Lars Sullivan

The effect of physical training on insulin production in obesity

Abstract Ten obese patients were subjected to physical training, which resulted in an increased maximal oxygen consumption and an increased isometric muscle strength. Body weight increased, due primarily to an increase in body fat, but also, in some cases, to an increase in body cell mass, determined by isotope dilution techniques. Fat cell diameter was unchanged. Peroral glucose tolerance test with plasma radioimmuochemically determined insulin in these patients showed no changes in blood glucose values after training but a marked decrease in insulin values. This was interpreted to be due to an increased insulin sensitivity of tissues. Since the body fat mass was not decreased it was not considered likely that the increased insulin sensitivity was due to adipose tissue factors. This augmentation of insulin sensitivity was furthermore not related to the increase in body cell mass and therefore probably not to an increase in muscle mass. It was concluded that muscle probably is an important determinant for insulin sensitivity in obesity.

Effects of long-term physical training on body fat, metabolism, and blood pressure in obesity.

Twenty-seven women with varying degrees of obesity were physically trained for 6 mo on an ad lib. diet. Body fat changes were positively correlated with the number of fat cells in adipose tissue. Obese women with fewer fat cells decreased in weight during training whereas women with severe obesity and an increased number of fat cells even gained weight. Blood pressure decreased consistently after training. Blood pressure elevation was not associated with body fat mass, nor was a decrease in blood pressure associated with a decrease in body fat or with pretraining blood pressure level. There were, instead, correlations between decreases in blood pressure on the one hand and initial concentrations and decreases in plasma insulin and triglycerides and blood glucose on the other. These results suggest an association between elevated blood pressure and metabolic variables. The possibility of treating and preventing early essential hypertension with methods that also correct the metabolic derangement, such as diet and exercise, should be given high priority in further research.

Influence of the sympathetic nervous system on insulin sensitivity and adipose tissue metabolism : a study in spinal cord-injured subjects

To evaluate insulin sensitivity and adipose tissue metabolism, seven spinal cord-injured (SCI) subjects (age, 43 +/- 6 years; body mass index, 22.8 +/- 1.4; mean +/- SE) and their seven siblings (age, 45 +/- 6 years; body mass index, 24.8 +/- 0.8) were studied using oral glucose (100-g) tolerance tests (OGTTs), euglycemic insulin clamps (insulin infusion, 1 mU/kg.min), and microdialysis of the subcutaneous tissue. Blood glucose and insulin after oral glucose were significantly increased in SCI subjects as compared with their siblings. During insulin clamping, plasma adrenaline increased significantly in controls, but not in SCI subjects. However, the rates of glucose production (2.02 +/- 0.36 v 1.59 +/- 0.09 mg/kg.min) and utilization (5.13 +/- 0.71 v 5.78 +/- 0.34) were similar in the two groups. Furthermore, interstitial subcutaneous glycerol and lactate concentrations before and after oral glucose were similar in the two groups, even in neurally decentralized tissue with broken connection between the central nervous system and peripheral sympathetic nerves. The data suggest that (1) well-mobilized SCI subjects show minor insulin resistance, and (2) sympathetic nervous activity has a minor influence on adipose tissue metabolism in the postabsorptive state, but may affect insulin sensitivity during euglycemic clamping.

Physical training in human hyperplastic obesity. IV. Effects on the hormonal status

Severly obese subjects and sex- and age-matched controls underwnet physical training during a 6-wk period. Evidence of training was shown in all subjects by increased aerobic power. Before training the obese subjects were characterized by the following abberations: decreased glucose tolerance, hyperinsulinemia, elevated blood glycerol and plasma free fatty acids, and a blunted plasma growth hormone response during glucose tolerance. Noradrenaline output was elevated, a finding of potential interest for the explanation of increased lipolysis, blood pressure, and heart size in obesity. With training the following changes were found:In the controls there was evidence for the beginning of a decrease of adipose tissue mass. In the obese, however, body weight, body fat, or fat cell size did not decrease during training. Plasma insulin decreased, and a corresponding increase of plasma glycerol was seen. Glucose tolerance was not changed, and this, together with decreased plasma insulin, indicated an increase insulin sensitivity of the periphery. Changes in noradrenaline or growth hormone during training could not explain this increased sensitivity. Urinary cortisol output was found to decrease after training in the obese; this might be interpreted as a decrease in cortisol secretion allowing a more effective insulin action on the periphery.

Physical Training in Human Obesity II. Effects on Plasma Insulin in Glucose-Intolerant Subjects without Marked Hyperinsulinemia

Five severely obese subjects with decreased glucose tolerance but without marked hyperinsulinemia were trained physically, producing a slight circulatory adaptation and an increase in muscle aerobic enzyme activity. The patients ate ad libitum, and no decrease of body fat was found after training. Glucose tolerance did not change. Fasting plasma insulin, as well as the sum of insulin values, decreased after an intravenous glucose tolerance test, but not after a peroral glucose tolerance test. Excretion of 17-ketogenic steroids was unaltered. It was concluded that physical training can cause a decrease in plasma insulin in glucose-intolerant patients without marked hyperinsulinemia, concomitant with minor effects on oxygen transport system, and no effects on body fat, glucose tolerance, enteric insulinogenic factors, and 17-ketogenic steroid excretion.

Physical training in human obesity. III. Effects of long-term physical training on body composition

Abstract Eight severely obese patients with adipose tissue hypercellularity, elevated body cell mass, and a juvenile onset of obesity were subjected to physical training during 6 mo without dietary restrictions. The training program was of 35-min duration three times weekly and followed a fixed schedule individualized to the working ability of each subject, so that the heart rate was 10–15 beats below maximal during three 5-min periods of each training session. Body weight, body cell mass, and body fat showed no significant changes after 3 or 6 mo of training. Fasting plasma insulin decreased after 3 mo of training, but fasting blood glucose was not changed. After 6 mo plasma insulin values were still decreased. Now glucose tolerance had also improved, and plasma triglycerides showed a trend to lower values. The results suggest that the lack of body fat decrease after the long training period might be characteristic for subjects with the type of severe obesity studied, because in a previous study 1 a similar, although lighter, training procedure produced a marked body fat decrease in patients without severe obesity.

Peripheral afferent stimulation of decentralized sympathetic neurons activates lipolysis in spinal cord-injured subjects

Spinal cord-injured (SCI) subjects exhibit a normal lipolytic rate despite the failure of centrally mediated sympathoexcitatory stimuli to activate lipolysis. Peripheral afferent stimulation below the lesion level induces an exaggerated autonomic reaction in SCI with lesion levels above T5, ie, so-called autonomic dysreflexia. The metabolic effects of induced dysreflexia were investigated in five SCI subjects (age, 35 +/- 8 years; duration of paresis, 15 +/- 7.5 years [mean +/- SD]; lesion level, T3 to T4, n = 2, C7, n = 3) following bladder stimulation. Subcutaneous glycerol concentrations were measured by microdialysis above and below the lesion level. Diurnal plasma noradrenaline (NA) and adrenaline levels were continuously monitored in seven SCI subjects (lesion level T3 to T4, n = 2; C4 to C7, n = 5). Bladder stimulation resulted in an increased mean arterial pressure ([MAP] 81 +/- 8 to 114 +/- 11 mm Hg, P < .05), a decreased heart rate (70 +/- 3 to 54 +/- 4 beats/min, P < .05), and an increased plasma NA (0.70 +/- 0.49 v 3.27 +/- 1.56 nmol/L, P < .05). Interstitial glycerol was increased in the decentralized region (89 +/- 12 to 135 +/- 21 mumol/L, P < .05), whereas no reaction was found in the centrally innervated region. Plasma concentrations of glycerol and insulin increased. Diurnal monitoring showed periods of increased plasma NA sufficient to induce lipolysis (> 1.4 nmol/L) during 20% of the registration period. The data suggest that peripheral afferent stimulation below the lesion level increases NA release and activates lipolysis and that frequent episodes of activation are found in SCI subjects with tetraplegia or high paraplegia.