If we're talking about the same study from 1984, the conclusion was that it was the 300iu/day for 5 days that lead to double the Testosterone levels:
Smals AG, Pieters GF, Boers GH, Raemakers JM, Hermus AR, Benraad TJ, Kloppenborg PW. Differential effect of single high dose and divided small dose administration of human chorionic gonadotropin on Leydig cell steroidogenic desensitization. J Clin Endocrinol Metab. 1984 Feb;58(2):327-31.
This study compared the effect of a single high dose of hCG (1500 IU) with that of the same dose administered in multiple small doses (300 IU, once daily for 5 days) on Leydig cell steroidogenesis. Administration of a single high dose of hCG to seven healthy men raised the mean plasma testosterone (T) level to peak levels 2.1 ± 0.2 (SEM) x the baseline value at 48 h. Thereafter plasma T decreased to below normal (0.7 ± 0.1 x baseline) 7 days after the injection. The mean 17-hydroxyprogesterone (17-OHP) level peaked at 24 h (2.5 ± 0.2 x baseline) and then also fell to a nadir value of 0.6 ± 0.2 x baseline on day 7. Reflecting the early accumulation of 17-OHP over T, the 17 OHP/T ratio reached its maximum (1.6 ± 0.1 x baseline) at 24 h at the same time when plasma estradiol [(E2) 4.4 ± 0.6 x baseline] and the ratio E2/T (2.7 ± 0.3 x baseline) achieved their maximal values. Administration of 1500 IU hCG in five divided doses of 300 IU daily increased the mean plasma T levels to peak value of 2.1 ± 0.2 x baseline at 5 days and the levels remained elevated thereafter. The response of T as reflected by the area under the curve was almost twice as great as in the single dose study (2844 ± 360 vs. 1647 ± 214). In contrast to the single high dose experiment, mean plasma 17-OHP levels in the divided dose protocol did not peak at 24 h but only gradually increased. As the increase of T exceeded the 17-OHP increase at almost all time intervals, no accumulation of 17-OHP over T occurred as in the single dose experiment. Instead the 17-OHP/ T ratio fell to a nadir value of 0.6± 0.1 x baseline on day 7. The initial E2 peak was absent in the divided dose protocol and the E2/T ratio only marginally increased. Considering both experiments together a close relation was found between the hCGinduced increases in E2 and 17-OHP (r = +0.88, P < 0.001), as well as the ratio 17 OHP/T (r = +0.64, P< 0.02). Multiple small dose hCG administration in contrast to a single high dose does not desensitize but rather enhances Leydig cell steroidogenesis, probably by preventing the early accumulation of E2 and thereby the steroidogenic enzyme suppression which occurs after massive doses of hCG.