immersion versus that of cold exposure per se. It was not until 1909 that Gibson (1909) demonstrated an increase in urine flow to be the direct result of cold exposure. In 1940 Bazett and associates published a field study that confirmed that an increase in urine flow occurred with cold exposure, but also demonstrated commensurate reductions in plasma and blood volume.
Bader et al. (1952) demonstrated that confounding factors could influence the magnitude of CID and determined whether or not a diuresis occurred during cold exposure. They found that CID could be avoided if moderate exercise was performed during the exposure to cold. Subsequent investigations demonstrated that CID can be influenced by other factors such as: (1) the intensity and (2) duration of cold exposure, (3) hydration status, (4) body posture during cold exposure, (5) performance of exercise, (6) diet, (7) gender, (8) age, (9) body composition, and (10) the time of day.
Lennquist et al. (1974) attempted to determine the mechanism(s) responsible for CID. They hypothesized that CID was not the result of a fall in antidiuretic hormone (ADH) as was previously suggested (Bader et al., 1952; Eliot et al., 1949) and commonly believed. During this decade, the notion reemerged that CID was simply a pressure diuresis, the logic being that the increased systemic arterial blood pressure would increase renal blood pressure and thereby reduce tubular reabsorption of both water and solute (i.e., electrolytes). Wallenberg and Granberg (1976) demonstrated that increases in blood pressure during cold exposure were correlated to sodium excretion (r ~ 0.60). Hence, they speculated that the mechanism for CID was, at least in part, the result of an increase in blood pressure. The hypothesis that CID is a pressure diuresis is still favored by many investigators today, and little direct evidence has suggested otherwise.
Combined data in two publications from a study conducted at the U.S. Army Research Institute of Environmental Medicine (Muza et al., 1988; Young et al., 1987), however, suggest that CID may not be a pressure diuresis. Data for the two papers came from the same experiments in which subjects were immersed in cold water prior to and following a 5-wk cold-water acclimation program. Young and colleagues (1987) reported that the CID response to cold-water immersion was not affected by the cold-water acclimation regime. That is, the magnitude of diuresis was the same during the initial pretest as it was during the posttest. When reporting the cardiovascular data, Muza et al. (1988) showed that while mean arterial blood pressure was markedly increased during the initial cold-water exposure (pretest), it did not increase during the posttest. Together, these data provide evidence that CID and blood pressure responses can be disassociated and, hence, raise questions about the pressure diuresis hypothesis.