Athletes &

Stress-fractures

 

 

 

 

 

 

 

The problem for athletes is that “the calcium hormones” serve two purposes:

-   regulating blood-calcium level

-   maintaining bone health

 

In athletes loading is increased and thus more micro-fractures have to be repaired and more damaged cells (due to the increased loading) have to be replaced by new ones. The damaged cells are decomposed and the calcium is deported by osteoclasts. New cells must replace damaged cells to maintain bone health. Thus osteoblasts have to compose more pre-calcified bone-matrix. This requires increased activity of osteoblasts, and thus osteoblast apoptosis is also increased in athletes. (exercise induces osteoblast apoptosis. (1))

 

So far - so good.

 

But the hormones that regulate bone formation and resorption to maintain bone-health, also regulate blood-calcium level. If considerable calcium is consumed, more calcium has to be temporarily stored in the bones prior to excretion to prevent elevation of blood-calcium level (excessive calcium in the blood blocks respiration because it blocks muscle functioning)  

 

This extra calcium can only be temporarily stored in the bones if it can precipitate on pre-calcified bone matrix which osteoblasts composed for this purpose. This calcium will subsequently be deported to be excreted because it is redundant calcium that is being temporarily absorbed for the sole purpose of preventing elevation of the blood-calcium level. Redundant calcium is deported according to the body's designed plan for the bones.

 

The loading on bones is so intense in athletes that maximum capacity of osteoblasts to compose new bone matrix is met. A small percentage of the total bone cells is damaged every training session. If remaining undamaged cells must compose new matrix to absorb redundant calcium, their osteoblasts will not be able to keep up with composing new matrix the next day when the cells are damaged due to loading.

Sot the repairing of microfractures will not be complete because regulating the blood-calcium level has top-priority.

 

You can compare it to an athlete that has to train every day but also has to do hard labor to make a living; such an athlete will never be able to increase muscle strength because he lacks time to recover.

 

If the bones (osteoblasts) of an athlete must recover and also must process redundant calcium to prevent excessive calcium in the blood, the osteoblasts' productivity will be insufficient to do both.

In athletes, especially, it is essential to prevent any unnecessary processing of calcium. This means that the athletes should not absorb any more calcium than they need to maintain bone-health.

It is also essential that athletes never consume large amounts of calcium in one meal (or supplement!); the more calcium consumption is spread through the day, the less redundant calcium will need to be temporarily absorbed in the bones.

 

 

Female athletes

Estrogen levels are decreased in female, because intense physical exercise makes the body produce less estrogen. (2)

Unfortunately, estrogen maintains bone health by inhibiting both uptake of calcium into the bones (3) and deportation of calcium (also indirectly through inhibiting PTH secretion) Thus the lower the estrogen level, the more devastating the effect of excessive calcium intake will be. Logically, exercise can never ‘compensate’ for the side effects of reduced estrogen levels. (4)

If estrogen levels are low, more calcium will be actually absorbed into the bones, increasing osteoblast activity and apoptosis.

The necessity of adequate estrogen levels is less strong if less calcium is consumed.

 

 

 

 

 

© 2000 Copyright Artists Cooperative Groove Union U.A.     

 

 

 

 

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Excessive Calcium Causes Osteoporosis

 

 

 

Sources

Abstracts of most sources can be found at the National Library of Medicine ;

 

(1) Meyer T, et al, Identification of apoptotic cell death in distraction osteogenesis. Cell. Biol. Int.1999 / 23 (6) / 439-446. , Landry P, et al, Apoptosis is coordinately regulated with osteoblast formation during bone healing. Tissue Cell 1997 / 29 (4) / 413-419.

(2) attiv A, Stress fractures and bone health in track and field athletes. J. Sci. Med. Sport 2000 / 3 (3) / 268-279. , Hobart JA, et al, The female athlete triad. Am. Fam. Physician 2000 / 61 (11) / 3357-3364, 3367. , Anderson JM, The female athlete triad: disordered eating, amenorrhea, and osteoporosis. Conn. Med. 1999 / 63 (11) / 647-652.

(3) Bryant HU, et al, An estrogen receptor basis for raloxifene action in bone. J Steroid Biochem Mol Biol 1999 / 69 (1-6) / 37-44. , Jilka RL, et al, Loss of estrogen upregulates osteoblastogenesis in the murine bone marrow. Evidence for autonomy from factors released during bone resorption. J. Clin. Invest. 1998 / 101 (9) / 1942-1950. , Sims NA, et al, Estradiol treatment transiently increases trabecular bone volume in ovariectomized rats. Bone1996 / 19 (5) / 455-461.Smith, G.R. et al, Inhibitory action of oestrogen on calcium-induced mitosis in rat bone marrow and thymus. J. Endocrinol. 1975 / 65 (1) / 45-53.

(4) Pettersson, U., et al, Low bone mass density at multiple skeletal sites, including the appendicular skeleton in amenorrheic runners. Calcif. Tissue Int. 1999 / 64 (2) / 117-125.