• Expert opinion
  • 2013

The importance of vitamin D for athletes

Published on

01 September 2013

Daniel J. Owens and Graeme L. Close, Liverpool John Moores University, Research Institute for Sport and Exercise Science, Liverpool, United Kingdom

“The importance of sunlight for physical performance has been known for centuries. Indeed ancient Greek Olympians were encouraged to train under the sunrays presumably due to the benefits to physical health described by the Greek physician Antyllus. However, only in recent times and with the development of scientific principles has the data pointed our understanding of the beneficial effects of sunlight exposure for muscle health, and potentially athletic performance, to vitamin D. It is now apparent that its effects may be explained by the vitamin’s regulation of genomic and non-genomic cellular pathways inside skeletal muscle tissue (1). This field of research is however in its infancy; and given the complexity of cell signaling and control of gene expression, which vitamin D appears to mediate, there are many questions yet to be answered.

Epidemiological data indicates poor vitamin D status is widespread around the globe, even in sun-rich environments. The classification of vitamin D deficiency is a highly debated topic, with much disparity as to what serum 25-hydroxyvitamin D (or 25[OH]D) concentrations constitute a deficiency, what is ‘optimal’ and what is a safe concentration. If we consider the US Institute of Medicine’s guidelines for vitamin D status classification, deficiency is defined as concentrations below 30 nmol/L. However, such recommendations are considered by many to be too conservative with some authors suggesting that 100–250 nmol/L is the optimal level for human health (2). Observational studies indicate that vitamin D deficiency (below 30 nmol/L) and inadequacy (below 50 nmol/L) – as defined by the US Institute of Medicine – are prevalent in athletes (3–12). Furthermore, these observations appear to be irrespective of competition standard and geographic location. Such findings are likely attributable to a predominantly sun-shy lifestyle in developed countries, few foods containing vitamin D, severe cloud cover at northerly latitudes, sub-optimal solar zenith for cutaneous vitamin D synthesis during winter months and covering the majority of one’s skin with clothing.

There appear to be a number of ways in which vitamin D affects cellular processes that may potentially impact cellular physiology. It is generally accepted that these processes fall into two main categories: 1) genomic effects mediated by interaction of 25(OH)D with the vitamin D receptor (VDR) and 2) non-genomic effects mediated by numerous transmembrane signaling pathways initiated by 25(OH)D. Available evidence suggests that the impact that vitamin D may have on muscle fibers (myotubes) and subsequently muscle function, may be more dependent on rapid non-genomic mechanisms than alterations in gene expression mediated by the VDR (13) and indeed it is currently unknown whether the vitamin D receptor exists in fully differentiated muscles as recent investigations have failed to identify the receptor. One major mechanism mediated by 25(OH)D that may impact upon muscle function is its role in calcium homeostasis (14). As calcium is essential for interaction of actin and myosin, it is paramount that intracellular calcium concentra-tions remain within the physiological range for normal muscle contraction. A further mechanism by which vitamin D may mediate the function of muscle, has been provided by investigations demonstrating a role for 25(OH)D in phosphate uptake of skeletal muscle tissue (14). Like calcium, phosphate is a key substrate for muscle contraction involved in cross bridge cycling. There is also evidence to suggest that vitamin D may directly influence contractile components of skeletal muscle tissue.

Emerging data suggests that adequate vitamin D concentration is important for skeletal muscle regeneration following damage. In vitro experiments and animal studies have shown that expression of the VDR gene is increased significantly following injury in skeletal muscle tissue (15). In addition, 25(OH)D3 induced the synthesis of factors related to the generation of new muscle tissue (16). Moreover, recent data suggests that 25(OH)D seems to stimulate the proliferation and differentiation of muscle cells and the formation of new blood vessels (angiogenesis), a key process in tissue development and repair (17).

Taken together, the evidence described above suggests a firm link between vitamin D and the function and health of skeletal muscle tissue. However in order to fully establish this link, we must consider if such data translates into whole muscle/whole body physical performance. Such data is lacking in young healthy and particularly ‘athletic’ populations. There is however data from elderly populations that directly suggest that poor vitamin D status is associated with poorer physical performance and that this may be attributed to aberrant muscle function, muscular disease (myopathy) and in some cases muscle loss (atrophy) (18–22). Recent well-controlled and designed studies suggest vitamin D may have a role in moderating the age related decline in muscle function (23-28).

Oral supplementation with vitamin D3 is an effective method for elevating serum 25(OH)D concentrations responding in a dose dependent fashion (29). Furthermore, it should be noted that D3 is more effective than D2 in elevating and maintaining serum 25(OH)D concentrations (30) particularly during the winter months. Trials in young healthy and active cohorts reveal deficiency is reversible with oral supplementation (31). The data provided thus far demonstrate the positive effects of supplementing with high doses of vitamin D, but toxicity from vitamin D supplementation must also be considered when supplementing with vitamin D. The US Institute of Medicine has set the ‘no observed effects level’ (NOAEL) for vitamin D intake at 4,000 IU per day (32). However, in review of scientific literature it is apparent that no side effects have been reported at daily doses of 10,000 IU a day (33). It is clear that vitamin D deficiency is treatable with oral supplemen-tation as evidenced by the data provided. However, further work is warranted to establish the effect of varying vitamin D concentrations on muscle function, from a functional and molecular perspective.”


1. Ceglia L. and Harris S. S. Vitamin D and its role in skeletal muscle. Calcified tissue international. 2013; 

2. Heaney R. P. and Holick M. F. Why the IOM recommendations for vitamin D are deficient. J Bone Miner Res. 2011; 26(3):455–457.

3. Lehtonen-Veromaa M. et al. Physical activity and bone mineral acquisition in peripubertal girls. Scand J Med Sci Sports. 2000; 10(4):236–243.

4. Ducher G. et al. Vitamin D status and musculoskeletal health in adolescent male ballet dancers a pilot study. J Dance Med Sci. 2011; 15(3):99–107.

5. Hamilton B. et al. Vitamin D deficiency is endemic in Middle Eastern sportsmen. Public Health Nutr. 2010; 13(10):1528–1534.

6. Halliday T. M. et al. Vitamin D status relative to diet, lifestyle, injury, and illness in college athletes. 

Med Sci Sports Exerc. 2011; 43(2):335–343.

7. Lovell G. Vitamin D status of females in an elite gymnastics program. Clin J Sport Med. 2008; 18(2):

8. Morton J. P. et al. Seasonal variation in vitamin D status in professional soccer players of the English Premier League. Appl Physiol Nutr Metab. 2012; 37(4):798–802.

9. Bescós García R. and Rodríguez Guisado F. A. Low levels of vitamin D in professional basketball players after wintertime: relationship with dietary intake of vitamin D and calcium. Nutr Hosp. 2011; 26(5):945–951.

10. Close G. L. et al. Assessment of vitamin D concentration in non-supplemented professional athletes and healthy adults during the winter months in the UK: implications for skeletal muscle function. J Sports Sci. 2013; 31(4):344–353.

11. Wilson G. et al. Markers of bone health, renal function, liver function, anthropometry and perception of mood: a comparison between Flat and National Hunt Jockeys. Int J Sports Med. 2013; 34(5):453–459.

12. Wolman R. et al. Vitamin D status in professional ballet dancers: Winter vs. summer. J Sci Med Sport. Published online February 2013.

13. Nibbelink K. A. et al. 1,25(OH)2-vitamin D3 actions on cell proliferation, size, gene expression, and receptor localization, in the HL-1 cardiac myocyte. J Steroid Biochem Mol Biol. 2007; 103(3–5):533–537.

14. Girgis C. M. et al. The roles of vitamin D in skeletal muscle: form, function, and metabolism. Endocr Rev. 2013; 34(1):33–83.

15. Srikuea R. et al. VDR and CYP27B1 are expressed in C2C12 cells and regenerating skeletal muscle: potential role in suppression of myoblast proliferation. Am J Physiol Cell Physiol. 2012; 303(4):396–405.

16. Stratos I. et al. Vitamin D increases cellular turnover and functionally restores the skeletal muscle after crush injury in rats. Am J Pathol. 2013; 182(3):895–904.

17. Garcia L. A. et al. 1,25(OH)(2)vitamin D(3) enhances myogenic differentiation by modulating the expression of key angiogenic growth factors and angiogenic inhibitors in C(2)C(12) skeletal muscle cells. 
J Steroid Biochem Mol Biol. 2013; 133:1–11.

18. Wicherts I. et al. Vitamin D status predicts physical performance and its decline in older persons. J Clin Endocrinol Metabol. 2007; 92:2058–2065.

19. Mowe M. et al. Low serum calcidiol concentration in older adults with reduced muscular function. J Am Geriatr Soc. 1999; 47:220–226.

20. Houston D. et al. Association between vitamin D status and physical performance: The InCHIANTI Study. J Gerontol. 2007; 62A:440–446.

21. Bischoff-Ferrari H. et al. Higher 25-hydroxyvitamin D concentration are associated with better lower-extremity function in both active and inactive persons aged >60y. Am J Clin Nutr. 2004; 80:752–758.

22. Bischoff H. et al. Muscle strength in the elderly: its relation to vitamin D Metabolites. Arch Phys Med Rehab. 1999; 80:54–58.

23. Visser M. et al. Low Vitamin D and high parathyroid hormone levels as determinants of loss of muscle strength and muscle mass (Sarcopenia): The Longitudinal Aging Study Amsterdam. J Clin Endocrinol Metabol. 2003; 88:5766–5772.

24. Bischoff H. et al. Effects of vitamin D and calcium supplementation on falls: a randomized controlled Trial. J Bone Min Res. 2003; 18:343–351.

25. Gerdhem P. et al. Association between 25-hydroxy vitamin D levels, physical activity, muscle strength and fractures in the prospective population-based OPRA study of elderly women. Osteoporosis Int. 2005; 16:1425–1431.

26. Bunout D. et al. Effects of vitamin D supplementation and exercise training on physical performance in Chilean vitamin D deficient elderly subjects. Exp Gerontol. 2006; 41:746–752.

27. Dhesi J. et al. Vitamin D supplementation improves neuromuscular function in older people who fall. 
Age Ageing. 2004; 33:589–595.

28. Verhaar H. et al. Muscle strength, functional mobility and vitamin D in older women. Ageing Clin Exp Res. 2000; 12:455–460.

29. Lagari V et al. The role of vitamin D in improving physical performance in the elderly. J Bone Miner Res. Published online April 2013.

30. Heaney R. P. et al. Vitamin D3 is more potent than vitamin D2 in humans. The Journal of clinical endocrinology and metabolism. 2011; 96(3):447–452.

31. Watkins C. M. and Lively M. W. A review of vitamin d and its effects on athletes. Phys Sportsmed. 2012; 40(3):26–31.

32. Institute of Medicine. Dietary Reference Intakes for calcium and vitamin D. Report Brief. November 2010.

33. Glade M. J. A 21st century evaluation of the safety of oral vitamin D. Nutrition. 2012; 28(4):344–356.

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