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The present study examined fasting serum insulin levels in relation to body composition and dietary intake during the initial 4 weeks of a 12-week physical training programme in 26 previously sedentary men. Fasting serum insulin concentrations decreased markedly during the first 4 weeks of training and remained at these reduced levels for the rest of the study. The early fall in serum insulin concentration was significantly correlated with the concomitant decrease in body fat, the increase in lean body weight and the age of the subjects. Body weight and reported dietary intake on the other hand, did not change significantly over this period. These results indicate that the decrease in fasting serum insulin in previously sedentary men with physical training is associated with the concomitant changes in body composition. Increased muscle tissue in particular may contribute to this training-induced decrease in serum insulin.

Twenty-six consecutive patients had measurement of ejection fraction by gated blood-pool imaging at rest and during isometric exercise, following recovery from an uncomplicated myocardial infarction. We found there was a highly significant fall in ejection fraction at rest from 56 +/- 3% to 43 +/- 3% during isometric exercise (p less than 0.0001). There was a dramatic fall in ejection fraction during isometric exercise in some patients with a normal resting value. These patients may be a cause for concern. Our preliminary findings suggest these latter patients are at risk for future cardiac events such as, unstable angina, further myocardial infarction and future coronary bypass surgery.

Twenty-three apparently normal untrained men aged 20--55 participated in a 4-month self-regulated training programme ending in a marathon run. Fasting plasma and lipoprotein lipid concentrations, adipose tissue lipoprotein lipase activity, anthropometric data, alcohol consumption, smoking habits, weekly mileage run and performance on a bicycle ergometer were recorded before and after the training period. Training induced an increase in high density lipoprotein cholesterol (HDL-C) concentration which was not directly related to concomitant decreases in mean very low density lipoprotein cholesterol (VLDL-C) concentration or mean total skinfold thickness. The degree of the changes in VLDL lipids and HDL-C levels were related to pretraining values, and changes in HDL-C and VLDL triglycerides (VLDL-TG) were also associated. Initial total skinfold thickness correlated inversely with the change in VLDL-TG levels during training. The pretaining concentration of VLDL-C was related to the corresponding value for HDL-C after training. The magnitude of exercise-induced changes in VLDL-C and HDL-C levels are more related to pre-training levels than to changes in measured exercise parameters, indices of obesity or adipose tissue lipoprotein lipase activity. However, the level of adiposity of subjects at the beginning of the study influenced the response of VLDL-TG levels to increased physical activity. The data suggest that VLDL contributes to the increase in HDL-C levels with exercise but is not the major source of the increment.

Twenty-three moderately active apparently normal men aged 20-55 participated in a 4-month stamina training programme ending in a marathon run. Fourteen men decreased their training levels and 5 men continued training at the same level in the subsequent 2 months. Fasting lipoprotein lipid concentrations, anthropometric data, performance on a bicycle ergometer, reported values for alcohol consumption, smoking and weekly distance run were recorded at each phase of the study. Both groups of men showed significantly increased levels of plasma triglycerides (TG) and very low density lipoprotein triglycerides (VLDL-TG) during the detraining and continued training period. At the same time, plasma total cholesterol (TC), low density lipoprotein cholesterol (LDC-C) and very low density lipoprotein cholesterol (VLDL-C) increased significantly only in men who decreased their level of training. However, final mean values for plasma lipids and lipoproteins did not significantly differ between the 2 groups of men. It is concluded that levels of plasma lipids and lipoproteins, excepting VLDL-C, do not return to pretraining values during 2 months of detraining.

Four months physical training significantly raised the mean proportions (%) of lauric (+0.64), myristic (+0.52), stearic (+2.06) and linoleic (+1.69) acids and lowered the mean proportions of palmitic (-1.46) and oleic (-3.46) acids in adipose tissue of 20 apparently normal men aged 20-55 yr. These changes were dependent on pretraining proportions of the fatty acids. In addition, the decreases in palmitic acid and oleic acid proportions were positively correlated (rho = 0.905, P less than 0.01, tau = 0.758, P less than 0.01). The pattern of significant correlations among adipose tissue fatty acids was altered as a result of training. We suggest that preferential mobilisation of fatty acids from adipose tissue is responsible for the change in adipose tissue fatty acid composition with increased physical training. The significant increase in adipose tissue linoleic acid proportions may be linked with the reduced risk of coronary heart disease which has been previously associated with increased physical activity.

Plasma post-heparin hepatic lipase (PHHL) activity, plasma lipids, and high density lipoprotein cholesterol (HDL-C) levels, pulse rate at submaximal workload, and body weight were measured in 12 men during the 18 weeks physical training for their first marathon run. Reduced pulse rate at submaximal workload indicated that the men increased their physical fitness during the training period. Plasma HDL-C levels (+27%) and PHHL activity (+29%) also increased significantly after 18 weeks training. These changes were not in accord with the inverse correlation between plasma HDL-C levels and PHHL activity which was observed before training. The results of this study do not support the concept that reduced PHHL activity is mainly responsible for increased levels of plasma HDL-C with training.