) and then sat quietly in an armchair for 3h. A control trial without any exercise was also performed in a counterbalanced research design. The VO2, carbon dioxide output (VCO2), pulmonary ventilation (VE), respiratory exchange ratio (RER), heart rate (HR) and blood lactate concentration (LA) were measured before exercise, during exercise and during the 3-h recovery period. The mean VO2 after intermittent trial at 150%VO2max were higher than these of the control trial and the continuous trials at 105%VO2max for 3-h recovery periods (p<0.05). The 3-h EPOC value for intermittent exercise trial (10.5±2.4L) was significantly greater than that of continuous exercise trial (4.8±2.7L) (p<0.05). The mean RER values for intermittent exercise trial were significantly lower than those of the control trial during 60-180 min post-exercise (p<0.05). We examined the effect of supramaximal exercise intensity on the magnitude of 3-h EPOC after 12-fasting. In the present study, 3-h EPOC was significantly greater for supramaximal intermittent exercise compared with the supramaximal continuous exercise when the amounts of work output performed are same. Therefore, our results indicate that exercise intensity may be a primary factor of 3-h EPOC even in a supramaximal exercise and that one of mechanisms for the 3-h EPOC would be related to the promoted lipid metabolism.