There is a well documented association between strenuous exercise and menstrual irregularities in women.
Some authors have argued this should not be considered pathological since the effect is temporary and relieved by cessation of exercise so is rather an adaptation to demands placed on the body.
There is also a related condition called the female athlete triad which consists of:
- osteoporosis
- amenorrhea
- disordered eating
Why do we see secondary amenorrhea in these individuals?
FHA manifests from many factors influencing the complex hypothalamic–pituitary–ovarian axis. When energy stores fail to meet the energy requirements of the body, there are numerous downstream effects. At the level of the hypothalamus, gonadotropin-releasing hormone (GnRH) secretion decreases, leading to less follicle-stimulating hormone (FSH), luteinizing hormone (LH), follicular development, and estrogen secretion. Serum testing of FSH and LH levels in a female with FHA falls in the low-normal to pre-pubertal range reflecting this physiologic change. Cortisol and stress affect this axis, as increasing levels of cortisol inhibit GnRH secretion. This action helps to explain why times of high stress can lead to irregular menses and amenorrhea.
So we can see low energy stores causes abnormalities in the female HPG axis.
Males also have a HPG axis so is there a similar situation in the male? There is less literature on this probably owing to endocrine abnormalities having more obvious consequences in women. But the answer appears to be yes.
Cross-sectional reports of hypogonadotropic hypogonadism have been reported in male athletes, particularly in those athletes participating in endurance sports, and include evidence of low testosterone [49–52], poor semen quality/oligospermia [53, 54], and low libido [55, 56].
I recommend reading this paper as there is much more detail than I can include in an answer. However some highlights:
Interestingly, it is primarily in “extreme” situations consisting of high intensity, long duration exercise or simultaneous exposure to multiple stressors that significant reductions in metabolic and reproductive hormones are observed.
In cross-sectional studies of chronic strenuous exercise training, it seems that very high training loads are required for impairments to be translated to the HPG axis, presumably through poor energetic status. We found that high mileage runners (108.0 ± 4.5 km/week), compared to moderate distance runners (54.2 ± 3.7 km/week) and controls, had lower testosterone levels as well as poor semen quality, including decreased sperm motility, an increased immature sperm number, and decreased bovine cervical mucus penetration, all of which are associated with infertility [53]. It is important to note that the moderate mileage runners in our study maintained a gonadal and semen profile that was similar to that of the sedentary control group, despite running approximately 40–60 km/week. We concluded that in male athletes participating in high-volume training, the findings of decreased testosterone and abnormal semen profiles (Table 1) likely reflect the failure of these athletes to increase energy intake in a manner that accommodates the increased energy expenditure associated with a high training volume [53, 54].
So, to summarise, yes there can be pathological effects to these lifestyles. They are chiefly associated with the combination of very low energy input and high energy output in the form of exercise. The effect is more widely seen in women but can occur in males who are engaged in extremely strenuous exercise, especially with concomitant stressors like sleep deprivation and psychological stress. The dysfunction involves disruption of the HPG axis causing either hypoandrogenic or hypoestrogenic states in males and females respectively.
As discussed in this paper hypogonadotrophic hypoestrogenic states in women can result in anovulation and decreased libido which can result in infertility.
Other adverse effects discussed include:
low bone mineral density, osteoporosis and stress fractures, psychologic effects, diminished athletic performance, and morbidity or even death due to disordered eating patterns