Inactivity and excessive and inappropriate caloric intake stimulate development of visceral obesity that is associated with increased risks of type 2 (non-insulin-dependent) diabetes, hypertension, and coronary heart disease (CHD). Both exercise and dietary restriction have been successfully used as a means of body fat loss. In addition, exercise, with or without fat loss, can reduce risks of diabetes, hypertension, and coronary heart disease but its effects have not been consistent. In particular, there is little consensus regarding the effects of exercise intensity on either body fat loss, insulin sensitivity, or risks of hypertension and CHD. Our premise is that if exercise is to be used effectively to prevent or reduce different health risks or to be used as a tool in mechanistic analyses of hormone action, a better understanding of dose-dependent effects of exercise intensity is needed. Our pilot study, initiated two years ago, focused on the question of whether exercise training at high walking intensities could increase basal pulsatile growth hormone (GH) secretion. This hypothesis was supported by our results (8,9), but in addition, we discovered that exercise intensity bears an inverse relationship to body fat loss (assessed by indirect, anthropometric methods), has an apparent diabetogenic effect (assessed with an indirect measure of insulin sensitivity), and is associated with increased androgenic action (ratio of plasma testosterone to sex-hormone-binding globulin, SHBG). Since all three observed changes, the accumulation of visceral body fat (6,44), GH oversecretion, and increased androgenic index (47), either antagonize insulin action (GH oversecretion) or are accompanied by increased risk of diabetes, hypertension, and CHD (high androgenic index and increased postprandial insulin response), our results suggested that exercise intensity during 15 weeks of training had a deleterious effect on at least two risk factors: it was inhibitory to body fat loss and to peripheral sensitivity to insulin. These serendipitous observations redirected our interest from the role of exercise in alleviating somatopause, the exponential decline in spontaneous GH secretion with age, to the mechanism by which exercise intensity affects insulin resistance, hypertension and CHD in postmenopausal women.
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