However, the abrupt hormonal changes induced by medical treatment in intersex/DSD or transgender individuals may be telescoped compared with male puberty where circulating testosterone concentrations increase irregularly and incompletely for some years. These facts explain the clear sex difference in athletic performance in most sports, on which basis it is commonly accepted that competition has to be divided into male and female categories. However, obtaining ethical approval to administer supraphysiological testosterone doses that maintain circulating testosterone in the male range for sufficiently prolonged periods, as well as the practical difficulties in recruitment, are likely to remain obstacles to definitive resolution of this question. In creating a threshold for eligibility for female events it is also necessary to make allowance for women with polycystic ovary syndrome (PCOS) and nonclassical adrenal hyperplasia. A reliable threshold for circulating testosterone must be set using measurement by the reference method of liquid chromatography–mass spectrometry (LC-MS) rather than using one of the various available commercial testosterone immunoassays. Unsurprisingly, this dilemma has always been highly contentious since it first entered international elite sports in the early 20th century, and it has become increasingly prominent and contentious in recent decades; nevertheless, the requirement to maintain fair play in female events will not disappear as long as separate female competitions exist. The proposal that the sex difference in muscle mass and function might be due to sex differences in endogenous GH secretion (116) is refuted by the extensive and conclusive clinical evidence that endogenous GH secretion in young women is consistently higher (typically twice as high) as in young men of similar age (163–170). It has also been proposed that the sex difference in athletic performance may be due to genetic effects of an unspecified Y chromosome gene that may dictate taller stature (154), as height is correlated with men’s greater muscle mass. One proposal has been that, as men are taller than women, height differences may explain the sex differences in muscle mass and function, which explains some athletic success (116). Additionally, whereas passing through puberty enhances male physical performance, the widening of the female pelvis during puberty, balancing the evolutionary demands of obstetrics and locomotion (136, 137), retards the improvement in female physical performance, possibly driven by ovarian hormones rather than the absence of testosterone (138, 139). Analogous findings were reported for testosterone treatment effects in postmenopausal women where the highest dose (25 mg weekly) of testosterone, which increased mean serum testosterone to 7.3 nmol/L, had the largest increase (3%) in blood hemoglobin and hematocrit (112). Furthermore, from 2016 to 2023, there was a surfing population increase of 46% among people aged 18 years or older (2). We discuss this in the context of thermal regulation, hormone profile change, and the subsequent expression of "power" on waves—a key criteria that surfers are scored for. However, surfing is a unique sport in that it is undertaken both above and below water. Kennelly, who was one of the first openly gay women in pro surfing and was dropped by most of her sponsors when she came out in 2008, is more scathing. And when they do back female surfers, brands have long favoured a bikini-clad feminine ideal. "It’s really hard to find sponsors that see the value in big-wave surfing," says Alms. Unlike regular surfing, which has dozens of events, there are fewer major big-wave competitions. Change in the core body temperature as a proportion of the baseline (start of the warm-up) core body temperature. Significantly greater than all the time points prior, including the second competition set of waves (p Significantly greater than all the prior time points but not the start of second set of competition waves (p Given the categorical nature of the data, a non-parametric statistical analysis was most suitable. As a result, it is not feasible to produce a sufficient increase in circulating testosterone in women either by direct ovarian stimulation or indirect reflex effects to test this hypothesis even if doing so were deemed ethical and safe. However, similar mechanisms do not operate in women, in whom circulating testosterone originates from three different sources (adrenal, ovary, extraglandular conversion of androgen precursors), none of which is subject to tight testosterone negative feedback control. In healthy men, circulating testosterone originates almost exclusively from a single source (testicular Leydig cells) and is subject to tight hypothalamic negative feedback control, so that either direct stimulation (by human chorionic gonadotropin) or indirect reflex effects (e.g., from estrogen blockers operating via negative feedback) to enhance Leydig cell testosterone secretion are feasible. Although the dose-response relationship in women may be similar to what is seen in men, there is also anecdotal evidence that the dose-response curves may be left shifted so that testosterone has greater potency in women than in men at comparable doses and circulating levels. These studies did not report muscle strength, but other studies of testosterone dose-response relationships for muscle mass and strength show consistently positively correlation (65, 93, 117, 119), although with disproportionately greater effect on muscle strength than on muscle mass. Conversely, in 17 transmen (F2M transgender) treated for the first time with testosterone for 12 months (which increased circulating testosterone levels to a mean of 31 nmol/L), muscle mass increased by 19.2% and hemoglobin by 15% (114). Similarly, among elite athletes with circulating testosterone in the male range due to DSDs, comparable findings of athletic performance reduced by an average of 5.7% when circulating testosterone was suppressed from the male range to 176).
