1. Ten male subjects were cooled on three occasions to a rectal temperature of 35°C by immersion to the neck in water at 11·3°C. The subjects were rewarmed for 60 min, once by metabolic heat production alone (shivering), once by inhalation rewarming with spontaneous breathing of saturated air at 47°C (control) and once by inhalation rewarming with ventilation regulated at 40 litres/min by respiring a controlled fraction of CO 2 (hyperventilation). 2. Metabolic heat production was substantially reduced by inhalation rewarming ( P < 0·05), from 913 kJ when shivering to 766 kJ (control) and 613 kJ when hyperventilating. The fall in metabolic heat production was greater than the corresponding respiratory heat gain, which increased from a loss of 41 kJ when shivering to gains of 85 kJ (control) and 169 kJ (hyperventilation). 3. As differences in mean skin temperatures were small (<1·0°C), it is concluded that the lower metabolic heat production in response to increased respiratory heat input must result from more rapid central temperature gains. This conclusion is supported by the relative values of rectal and tympanic temperatures. It was calculated that the percentage of the total heat supply which was donated to the core increased from 13% during shivering to 16% for the control and 23% in hyperventilation. Results imply that respiratory heat input is more efficient than metabolic heat production in elevating central temperature.

1. The present experiments were designed to elucidate the reasons for the fall in central body temperature during hypoglycaemia. 2. The first experiment was carried out at a room temperature of 25 °C on 11 male subjects. Hypoglycaemia was induced by infusion of insulin. Heat production (calculated from respiratory gas exchange) rose from a baseline of 5.10 ± 0.13 kJ/min (mean ± sem ) to a peak of 6.25 ± 0.21 kJ/min ( P < 0.001), but core temperature fell concurrently by 0.51 ± 0.08°C and skin temperature fell by 1.1 ± 0.2°C. The net heat loss was due to peripheral vasodilatation and sweating. 3. To determine the effect of insulin-induced hypoglycaemia on thermoregulation in a cool environment, the experiment was repeated at a room temperature of 18–19°C on five of the subjects who had air blown over them until shivering was sustained. During this time heat production rose to 10.13 ± 1.67 kJ/min, but core temperature remained constant. Shivering stopped as plasma glucose fell below 2.5 mmol/l during insulin infusion and the subjects said they no longer felt cold. 4. During hypoglycaemia in the cold peripheral vasodilatation and sweating occurred, skin temperature fell by up to 0.8°C and core temperature fell below 35°C, so subjects had to be rewarmed. 5. Recovery of plasma glucose after hypoglycaemia in the cold was impaired at low body temperatures, but shivering was restored within seconds when glucose was given intravenously.

1. Hypothermia to a temperature of 30°C was induced in both shivering and non-shivering groups of dogs. 2. There was a sustained increase in oxygen consumption in the dogs allowed to shiver and this was up to 300% greater than the oxygen consumption in the relaxed dogs. 3. The increased tissue requirement for oxygen was met both by increased cardiac output and increased oxygen extraction from haemoglobin. 4. Oxygen utilization remained adequate in hypothermia, as shown by the absence of hypoxic acidosis. 5. Heart rate fell during cooling and stroke volume increased to meet the increased oxygen demands associated with shivering during the induction of hypothermia.

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.