Experimental Evidence Supporting the Conception of “adaptation Energy”

It has been shown that when an organism is exposed to a stimulus to the quality or intensity of which it is not adapted, it responds with a reaction which has been termed the “general adaptation syndrome” (Selye, 1936a, 1937a, 1938a). The symptoms of this syndrome have been described elsewhere (Harlow and Selye, 1937; Howlett and Browne, 1937; Karady et al., 1938; Schacher et al., 1937; Selye, 1936b, 1937b, 1937c; Selye et al., 1936). They are largely independent of the specific nature of the agent to which adaptation occurs, so that the reaction has been regarded as the somatic expression of damage as such. The general adaptation syndrome develops in three distinct stages which have been termed: 1, the stage of the alarm reaction; 2, the stage of resistance, and 3, the stage of exhaustion. The symptoms of the alarm reaction, among which thymus atrophy and adrenal hyperplasia are particularly conspicuous, disappear during the stage of resistance in spite of continued treatment with a uniform damaging stimulus (a drug, exposure to cold, excessive muscular exercise, etc.) but these same symptoms reappear during the so-called stage of exhaustion and finally death ensues. A similar three stage reaction was recently observed by Giragossintx and Sundstroem (1937) in rats kept under low oxygen tension. In these experiments, the loss of acquired adaptation during the stage of exhaustion is difficult to explain but as a working hypothesis, it was assumed that every organism possesses a certain limited amount of “adaptation energy” and once this is consumed, the performance of adaptive processes is no longer possible (Selye, 1938c). Previous observations (Karady et al., 1938; Selye, 1938a, 193813) showed that during the alarm reaction, the resistance of the organism is increased, not only to the stimulus with which the alarm reaction had been elicited but also to agents of a different nature. However during the second stage of the adaptation syndrome, this non-specific resistance vanishes rapidly at a time when the specific resistance to the agent with which the animal had been pretreated, is still very high. These findings