A recent theory (Gerontology 2004; 50:265-290) defines aging as any change in an organism over time, including not only the loss of efficiency due to senility, but also the changes associated with the period of growth and puberty. 

The speed of these changes would be related to the progression of aging, which would therefore be highest in the fetal period. 
The second most rapid aging period is the first year of life, during which the body size doubles. A slowdown in growth (and aging) then occurs until puberty, the period between 11-13 and 16-18 years of age when body mass doubles in five years. 
The next period, typically lasting 15-20 years, is one in which the reproductive function is maximum and is one in which the changes and thus the aging process are minimal. 
When the reproductive function starts to decline, in the 4th decade of life, changes in body composition and functions begin to show up again therefore speeding up aging one more time. 

It is mainly SEX HORMONES that determine the rapid development of the fetus, the periods of postnatal growth and puberty and, according to this theory these same hormones are responsible for the decline manifest in aging. 
The hormones produced by the hypothalamus (GnRH) from the pituitary (LH and FSH) and gonads (testosterone and estrogen) are the protagonists of the changes that come with aging. 
Their production is modulated by "Activins" (produced by many organs and tissues) and "Inhibins" (produced in the gonads). 
When the body size increases, both the production of "Activins" and the production of sex hormones (testosterone in males and estrogen in females) intensify. 
With the decline of reproductive functions, gonads reduce their ability to produce sex hormones and "Inhibins" with the result of an increase in LH and FSH, in the futile attempt to maintain the reproductive capacity. 
Menopause in females and andropause in males are characterized by high levels of LH and FSH: in old sedentary subjects, gonadotropins determine an alteration of lipid metabolism leading to increased triglycerides, LDL-cholesterol and abdominal fat. 

The fact that fertility hormones determine the rate of aging is confirmed by scientific evidence that the decline in fertility caused by lack of food (caloric restriction) is accompanied by an increase in longevity, both in humans and animals. 
The caloric restriction in fact induces a reduction of LH, FSH and "Activins", all mitogenic factors that drive growth and cell replication that in senescence may lead to the development of neoplasms, cardiovascular disease, obesity. 
The lower life expectancy of males compared to females may be due to increased body size and hence a greater production of "Activins" resulting in increased production of sex hormones in the course of life. This would be confirmed by the fact that men and women of the same size have similar longevity. 

If it is true that senescence is a positive process for the survival of the species (the death of the elderly means lower reduction in resources for fertile individuals...), single individuals have an interest in delaying the effects of aging. 
Since the fertile period is one in which there are fewer changes (and therefore aging), a strategy would be to try and extend the reproductive period by offering a "hostile environment to breeding", such as caloric restriction (eating less), exposure to cold, and vigorous exercise. 
In menopause - andropause is useful to reduce the caloric intake, increase physical activity, reduce body fat and eventually take small doses of estrogen - testosterone and/or "Inhibin" in order to reduce the values of gonadotropins back to those of the reproductive period. 

Athletes during the reproductive age may find that high levels of gonadotropins could improve endurance performances. 
LH in fact is able to activate the two types of lipase (HSL and LPL) which determine an increase of the use of fat as muscle fuel, with a consequent saving of glycogen and increased resistance. 
Some Authors (Med Hypotheses 2007; 68:735-749) argue that high levels of gonadotropins and prolactin resulting from orchiectomy may explain the improvements of Lance Armstrong in three-week stage races, in which an increased use of lipids - saving of glycogen allows a better recovery and thus better performances. 
If this is true, the intake of exogenous testosterone in endurance activities would be useless (J Endocrinol 2001, 170:27-38) if not detrimental to the performance...