We studied the effect of aerobic training and detraining on insulin-stimulated glucose disposal and on erythrocyte insulin receptor binding. Seven endurance-trained athletes were studied at 12 h, 60 h, and 7 days after cessation of training and compared with three untrained, age- and weight-matched controls. The metabolic clearance rate of glucose as measured by the euglycemic clamp technique was 15.6 +/- 1.8 ml/kg/min (mean +/- SEM) in the trained subjects 12 h after the last bout of exercise compared with 7.8 +/- 1.2 ml/kg/min in the untrained control group. When the trained subjects refrained from physical training, the metabolic clearance rate decreased to 10.1 +/- 1.0 ml/kg/min at 60 h and further to 8.5 +/- 0.5 ml/kg/min after 7 days of detraining. The percentage of specific insulin binding to young erythrocytes (density 1.089-1.092), isolated by density gradient centrifugation, decreased from 10.4 +/- 0.9 at 12 h after the last exercise to 8.1 +/- 0.7%/3 X 10(9) cells after 60 h of detraining (P less than 0.001). The decrease in insulin binding to erythrocytes was almost entirely accounted for by a decrease in the number of insulin receptors. We conclude that the increase in peripheral insulin action seen in trained athletes is rapidly reversed, possibly by a mechanism separate from other phenomena associated with chronic training. The parallel findings of decreased in vivo insulin action and decreased insulin binding in young erythrocytes suggest that modulation of in vivo insulin response by detraining may be at least partially mediated by changes in insulin receptor number.(ABSTRACT TRUNCATED AT 250 WORDS)

The present study was undertaken to examine the energy cost of prolonged walking while carrying a backpack load. Six trained subjects were tested while walking for 120 min on a treadmill at a speed of 1.25 m.s-1 and 5% elevation with a well fitted backpack load of 25 and 40 kg alternately. Carrying 40 kg elicited a significantly higher (p less than 0.01) energy cost than 25 kg. Furthermore, whereas carrying 25 kg resulted in a constant energy cost, 40 kg yielded a highly significant (p less than 0.05) increase in energy cost over time. The study implies that increase in load causes physical fatigue, once work intensity is higher than 50% maximal work capacity. This is probably due to altered locomotion biomechanics which in turn lead to the increase in energy cost. Finally, the prediction model which estimates energy cost while carrying loads should be used with some caution when applied to heavy loads and long duration of exercise, since it might underestimate the actual energy cost.

An increase in endogenous androgen production has been observed following long-term physical training and the beneficial effects of training have been attributed in part to this phenomenon. Other investigators, however, found, in contrast lower testosterone levels in trained compared with untrained subjects. The purpose of the present study was to follow the long-term changes in total testosterone (T) and cortisol (C) levels in intensely training individuals. The changes in the body's anabolic state, induced by intense long-term physical training, were determined using the plasma resting T/C ratio. T and C levels of 35 young untrained subjects were measured at 6 week intervals during 18 weeks of strenuous physical training. All samples were drawn within one half hour of awaking (05.30-06.00). Mean serum T levels increased significantly at 6 weeks (28.7%, p less than 0.02) and decreased significantly at 12 weeks (20.6%, p less than 0.02), but did not differ at 18 weeks compared with levels before training was commenced (mean +/- SE, 16.9 +/- 0.2, 21.8 +/- 0.3, 12.8 +/- 0.2 and 17.3 +/- 0.2 nmol/l at 0, 6, 12, and 18 weeks, respectively). Mean serum C was increased significantly (21.3%, p less than 0.005) at 18 weeks (463.5 +/- 19.3, 507.7 +/- 22.1, 480.1 +/- 19.3, and 565.6 +/- 22.1 nmol/l). T/C ratio decreased significantly after 12 and 18 weeks of training. Our results do not support an association between reduced total testosterone levels and prolonged training. However, hypercorticolism with a relative catabolic state may occur.

The effect of acute exercise on insulin action has been studied in six obese (150-250% ideal body weight) non-insulin-dependent diabetics (OD), seven obese normoglycemics (ON), and six lean healthy controls (LC). Using a three-stage euglycemic clamp, the metabolic clearance rate (MCR) of glucose under increasing insulin concentrations was measured. The insulin dose-response curve was assessed on two separate occasions: 1) a base-line test and 2) 1 h after aerobic treadmill exercise at a steady-state heart rate of 150-160 beats/min. In the base-line test, under all insulin levels, glucose MCR was significantly lower in obese compared with lean individuals (P less than 0.01). Exercise increased glucose MCR at the highest hormonal concentrations applied to 124 and 134% of base line in OD and in ON, respectively (P less than 0.05); the insulin concentration required for one-half of the maximal clearance rate of glucose achieved in this study decreased from 200 to 130 and from 160 to 95 microU/ml in OD and ON, respectively (P less than 0.05). The changes in these parameters were insignificant in LC. It is suggested that acute exercise affected the insulin dose-response curve in OD and in ON but not in LC; although enhanced by exercise, glucose MCR remained significantly lower in both obese groups compared with control subjects. We concluded that insulin resistance, which accompanies extreme obesity, could be markedly decreased but not completely reversed by one bout of exercise.