A brief review of bone dynamics is included below to illustrate the relationship between mineral metabolism and hormones.
Bone tissue contains cells that are responsible for bone formation and degradation of its matrix (resorption). These cells (osteocytes) are dependent upon an adequate supply of nutrients. During times of growth and exercise a cell’s requirement for nutrients increases. The rate of bone formation remains constant throughout life. Long bones growth determines heights and is genetically determined.
Bone resorption increases as athlete’s age. The resorption and subsequent rebuilding of bone occurs at a relatively high rate during periods of growth. Growth is thus a result of increased activity of osteoblast (cells that form bone), which dominate over the osteoclasts or cells responsible for the degradation of bone.
When an athlete finishes growing and skeletal growth stops, bone to remain vital must undergo the process known as bone remodeling.
Remodeling is the result of a balance between bone destruction and new formation. Aging causes osteoclast activity to exceeds that of osteoblast activity.
Once an athlete loses the ability to form new bone to replace the bone lost during degradation, osteoporosis has developed. This net decrease in bone mass present significant concerns to female athletes.
Bone is a dynamic tissue categorized as cancellous or cortical bone. Cancellous (trabecular or spongy bone) differs from cortical (compact or dense) bone in being more metabolically active. Cancellous bone undergoes constant turnover and are thus metabolically very active, as bones go.
Individual bones are formed by bone-modeling. Each bone contains a different proportion of cortical and cancellous bone.
Vertebral (spinal) bones contain much higher amounts of cancellous (spongy) bone tissue than any other bone in the body. They are metabolically very active.
The ends of long bones that join other bones (knee, hip, wrist and ankle, shoulder) contain significantly more cancellous bone than the shaft of the bone contains.
Due to the high metabolic rate of cancellous bone, during menopause when bone resorption predominates, those sites with high cancellous bone tissue (more active resorption) results in loss of bone mass.
During growth, modeling of the long bones in the limbs results from new bone formation at the epiphysis or ends of the bone. The cells first produce cartilage, which is ultimately replaced by the mineralized tissue, bone.
Skeletal growth determines height and is completed by the age of 18 in females and 22 in males. After growth stops, remodeling becomes the sole process through which bone is modified.
Bone remodeling then only occurs as osteoclast resorption of bone precedes new bone being formed.
The loss of bone mass that occurs during the early post-menopausal period is inevitable and results from a cessation of the normal ovarian production of estrogen.
The estrogen that is produced is estrone, instead of estradiol and is due to its synthesis from testosterone and androstenedione.
Osteoclast activity predominates in this estrogen depleted environment, which accelerates bone loss.
The loss of bone in healthy females athletes occurs despite an adequate or even supranormal intake of calcium.
During the later decades of a life (menopause), osteoblast activity is unable to keep pace and replace the bone lost. Each remodeling cycle causes a further net loss in bone mass.
Loss of bone mass increases a menopausal athlete’s susceptibility to experience fractures in these bones (hips, knee, wrists and ankles).
Women who have strong bones at the start of menopause, stand a better chance of keeping their bones strong and remaining injury free.
Athlete’s who enter the post-menopausal period with already high bone mass levels and increased lean body mass, will delay their entry into the fracture risk group by more than a decade.
To counter the inevitable decline in bone mass, The Athlete’s Diet recommends that female athletes prepare their body through a program of exercise and dietary supplements while they are young.
One of the benefits of intense exercise is the stimulation of osteoblast. They form bone in response to stress, thereby increasing its bone mass.
Bone is a mineralized tissue that gains strength form the addition of the mineral, calcium. The more calcium incorporated into its matrix, the stronger the bone.
Calcium homeostasis is maintained through the opposing actions of the two calcium-regulating hormones (parathormone and calcitonin).
Parathormone regulates both calcium and phosphate concentrations in the blood through direct effects on bone resorption and the excretion of calcium by the kidneys.
Parathyroid hormone (parathormone) is secreted by the parathyroid gland whenever calcium ion concentration in the blood is lowered. The increase in circulating parathyroid hormone causes the removal of calcium from the skeleton. The result is a loss of mineralization of bone.
Parathyroid hormone also stimulates the conversion of vitamin D to its active form (1,25 dihydroxycholecalciferol) in the kidney. Active vitamin D initiates production of calcium-binding protein, which aids in the absorption of calcium from the intestine. The effect of parathormone is to increase the level of blood calcium ions at the expense of skeletal assets.
Parathyroid hormone is composed of a single polypeptide chain containing 84 amino acids. It is formed from a larger precursor molecule (pro-PTH) illustrating the general phenomena that secreted proteins and hormones are first synthesized in larger precursor forms.
Post-menopausal athletes have impaired calcium absorption due to the lack of ovarian estrogen. The lack of estrogen results in lower calcium ion concentration in the blood, which triggers more parathyroid hormone release. Parathyroid hormone continues to demineralize bone and further reduces bone mass.
The belief, that calcium supplementation by post-menopausal women can prevent osteoporosis is probably wrong.
Phosphorous intake always exceeds that of calcium because all foods contain plentiful amounts of phosphorous, but only a few contain calcium.
A high phosphorous diet lowers the calcium level of the blood, which in turn stimulates parathyroid hormone secretion.
Low calcium to phosphate ratios causes a perpetual elevation in parathyroid hormone. Parathyroid hormone reduces bone density by removing calcium. Many foods contain phosphate in the form of additives.
Diets, that avoid dairy product due to their fat and caloric content, increase the risk of accelerating bone loss.
Vitamin D is involved in calcium absorption. A significant percentage of elderly athletes are deficient in vitamin D.
The primary reasons for lowered levels of vitamin D are insufficient exposure to ultraviolet light, which is required for skin biosynthesis of vitamin D and limited dietary intake of vitamin D rich dairy products.
Vitamin K, the clotting vitamin, is also required in the synthesis of the extracellular bone protein, osteocalcin.
Osteocalcin is involved in the initial stages of the mineralization of collagen. Collagen (the organic matrix of bone) and calcium mineralization maintain proper bone density.
Vitamin K is thus important for bone health throughout life and supplementation prior to menopause may be beneficial. The goal being to to reduce the risk of incurring fractures.
The Athlete’s Diet relies on physical activity and sport to increase bone mass prior to a woman’s entry into menopause.
It’s program stresses exercise early on in life, to prevent diseases later on.
Its foods contain an abundance of calcium, protein and vitamins to maintain and stregnthen bone. Its goal of increased bone mass is also achieved by athletes losing less bone.
This can occur by increasing circulating levels of calcium and incresing the mineralization of bone with daily calcium supplements.
The theory assumes that athletes who obtain adequate amounts of calcium before menopause and maximize their bone density while young can delay the damaging consequence of menopause.
The Athlete’s Diet is a preventative approach. It is based on acquiring increased density and mass of bone through intense exercise and sound nutrition.
The earlier a program is initiated the longer an athlete can delay entering this critical period of life.