Effects of the Menstrual Cycle on the Acquisition of Peak Bone Mass

Bone Composition, Physiology, Function, and Interaction with Ovarian Hormones

Menstrual disturbances File photo | Credit: NICHDOpens in new window

The menstrual cycle has huge implications on the building, maintenance, and break down of skeletal bone in women. Due to the fluctuating level of female hormones, the menstrual cycle plays a different role during various times of the month which in turn affects bone health.

Estrogen is a crucial hormone for bone turnover/remodeling which, when released, provides a protective mechanism against the process of natural bone loss due to aging.

Acquiring a high amount of peak bone mass during adolescence helps to protect the female athlete against rapid degradation of bone due to the decline of estrogen around menopause. Therefore, taking appropriate steps years before and after menopause is crucial in order to preserve bone mass in females.

Skeletal tissue is one of the hardest and strongest tissues in the body. Bone is mineralized connective tissue comprised of specialized cells, along with noncellular substances, organic matrix (35 % by weight), and inorganic mineral (65 %).

Two key types of bone cells are osteoblasts, which are involved in bone formation, and osteoclasts, which are involved in bone resorption. Components making up the organic matrix include glycoproteins, collagen (Type I), elastin, and protein (90 % collagen), bathing in a sea of gelatin-like mucopolysaccharide (ground substance).

Bone can be classified into two categories: cortical, representing 80 % of bone mass, and trabecular, representing only 20 % of bone mass but comprising 80 % of bone surface area.

Collage fibers in the bony skeleton represent specific sites where inorganic calcium/phosphate hydroxyapatite crystals are deposited prior to the mineralization process of bone. Ninety-eight to ninety-nine percent of the body’s total calcium is sequestered in the skeletal framework, which serves as a mineral bank and releases calcium into the bloodstream to keep serum calcium levels constant.

Because the quantity of calcium is tightly regulated, the body will rob calcium from its main reservoir, bone, to maintain adequate blood levels in order to carry out essential, vital tasks such as blood clotting and muscle contraction. Calcium, however, cannot be absorbed and incorporated into bone unless vitamin D is readily available.

Ovarian hormones play an important role in the metabolism of calcium and vitamin D. Indeed, estrogen helps to regulate the absorption of calcium, subsequently contributing to bone formation, as already discussed above. In effect, any irregularities in the menstrual cycle will negatively affect bone disposition in the long run by negating estrogen’s positive influence on calcium balance.

Bone remodeling cycle Figure X-1. Bone remodeling cycle | Source: IOFOpens in new window

Additionally, with the loss of protection from estrogen, osteoclasts will be affected to a greater extent than osteoblasts, resulting in an uncoupling effect. This dissociation between osteoblasts and osteoclasts causes undesirable bone loss, which could manifest itself as early osteoporosis (Figure X-1).

Peak Bone Mass

Peak bone mass (PBM) signifies the maximal quantity of bone which can be gained primarily during the adolescent years (with the critical window being between 9 and 20 years), while the skeleton is undergoing an accelerated growth in both size and density.

By age 7, females have reached 80 % of their adult height but only 40 % of their PBM. This “adolescent growth spurt” occurs 1 – 2 years preceding the rapid deposition of bone into the skeleton.

In females, up to 90 % of PBM is accumulated by 18 years of age. After this prime period, bone can still continue to grow in terms of strength and density, up until about age 25 – 35, at which time true PBM is reached. However, some researchers have shown that this PBM acquisition may occur as young as the late teens.

After attainment of peak bone mass, measures to maintain bone density are of paramount importance since physiologic bone loss will inevitably occur gradually over time. In fact, prior to reaching menopause in their fourth or fifth decade, females lose about 0.3 % of their entire skeleton each year after the final acquisition of peak bone mass (Figure X-2).

Figure X-2 Rate of bone loss through a woman’s lifetime Figure X-2 Rate of bone loss through a woman’s lifetime

The quantity of bone deposited in the skeleton is influenced by both genetics (uncontrollable) and environmental (controllable) factors. Mechanical loading in the form of weight-bearing/resistance exercise; appropriate and adequate nutrition (i.e., sufficient consumption of key bone building nutrients such as calcium, magnesium, zinc, vitamins C and D); and normal, regular menses all contribute to optimal bone health.

Endocrine function is highly dependent on the amount of available energy. Energy availability is the quantity of energy remaining after physiological energy is utilized (i.e., energy for everyday movement and activity).

As long as energy availability is maintained, the endocrine system will function optimally with normal hormone serum levels. However, without adequate energy the endocrine system is altered, primarily affecting the hypothalamic production of hormones.

Insufficient energy will adversely affect the pulsatile secretion of LH. This casuses a decrease in hormones such as estrogen, testosterone, GH, and IGF-1. On the other end of the spectrum, an extreme excess of available energy, as seen in obesity, will tend to cause hormone level alteration as well. In short, any aberrant serum levels of sex hormones will alter the menstrual cycle and ultimately affect bone balance.

A delay in menarcheOpens in new window (initiation of menses), dysmenorrheaOpens in new window (irregular menstruation), oligomenorrheaOpens in new window (insufficient number of cycles per year), or amenorrheaOpens in new window (absence of menses) all will interfere with the final attainment of peak bone mass by causing more rapid bone loss. Bone mass density steadily declines, particularly in non-weight-bearing limbs, as the number of missed menses increases and this loss of BMD may not be completely reversisble.

Irregular menses is primarily due to a deficiency of estrogen and, if not corrected promptly, ultimately will result in premature osteoporosis. Such menstrual irregularities/disorders could be caused by various weight loss, excessively intense exercise, and disorderd eating, along with associated extreme physical and/or psychological stress.

Specifically, women with menstrual disorders will lose as much as 2 % of their skeleton per year, almost tenfold more than the usual, natural rate. In other words, exercising excessively can negatively affect both the reproductive and the skeletal systems, altering the body’s normal hormonal milieu and causing a reduction in bone mass.

One study has found that total, vigorous, intense training for more than 8 h per week could lead to amenorrhea and, subsequently, osteoporosis with its inherent risks. Physical activity affects the skeleton differently during the various stages of puberty.

Studies have shown that estrogen increases skeletal sensitivity to mechanical loading, suggesting that early and mid-puberty are optimal times for skeletal benefit as far as bony deposition is concerned.

Female athletes, particularly in sports such as running, gymnastics, and swimming, reach menarche later than non-athletes. A study conducted on sisters found menarche occurred later in swimmers than their sedentary siblings, thus may potentially affect bone mass negatively.

Concluding Remark

A regular, well-functioning monthly cycle is of paramount importance in bone deposition during the adolescent growth spurt and then in prevention of bone loss after peak bone mass is achieved in the second decade of life.

The main hormone involved in bone regulation is estrogen which is secreted by the ovaries, affecting both the osteoclasts and the osteoblasts, keeping these two types of bone cells in balance in terms of their function on skeletal resorption and formation, respectively.

Additionally, the organs involved with controlling the menses are the hypothalamus, anterior pituitary and, of course, the ovaries. Each organ secretes different hormones, which interact in a complex, loop-type feedback mechanism to regulate the monthly cycle, in order to maximize bone deposition and minimize bone loss.

If menarche is delayed or if menstrual dysfunction occurs or menses disappears entirely, then the protective mechanism of estrogen on bone is lost. If this menstrual disturbances is not corrected fairly promptly, it will eventually result in osteopenia or frank osteoporosis, ultimately increasing one’s susceptibility to fractures. In fact, osteoporotic prevention starts as early as the initial onset of menarche during adolescence.

Additionally, other factors, such as lifestyle habits (nutrition, training, etc.), also play a very essential part in contributing to bone building (formation) or bone loss. As such, measures taken to ensure that the monthly female menstrual cycle is functioning correctly and optimally are of utmost importance to positively influence the final attainment of peak bone mass.

  1. Elgan C, Dykes AK, Samsioe G. Bone mineral density changes in young women: a two year study. Gynecol Endocrinol. 2004; 19(4): 169 – 77.
  2. Perez-Lopez FR, Chedraui P, Lopez-Cuadros JL. Bone mass gain during puberty and adolescence: deconstructing gender characteristics. Curr Med Chem. 2010;17:454 – 66.
  3. Clarke BL, Khosla S. Female reproductive system and bone. Arch Biochem Biophys. 2010;503:118 – 28.
  4. Brown S. Better Bones at every age. Lets Live Magazine, Oct 2000.
  5. Lebrum C. Menstrual cycle dysfunction. American Collage of Sports Medicine, Oct 2000.
  6. Nichols D. Bonnick S, Sanborn C. Bone health and osteoporosis. The Athletic Woman. 2000;19(2):233 – 49.
  7. Duncan CS, Blimki CJR, Cowell CT. Burke ST. Briody JN, Howman-Giles R. Bone mineral density in adolescent female athletes: a relationship to exercise type and muscle strength. Med Sci Sports Exerc. 2002;34:286–94.
  8. Galuska DA, Sowers MR. Menstrual history and bone density in young women. J Womens Health Gend Based Med. 1999;8(5):647–56.
  9. Thys-Jacobs S. Micronutrietns and the premenstrual syndrome: the case for calcium. J Am Coll Nutr. 2000;19(2):220–7.
  10. Brooks GA, Fahey TD, Baldwin KM. Exercise physiology: human bioenergetics and its applications. 4th ed. New York, NY: McGraw-Hill;2005.
  11. Women’s Health Orthopaedic Edition. Assessing health in young female athletes. 2000 November–December;3(6):205–7.
  12. Slemenda C, Longcope C, Peacock M, Hui S, Johnston C. Sex steroids, bone mass, and bone loss. J Clin Invest. 1996;97(1):14–21.
  13. Warren MP, Stiehl AL. Exercise and female adolescents: effects on the reproductive and skeletal systems. J Am Med Womens Assoc. 1999;54(3):115–20.
  14. Beals KA, Hill AK. The prevalence of disordered eating, menstrual dysfunction, and low bone mineral density among US collegiate athletes. Int J Sport Nutr Exerc Metab. 2006; 16(1):1–23.
  15. Zanker CL, Osborne C, Cooke CB, Oldroyed B, Truscott JG. Energy balance, bone turnover and menstrual history of sedentary female former gymnasts, aged 20–32. Osteoporos Int. 2004;15:145–54.
  16. Bonjour JP, Carrie AL, Ferrari S, Clavien H, Slosman D, Theintz G, et al. Calcium enriched foods and bone mass growth in prepubertal girls: a randomized, double-blind, placebo-controlled trial. J Clin Invest. 1997;99:1287–94.
  17. Bailey CA, Brooke-Wavell K. Exercise for optimizing peak bone mass in women. Proc Nutr Soc. 2008; 67:9–18.
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