The effects of prolonged muscular exercise on the metabolism
- 2 March 1936
- journal article
- research article
- Published by The Royal Society in Proceedings of the Royal Society of London. B. Biological Sciences
- Vol. 119 (815) , 381-439
- https://doi.org/10.1098/rspb.1936.0014
Abstract
Expts. were carried out on the authors at a sufficient interval after food intake to ensure a post-absorptive state. During a preliminary rest, a 10 mile walk at 4.5 miles per hr. on the level, and a subsequent rest period the respiratory exchange, alveolar CO2, body temp., blood CO2-combining power, lactic acid, ketone bodies and sugar, urine ketone bodies and total N were detd. at suitable intervals. With the subjects on their normal diets, the average initial R. Qs. of 0.79 and 0.81 rose to 0.83 and 0.84 after 2 miles, decreased to 0.80 and 0.81 at the end of 10 miles, to 0.76 and 0.73 at the cessation of exercise and maintained this low value for as long as 9 hrs. during rest, the oxygen consumption during the post-exercise period remaining higher, and the CO2 output the same as, or lower than the pre-exercise values. The fall of the quotient during the exercise cannot be accounted for by temp, changes, by the slight temporary increases in lactic acid in the blood, and in CO2-combining power, or by ketosis which develops only after exercise. Protein metabolism, calculated from total urine N, amounted to about 3.3 gms. per hr., implying a CO2 output of 43 cc. and oxygen consumption of 53 cc. per min., this correction for protein metabolism altering the above R. Qs. only when their value is below 0.76. The R. Qs. during exercise must therefore be an index of the carbohydrate to fat ratio oxidised, and show a rise in this ratio from 1:1.2 in the early stages of exercise to 1:2.0 later. Alveolar CO2 usually remained unchanged throughout, blood sugar within the normal limits. Ketone bodies in the blood and urine increased after exercise, and decrease in CO2-combining power was correlated with increase in ketones. In expts. in which the walking rate was slowed, the R. Q. did not rise above the resting value, but feil during the course of the expt. Ketonuria developed as before, seeming to depend rather on the total amt. of work than the rate. High carbohydrate diet during the day preceding an expt. resulted in a qualitatively similar behavior of the R. Q., but at a higher level throughout, and without ketosis or loss of CO2-combining power. Ketonuria developed after exercise could be abolished by ingesting sugar during the post-exercise resting period. The ingestion of 50 gms. glucose or fructose just previous to exercise resulted in high R. Qs. of 0.91 and 0.97 during pre-exercise rest, falling steadily during exercise so that at the end of the expt. the R. Q. was the same as in the post-absorptive subject on normal diet. Post-exercise ketonuria developed. The effect of a diet rich in carbohydrate on the day preceding the expt. has a greater influence on the ketonuria than ingestion of readily assimilable carbohydrate just previous to work. Pre-exercise administration of NaH2PO4 up to 15 gms. had no appreciable effect. The non-protein R. Q. was never sufficiently low to indicate conversion of fat into stored carbohydrate. The ketosis and persistent low R. Q. after exercise must be due to the low ratio of carbohydrate to fat oxidised. A second walk following a short period of rest resulted in a rise in R. Q. during the exercise, showing that the carbohydrate stores of the body had been depleted by the first 10 mile walk. The ketosia developed during the intervening rest period was maintained during the 2d walk, and increased during subsequent rest. Ingestion of glucose, sucrose or fructose in post-exercise periods showed a lowered sugar tolerance as measured by changes in R. Q. It is suggested that the changes in carbohydrate metabolism due to exercise may result from the activity of the endocrine organs controlling sugar metabolism being correlated with the activity of the muscles.This publication has 20 references indexed in Scilit:
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