J. DUNCAN MACDOUGALL, AUDREY L. HICKS, JAY R. MACDONALD, ROBERT S. MCKELVIE, HOWARD J. GREEN, AND KELLY M. SMITH Department of Kinesiology, McMaster University, Hamilton, Ontario, Canada L8S 4K1
MacDougall, J. Duncan, Audrey L. Hicks, Jay R. MacDonald, Robert S. McKelvie, Howard J. Green, and Kelly M. Smith. Muscleperformance and enzymatic adaptations to sprint interval training. J. Appl. Physiol. 84(6): 2138–2142, 1998.—Our purpose was to examine the effects of sprint interval training on muscle glycolytic and oxidative enzyme activity and exercise performance. Twelve healthy men (22 2 yr of age) underwent intense interval training on a cycle ergometer for 7 wk. Training consisted of 30-s maximum sprint efforts(Wingate protocol) interspersed by 2–4 min of recovery, performed three times per week. The program began with four intervals with 4 min of recovery per session in week 1 and progressed to 10 intervals with 2.5 min of recovery per session by week 7. Peak power output and total work over repeated maximal 30-s efforts and maximal oxygen ˙ consumption (VO2 max) were measured before and after thetraining program. Needle biopsies were taken from vastus lateralis of nine subjects before and after the program and assayed for the maximal activity of hexokinase, total glycogen phosphorylase, phosphofructokinase, lactate dehydrogenase, citrate synthase, succinate dehydrogenase, malate dehydrogenase, and 3-hydroxyacyl-CoA dehydrogenase. The training program resulted in signiﬁcant increases in peakpower ˙ output, total work over 30 s, and VO2 max. Maximal enzyme activity of hexokinase, phosphofructokinase, citrate synthase, succinate dehydrogenase, and malate dehydrogenase was also signiﬁcantly (P 0.05) higher after training. It was concluded that relatively brief but intense sprint training can result in an increase in both glycolytic and oxidative enzyme ˙ activity, maximum short-term poweroutput, and VO2 max. Wingate protocol; muscle biopsy; glycolytic enzymes; oxidative enzymes
termed ‘‘sprint training’’ as well as to problems in simulating maximal sprinting efforts with certain animal models. Suggestions that sprint training does not induce increases in muscle enzyme activity are somewhat perplexing, since in most studies in which a performance measure was included suchtraining has been shown to result in an improvement in short-term power output (4, 5, 23, 28). Therefore, we decided to reexamine this issue by investigating glycolytic and oxidative enzyme activity in a group of healthy, physically ﬁt young adults before and after they underwent a program of intense sprint interval training, similar to that previously found to result in enhanced short-term poweroutput (21, 22).
IT IS WELL KNOWN that a program of endurance exercise training can result in signiﬁcant increases in muscle mitochondrial density (14, 15) and oxidative enzyme activity (13, 24) but has minimum effect on glycolytic enzymes (12). In studies with humans and animals, the changes in oxidative enzyme activity are often three- to ﬁvefold greater than the increases observed inmaximal ˙ oxygen consumption (VO2 max) (5, 6, 8) and display a close correlation with improvements in endurance exercise capacity (6). The issue as to whether a program of anaerobic or sprint training can result in an increase in the maximal activity of either glycolytic or oxidative enzymes is somewhat more controversial. Whereas the majority of investigators have noted increases in glycolyticenzyme activity after sprint training (2, 4, 16, 25), some have not (9, 11). Moreover, there are reports in the literature that sprint training has either no effect (4, 17) or a lesser effect (27) on mitochondrial enzyme activity than does endurance training. It is possible that many of these disparities (see Table 1) may be due to the differing intensities and durations of exercise