Nine previously sedentary middle-aged males underwent cycle endurance training 45 min/day for 9 wk with an average attendance of 4.1 days/wk. Seven males served as controls. Before and after the training period, the subjects performed three cycle ergometer tests. Work rate was incremented by 15 W/min, to the limit of the subjects' tolerance, in the first two tests; the third test consisted of contant-load cycling at an O2 uptake (VO2) just below the pretraining anaerobic threshold (AT). After training, the AT increased significantly by 44%, expressed as absolute VO2, and by 15%, expressed relative to VO2 max. Significant increases were also noted in VO2max (25%), maximal minute ventilation (19%), and maximal work rate (28%). The test-retest correlation coefficients for the AT (%VO2max) were 0.91, pre- and posttraining. Training did not alter steady-state VO2 during the submaximal exercise test whereas significant decreases occurred in CO2 output, VE, respiratory quotient, and VE/VO2. No changes occurred in the control subjects during this period. These results demonstrate that the AT is profoundly influenced by endurance training in previously sedentary middle-aged males.

1. Monkey renin and human renin, but not hog, dog, or rabbit renins, were pressor in the monkey. Monkey renin was neutralized by antirenin to human renin, but not by antirenin to hog renin or antirenin to dog renin. 2. Experimental renal hypertension developed consistently in the monkey after unilateral 3:1 renal artery constriction and became more marked after contralateral constriction or nephrectomy. Hypertension usually persisted when the second kidney was left untouched. 3. Chronic experimental renal hypertension in the monkey was treated with partial success by crude human renin. Semipurified hog renin was not therapeutically effective. 4. Chronic experimental renal hypertension was treated successfully by passive administration of dog serum containing antirenin to human renin, but not by dog serum containing antirenin to hog renin or dog serum without antirenin. 5. Prophylaxis of experimental renal hypertension with crude human renin was partially successful in preliminary experiments. 6. Attempts to alter the antigenicity of hog renin through chemical treatment so that the antibody to it would neutralize human renin were not successful. Antihypertensive effects were not observed during treatment or prophylaxis experiments with chemically treated semipurified hog renin. 7. The interfering effects of renal medulla seen in the treatment of renal hypertension in dogs with hog renin were not observed in monkeys treated with human renin. 8. During each individual experiment involving treatment of the renal hypertensive monkey with human renin, correlation was observed between the extent of the antihypertensive response and the antirenin titer to human renin. On the other hand, correlation was not apparent when the antihypertensive response and the maximum antirenin titers of different experiments were compared. However, rough correlation between antihypertensive responses and maximum antirenin titers was observed in passive administration experiments with antirenin to human renin. 9. Passive administration of dog serum containing antirenin to human renin to renal hypertensive monkeys was followed by antihypertensive responses which were substantially more marked than in monkeys in which comparable antirenin titers were produced by daily injections of human renin. Passive administration of normal dog serum or dog serum containing antirenin to hog renin was not followed by decreases in blood pressure during initial experiments with dog serum. Sensitization to dog serum was a complicating feature of passive administration experiments after the initial experiment. 10. With both active and passive treatment, the minimum titers of antirenin to human renin required for minimal antihypertensive responses in the monkey were lower than the minimum effective titers of antirenin to hog renin observed previously in dogs. 11. The chief postoperative complication after renal artery constriction in the monkey was congestive heart failure. Malignant hypertension with necrotizing arteriolar lesions occurred infrequently. Atherosclerosis and cardiac hypertrophy were common findings after a year or more of hypertension. Arteriolar lesions were absent or minimal. Significant nephrotoxic effects did not appear to result from daily injections of crude human renin or from passive administration of dog serum containing antirenin to human renin. 12. These results support the hypothesis that renin (or a closely related protein) plays a role in the pathogenesis of primate experimental renal hypertension. 13. Passive administration experiments with antirenin to human renin to determine the possible role of renin in the pathogenesis of essential hypertension are a practical possibility.

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TRANSLATORS' NOTE Carl Ludwig (1816-95) published the second edition of his Lehrbuch der Physiologie in 1858-61, at the onset of the political and industrial ascendency of Germany in Europe and the beginning of 'the greatest ferment of ideas and revolution in attitudes since the middle ages.'" In Ludwig's laboratories physiology, still only an 'embellishment' of anatomy, joined with the burgeoning physics and chemistry of the day to form a new, independent, science. The two volumes of the Lehrbuch presented the first fruits of that merger. Even as Claude Bernard in Paris conducted his investigations in a damp basement, the physiological institutes of Germany multiplied and grew strong, so that by 1879 an unnamed observer was able to describe the 'development of physiology during the last quarter century in Germany' as 'by general acknowledgement unprecedented in the history of science."' 'Ludwig's Physiology,' wrote Wilhelm His, 'appeared like a meteor on the scientific horizon. It attacked the scientific knowledge of the day, demolishing former theories and conceptions with critical severity."9 The physical movement in physiology was quantitative and objective in outlook, in contrast to the older trend, which was descriptive, impressionistic and vitalistic. According to Burdon-Sanderson, the book exerted an 'extraordinary influence." It 'gave the coup de grace to vitalism in the old sense of the word."' The treatise began with a 'discussion of the elementary endowments of the structure or framework of the living body, and of the processes in which these endowments manifest themselves; seeking to arrive at a clear conception of each vital function by regarding it as a complex of constituent processes severally definable in chemical or physical terms. The book set forth no 'biological principles,' and therefore had no interest for the general reader. It was for students and for students only, but for them it was a revelation, a forecasting of the physiology of the future for those who were about to make it."4 The Introduction to the Lehrbuch was especially influential and sums up the essential argument of that work. Unlike that of his colleague Emil Du Bois-Reymond, the fame of Ludwig did not spread far beyond his field. He never became a major public figure. Nevertheless, his enormous capabilities and his versatility, both as an investigator and as a teacher, attracted students to his laboratories from all over the civilized world, with the end-result that the schools of physiology which arose during the latter half of the nineteenth century in Germany, England, America, Austria, Italy, Russia, and Scandinavia bore the stamp of his influence. At the turn of the century nearly every important physiologist then active had once been a student of Carl Ludwig. Ludwig's disciples have not been entirely unanimous in regard to the outlook put forward in the Lehrbuch. According to Robert Tigerstedt, Ludwig wrote as a mechanist, that is, he tried to give a 'purely mechanical explanation of life."' William Stirling wrote th...