Bone Health
Introduction
Bone health is an important but often overlooked subject for athletes, as well as the general population. Bone density is a critical component to overall health and function throughout the lifespan.
Maximizing bone mineral density is crucial because females are particularly susceptible to low bone mineral density, known as osteopenia and osteoporosis.
The following information will provide a brief overview of bone physiology, growth and remodeling, the impact of energy and micronutrient intake on bone health, and practical applications to support athlete bone health.
Bone physiology
The human skeleton is made up of cartilage and bone. It provides the structure of the human body, protects vital organs, serves as an attachment point for muscles, and stores calcium.
Bone is one of the hardest materials within the human body, yet it is also very light in weight. The composition of bone includes water, calcium phosphate in the form of hydroxyapatite, and protein in the form of collagen. The structure of healthy bones largely differs to that of osteoporotic bone (i.e., during osteopenia and osteoporosis), as shown below.
Normal bone vs. osteoporotic bone
Stage 1
Normal bone density
Stage 2
Osteopenia
Stage 3
Osteoporosis
Stage 4
Severe osteoporosis
Bone formation and turnover
Bone health is regulated by the endocrine system, with multiple hormones influencing the building, maintenance and breakdown of bone, including, but not limited to, parathyroid hormone (PTH) and estrogen.
The information below describes the process when the endocrine system is functioning as designed, with adequate energy availability and micronutrient intake from the diet.
Bone modeling and remodeling
Bone modeling is the process of building new bone tissue, and bone remodeling is a process of continuous breakdown and formation. In youth, longitudinal bone modeling occurs at the sites of the epiphysial (growth) plates. Peak bone density is achieved in the first few decades of life. With mechanical loading, bone diameter can continue to grow into adulthood. Specific cells called osteoclasts, osteocytes and osteoblasts (click below for more information on each) are responsible for development, growth and remodeling of bone tissue. The process of bone modeling and remodeling can be seen below.
Osteoctyes are the most common cells found within the bone tissue. They monitor the health of the bone and when stressors are placed on the bone. If the bone tissue becomes damaged, osteocytes are responsible for sending signals to the osteoclasts and osteoblasts, to remove damaged bone tissue and build new bone tissue, respectively.
Osteoclasts:
When old or damaged bone tissue is present, osteoclasts release enzymes that dissolve that bone tissue. Osteoclasts will only break down tissue identified by osteocytes.
Osteoblasts:
Osteoblasts are activated by hormones and deposit a bone matrix (collagen, calcium, phosphate and other minerals) onto areas of the bone that either need to grow or be repaired. The bone matrix then hardens to become new healthy bone. Once the new bone tissue has been laid, osteoblasts will either transform into osteocytes, or die.
Bone remodeling
There are two primary factors that impact how the bone is remodeled and the strength of the bone throughout adulthood:
1
The availability of calcium in the blood
The human body tightly regulates serum calcium levels and will sacrifice bone tissue to maintain calcium homeostasis. Without adequate calcium ingestion, calcium is not available to be deposited into the bone tissue. In youth and early adulthood, if inadequate amounts of dietary calcium are consumed, bone formation may be compromised. In addition, existing bone tissue may be broken down to release stored calcium back into the blood to maintain serum calcium levels. Prolonged breakdown of bone tissue can compromise bone density in both youth and adulthood.
2
The pull of gravity and muscles on the skeleton
Exercise is classed as weight bearing when the person is on their feet and the skeleton is supporting their body weight. Exercises like walking, running, dancing, as well as sports involving running or jumping (e.g., tennis, soccer, basketball, etc), are all considered weight bearing. The mechanism of weight bearing activity causes muscles and tendons to put stress on the bone tissue. This stimulates bone formation and strengthens bones.
Bone health
throughout the lifespan
Bone is a dynamic and active tissue. The greatest amount of growth in bone length and diameter occurs during puberty, until the epiphyseal (growth) plates close. (see below). During this period, over 90% of an individual’s total bone density is acquired.
Bone mass can also be accrued through the third decade of life through a combination of load bearing physical activity and adequate dietary intake. After this point, the focus shifts to the maintenance of bone mineral density.
Osteoporosis and its pre-cursor, osteopenia are health conditions characterized by low bone mineral density. Osteoporosis is generally considered an aging disease. However if peak bone mineral density is not acquired during puberty, and there is continued inadequate energy and/or micronutrient intake, it is possible for athletes to develop osteopenia and osteoporosis at a younger age.
Porous and brittle bones are not compatible with life as a competitive athlete and can cause an early end to promising careers.
Bone density throughout the lifespan
As over 90% of bone mineral density is acquired in the first two decades of life, providing adequate calcium to maximize bone density during this time is critical to lifelong bone health.
Critical time points
Puberty
Throughout childhood and adolescence, cells called chondrocytes within the epiphysial plates are continuously producing new cartilage. The cartilage will ultimately be replaced by mature osteocytes when the epiphysial plates ossify or ‘close.’ At the same time, modeling and remodeling of existing bone is also occurring. Bone modeling is closely related to the production of sex steroid hormones, particularly estrogen in females.
Menopause
Bone loss with aging is not an unexpected phenomenon, but effort should be made to minimize losses in bone mineral density. In females, estrogen production significantly decreases with the onset of menopause. This decrease, when combined with lack of weight bearing exercise and low intake of dietary calcium, vitamin D and magnesium, can significantly increase the risk of the development of osteopenia or osteoporosis. The risk is even greater if an individual already has weak and porous bones prior to menopause.
Nutrition and bone health
Energy balance
Adequate energy intake supports the overall health of bone. When in prolonged energy restriction, disruptions occur within the endocrine system that can ultimately have a negative impact on bone health. See
for more information on the impact of energy restriction on bone health.
Protein
Protein plays an important role in the production and action of Insulin-like Growth Factor (IGF-1), which is necessary for bone formation. IGF-1 stimulates the absorption of the bone mineral elements calcium and phosphate in the intestines, as well as the renal tubular reabsorption of phosphate. Without adequate protein intake during puberty, the production and action of IGF-1 are impaired, which can negatively impact bone mineral density.
In older athletes, particularly post-menopause, bone strength is positively correlated with greater dietary protein intake. In addition to bone health, adequate protein intake with aging can also reduce the risk of muscle weakness and loss (sarcopenia).
See
for more information.
Micronutrients
Calcium
Calcium is the primary mineral found in bone tissue. When adequate calcium is consumed during both the development and maintenance phases of bone formation, bone mineral density is maximized and subsequently the integrity of the bone is maintained throughout the lifespan.
Recommended daily intake
9-13 years
1300 mg
14-18 years
1300 mg
19-50 years
1000 mg
51-70 years
1200 mg
70+ years
1200 mg
Insufficient intake
When serum calcium falls below a certain level and no exogenous calcium is consumed, the calcium that is stored within the bone can be removed to maintain serum calcium homeostasis. Continuous removal of calcium is detrimental to the integrity of the bone structure if not replaced.
Excess intake
Hypercalcemia (too much calcium in the blood) is most frequently caused by issues with the parathyroid hormone, or other medical conditions. Excess supplemental intake of calcium (>2000 mg/d) can also cause hypercalcemia which, in turn, can cause weakness in the bone or bone pain.
Vitamin D
Vitamin D is a critically important micronutrient for bone health. Vitamin D and its metabolites are a key component to endocrine regulation of serum calcium through the mechanisms of intestinal absorption, stimulating the breakdown of bone tissue and renal absorption of calcium.
Recommended daily intake
9-13 years
600 IU (15 µg)
14-18 years
600 IU (15 µg)
19-50 years
600 IU (15 µg)
51-70 years
600 IU (15 µg)
70+ years
800 IU (20 µg)
Due to the limited number of natural sources of vitamin D and limited exposure to UV rays from the sun, supplemental intake of vitamin D3 may be warranted after consulting with a physician. See the vitamin D section of ‘Micronutrients’ for more detail.
Insufficient intake
Inadequate Vitamin D intake and subsequent Vitamin D deficiency negatively impacts the regulation of calcium, which can result in poor bone health. Other symptoms of Vitamin D deficiency include muscle weakness, muscle aches, fatigue, joint pain, and increased suseptibility to illness.
Excess intake
Toxicity is rare but generally occurs with excessive supplemental intake of Vitamin D. Hypervitaminosis D can result in hypercalcemia in the blood due to disruptions in calcium regulation.
Magnesium
From an endocrine standpoint, magnesium indirectly impacts bone health because it is an essential co-factor in the activation of Vitamin D (1,25[OH]2D or calcitriol). Consuming adequate amounts of magnesium is necessary in order to achieve the optimal benefits of Vitamin D.
Recommended daily intake
9-13 years
240 mg
14-18 years
360 mg
19-50 years
310-320 mg
51-70 years
320 mg
70+ years
320 mg
Insufficient intake
Based on NHANES data, nearly half of all Americans consume less magnesium than recommended. Diagnosing a magnesium deficiency is difficult though since serum magnesium status does not always reflect total body magnesium.
Excess intake
Toxicity generally occurs with excess supplementation of magnesium, or in individuals with renal issues. Excess magnesium intake from food does not pose a risk in healthy individuals because the kidneys eliminate excess amounts in the urine.
Phosphorus
Phosphorus is another mineral involved in the mineralization of bone tissue as part of hydroxyapatite. Approximately 85% of phosphorus in the human body is found within the skeleton. It is a necessary mineral for osteoblasts to work and osteocytes to form.
Recommended daily intake
9-13 years
1250 mg
14-18 years
1250 mg
19-50 years
700 mg
51-70 years
700 mg
70+ years
700 mg
Insufficient intake
Phosphorus deficiency is rare in adults. According to NHANES data, most Americans consume more than the recommended daily intake for phosphorus.
Excess intake
Excess phosphorus intake may lead to hypocalcemia or low serum calcium due to the affinity of phosphorus for binding to calcium in the digestive tract, reducing calcium absorption and availability for building bone structure. High dietary phosphorus intake may also increase PTH secretion, which in turn can lead to increased bone resorption or breakdown to release calcium into the bloodstream.
Practical suggestions
Adequate energy intake can help to minimize the risk of micronutrient deficiencies, particularly when a wide variety of foods are consumed.
Female athletes should be encouraged to eat regularly throughout the day, between 4-6 meals including multiple food groups at each meal.
Protein intake is also critically important when it comes to developing and maintaining bone mineral density. It is highly recommended to screen female athletes for low energy availability/REDs, particularly those at high risk.
This can help to identify athletes who are in need of intervention and education.
See
for more information on screening for low energy availability.
bone health
References
Ballabriga, A. (2000). Morphological and physiological changes during growth: An update. European Journal of Clinical Nutrition, 54 Suppl 1, S1-6.
Benedetti, M. G., Furlini, G., Zati, A., & Letizia Mauro, G. (2018). The Effectiveness of Physical Exercise on Bone Density in Osteoporotic Patients. BioMed Research International, 2018, 1–10.
Bhattarai, H. K., Shrestha, S., Rokka, K., & Shakya, R. (2020). Vitamin D, Calcium, Parathyroid Hormone, and Sex Steroids in Bone Health and Effects of Aging. Journal of Osteoporosis, 2020, 9324505.
Bonjour, J.P., & Chevalley, T. (2014). Pubertal timing, bone acquisition, and risk of fracture throughout life. Endocrine Reviews, 35(5), 820–847.
Feng, X. (2009). Chemical and Biochemical Basis of Cell-Bone Matrix Interaction in Health and Disease. Current Chemical Biology, 3(2), 189–196.
Fleet, J. C. (2017). The Role of Vitamin D in the Endocrinology Controlling Calcium Homeostasis. Molecular and Cellular Endocrinology, 453, 36–45.
Rizzoli, R., Biver, E., Bonjour, J.-P., Coxam, V., Goltzman, D., Kanis, J. A., Lappe, J., Rejnmark, L., Sahni, S., Weaver, C., Weiler, H., & Reginster, J.-Y. (2018). Benefits and safety of dietary protein for bone health-an expert consensus paper endorsed by the European Society for Clinical and Economical Aspects of Osteopororosis, Osteoarthritis, and Musculoskeletal Diseases and by the International Osteoporosis Foundation. Osteoporosis International: A Journal Established as Result of Cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA, 29(9), 1933–1948.
Rondanelli, M., Faliva, M. A., Tartara, A., Gasparri, C., Perna, S., Infantino, V., Riva, A., Petrangolini, G., & Peroni, G. (2021). An update on magnesium and bone health. Biometals: An International Journal on the Role of Metal Ions in Biology, Biochemistry, and Medicine, 34(4), 715–736.

Shaker, J. L., & Deftos, L. (2000). Calcium and Phosphate Homeostasis. In K. R. Feingold, B. Anawalt, M. R. Blackman, et al. (Eds.), Endotext. MDText.com, Inc.; May 17, 2023.
Shanb, A. A., & Youssef, E. F. (2014). The impact of adding weight-bearing exercise versus nonweight bearing programs to the medical treatment of elderly patients with osteoporosis. Journal of Family & Community Medicine, 21(3), 176–181.
Uwitonze, A. M., & Razzaque, M. S. (2018). Role of Magnesium in Vitamin D Activation and Function. The Journal of the American Osteopathic Association, 118(3), 181–189.