Abstrakt
The literature clearly documents the existence of nonshivering thermogenesis of adrenergic origin in adult humans. This thermogenesis is activated in cold exposed individuals, during the early phase of cooling, prior to shivering and equals to about 25% of the basal MR (0.29 W kg-1).
This amount of heat can compensate for the heat loss from the body when the air temperature is about 5oC below the thermoneutral zone. Human nonshivering thermogenesis is probably based on thermogenic actions both of adrenaline and noradrenaline.
Relative participation of adrenaline or noradrenaline in the thermogenic response is not known and the mode of action of the amines may differ. Adrenaline themogenesis, in contrast to noradrenaline thermogenesis, can be potentiated by cold adaptation to the level corresponding to the total capacity of β-adrenergic (isoprenaline) thermogenesis (0.58 W kg-1).
Adrenaline thermogenesis is located in skeletal muscles and probably also in white fat. Diffused brown fat cells present in white fat pads may be also involved, however.
Although several molecular mechanisms have been suggested, the discrete mode of catecholamine thermogenic action in organs other than the brown adipose tissue remains unknown. Participation of various subtypes of adrenoceptors and uncoupling proteins must be considered, although the direct evidence for their involvement in human adrenaline thermogenesis is still lacking.
Thus the cellular mechanisms of human nonshivering thermogenesis may differ from those found in small mammals. Physiological regulatory mechanisms, namely changes in the blood flow, could be involved in inducing adrenergic thermogenesis in human muscle.
Thus, the regulation of MR by catecholamines may not be solely dependent on biochemical mechanisms related to the uncoupling of oxidative phosphorylation but may also rely on physiological processes.