1. Gluteal adipose tissue was examined in 13 patients with generalized adiposis dolorosa, a clinical condition characterized by painful adiposity with a chronic intractable course. The total metabolic activity of fat cells, isolated by collagenase and suspended in Krebs-Ringer bicarbonate buffer with glucose and insulin, was assessed by the measurement of heat production at 37°C using microcalorimetry. 2. Fat cells were markedly enlarged; their metabolic activity expressed in terms of μW/g, but not in pW/cell, was significantly decreased when compared with both lean and weight-matched non-painful subjects. Both mean values were, however, significantly higher than in grossly obese subjects with similar mean cell size. Heat production as expressed per g of tissue, but not per cell, was inversely correlated with body mass index. One additional patient had unilateral disease, and fat cells from the painful side had a lower heat production than cells from the unaffected side. 3. The fatty acid composition of adipose tissue, as determined by g.c., revealed a significantly increased proportion of monounsaturated (18:1 and 16:1) at the expense of saturated (14:0 and 18:0) fatty acids compared with healthy control subjects. The activity of adipose tissue lipoprotein lipase was slightly, but not significantly, decreased. 4. It is concluded that a metabolic pathogenetic factor cannot be ruled out in adiposis dolorosa. As the results do not explain the nature of the diffuse pain, further studies need to be performed.

1. The influence of β-adrenoceptor-blockade on skeletal muscle was studied in ten healthy males with propranolol, atenolol and pindolol randomly given for 8 days each in a cross-over double blind test. After 7 days on each drug, muscle function was tested by an isokinetic dynamometer. Thermogenesis in biopsy samples taken from vastus lateralis muscle after a low grade exercise was studied after 8 days on each drug by direct calorimetry with a perfusion microcalorimeter. 2. Before drug administration, a median heat production rate of 0.67 mW/g of muscle was measured. This value was significantly reduced by 25% during propranolol, but no significant change was found during atenolol or pindolol administration. 3. Peak torque decline during isokinetic endurance test changed significantly in knee flexor but not in extensor muscles, from 15% to 27% after propranolol and from 15% to 23% after pindolol. Maximum dynamic strength was unaltered. 4. Our data suggest that blockade of sympathetic β 2 -receptors decreases thermogenesis in human skeletal muscle and impairs isokinetic endurance.

1. Different microcalorimetric techniques have been compared for the assessment in vitro of the total metabolic activity of resting skeletal muscle. Human fibre bundles were suspended in Krebs-Ringer-phosphate buffer containing glucose and insulin and the heat evolution was continuously monitored for 2–6 h. Palmitate as substrate was also tested. 2. The power signals declined rapidly when a static calorimetric method (A) was used. Two different perfusion methods (B, C) gave higher power values. Long-lasting steady states were observed with method C, where the sample was contained in a cage acting as a stirrer. 3. Significant differences were found for fibre bundles from different human muscles as well as age- and sex-related differences. The heat production in samples from the rectus abdominis muscle (method B), 0.73 mW/g muscle wet wt., was significantly higher than for the obliquus internus muscle, 0.44 mW/g, and the vastus lateralis muscle, 0.55 mW/g, but not different from the heat production value of vastus medialis, 0.66 mW/g. 4. In method C particularly, the fibre bundles are believed to be in adequate contact with the surrounding medium. With the use of a multichannel calorimeter it is possible to perform up to four experiments simultaneously, e.g. involving the calorigenic effects of pharmacological substances. The technique provides a new approach for detailed studies of muscle metabolism in physiological and pathological conditions.

1. Twenty lightly anaesthetized dogs were cooled to 29°C by cold-water immersion. Ventilation was spontaneous and the animals were allowed to shiver freely. Metabolic heat production and respiratory heat exchange were measured during rewarming. 2. The animals were divided into four groups each of five dogs and each group was rewarmed by a different technique. The control group was allowed to rewarm spontaneously; a second group was given warm (45–50°C) fully humidified air to breathe in addition; a third group was rewarmed in a hot-water bath (42–44°C) and the remaining group was given a muscle relaxant to abolish shivering and rewarmed by warm inspired air only. 3. The group rewarmed in hot water achieved normal core temperature most rapidly but there was no difference in the rewarming rates of the group rewarmed spontaneously and of the group given warm air to breathe in addition. 4. The group given a muscle relaxant and rewarmed with warm inspired air required 12 h to achieve the same core temperature as the shivering groups achieved in 2 h. Compared with the heat produced by shivering the amount of heat which it was possible to transfer across the respiratory tract was so small that it did not materially influence the rate of rewarming.