In contrast to the brilliant successes that science has won in the study of nitrogen equilibrium, there is a rather discouraging inconclusiveness in the work that has been done on the factors that regulate the nutritive balance of the fat tissue of the body, and the balance between the total intake and total output of potential and kinetic energy in the adult warm-blooded organism. We do not yet know what mechanism there is to prevent the unlimited accumulation of potential energy in the form of an overload of adipose tissue. Is nerve regulation through changing appetite the only guide, or does the body vary its destruction of fats and carbohydrates in accordance with their fluctuating intake, somewhat after the manner that it varies its nitrogen exchange?The best road to a true solution is probably in a study of selected contrasting individuals of the over-fat and under-fat body habits, or better still, of the easily fattening and difficultly fattening types.The problem was first drawn to my attention by observation of myself, and the experiments here reported were performed upon myself as a selected example of the "spare" or apparently non-fattening type. I had long noted my inclination toward a very copious diet of predominantly starchy nature, in spite of which my weight remained fairly constant, even on a moderate round of activity, at a figure well below the average for my stature. If the hereditary constitution is important in this connection, such family data as I possess seem to indicate that I am derived largely from non-fattening strains. It has long been recognized that food intake has a powerful effect on the rate of oxidation in the body. In the case of protein food, Rubner (1) distinguishes two such effects. The first of these is the oft discussed specific dynamic effect. The second is a change which appears more gradually, and is explained by him as a stimulus from plethora of nitrogenous products in the cell fluids. The specific dynamic effect occurs equally in well-fed and badly-fed animals, and so it cannot function as a safety valve for excessive intake. But the secondary or plethora effect may very well so function. According to Rubner, this effect shows itself as a cumulative increase in the specific dynamic effect of heavy protein meals, when they are administered on a series of days. He states that in spite of its cumulative character, this secondary effect is not in evidence during the hours when no food is being absorbed. Consequently a dog that has been over-fed in this manner shows no change in its basal metabolic rate, as ordinarily determined on an empty stomach (p. 260, loc. cit.).Similar results are reported by Dengler and Meyer (2) in their study of the basal metabolism of a man who was over-fed with protein. They found the basal rate changed to a surprisingly slight degree as a result of nitrogen accumulation, and hence conclude that the excess of stored nitrogen was in a non-stimulating form.A. Miiller (3), in tests on a young man, found that the secondary rise on a high prote...
The objective of this study was to evaluate the effect of altitude on arterial blood-gases and hematocrit in Angus-based calves. It was hypothesized that alveolar ventilation rate, as indicated by arterial pCO, would increase with altitude but hematocrit would not. Five Angus-based herds ( = 30 to 80 per cohort) located at 105 m, 1,470 m, 2,010 m, 2,170 m, and 2,730 m above sea level were enrolled in this prospective cohort study. A portable analyzer measured blood-gas tensions in coccygeal arterial blood. Calves at 1,470 m, 2,170 m, and 2,730 m were sampled twice, at approximately 4 mo and 7 mo of age. Calves at 105 m and 2,010 m were sampled once, at 7 or 4 mo of age, respectively. Linear regression analyses were used to determine the fixed effect of herd (a proxy for altitude) on the 4 outcome variables pCO, pO, pH, and hematocrit, while controlling for age and sex. As hypothesized, alveolar ventilation rate increased with altitude ( < 0.001). Hematocrit, however, did not show a clear association with altitude except for an increase from 105 m to ≥ 1,470 m ( < 0.001). Arterial pO decreased significantly with increasing altitude in calves at 4 mo and 7 mo of age ( < 0.001). The adjusted mean values of the 4 variables studied were similar at 4 and 7 mo of age for all of the herds studied. This indicates that suckling calves show minimal respiratory or erythrocytic adaptation to hypoxemia and hypocapnia with increasing age, regardless of altitude. We propose that the lack of an erythrocytic response in hypoxemic calves born and raised at high altitude prevents a deleterious increase in viscous resistance and, consequently, pulmonary arterial pressure. This physiological response, or lack thereof, may be a survival adaptation in a species predisposed to hypoxia-induced pulmonary hypertension.
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