Based on autopsy findings in these cases, the authors hypothesize that rather than a single mechanism or macroscopic finding that explains the causes of these deaths, the deaths were related to the findings of a combination of malignant brain swelling without herniation, cellular neuronal, and cerebral cardiorespiratory center dysfunction, resulting in posttraumatic apnea and fatal cardiac arrhythmia, which acted together to produce the atypical scenarios in these cases. Of these hypothesized mechanisms, the authors favor the mechanisms that underlie so-called "postexercise peril." Dinsdae et al. described the phenomenon of "postexercise peril." In their observations of 10 healthy men who underwent exercise testing, they report the rise in catecholamine levels, not only as a response during the exercise period, but also in the immediate postexercise period. A 10-fold increase of norepinephrine over baseline could have profound cardiac effects, especially in those with pre-existing cardiac disease. It could be hypothesized that persons with undiagnosed cardiac arrhythmogenic syndromes, which have been diagnosed as causes of sudden unexpected adult death, could place these individuals at increased risk of death under the circumstances of "post exercise peril." This natural physiological response could have placed the individuals in the cases cited at increased risk of death under the circumstances described. In addition, blood potassium concentrations also alter during exercise, increasing and then rapidly decreasing in the postexercise period. The combination of raised catecholamines and decreasing potassium levels in the presence of pre-existing cardiac disease may result in fatal cardiac arrythmias. 17 references