suggested that deep cooling might be of little importance in practice. However, it has been reported (Keatinge, 1960 a) that although the rate at which men's rectal temperatures fell in water at 150 C was closely related to their subcutaneous-fat thickness, their early metabolic response to the cold immersion was not, and the metabolic rates of thin men only rose substantially above those of the fat men during the later part of immersions, when the thin men's rectal temperatures fell. The present studies of fat and thin men in a steady state of heat exchange in water were designed partly to confirm or refute this evidence that stimulation of deep temperature receptors plays a major part in adjusting the metabolic rates of fat and thin men to their different rates of heat loss during prolonged exposures to cold. They were also designed to show whether fat and thin men have different critical ambient temperatures, at which physical temperature regulation is complete and below which the metabolic rate is increased (Rubner, 1902;Burton & Bazett, 1936;Scholander, Hock, Walters, Johnson & Irving, 1950).It was hoped that these experiments would also show whether cold vasodilatation substantially reduced the tissue insulation of fat men in near-freezing water. This seemed probable, as cold vasodilatation takes place eventually in cold extremities of even generally chilled people (Keatinge, 1957) and appears to be due largely to the direct effect of low temperatures on blood vessels (Keatinge, 1958). Physical exertion accelerates the fall in the rectal temperature of thin men in water at 160 C (Pugh & Edholm, 1955) and in water at 5 and 15°but not at 25 or 350 C

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