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Thyroid hormones were measured before, during and after acute exercise (60 min) or physical training (3 months) in obese women. Thyroid stimulating hormone concentration increased during acute work and decreased immediately after. No changes were seen during the two following days. An increase was seen after ten days as well as after three months of physical training. Thyroxine concentrations showed no changes. 3,5,3'-Triiodothyronine decreased slightly immediately after acute exercise, and after three months of physical training, 3,3',5'-triiodothyronine (reverse triiodothyronine) increased slowly during and after acute exercise. A negative correlation was found between changes in fasting insulin and thyroxine and a positive correlation between changes in blood pressure and triiodothyronine after training. Lack of agreement in previous reports is probably due to methodological differences such as methods more or less susceptible to fatty acid interference, and thyroid hormones changing differently during acute work and before and after physical training. The duration of the study may also be of importance, even 3 months possibly being too short for attaining equilibrium in thyroid homeostasis.

The purpose of this study was to determine, in exercising patients, how much diaphragm force increases before electromyographical evidence of diaphragm fatigue occurs. The study was performed in ten male patients with complete cervical cord injury (CCI) at the C5 to C8 levels, and five male patients with prior poliomyelitis infection (PPI) requiring chronic treatment with intermittent positive pressure ventilation (IPPV) at night. We studied the time course of the diaphragmatic tension-time index (TTdi), the centre frequency (CFdi) of the diaphragm electromyogram (EMGdi) power spectrum, and the ventilatory parameters, during steady-state submaximal arm/leg exercise. During exercise, early signs of diaphragm fatigue were present in seven out of 10 CCI patients and in four out of five PPI patients, as indicated by a reduction in CFdi. The increase in TTdi achieved before reductions in CFdi occurred was twofold in both the CCI and PPI patients. All patients except for the PPI patients, who demonstrated a reduction in CFdi, showed an increase in minute ventilation (VE), achieved by increasing both their tidal volume (Vt) and the breathing frequency (fb). The PPI patients demonstrating reductions in CFdi during exercise also increased their VE however, this was achieved by increasing fb while Vt remained constant. Following the reductions in CFdi, the CCI patients further increased their TTdi throughout the exercise test, while the PPI patients reduced their TTdi values.(1) During exercise, electromyographical evidence for diaphragmatic fatigue frequently occurred in the CCI and PPI patients studied; (2) Compared to the eightfold increase in TTdi seen in healthy subjects before reductions in CFdi occur, the TTdi values increased only two-fold before electromyographical evidence of diaphragm fatigue was present in these patients; (3) There is a clear discrepancy between the CCI and PPI patients who demonstrate electromyographical evidence of diaphragm fatigue, in terms of their ventilatory and TTdi responses.

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.

Centrally mediated sympathetic stimulation of subjects who have suffered a spinal cord injury (SCI) does not activate the decentralized part of the body below the level of the lesion, whereas experimental data indicate an exaggerated response above the level of the lesion. SCI subjects may exhibit an autonomic dysreflexia reaction following afferent stimulation below the level of the lesion. In order to investigate the function of the sympathetic nervous system above and below the level of the lesion, regional noradrenaline spillover was measured by means of steady-state isotope dilution technique above (forearm) and below (leg) the level of the lesion at baseline, during mental stress and following bladder stimulation in nine SCI subjects (mean age 41 years; level of injury C7-T4; mean duration of injury 13.8 years). The results from the SCI subjects were also compared with those from 10 weight- and age-matched control subjects, both at rest and during mental stress. Body composition was determined by dual energy X-ray absorptiometry scanning and arm/leg blood flow by occlusion plethysmography. At baseline, total and regional noradrenaline spillover did not differ between the groups. Mental stress increased mean arterial pressure in both groups. Heart rate (76 versus 64 beats/min; P < 0.05) and arm noradrenaline spillover (2.73 versus 1.71 pmol/min/100 g; P < 0.05) increased more in spinal cord injury subjects than in control subjects, whereas total body (2826 versus 3783 pmol/min; P < 0.01) and leg noradrenaline spillover (0.23 versus 0.41 pmol/min/100 g; P < 0.05) increased only in the control group. During bladder stimulation, SCI subjects reacted with a marked increase in mean arterial pressure and leg noradrenaline spillover (from 0.06 to 0.91 pmol/min/100 g; P < 0.05) and their leg blood flow decreased. Regional and total noradrenaline clearance were similar in the two groups. In conclusion, peripheral afferent stimulation below the level of the lesion in spinal cord injury subjects gives rise to a marked noradrenaline spillover from the decentralized part of the sympathetic nervous system suggesting a remaining, but qualitatively altered, neuronal function. Centrally mediated stimulation induced an exaggerated response above the level of the lesion.

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.

To evaluate the regulation of lipolysis by the sympathetic nervous system, eight spinal cord-injured (SCI) subjects with a lesion above T5 resulting in a decentralization of the lower-body sympathetic nervous system and adrenal medulla (age, 36 +/- 2 years; weight, 82 +/- 5 kg; body fat mass, 26.8 +/- 3.0 kg; all mean +/- SE) and nine control subjects (age, 33 +/- 2; weight, 80 +/- 3; NS; body fat mass, 16.1 +/- 1.5 kg; P.01) were investigated after fasting overnight. Each subject was studied with subcutaneous microdialysis and 133Xe-clearance adipose tissue blood flow (ATBF) in the umbilical and clavicular regions during postabsorptive rest and after sympathoexcitatory stimulation by means of mental stress and isometric handgrip exercise. SCI subjects had an increased body fat mass, hyperinsulinemia, and an elevated lipolytic rate at rest compared with control subjects. ATBF and lipolysis were activated to a normal extent following mental stress and isometric handgrip exercise in the umbilical region in control subjects. ATBF was increased in tissue above but not below the lesion level in SCI subjects following mental stress. Glycerol release was not different between groups in either tissue region despite significantly lower noradrenaline and adrenaline levels in SCI subjects. This finding argues against a significant adrenergic control of the lipolytic rate at rest. Furthermore, the small differences in stimulated glycerol release between groups, as well as the increased plasma glycerol levels in SCI subjects, cast doubt on the view that interruption of adrenergic activity below the lesion is the sole mechanism underlying the increased body fat mass in SCI subjects.

We administered capsaicin, a neurotoxic substance causing a reversible suppression of C fiber afferent neuronal activity, in an attempt to decrease bladder hyperreflexia.Capsaicin solution (2 mM.) dissolved in 30% alcohol was instilled into the bladders of 10 men with traumatic chronic spinal lesions and left in place for 30 minutes. Effects on bladder function, including response to cold stimulation, were recorded during treatment, immediately after instillation and at followup.Bladder function improved in all but 1 patient, which was expressed as an increase in cystometric capacity and/or a decrease in maximal detrusor pressure. The effects lasted for 2 to 7 months. Immediately after capsaicin administration the ice water test was negative in half of the patients.The positive effects on bladder function of capsaicin treatment can be explained by the blocking of C fiber afferents. The optimum dose and treatment interval are presently not established. The ice water test might possibly be used as an instrument to monitor the ideal dosage.

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.

Severely obese subjects and sex- and age-matched controls underwent 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.

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.

Blood coagulation, fibrinolysis and platelet function before and after a maximal work load was investigated in a group of obese subjects compared to age and sex matched controls. At rest the obese subjects had higher plasminogen, total antifibrinolytic activity, fibrinogen and factor II-VII-X activity than the controls. After maximal work the increase in fibrinolytic activity was less pronounced in obese than in controls both in the euglobulin fraction and in whole plasma. After stasis of the arm the increase in fibrinolytic activity in the euglobulin fraction was as high in obese as in controls but in whole plasma it tended to be lower in obese than in controls. Factor II-VII-X activity increased and recalcification time of citrated plasma decreased significantly more after a maximal work load in the controls than in the obese. Hematocrit also increased significantly more after exercise in controls than in obese. Both groups worked at a maximal level as evaluated from heart rate and oxygen consumption. Five of the obese subjects were trained physically for 7 months. After the training period the increase in hematocrit and factor II-VII-X after a maximal work load were almost as great in the obese as in the untrained controls. The insufficient increase of fibrinolysis, however, persisted. The less pronounced increase in fibrinolysis after exercise in the obese is probably partly due to a higher concentration of plasma-antifibrinolytic activity, but this cannot be the only explanation. Differences in serum lipids is, however, not decisive.

The explanatory value of total fat cell number, resting metabolic rate, mean heart rate during sleep, and peripheral insulin while seeing and smelling food were examined in relation to weight reduction in 19 obese women on a 1100-kcal/day diet. The insulin response while seeing and smelling food was expressed as the insulin area (mU · min · 1−1) over the baseline level. Food was presented in front of the patient for 5 min. Insulin was determined in short intervals 20 min before and 20 min after start of food presentation. Fat cell number, resting metabolic rate, and mean heart rate during sleep were determined with standard techniques. All patients went through a period of weight loss, a plateau phase, and a period of weight regain. Body weight, fat cell number, resting metabolic rate, and/or heart rate correlated significantly with degree and rate of weight loss, duration of plateau phase, and rate of regain. In multiple regression analysis fat cell number and resting metabolic rate explained 81% of the variance for weight loss, 66% for rate of regain, and 29% for duration. For duration, only fat cell number contributed significantly. The variance of rate of weight loss was explained up to 49% by metabolic rate and insulin response while seeing and smelling food. The possibility of predicting weight reduction to a certain target weight is of great practical importance since the patients can obtain a realistic goal for their efforts to reduce body weight. Hopefully systematic investigations of factors associated with the inability of obese subjects to maintain weight reduction will improve treatment in the future.

This chapter examines the value of physical training programmes in the prevention and management of obesity and its commonly associated conditions, including diabetes, hypertension and vascular disease. Physical exercise can be divided into two main types. One of these is largely static, engaging anaerobic pathways and muscle fibres of the white type rich in glycogen. Glucose is utilized and lactate is produced. The kind of athletic activity typical of this type of exercise is weight-lifting, short-distance running and wrestling. The other type of exercise is more dynamic; it involves the aerobic pathways and muscle fibres richer in aerobic enzymes and myoglobin. More fat substrate is utilized for energy purposes. The typical athletic activities here are the long-term, long-distance competitions, for example, running, swimming or cycling.

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.

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 aerobi...