Succinate dehydrogenase (SDH) and cytochrome oxidase activities in the lateral vastus of the human quadriceps femoris muscle together with total body VO2 max were followed during an 8-10 week period of endurance training (n = 13) and a successive 6 week period without training (n = 8). During the training period there was a gradual increase in both VO2 max and muscle oxidative enzyme activities, all being significantly different from the pre-training levels after 3 weeks of training. After 8 weeks of training VO2 max was 19%, vastus lateralis SDH 32%, and cytochrome oxidase activity 35% above the pre-training levels respectively. 6 weeks post training VO2 max was still 16% above the pre-training level, and not significantly different from the level at the end of training (p greater than 0.2). In contrast vastus lateralis SDH activity had returned to the pre-training level. Cytochrome oxidase activity had returned to the pre-training level within two weeks post-training. The significantly faster post-training decline in skeletal muscle oxidative enzyme activities in contrast to that of the VO2 max indicates that an enhancement of the oxidative potential in skeletal muscle is not a necessity for a high VO2 max. Moreover, the fast return to the pre-training level of both SDH and cytochrome oxidase activities indicate a high turnover rate of enzymes in the TCA cycle as well as the respiratory chain.

The effect of 7 to 8 weeks of physical training on oxidative and glycolytic enzyme activities in the 2 major fibre types of human quadriceps femoris muscle has been investigated. 2 groups of 4 and 5 subjects respectively were trained at the same total work-load on a bicycle ergometer 3 days per week using interval exercise with maximal intensity (I.T.) or continuous exercise with submaximal intensity (C.T.). Succcinate dehydrogenase (SDH) and phosphofructokinase (PFK) activities were determined on crude homogenates of muscle biopsy samples and on pools of type I and type II fibres dissected from freeze-dried samples taken before and after training. Crude homogenate SDH activity increased to the same extent in both groups, average increases were 27.5% (I.T.) and 22% (C.T.) respectively. Only type I-SDH increased in the C.T. group (p less than 0.01), the average increase being 32%. On the other hand only type II-SDH increased in the I.T. group (p less than 0.01), with an average increase of 49%. No changes in PFK activity could be detected. The results of the present study emphasize the great adaptability in oxidative potential of both the two major human skeletal muscle fibre types and further that this adaptation seems to be related to the pattern of fibre recruitment during exercise.

Six obese patients with recent-onset, non-insulin-dependent diabetes underwent assessment of glucose tolerance, insulin secretory capacity, and insulin-induced glucose disposal before and after 6-10 wk of intensive aerobic training while maintaining body weight. Fasting plasma glucose declined in every subject (average = -33 mg/dl), and oral glucose tolerance (3 h integrated plasma glucose) improved in five of the six (average = -74 mg X 3 h/dl) after training. Individual improvement in control of plasma glucose was directly proportional to degree of hyperglycemia before training and correlated well with an observed improvement in the early (30-min) plasma insulin response to oral glucose (all six subjects). The response of insulin action to training was highly variable; although the observed increase in average insulin-induced glucose disposal rate (M) during the euglycemic clamp did not reach statistical significance in our small cohort, the relative change in M was directly related to reduction in fasting insulin levels after training. Our results show that regular endurance exercise is effective in improving glucose homeostasis and may serve as an adjunct to other modes of treatment in recent-onset, non-insulin-dependent diabetic individuals.