It still doesn’t change the fact that, although the numbers are small, it appears CAIS is over represented at elite athlete level by a factor of 20, showing that even without the androgenising effects of testosterone, a Y chromosome proffers advantage.
Um now we're onto Y chromosomes!?
Make your mind up.
You seem to have an awful lot of unevidenced assumptions. In particular the idea that they werent diagnosed at the Olympics.
The text you link to is clear
"All had full physical examinations and
recommendations for follow-up care, including estrogen re-placement and appropriate surgical intervention"
They did SRY screening following which they had full examinations of those who were SRY+.
This has continued till the last decade
[2013 report]
"our elite young amenorrheic athletes with hyperandro-genism were referred to our Reproductive Endocrinology Department. Case 1 was identified through an abnormal
urine steroid profile and clitoral hypertrophy reported by
the antidoping officer, whereas cases 2 and 4 through in-
creased plasma T, and free androgen index and LH results
collected as a part of the Athlete Biological Passport (3).
Case 3 was directly referred to the international federation
medical department by her national federation doctor."
"The 4 young amenorrheic women, respectively, 18, 20, 21,
and 20 years of age at diagnosis, were from rural or moun-
tainous regions of developing countries. They had never
menstruated and this primary amenorrhea had never been
evaluated. Consanguinity was confirmed for 3 of them
(first cousins in cases 2 and 3 and siblings in case 4) and
was suspected in the fourth case (case 1), with the 2 parents
originating from neighboring villages (Table 1). All had
several brothers and sisters, including 1 sister who had
been surgically treated for a DSD (nonverified; case 2) and
1 infertile (case 3) (Table 1). They all reported unexpected
virilization at puberty with excessive pubic hair or clitoro-
megaly. In all cases, they had manifested strong motiva-
tion and high tolerance to intensive daily training, which
had made them good candidates for elite sports competi-
tion. However, none of them reported male sex behavior.
The clinical characteristics were quite similar, with all
presenting as tall, slim, and muscular young women but
with a complete lack of breast development and android
bone morphotype (high biacromial/bitrochanteric diam-
eter ratio) (Table 1). Axillary hair growth was slight and
pubic hair was female triangular, and none presented with
hirsutism. Clinical inspection of the external genitalia re-
vealed clitoromegaly in all cases, almost complete labial
fusion in cases 2 and 4, partial fusion in cases 1 and 3, and
a single urogenital orifice in cases 2 and 4 (types 2– 4 of the
Prader classification) (Table 1). Clinical palpation of the
major labia or inguinal region and MRI of the abdominal-
pelvic region determined the nature and size of the testes
and localized them at the inguinal orifice in cases 1 and 2,
intralabial in case 4, and 1 at the inguinal orifice and the
other sublabial in case 2"
"a short blinded vagina (22 mm) was identified in cases 1,
2, and 3"
"In contrast to the tendency to request gender change, our 4 athletes wished to maintain their female identity and
had many questions about menstruation, sexual activity, and child-bearing. Although leaving male gonads in SDRD5A2 patients carries no health risk, each athlete was
informed that gonadectomy would most likely decrease
their performance level but allow them to continue elite
sport in the female category. We thus proposed a partial
clitoridectomy with a bilateral gonadectomy, followed by
a deferred feminizing vaginoplasty and estrogen replace-
ment therapy, to which the 4 athletes agreed after in-
formed consent on surgical and medical procedures.
Sports authorities then allowed them to continue compet-
ing in the female category 1 year after gonadectomy."
So it's quite clear that in the past these athletes have come through, been identified during routine testing in most cases, and been directed to have gonadectomies in order to compete.
Which obviously they did, and in many cases I believe they will fallen away post-gonadectomy and not been competitive. E.g. Annet Negesa, who is probably one of the athletes mentioned above.
As far as CAIS goes the point was that androgen insensitivity is diagnosed by lack of virilization, which is subjective. It's not always associated with an androgen receptor gene mutation or deletion . So it's not clear that a CAIS Vs PAIS diagnosis is all that absolute, and hence whether in fact these athletes are benefitting in some way from the testosterone.
It does not seem plausible that such an overrepresentation is linked only to having a Y chromosome, whereas cases of pre-pubertal gonadectomy followed by oral oestrogen result in shorter adult heights than where no gonadectomy is performed, and oestrogen is endogenous, aromatized from testicular testosterone. I.e. they experience lower than XX female levels of oestrogen resulting in later bone maturation/taller height, and associated overrepresentation cf. XX female.
It doesn't seem that overrepresentation of athletes who had low levels of oestrogen because of not having ovaries is inherently problematic but the inclusion of athletes who have testes and who are significantly virilized is much more so.