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weight of wheat) and cod liver oil (compare Sherman, '37). The animals were kept in a room of fairly constant temperature (about 24" to 28'C.). Post-mortem examinations showed that no obvious abnormalities were present. Living conditions in the colony were favorable and had remained relatively constant for many generations.

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Sweating of human volunteers immersed to the neck in hot water declined markedly after reaching a peak in the 1st hr of exposure. This decline always occurred in fresh water regardless of level of thermal stress. Sweating in the 3rd hr of exposure was about the same whether the water was hot in the 1st 2 hr (sweat glands active) or cool (sweat glands inactive). Thus “fatigue” was not responsible for the decline. It is suggested that observations of decline of sweating in warm-humid air environments, attributed to “sweat gland fatigue,” in reality may have been owing to soaking of the skin with sweat. The mechanism of suppression appears more complex than blockage of the sweat ducts by swelling of the corneum. Rather, there is an association between the amount of decline and conditions favoring diffusion of water to deeper strata of the skin. For example, adding salt to the water reduced the decline; no decline occurred in 15% NaCl. Submitted on March 6, 1961

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