Vitamin D in athletes

Vitamin D remains a recurring topic in sport because low vitamin D status is common in athletic populations, particularly during winter at higher latitudes, and because vitamin D has well-established roles in calcium–phosphate homeostasis and skeletal health. Interest has expanded beyond bone, driven by mechanistic evidence that vitamin D receptors are expressed in multiple tissues (including skeletal muscle and immune cells) and by observational reports linking low vitamin D status to outcomes relevant to training consistency (illness burden), tissue repair, and possibly muscle function. At the same time, the field is characterised by disagreement over cut-off values, heterogeneity in study design and outcomes, and a tendency for applied narratives to drift, extreme views on supplementation, and claims beyond what the intervention evidence can support. In a series of blogs with Graeme Close and Dan Owens, we will remove confusion and come up with clear guidelines for sports practice.

This first blog provides the foundation: what vitamin D is, why athletes frequently present with low status, what the evidence suggests vitamin D can plausibly influence, and where the claims exceed the data. The second blog will focus on assessment (what to measure, how to interpret results, and common methodological/practical errors). The third blog will translate the evidence into applied supplementation strategies.

What vitamin D is and why winter status is predictable

Vitamin D is obtained primarily through skin synthesis following ultraviolet B (UVB) exposure, with smaller contributions from diet and supplements. Following synthesis or ingestion, vitamin D is converted in the liver to 25-hydroxyvitamin D [25(OH)D], the main circulating metabolite used to assess status, and then further hydroxylated to 1,25-dihydroxyvitamin D [1,25(OH)₂D], the biologically active hormone, primarily in the kidney (with additional tissue-level activation in multiple organs) (1). 

For athletes, the key practical point is that UVB availability is seasonal and latitude-dependent. At temperate latitudes (around ~40° north/south and above), there are months where ambient UVB is insufficient for meaningful dermal vitamin D synthesis, even on bright days, because solar zenith angle reduces the UVB reaching the earth’s surface. An often-used rule of thumb is that if your shadow is longer than you are tall, you are not making vitamin D.

If your shadow is longer that you are tall, you are not making Vitamin D.

This should be treated as a rule-of-thumb, not a diagnostic test, but it is directionally consistent with the seasonal physiology. This “vitamin D winter” helps explain why team screening frequently finds lower 25(OH)D values late in winter, particularly in athletes who train indoors, wear extensive clothing, or have limited habitual sun exposure.

A second predictable determinant is skin pigmentation. Higher melanin content reduces the efficiency of vitamin D synthesis for a given UVB exposure. Consequently, athletes with darker skin living or training at higher latitudes are at increased risk of low 25(OH)D, especially in winter. This is relevant to screening and risk stratification, and it also becomes relevant to interpretation in ethnically diverse squads (discussed later in the series).

The "classic" role: bone health

The best-established physiological role of vitamin D is regulation of intestinal calcium absorption and maintenance of calcium–phosphate balance, supporting bone mineralisation and skeletal integrity. In the general population, severe deficiency is associated with osteomalacia in adults and rickets in children.

In the general population, severe [vitamin D] deficiency is associated with osteomalacia in adults and rickets in children.

In athletic populations, overt rickets/osteomalacia are uncommon, and the relationship between 25(OH)D and bone outcomes can be less clear than in sedentary cohorts because mechanical loading is strongly osteogenic. Nonetheless, avoiding low vitamin D status remains a sensible component of bone health risk management, particularly in sports with high stress-fracture risk, periods of high training load, low energy availability, or limited sunlight exposure. This is not a claim that vitamin D alone prevents bone injury; it is the narrower and more defensible claim that deficiency should be avoided in athletes whose skeleton is repeatedly stressed (1). 

Vitamin D, muscle function and illness

The interest in Vitamin D in sports is dominated by potential extra-skeletal effects, mainly:

• Muscle function and recovery.

• Recovery and muscle repair following damaging exercise.

• Immune function and respiratory illness risk.

Mechanistically, these interests are plausible. Vitamin D signalling can influence gene transcription, inflammatory pathways, and cellular processes relevant to muscle remodelling and innate immunity. The existence of plausible pathways, however, does not establish that increasing vitamin D status improves performance in already-adequate athletes. The quality of inference depends on intervention trials, and those trials have limitations in athlete populations (sample sizes, baseline status, outcome selection, and confounding factors).

Performance: the consistent pattern is a "threshold" effect

A recurring pattern across the broader literature is that vitamin D supplementation is unlikely to improve muscle strength when baseline status is already adequate, and any benefits, when observed, tend to appear in those with genuinely low status. A systematic review/meta-analysis reported no significant strength benefit in vitamin D–replete adults (baseline 25(OH)D >25 nmol/L), while reporting improvements in a limited number of studies involving deficient participants (<25 nmol/L). This supports a “threshold” interpretation: deficiency is where risk and responsiveness are most likely, not an argument that pushing status higher yields incremental performance benefits (2).

This matters in applied sport because it directly challenges common marketing narratives. The most evidence-consistent message is not “vitamin D boosts performance,” but rather: avoid being low, especially during winter and in high-risk athletes, because low status may compromise aspects of musculoskeletal function and resilience.

Avoid being [vitamin D deficient], especially during winter and in high-risk athletes, because low [vitamin D] status may compromise aspects of musculoskeletal function and resilience.

Recovery and muscle repair: plausible, but definitive performance trials are limited

In applied sport, the recovery argument is often more compelling than direct ergogenic claims. The reasoning is that if vitamin D status influences pathways involved in muscle regeneration and immune function, then low status could impair recovery from damaging training, blunt adaptation, or increase time lost to illness/injury—effects that matter even if acute performance is unchanged.

The athlete-focused review by Owens, Allison, and Close emphasises this framing: vitamin D is not positioned as a “new ergogenic aid,” but as a factor that may influence recovery from damaging exercise and infection risk, while also highlighting the challenges in defining thresholds and the risks of extreme dosing practices (1).

The practical implication is conservative: correcting low vitamin D status is a reasonable health and resilience strategy, while claims of performance enhancement in vitamin D–replete athletes remain inadequately supported.

Illness: associations exist, but vitamin D is not an antiviral shield

Respiratory illness is a major disruptor of training continuity. Even “mild” upper respiratory tract illness can reduce sleep quality, appetite, training intensity, and competition readiness. Observational work in endurance athletes monitored across winter has reported associations between vitamin D status and upper respiratory tract illness incidence and immune markers. For example, He and colleagues examined endurance athletes during a 16-week winter period and assessed relationships between 25(OH)D and illness/immune outcomes (3). Such studies do not prove causality, but they support the pragmatic goal of preventing athletes from drifting into low status during a period when illness risk and training load often converge.

The key is to maintain scientific discipline in the message: vitamin D is not a universal protective factor against viral exposure, and it cannot compensate for inadequate sleep, excessive training stress, low energy availability, or poor hygiene. It is best considered one modifiable contributor to the broader resilience picture.

Vitamin D cannot compensate for inadequate sleep, excessive training stress, low energy availability, or poor hygiene.

What we should not overpromise: three recurring errors

1. Equating association with causation. Many studies linking low vitamin D status to poorer outcomes are observational. Confounding is likely: athletes who spend more time outdoors may have higher vitamin D status and different training or lifestyle characteristics.

2. Ignoring baseline status. The “threshold effect” pattern means that supplementation benefits are most plausible in deficient individuals, not as an across-the-board performance enhancer (2).

3. Assuming universal cut-offs and simple interpretation. Vitamin D thresholds vary between organisations and contexts, and interpretation may be more complex in ethnically diverse squads (1).

Practical takeaways

• Treat vitamin D as risk management, not a “magic” performance supplement (3).

• Low status is most likely in athletes who are:

  • Training predominantly indoors.

  • Living/training at higher latitudes in winter.

  • Using extensive skin coverage or having limited sun exposure.

  • And (often) athletes with darker skin at higher latitudes.

• Athletes are not just looking to “avoid a deficiency” (i.e. avoid deficiency symptoms), they want levels for “optimal health and performance”.

• Evidence linking vitamin D to illness burden and recovery is biologically plausible and supported by observational work, but intervention evidence in athletes is still limited and does not justify very high dosing.

• The recommendations for optimal function are higher than just preventing deficiency. Managing vitamin D in athletes is therefore important and this will be discussed in more detail in the following two blogs.

References

1. Owens DJ, Allison R, Close GL. Vitamin D and the Athlete: Current Perspectives and New Challenges. Sports Med. 2018;48(Suppl 1):3–16. 

2. Stockton KA, Mengersen K, Paratz JD, Kandiah D, Bennell KL. Effect of vitamin D supplementation on muscle strength: a systematic review and meta-analysis. Osteoporos Int. 2011;22(3):859–871. 

3. He CS, Handzlik M, Fraser WD, et al. Influence of vitamin D status on respiratory infection incidence and immune function during winter training in endurance athletes. Exerc Immunol Rev. 2013;19:86–101.

4. Willis KS, Peterson NJ, Larson-Meyer DE. Should we be concerned about the vitamin D status of athletes? Int J Sport Nutr Exerc Metab. 2008;18(2):204–224.