Abstract
Conclusions
It is clear that the worst that can be said of swimming shortly after diphosgene gassing at mid- or somewhat above mid-lethal doses is that it had no influence on final mortality among mice and rats or on survival time in dogs. There was, in fact, some indication, especially from the finding of a significant difference between survival of moderate early and late exercised mice, that moderate early swimming was beneficial or late swimming deleterious or both. It is striking that in all of the pooled data (see tables), and very often in individual experiments, differences noted, though not statistically significant, are consistently in the direction of increased survival for moderate early exercise in all 3 species, and in the direction of increased mortality for moderate or heavy late exercise in mice and heavy early exercise in dogs.
The dog survival times and lung weights suggest that “moderate” and “heavy” exercise as distinguished in these experiments are physiologically as well as quantitatively, of different orders of magnitude. Similarly, in the mouse experiments there is no indication of any effect, beneficial or deleterious, of heavy early swimming, as opposed to the indicated beneficial influence of moderate exercise.
Swimming seems a justifiable test of the effects of more natural types of exertion. The control experiments on mice show that the indifferent role of swimming or the perhaps beneficial effect of moderate early swimming does not represent an overcompensation of harmful exercise by a protective action of immersion in tepid water. If anything, swimming, as already indicated, may be responsible for the apparent ill effect of heavy “exercise” in dogs judged by the significantly greater pulmonary edema of heavy swimmers as opposed to controls.
Finally, it may be pointed out that exercise by a diphosgene patient or other pulmonary irritant patient during the clinical latent period need not be expected a priori to be adding insult to injury. The water and blood demands of muscle during exercise could tend to delay the onset of edema. Once edema and attendant anoxaemia set in, however, increased oxygen demand becomes an undesirable feature of exercise. Since the time of onset of edema is variable, depending mainly on severity of exposure, which is in turn a function of more than just gas concentration and exposure duration, no particular time can be set as the limit of a safe period.
Get full access to this article
View all access options for this article.
