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Fluctuations in the skin temperature of volunteers in water, of up to +/- 1.5 degrees C, were induced by circulating water through a tube suit at a fluctuating temperature for 80 min. Fluctuations with a cycle length of 2.5, 5.0 or 10.0 min all slowed the fall in core temperature that otherwise occurred in water at 29 degrees C, and reduced thermal comfort. Metabolic rate increased. Symmetrical fluctuations, or ramp fluctuations with either slow cooling and rapid warming phases or slow warming and rapid cooling phases, were all effective. Similar but less clear effects on core temperature were usually produced by fluctuating skin temperature in water at 25 and 33 degrees C; metabolic rate tended to increase during fluctuation in the 25 degrees C experiments, but not in the 33 degrees C experiments. Stability of the temperature of cutaneous receptors appears to be factor in insidious hypothermia produced by immersion in mildly cool water.

1. Four naïve subjects clothed in protective suits were immersed up to the neck in water on twenty-two occasions, the minimum skin temperature was 20 degrees C and the average skin temperature 26 degrees C. Subjects at first rested, initially demonstrating an increase in thermal muscular tone which did not lead to perceptible limb movements. Later, while resting, visible shivering with small unco-ordinated limb movements supervened. The subjects then exercised while still immersed by stationary cycling. 2. Steady-state minute oxygen consumption (VO2) and minute ventilation (VE) were measured on 152 occasions by timed collection of expired air. 3. The first collection was made at least 5 min after initial immersion. Hyperventilation due to recent immersion in cold water was not demonstrated. 4. The same linear relationship between VE and VO2 was demonstrated whether the increased oxygen consumption was due to shivering alone or to a combination of shivering and exercise. 5. VE was matched to VO2 in spite of an increase in the work of breathing as well as any ventilation-perfusion mismatching as a consequence of head-out water immersion. 6. Minute ventilation was not influenced by the large co-ordinated limb movements which only occurred during exercise. These results reinforce previous findings which have shown that in conscious man VE can be closely matched to VO2 below the anaerobic threshold despite large variations in the type and intensity of limb movements. 7. When VO2 is increased by thermal muscular tone VE is increased in direct proportion in a situation when the limbs are not perceptibly moving at all.

The rate at which alveolar PCO2 (PA, CO2) rises during expiration has been measured in seven healthy medical students. PA, CO2 rate of rise [delta PA, CO2/delta t] was measured by a method utilizing constant expiratory flow rates in individual breaths in two subjects, and was calculated from airway PCO2 and expiratory tidal volume in the remaining five subjects. Steady-state runs were recorded at two or more metabolic rates with the subject making no special effort to control mean lung volume. This was done to establish the relationship between delta PA, CO2/delta t and the rate of CO2 production (VCO2) at normal lung volume in individual subjects. Steady-state runs were also recorded at high lung volume. In each subject delta PA, CO2/delta t was less than would have been obtained at normal lung volume. Inversion of a hypothetical relation between delta PA, CO2/delta t, VCO2 and average lung volume (VLa; DuBois, Britt & Fenn, 1952) yielded calculated values of VLa for both the normal and the high lung volume states. Lung gas volume was measured in a whole body plethysmograph, ('box volume') both for the normal and high lung volume states, in each subject. Mean VLa and 'box volume' estimates showed only moderately good agreement, whereas the estimated differences between normal and high lung volume obtained by the two methods were virtually identical. These experiments suggest that the expiratory PA, CO2 rate of rise is determined, in the steady state, partly by the rate of CO2 production (a directly proportional relationship) and partly by the mean lung volume (an inversely proportional relationship).

1. The purpose of the study was to see whether the rate of rise of alveolar PCO2 (PA, CO2) in expiration was directly proportional to the rate of pulmonary elimination of CO2 (VCO2) in man in the steady state. 2. Alveolar ventilation at rest and during exercise in man was calculated from the difference between total ventilation and dead space ventilation, and from the ratio of the rate of pulmonary CO2 elimination to the mean expired alveolar CO2 (total) fraction. The results were indistinguishable. In agreement with other workers' findings alveolar ventilation changed in direct proportion to the rate of carbon dioxide elimination, confirming the isocapnia of exercise ventilation in man. 3. The rate of rise of expiratory alveolar PCO2 in individual breaths has been obtained by two methods. In the first, a pattern of respiration with constant expiratory flow in each breath brought expiratory alveolar profiles to the outermost end of the airway. In the second method, the early part of the alveolar PCO2 during normal expiration was calculated from airway PCO2 and expired volume. 4. The data obtained with both methods show that, in the steady state, expiratory alveolar PCO2 rises at a rate which is directly proportional to the rate of CO2 production.