Although calcium is best known for its role in bone health, other factors including vitamin D, vitamin K, protein and fatty acids as well as fruit and vegetable intake, high-salt diets, caffeine and alcohol also have an influence (for more information, refer to Chapter 19). Exercise, particularly high-impact or weight-bearing exercise and to a lesser extent resist-ance exercise, provide some protection to bone health by improving bone mineral density (BMD). However, when exercise in combination with a low energy intake induces amenorrhoea, bone health is compro-mised; bone mass is lost and ultimately cannot be fully replaced. In this situation, calcium and vitamin D exert a weak effect in treatment but are essential for
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building bone mass and subsequently help to prevent stress fractures. Resumption of menstrual function, increasing energy availability and decreasing training load are important in protecting from further losses in BMD.
Calcium
Calcium is an important mineral for bone health. It maintains the structural or mineral content of bone and, in the presence of adequate intake, reduces bone resorption. Other functions of calcium in metabolism (in its ionised state) include regulation of muscle contraction, nerve conduction and normal blood clotting (see Table 8.2). Adequate dietary calcium during the growing years is essential for optimising peak bone mass; in adult years it helps in bone maintenance and slows the rate of bone loss. Bone loss of around 1% per year is a normal physiological process in both cortical and trabecular bone in both male and female, although women tend to lose cortical bone faster than men.
Weight-bearing or high-impact exercise, and to a lesser extent resistance exercise involving muscle pull on the loaded limb, increases bone mass at the skeletal site at which the strain is applied. Athletes who participate in impact sports like gymnastics, basketball and volleyball typically have higher BMD than sedentary controls and weight-supported sports.
Weight-supported activities like swimming and cycling do not provide enough gravitational forces or mechanical loading on the skeleton to significantly improve bone mass. Reduced BMD has been reported in elite cyclists. Disrupted bone turnover that involves reduced bone formation and increased bone breakdown can occur in cyclists during stage racing.
Inadequate energy intake relative to expenditure during racing (and training) may be one possible cause of low BMD among cyclists. Other causative factors implicated include low body weight, increased loss of calcium through sweat, and substantial time spent training.
Female athletes are at higher risk of low BMD, which is more strongly associated with disturbed menstrual function than low-energy diets, low cal-cium intakes or high calcal-cium turnover. Female run-ners are a high-risk group for low BMD if they have amenorrhoea. Despite the benefits of weight-bearing exercise on bone mass, the high prevalence of amen-orrhoea or oligoamenamen-orrhoea in females involved in elite sport negates this benefit.
Consequences of inadequate calcium intake and amenorrhoea in athletes
Inadequate intakes of calcium and potentially other micronutrients involved in bone health, in combina-tion with inactivity and low-energy diets, particularly in the bone-forming years can impair optimal skeletal development and increase the risk of stress fractures.
The age of reaching peak bone mass is genetically determined and highly variable, and occurs in late adolescence or early adulthood after cessation of bone growth (between 16 and 28 years). Once peak bone mass is reached, it is mainly the mechanical forces acting on the skeleton that consolidates BMD.
The highest prevalence of stress fractures is reported in athletes with menstrual disturbances including those with delayed menarche, oligoamen-orrhoea and amenoligoamen-orrhoea. Adolescents, irrespective of gender, are also at high risk of stress fractures during the growth spurt when BMD is lowest. In the USA, there has been a doubling of fractures in children over the last three decades, which is attrib-uted to low levels of physical activity, suboptimal calcium intakes and subsequent low BMD. Failure to achieve peak bone mass characterised by low BMD, whether due to menstrual dysfunction or to dietary or lifestyle issues in adolescence or early adult years, may also hasten the onset of osteoporosis in later life.
Although exercise offers some protection at weight-bearing sites in both adults and adolescents, it is not sufficient to negate the adverse effects of delayed menarche and the consequences of prolonged untreated amenorrhoea or oligoamenorrhoea on bone health.
In summary, a history of menstrual irregularity or delayed menarche impairs the attainment of peak bone mass and increases the risk of stress fractures, independent of calcium intake. Inadequate calcium intake, in combination with a low-energy diet during adult and adolescent years, can hasten the rate of bone loss and predispose an athlete to early osteopenia, stress factures and increase the risk of osteoporosis later in life.
Are calcium intakes inadequate in athletes?
Calcium intakes in adolescent and young adult female athletes are often far below the intakes required to optimise peak bone mass or prevent further bone loss. The prevalence of a negative calcium balance has increased in children and young
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females in western countries and is one reason for the increased incidence of stress fractures in children and adolescents. However, low energy availability associ-ated with very low energy diets and amenorrhoea is a more predictive determinant of low BMD than suboptimal calcium intake.
Are calcium requirements higher in athletes than non-athletes?
Little is known about calcium requirements in physically active people, although calcium losses and bone turnover may be higher than in sedentary people. Calcium losses in sweat are substantial in men undertaking vigorous exercise (100–300 mg per session) but much less in women (around 90 mg after 1 hour of vigorous exercise). These lower values are probably associated with lower sweat rates, although few studies have been published in female athletes to confirm these differences. Calcium requirements may therefore be higher in athletes who sweat profusely. Obligatory calcium losses in urine in both men and women can be substantial (>200 mg/day) but are largely unaffected by exercise. High-protein diets, high-salt diets, smoking and alcohol increase urinary calcium excretion, although losses vary among individuals and depending on diet, lifestyle and genetic influences. There is some evidence that sports people can compensate for potentially high calcium requirements by absorbing more calcium, even with low calcium intakes. Although calcium is under homeostatic control, this mechanism does not fully compensate for very low calcium intakes or high calcium losses.
Calcium recommendations in athletes
In the absence of specific recommendation for calcium intakes for athletes, the appropriate pop-ulation reference value, i.e. Adequate Intake (AI), can be used to estimate the probability of adequate (or inadequate) calcium intake in individual athletes, with caution. Population reference values for calcium have increased in western countries for all age groups over the last 10–15 years. The AI for maximal calcium retention for those aged 9–18 years is 1300 mg calcium daily, which was based on data from white females, the highest risk group. In adult females, the AI decreases to 1000 mg calcium daily. The goal for determining the AI in the USA and Canadian DRIs was to maximise calcium retention to optimise bone
health in the highest risk group. In adolescents and children, calcium retention and BMD is higher in males than females, and higher in blacks compared with whites. Hence, white females are at highest risk of negative calcium balance and poor bone health.
Where menstruation is delayed or absent, which is not uncommon in females undertaking strenuous training programmes, calcium recommendations are even higher. Although there are only a few inter-vention trials with calcium supplements published in athletic populations, the recommended intake of calcium for athletes with amenorrhoea is 1500 mg/day. This amount is similar to population recommendations for post-menopausal women not taking oestrogen.
Calcium recommendations may be slightly lower in blacks and males. Limited data are available on other population groups and may not truly reflect requirements. The US and Canadian DRIs for calcium are under review. Recent research suggests that the current cut-offs are an underestimate for some risk groups, particularly post-menopausal women, which could apply as well to female athletes with amenorrhoea.
Do high calcium intakes or calcium supplements improve bone health?
The best intervention strategy for improving bone health in any population group is largely unknown and influenced by many environmental, genetic, dietary and individual factors. In terms of meeting calcium recommendations, there is insufficient evidence to confirm the efficacy of using calcium-rich food sources, calcium supplements or both. Calcium supplements and/or high calcium intakes can improve calcium retention and balance. High-protein diets and high salt intakes increase calcium excretion. The current evidence favours increasing calcium intakes from food sources, which appears to increase bone accretion more than supplementation. This improve-ment has been attributed to the presence of coexisting nutrients in food and from better compliance with food than with taking supplements. The increased availability of calcium-fortified products, particularly products in a wide range of dairy foods and milks, should help athletes meet calcium recommendations.
For those athletes at risk of poor bone health, particularly females with menstrual disturbances or those on low-energy diets or avoiding or limiting
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dairy foods, calcium supplements may be needed to improve calcium retention. However, the independent benefits of calcium supplementation on increasing BMD at all stages of the life cycle are weak but may be worthwhile for some individuals but not everybody.
In randomised controlled trials of pre-menopausal women without amenorrhoea, calcium supplements of around 1000 mg/day slightly increased bone mass (0–1.17% increase per year). In older post-menopausal women, calcium supplements assisted in maintenance of, but not gain in, bone mass. In a meta-analysis of randomised trials of older post-menopausal women, calcium supplements of 1000 mg/day prevented the expected 1% per year loss of both cortical and trabecular bone.
Little is known about the effects of calcium sup-plements or high calcium intake on improving bone mass in female athletes. In one study, supplemental calcium 800 mg/day taken for 1 year in 23 young adult female distance runners (without amenor-rhoea) prevented cortical but not trabecular bone loss compared with matched controls. The average calcium intake in these women from dietary sources was close to or exceeded the AI of 1000 mg/day but energy intake in both the control and experi-mental group was fairly low at an average of about 1500 kcal/day. The few trials using higher doses of calcium supplements (up to 1500 mg/day) to increase BMD in amenorrhoeic athletes have shown equivo-cal results at different skeletal sites and may not have been conducted for long enough.
Where calcium supplementation is recommended, the amount required is dependent on the usual amounts of dietary calcium consumed and its bioa-vailability, which highlights the importance of using a dietitian to estimate calcium intake and food com-binations to enhance bioavailability. Because of the interaction between calcium and vitamin D in bone health, a vitamin D supplement may also be needed for those athletes not exposed to adequate sunshine.
Moreover, any gains in bone mass associated with calcium supplementation are not maintained after supplementation has ceased unless dietary calcium intakes are high to compensate. Clearly in the pres-ence of amenorrhoea, other interventions including hormone replacement therapy and increasing energy availability are more important to conserving or pre-venting further losses in bone mass than calcium intervention alone.
Vitamin D
The prevalence of vitamin D deficiency or insufficiency has recently increased worldwide. Although the adverse effects of deficiency on bone health are well known, negative effects of deficiency on other body systems is just emerging. Low vitamin D status is expected to be highest in those athletes who train inside or have little exposure to the sun from living in high latitudes, are dark skinned, use sunscreen or wear protective clothing.
Vitamin D is both a hormone and a nutrient. It is manufactured in the liver and kidney from the action of ultraviolet (UV) rays from the sun (or other sources) reacting with the compound 7-dehydrocho-lesterol in the skin, where it converted to its inactive form called provitamin D3 or cholecalciferol. Once transported to the liver, this inactive vitamin D, together with the small amount of vitamin D derived from food sources, undergoes further transforma-tion into another form called 25-dihydroxyvitamin D3 (also called calcidiol). This form of vitamin D3 is finally transported to the kidney where it is converted to the primary activated form called 1,25-dihydroxy-vitamin D3 [1,25(OH)2D3] or calcitriol.
Role of vitamin D
Activated vitamin D (calcitriol) is essential in the reg-ulation of calcium homeostasis. A deficiency results in inadequate bone mineralisation which, if prolonged, leads to rickets in children and osteomalacia in adults.
Compromised vitamin D status does diminish bone health and increase fracture risk in elderly popula-tions but whether the same effects occur in younger populations and athletes is speculative. In early stud-ies of athletes with stress fractures, vitamin D status was overlooked as a risk factor and not measured.
However, the role of vitamin D goes beyond calcium and bone metabolism. There is now mounting evidence that vitamin D deficiency negatively influences muscle function, immune function, inflammation, cell differ-entiation and growth, and that deficiency increases the risk of chronic non-skeletal diseases including cardiovascular disease, hypertension and some type of cancers. Measuring vitamin D status in people with these conditions has been overlooked in clinical practice, until recently. There is also some speculation, given the multiple roles of vitamin D and the increased prevalence of vitamin D deficiency reported in several risk groups in the population (e.g. elderly in residential
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care, adolescents, dark-skinned and veiled women), that the recommended AI for vitamin D might be too low to maintain bone health and reduce chronic disease risk.
Vitamin D status in athletes
Only a few studies have been conducted on the vitamin D status or vitamin D intake of athletes. In these studies, 37–68% of athletes showed deficient status based on biochemical measures, which is similar to the prevalence in the general population and in the same at-risk groups. There is some evidence that those athletes who follow low energy intakes or vegan diets are also at risk of low vitamin D status but the reasons for this are unclear. Generally, dietary sources of vitamin D are a minor contributor to vitamin D status, compared with exposure to sunlight, but become a more important source during winter when the sun is not strong enough to provide enough UV rays. In Sydney, Australia during summer, exposure of the hands, face and arms for about 6–8 min daily is needed to prevent deficiency of vitamin D in light-skinned people. In winter, exposure time increases more than threefold during the hottest part of the day when the sun’s rays are strongest. Individuals with darker skin need longer exposure to UV rays for vitamin D synthesis to occur than fair-skinned people. Vitamin D synthesis via the sun is not possible during most of the winter months for people living at latitudes of more than 40°N or 40°S because the sun never rises high enough to provide the direct sunlight needed. Sunscreen with an SPF of 8 or more blocks UV light needed for vitamin D synthesis.
Does low vitamin D status affect bone health and performance?
Currently, there are no known studies that have investigated the potential effects of marginal vitamin D deficiency on bone health or athletic performance.
Given the multiple roles of vitamin D in human metabolism, a prolonged inadequate intake accom-panied by a low biochemical status could increase the risk for stress fractures in athletes.
Are vitamin D supplements required in at-risk groups?
To potentially protect bone health and fracture risk in older people, supplementation with 1000–2000 IU vitamin D daily may be needed to prevent deficiency
in those who are unable to gain adequate exposure to sunlight, particularly in the winter months (Table 8.6). The same recommendations could be applied to athletes at high risk of stress fractures or in similar environmental circumstances where exposure to sunlight is limited (e.g. female athletes with amenorrhoea). In the absence of adequate UV light or sunlight, dietary sources of vitamin D contain only small amounts of vitamin D, and are unlikely to be consumed in amounts that will maintain adequate vitamin D status. Mandatory fortification of foods with vitamin D has increased in recent times in several European countries, which is likely to improve intake from dietary sources. However, the number and range of foods fortified with vitamin D is highly variable and may not address the problem, particularly in those athletes with low energy intakes.
The recommended dosage of vitamin D to prevent deficiency in the absence of adequate exposure to sunlight is 200–600 IU/day.
Once diagnosed, treatment of moderate to severe vitamin D deficiency requires vitamin D doses of 3000–5000 IU/day. Guidelines on prevention and treatment for the general population are summarised in Table 8.6. More research is needed to determine the prevalence of vitamin D depletion in athletes and the efficacy of vitamin D supplementation on infection, illness and stress fractures and BMD in trained athletes.
In summary, recommendations for improving bone health in athletes include maintenance of normal menstrual cycles (or oral contraceptive intervention), increasing dietary energy and/or calcium intake to at least meet or exceed the current recommended intakes, and adequate exposure to sunlight. Where access to
Table 8.6 Recommended daily dosage of vitamin D2 (ergocalciferol) supplements for prevention and treatment of vitamin D deficiency.
Prevent deficiency (in absence of adequate sun)
5–10 μg 200–600 IU
Reduce fracture risk (in elderly)
25 μg 1000 IU
Treat moderate to severe deficiency
75–125 μg (for 6–12 weeks)
3000–5000 IU (for 6–12 weeks) Source: Working Group of the Australian and New Zealand Bone and Mineral Society, Endocrine Society of Australia, Osteoporosis Australia, 2005.
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sun is limiting and calcium intakes are suboptimal, a combination of vitamin D and calcium supplements may help to enhance peak bone mass in adolescents and young adults and help prevent further bone loss in adult women.