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Vitamin D Status Relative to Diet, Lifestyle, Injury, and Illness in College Athletes


Medicine & Science in Sports & Exercise: February 2011 - Volume 43 - Issue 2 - p 335-343
doi: 10.1249/MSS.0b013e3181eb9d4d
Applied Sciences

Vitamin D deficiency is endemic in the general population; however, there is much to be learned about the vitamin D status of athletes.

Purpose: The purposes of this study were to assess the prevalence of vitamin D insufficiency in collegiate athletes and to determine whether 25(OH)D concentrations are related to vitamin D intake, sun exposure, body composition, and risk for illness or athletic injury.

Methods: 25(OH) vitamin D concentrations were measured in 41 athletes (18 men/23 women, 12 indoor/29 outdoor athletes) throughout the academic year. Dietary intake and lifestyle habits were assessed via questionnaire, bone density was measured by dual energy x-ray absorptiometry, and injury and illness were documented as part of routine care.

Results: The 25(OH)D concentrations changed across time (P = 0.001) and averaged 49.0 ± 16.6, 30.5 ± 9.4, and 41.9 ± 14.6 ng·mL−1 (mean ± SD) in the fall, winter, and spring, respectively, and were higher in outdoor versus indoor athletes in the fall (P < 0.05). Using 40 ng·mL−1 as the cutoff for optimal status, 75.6%, 15.2%, and 36.0% of athletes had optimal status in the fall, winter, and spring, respectively. 25(OH)D concentrations were significantly (P < 0.05) correlated with multivitamin intake in the winter (r = 0.39) and tanning bed use in the spring (r = 0.48); however, status was otherwise not related to intake, lifestyle factors, or body composition. 25(OH)D concentrations in the spring (r = −0.40, P = 0.048) was correlated with frequency of illness.

Conclusions: Our results suggest that collegiate athletes can maintain sufficient status during the fall and spring but would benefit from supplementation during the winter to prevent seasonal decreases in 25(OH)D concentrations. Results further suggest that insufficient vitamin D status may increase risk for frequent illness. Future research is needed to identify whether vitamin D status influences injury risk during athletic training or competition.

Supplemental Digital Content is available in the text.

1Department of Family and Consumer Sciences, University of Wyoming, Laramie, WY; 2Department of Athletics, University of Wyoming, Laramie, WY; 3Laramie Pediatrics, Laramie, WY; and 4Medical University of South Carolina, Charleston, SC

Address for correspondence: D. Enette Larson-Meyer, Ph.D., R.D., FACSM, Department 3354, 1000 E. University Avenue, University of Wyoming, Laramie, WY 82071; E-mail:

Submitted for publication February 2010.

Accepted for publication May 2010.

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Web site (

Numerous studies have recently reported a high prevalence of vitamin D deficiency (25(OH)D < 20 ng·mL−1) and insufficiency (25(OH)D < 32 ng·mL−1) for all age groups worldwide (15,16,23,38). It is widely accepted that vitamin D is necessary for adequate bone health through up-regulation of the expression of genes that enhance calcium absorption and bone deposition (15). However, recent evidence has also linked low vitamin D status to various nonskeletal, chronic, and autoimmune diseases, including cardiovascular disease, hypertension, diabetes, inflammatory bowel disease, depression, multiple sclerosis, rheumatoid arthritis, and certain types of cancer (15,16,38). Furthermore, recent studies have found that vitamin D up-regulates gene expression of antimicrobial peptides (AMP) (12) and down-regulates expression of several inflammatory cytokines, including tumor necrosis factor α and interleukin 6 (24), and therefore may be an important component in immune function and inflammatory modulation (6,38). Although vitamin D is considered a vitamin, it is unique in that it may be obtained from the diet or synthesized in the skin in the presence of ultraviolet B (UVB) light (290-315 nm) (15,16). Unfortunately, only a few foods such as oily fish naturally contain vitamin D, whereas milk, selected fruit juices, breads, and cereals are among the few fortified food sources (5,8,15). Although sun exposure has the ability to provide the needed precursors for adequate status, wintertime latitude greater than 37° north or south (15,36), skin pigmentation (15), sunscreen use (15,22), and excess adiposity (25,29) all decrease endogenous vitamin D synthesis and bioavailability.

Despite the large number of studies conducted in the general population, much less is known about the vitamin D status of athletes. The few studies conducted have documented a surprisingly high percentage of vitamin D insufficiency or deficiency in athletes participating in outdoor (13,21; Willis, 2008, unpublished data) as well as indoor (2,13,19,20) sports. On the basis of our current understanding of vitamin D's role in bone health, inflammation, and immunity, it is plausible that suboptimal vitamin D status increases the risk of overuse and inflammatory injuries as well as the susceptibility to common upper respiratory tract infection (URI) and other illnesses. These adverse consequences could negatively impact athletic training and performance (in addition to impacting long-term risk for chronic disease).

The purposes of this study were to evaluate the prevalence of vitamin D insufficiency in National Collegiate Athletic Association (NCAA) Division I athletes throughout the academic year and to determine whether circulating concentrations of 25(OH)D are related to vitamin D intake, sun exposure, and body composition. A secondary purpose was to evaluate whether 25(OH)D concentration is linked to bone density, development of overuse or inflammatory injuries, and/or incidence of frequent illness. We hypothesized that athletes participating in indoor sports would have lower 25(OH)D concentrations compared with those participating in outdoor sports. Within the entire group of athletes, we further hypothesized that sun exposure, sunscreen use, and vitamin D intake (from food and supplements) would be predictive of 25(OH)D concentrations. In addition, we hypothesized that lower concentrations of 25(OH)D at any time point throughout the year would increase risk for low bone density, overuse and/or inflammatory injuries, and frequent illness.

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All male and female NCAA Division I college athletes ≥18 yr from the University of Wyoming (UW) (2195 m, 41.3°N) were invited to participate in the study, which was approved by both the institutional review board and the athletic department at UW. Before participation, interested athletes were fully informed about the study procedures and the possible risks before providing written informed consent. All athletes had undergone a routine preseason physical with the UW athletic department physician (KK) and were considered in good health. Participants were classified as either indoor or outdoor athletes on the basis of their sport. Athletes who trained and/or competed outdoors (football, soccer, cross-country or track and field, and cheerleading/dance) were considered outdoor athletes, whereas athletes who trained and competed exclusively indoors (wrestling, swimming, and basketball) were considered indoor athletes. In accordance with NCAA regulations, all athletes are allowed no more than 20 h·wk−1 to train and to compete during their competitive season and 8 h·wk−1 during their off season.

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Study design.

This longitudinal study tracked the vitamin D status of the athletes throughout the academic year. Blood samples for analysis of vitamin D (serum 25(OH)D) and parathyroid hormone (PTH) were collected in the fall (September/early October), winter (late February/early March), and spring (late April/early May). A vitamin D-specific questionnaire was administered at these same time points. At study completion (spring only), body composition and bone density of the hip, lumbar spine, and total body were evaluated via dual energy x-ray absorptiometry (DEXA) using standardized procedures. Illnesses and injuries that occurred in all UW NCAA athletes, including study participants, were documented throughout the academic year by the UW athletic training staff and the team physician.

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Vitamin D and PTH.

At each testing point (fall, winter, and spring), 5 mL of blood was collected in standard red top tubes (no additives), allowed to clot for 30-60 min at room temperature, and centrifuged at 3500 rpm for 15 min. Aliquots of serum were stored at −20°C until analysis. Serum was later analyzed for 25-hydroxy vitamin D and PTH via Diasorin 25(OH)D RIA and intact PTH IRMA, respectively, in an external laboratory (BH, Charleston, SC).

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Questionnaire and sun exposure during practice/competition.

The vitamin D-specific questionnaire completed at each of the three collection points focused on dietary and lifestyle habits that could impact vitamin D status. The questionnaire asked athletes how often (never or less than one time per month, one to three times per month, one time per week, two to four times per week, five to six times per week, one time per day, two to three times per day, four to five times per day, or six or more times per day) they consumed various vitamin D-containing foods, multivitamins (MVI), and other vitamin D-containing supplements including cod liver oil. The vitamin D-containing foods included cows' milk, soy or rice milk, eggs, vitamin D-fortified cereal, margarine, orange juice, and fatty fish (see SDC 1, Vitamin D questionnaire for full list of foods assessed in the study; Intake of vitamin D was estimated by multiplying the frequency midpoint by the average content of each vitamin D-containing food and expressed as IU per day. The vitamin D content of foods was obtained from Chen et al. (8), from the national nutrient database for standard reference (33), and from selected food labels. The questionnaire also asked athletes about the frequency of leisure time spent outside (never or <1 h·month−1, 1-3 h·month−1, 1 h·wk−1, 2-4 h·wk−1, 5-6 h·wk−1, 0.5-1 h·d−1, or >2 h·d−1), the frequency of tanning bed use (never or <10, 10-20, 20-30, 30-40, 40-50, 50-60, or >60 min·wk−1), the type and frequency of sunscreen applied (never, sometimes, usually, or always), and the type of clothing typically worn outdoors. Information on sun exposure during practice or competition was collected from records of team-specific training and competitions, which varied by season in accordance with the NCAA Division I regulations. For outdoor athletes, estimates of weekly time spent outside during practice or competition were estimated for fall (average of August, September, and early October) and spring (April) but not for winter (because little to no training occurred outdoors during these months). For indoor athletes, weekly time spent outdoors during practice or competitions was assumed to be zero. Total sun exposure was estimated from the sum of estimated practice or competition sun exposure and reported leisure time spent outdoors. At the first collection point (fall), participants reported on their summer location; at the second collection (winter), participants reported on their winter break location; and at the third collection (spring), participants reported on their spring break location.

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Athletic injury and illness.

Selected information contained within the athletes medical charts, including injury status and frequency of illnesses (URI, influenza, gastroenteritis, etc.) during the academic year, was collected by a certified athletic trainer (JT) who was blinded to the vitamin D status of the athletes. The total number of injuries that were likely to be subacute or overuse injuries (such as stress fractures and tendonitis) rather than the result of a specific mechanism were tallied for each athlete.

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Statistical procedures.

Statistical analyses were performed using the Statistical Package for the Social Sciences for Windows analysis software (PASW Statistics Version 17.0, SPSS Inc., Chicago, IL). Pearson correlations were used to assess the relations between serum 25(OH)D concentrations and continuous measured or estimated variables, including body weight, body fat percentage, PTH concentrations, and vitamin D intake, whereas Spearman rank correlations were used to assess the relations between serum 25(OH)D concentrations and noncontinuous variables, including frequency of intake of vitamin D-containing foods and supplements, leisure time spent outdoors, tanning bed use, and frequency of illness. One-way ANOVA was used to test differences between indoor versus outdoor and male versus female athletes. Repeated-measures ANOVA was used to assess differences over time (fall, winter, and spring). Alpha was set at 0.05.

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Eighteen men (mean ± SD: age = 20.1 ± 1.9 yr, height = 183.9 ± 11.2 cm, weight = 88.0 ± 19.6 kg, body mass index [BMI] = 25.9 ± 4.4 kg·m−2, 1 black, 0 Hispanic, 17 white) and 23 women (age = 19.9 ± 1.5 yr, height = 168.1 ± 9.6 cm, weight = 59.6 ± 10.2 kg, BMI = 20.9 ± 1.9 kg·m−2, 0 black, 1 Hispanic, 22 white) from a variety of intercollegiate athletic teams initially volunteered to participate in the study. The athletes who participated in basketball, wrestling, and swimming (n = 12) were classified as indoor athletes, whereas those that participated in soccer, football, cross-country or track and field, and cheerleading or dance team (n = 29) were classified as outdoor athletes. At the winter testing point, data were not collected on eight athletes because they were either no longer part of UW athletics (n = 4) or elected to discontinue participation in the study (n = 4). At the spring testing point, data were not collected on eight additional athletes because of scheduling conflicts with final examinations or team or personal travel. The study sample, therefore, was n = 41 in the fall, n = 33 in the winter, and n = 25 in the spring. Scheduling conflicts in the spring also prohibited measurement of body composition or bone density by DEXA in four of the 25 athletes (n = 21 for DEXA analysis).

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Vitamin D status.

As shown in Figure 1, 25(OH)D concentration changed significantly across time (P = 0.001) and averaged 49.0 ± 16.6 ng·mL−1 in the fall, 30.5 ± 9.4 ng·mL−1 in the winter, and 41.9 ± 14.6 ng·mL−1 in the spring. In the fall, 9.8% of athletes (n = 4) were vitamin D insufficient (25(OH)D concentration <32 ng·mL−1 but >20 ng·mL−1) (17), whereas one (2.4%) had 25(OH)D concentrations indicative of vitamin D deficiency (25(OH)D <20 ng·mL−1) (15,38). In the winter, 60.6% (n = 20) of athletes were vitamin D insufficient and 3.0% (n = 1) were vitamin D deficient. In the spring, 16.0% (n = 4) were insufficient and 4.0% (n = 1) were deficient. Using a cutoff of 40 ng·mL−1, thought to be the lower limit of optimal achieved by humans living naturally in a sun rich environment (6), 75.6% (n = 31), 15.2% (n = 5), and 36.0% (n = 9) of athletes had optimal vitamin D status in the fall, winter, and spring, respectively. As shown in Figure 2, vitamin D status was significantly higher in outdoor compared with indoor athletes in the fall (53.1 ± 17.4 vs 39.3 ± 8.9 ng·mL−1, P = 0.013) but not in the winter (31.9 ± 10.2 ng·mL−1, n = 25 vs 26.3 ± 5.0 ng·mL−1, n = 8; P = 0.15) or spring (44.6 ± 15.6 ng·mL−1, n = 19 vs 33.1 ± 4.8 ng·mL−1, n = 6; P = 0.09). Vitamin D status did not differ by sex at any of the time points (P = 0.10). In the entire group, 25(OH)D concentration in the fall was correlated with 25(OH)D concentrations in the winter (r = 0.85, n = 33, P = 0.0001) and spring (0.76, n = 25, P = 0.0001).





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PTH and relation with vitamin D status.

Serum PTH concentrations ranged between 7.7 and 54.4 pg·mL−1 (23.8 ± 10.9 pg·mL−1) in the fall, between 9.4 and 50.8 pg·mL−1 (25.4 ± 9.3 pg·mL−1) in the winter, and between 12.8 and 48.5 pg·mL−1 (28.1 ± 9.9 pg·mL−1) in the spring (normal range = 12-54 pg·mL−1) and did not change significantly across time (P = 0.18). PTH concentrations were not different between indoor and outdoor athletes in the fall (24.8 ± 12.5 vs 23.3 ± 10.4 pg·mL−1), winter (25.2 ± 12.1 vs 25.5 ± 8.3 pg·mL−1), or spring (22.6 ± 11.1 vs 29.8 ± 9.1 pg·mL−1) (P > 0.10). As shown in Table 1, PTH concentration was not correlated with 25(OH)D concentration at any time point.



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Intake of vitamin D-containing foods and supplements and relation with vitamin D status.

Frequency of consumption of selected vitamin D-containing foods and supplements along with their vitamin D content is shown in Table 2. Vitamin D status was correlated with MVI intake in the winter (r = 0.39, P = 0.025, n = 33) but not in the fall (r = 0.29, P = 0.062, n = 41) or spring (r = −0.14, P = 0.49, n = 25). In the fall, consumption of orange juice was negatively correlated with 25(OH)D status (−0.36, P = 0.02). No other correlations were found between vitamin D status and self-reported intake of vitamin D-containing foods.



Estimated vitamin D intake from food sources averaged 242 ± 161, 282 ± 206, and 204 ± 171 IU·d−1 from food sources in the fall, winter, and spring, respectively, and averaged 553 ± 471, 683 ± 610, and 489 ± 456 IU·d−1 when vitamin D supplements (including an MVI) were included. Neither total vitamin D intake nor intake from food alone differed across time or with sex or training location (indoor vs outdoor) (P > 0.05). Neither vitamin D intake from food nor food plus supplements was significantly correlated with vitamin D status in the fall (r = −0.05 and 0.03), winter (r = 0.02 and 0.00), or spring (r = −0.10 and 0.17) (P > 0.05), respectively. A very small percentage of athletes (4.9% in the fall, 6.1% in the winter, and 4% in the spring) consumed the current RDA of 600 IU from food alone. This increased to 26.8%, 18.2%, and 20% in the fall, winter, and spring when supplements were included. Interestingly, with the exception of two athletes during the winter, those who consumed >1000 IU·d−1 from food plus supplements had sufficient status (≥32 ng·mL−1).

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UV exposure and relation with vitamin D status.

Reported leisure time spent outdoors changed significantly across time (P = 0.001) and averaged 4.5 ± 1.8, 3.6 ± 1.7, and 4.0 ± 1.8 h·wk−1 in the fall, winter, and spring, respectively. Reported tanning bed use averaged 0.24 ± 0.89, 0.03 ± 0.17, and 0.24 ± 0.66 h·wk−1 and did not vary significantly across time (P = 0.08). Time spent outside during practice or competition averaged 7.8 ± 6.4, 0 ± 0, and 4.9 ± 4.7 h·wk−1 in the fall, winter, and spring, respectively. Leisure time spent outdoors was not significantly (P > 0.10) correlated with vitamin D status at any time point. However, tanning bed use was correlated with 25(OH)D concentrations in the spring (r = 0.48, P = 0.016) but not winter (r = 0.20) or fall (r = 0.17) (P > 0.05), whereas time spent outside during practice or competition and total time spent outdoors were correlated with vitamin D status in the fall (r = 0.40 and 0.42, P < 0.01) but not the spring (r = 30 and 0.21, P > 0.05), respectively. Leisure time spent outdoors was significantly lower in indoor versus outdoor athletes in the winter (2.4 ± 1.5 vs 3.9 ± 1.6 h·wk−1, P = 0.02) and spring (2.8 ± 1.2 vs 4.4 ± 1.8 h·wk−1, P = 0.068) but not in the fall (4.1 ± 1.5 vs 4.8 ± 1.8 h·wk−1, P > 0.05). Reported tanning bed use, sunscreen use, or SPF typically applied were not different between indoor versus outdoor athletes at any time point.

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Relation between vitamin D status and body composition.

Relations between vitamin D status and body mass, BMI, and percentage body fat are shown in Table 2. Pearson correlations between body mass or BMI were not found at any time point, although 25(OH)D concentrations tended to be correlated with body fat percentage in the fall and spring. When correlations were adjusted for sex, however, the relation between body fat and 25(OH)D concentration was significant in the fall (partial r = 0.44, P = 0.05) but not the winter (P = 0.19, P = 0.41) or spring (partial r = −0.33 P = 0.16).

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Relation between vitamin D status and bone density.

Vitamin D status was not correlated (P ≥ 0.05) with total body bone density (r = 0.02) or bone density in the lumbar spine (r = 0.06) or dual femur (r = 0.02), which was assessed only in the spring. PTH, however, was significantly correlated with bone density assessed in the total body (r = −0.66, P = 0.001), lumbar spine (r = −0.51, P = 0.03), and dual femur (r = −0.55, P = 0.01).

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Relation between vitamin D status and illness and injury.

Seven of 33 athletes who remained in the study at the winter collection point developed overuse injuries that were not due to contusion. This included one case of Achilles tendonitis, five stress reactions (two in the shin, two in the foot, and one in the femur), and a fracture of the foot, five of which occurred in athletes participating in cross-country or track and field. Frequency of injury was not related to vitamin D status but was significantly negatively correlated with total body bone mineral density (BMD; r = −0.50, P = 0.02).

Thirteen of 33 athletes also contracted at least one documented illness, which included the common cold, flu, or other URI, with 8 of the total contracting one illness, 3 contracting two different illnesses, and 2 contracting four. Vitamin D status in the fall, winter, or spring was not significantly correlated with incidence of injury but was significantly correlated with frequency of illness in the spring (r = −0.40, P = 0.048; Fig. 3) but not in the winter (r = −0.33, P = 0.065; Fig. 3) or fall (r = -0.15, P = 0.39).



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The purposes of this study were to examine the vitamin D status of male and female college athletes during the university academic year to determine if vitamin D status (circulating concentrations of 25-hydroxy vitamin D) was related to dietary intake, training, and lifestyle habits and/or body composition and to evaluate whether insufficient status was linked with compromised bone density or increased risk for illness or inflammatory injuries. We found that vitamin D status varied across the year, with a higher percentage of athletes having insufficient or deficient status (25(OH)D < 32 ng·mL−1) in the winter (63.6%) compared with the fall (12.2%) and spring (20%). Interestingly, 75.6% and 36.0% of athletes maintained status within the more optimal range (>40 ng·mL−1) in the fall and spring compared with only 15.2% in the winter. We also found that low vitamin D status in the spring was correlated with frequency of illness-including URI, the common cold, influenza, and gastroenteritis. Although vitamin D status was correlated with outdoor practice or competition time in the fall and spring, reported MVI consumption in the winter, and tanning bed use in the spring, status was otherwise not significantly related to vitamin D intake, lifestyle habits, or body composition.

The main finding from this study was that a surprisingly low percentage of college athletes had insufficient status (defined as a circulating 25(OH)D concentration <32 ng·mL−1) in the fall and spring and more importantly that a high percentage of those with sufficient status maintained stores in the more optimal range (>40 ng·mL−1). In contrast to our findings, several groups of researchers studying runners (19; Willis, 2008, unpublished data), gymnasts (19,20), and other athletes (2,13) found that at least 37%-100% of athletes are vitamin D insufficient and that 1%-83% are deficient (25(OH)D concentration <20 ng·mL−1), depending on sport, geographic location, and season tested. A recent study from our laboratory, for example, found that 42% of distance runners training in Baton Rouge, Louisiana (30.5°N), were vitamin D insufficient and ∼1% had concentrations low enough to be deficient (Willis, 2008, unpublished data). Another study in 93 Middle Eastern sportsmen training in Qatar (25.4°N) found that 90% were vitamin D deficient (25(OH)D < 20 ng·mL−1). Although incidence of vitamin D insufficiency in the current study increased in the winter, as might be expected in athletes living at >35°-37° north or south latitude (6,15), the low prevalence of insufficiency and the high prevalence with optimal status in fall and spring may be explained by the sunny and mild climate of Wyoming during the spring, summer, and fall months. Such conditions allow athletes to train and/or perform leisure activities outdoors at close to solar noon when vitamin D synthesis is most effective (6). It is further possible that the lack of cloud cover and pollution as well as Laramie's elevation of >2195 m above sea level (31) allows increased endogenous synthesis because of an increased fractional strength of UVB radiation.

In support of our hypothesis, we found that athletes participating in indoor sports such as wrestling, basketball, and swimming had lower circulating vitamin D in the fall than athletes participating in outdoor sports, including football, soccer, cross-country or track and field, and cheerleading, and that vitamin D status correlated with estimated weekly outdoor practice time in fall and spring. This finding suggests that athletes who practice indoors are at increased risk for vitamin D insufficiency and deficiency, as are athletes who practice outdoors only in the early evening (13) or early morning (Willis, 2008, unpublished data) or who diligently apply sunscreen (which can reduce cutaneous synthesis by >95% (22). Although we also expected that 25(OH)D concentration would correlate with reported leisure-time sunlight exposure, we found that vitamin D status correlated with reported frequency of tanning bed use, as previously suggested (32), but only in the spring. Self-reported data via questionnaires, however, may not be the most accurate method for obtaining data on effective sun exposure (i.e., between the hours of 10:00 a.m. and 2:00 p.m., nondaylight savings time) or tanning bed use. Effective sun exposure is complicated by factors such as cloud cover and sunscreen use (6,15), whereas commercial tanning beds vary considerably with the type of UV light emitted (i.e., only beds that emit adequate UVB promote cutaneous vitamin D synthesis [15,32]). In future studies, the frequency and the length of time spent in leisure time and practice or competition between 10:00 a.m. and 2:00 p.m. nondaylight savings time and sunscreen application frequency and type should be collected through more detailed questionnaires, logs, or direct documentation. Direct measurement of UVB exposure with UVB detection devices placed directly on skin would also be of interest.

Our lack of a relation between vitamin D status and both frequency of intake of vitamin D-containing foods and estimated vitamin D intake from food is not surprising given that vitamin D is limited in our food supply. Only a few foods, including oily fish, naturally contain vitamin D, whereas milk, some fruit juices, margarine, and ready-to-eat cereals are among the few fortified food sources (5). In addition, food intake tables for vitamin D are inadequate, which makes intake evaluation difficult (5). In the current study, reported vitamin D intake from food alone averaged 242 ± 161, 282 ± 206, and 204 ± 171 IU·d−1 in the fall, winter, and spring and while higher than that previously reported in athletic populations, including ski jumpers, gymnasts, soccer players, ice skaters and runners (3,9,19,26,37), was lower than the current RDA of 600 IU (27). When vitamin D from supplements (including an MVI) was included, intake increased to more than approximately 500 IU·d−1 in the fall and spring and to almost 700 IU·d−1 in the winter, approaching the higher intake level (of 1000-4000 IU·d−1) recommended by researchers (4,6,16,17). The lack of a correlation with total intake from vitamin D (including supplements), however, is unexpected but may be explained by the food frequency methodology and/or by the fact that most circulating 25(OH)D is thought to originate from sunlight exposure rather than from dietary sources (6,15). We were intrigued, however, by our weak but significant relation between frequency of MVI intake and vitamin D status in the winter (and tendency for this same association in the fall). Although these findings suggest that a vitamin D-containing MVI may help athletes maintain vitamin D status, it is important to stress that previous studies indicate that-in the absence of sun exposure-a daily MVI (which typically contains 400 IU) is not enough to maintain 25(OH)D concentrations in the sufficient range (14,16,19).

Vitamin D status in the current study also did not appear to be significantly influenced by body weight or adiposity, although the expected negative association with body fat percentage tended to be present in the fall and spring. Previous studies in nonathletes have found that 25(OH)D concentrations are inversely correlated with body fat percentage (within the typical range of sedentary individuals) (29) and are commonly depressed with obesity (along with elevated PTH concentrations) (25,29). In a cohort of 302 healthy adults, for example, Parikh et al. (25), found lower serum concentrations of 25(OH)D in obese compared with nonobese adults. The decrease in vitamin D bioavailability is thought to be due to sequestration of vitamin D in adipose tissue after cutaneous synthesis or dietary intake, although the exact mechanism is not yet known. The reason for a lack of a significant correlation between vitamin D status and adiposity in the current study is most likely explained by the reduced range of body fat of our collegiate athlete population. Future studies in larger athletic populations, however, should evaluate whether athletes with excessively high body fat stores are at increased risk for vitamin D insufficiency, particularly during certain seasons of the year.

The final purpose of the current study was to evaluate whether vitamin D status is linked to bone density, overuse injury, or illness throughout the academic year. Studies in healthy individuals have found that serum 25(OH)D concentrations correlate positively with BMD (4,34), with the greatest BMD observed when serum concentrations are close to 40 mg·dL−1 (4). Among military recruits, risk for bone fracture is significantly associated with reduced serum 25(OH)D (11,28) and elevated PTH concentrations (35) and is reduced by supplementation with 800 IU·d−1 of vitamin D plus calcium (18). Although less is known about overuse or inflammatory injuries, preliminary findings from our laboratory found that the inflammatory marker tumor necrosis factor α rises exponentially in runners when serum 25(OH)D concentrations fall less than 32 ng·mL−1 (Willis, 2008, unpublished data). A previous German report also documented that athletes undergoing an extensive 6-wk program of UVB irradiation experienced a reduction in chronic pain because of sports injuries (30). Although the current study was unable to provide evidence for a link between low vitamin D status and compromised bone health and athletic injury, additional studies are warranted because detection of injury due to vitamin D deficiency was not ideal in our athletic population that mostly maintained 25(OH)D concentrations more than the 32-40 ng·mL−1 throughout the year. Our results, however, highlight the role of high-normal PTH (which is typically elevated when serum vitamin D concentrations fall less than 20-30 ng·mL−1) (15,17) in bone health and the probable link between bone density and bone fracture.

The finding that 25(OH)D concentrations in the spring were significantly associated with frequency of illness, on the other hand, is consistent with research, indicating that vitamin D up-regulates naturally occurring-and broad spectrum-AMP (6,12). AMPs exert a powerful immune response by compromising the integrity of the cell membrane of invading pathogens (10). These results are in agreement with Aloia and Li-Ng (1), who found that supplementation with vitamin D3 for 3 yr reduced self-reported incidence of influenza and the common cold and in support of other evidence that influenza epidemics and other wintertime infections may be brought on by seasonal deficiencies of AMP secondary to seasonal deficiencies in vitamin D (7). Although illness in the current study was documented as part of routine medical care by a staff member who was unaware of the athletes' study participation or vitamin D status, further evaluation in larger athletic populations is of interest. Future studies should document the time course of illness in relation to vitamin D status as well as the duration and the frequency of illness.

In conclusion, the current study demonstrates that healthy athletes can achieve adequate to optimal 25(OH)D concentrations in the nonwinter months through routine sun exposure, dietary sources, and supplements (which surpass the newly revised RDA of 600 IU) (27). Athletes living at distances away from the equator, however, need supplemental vitamin D during the winter to prevent the seasonal reduction in serum 25(OH)D concentrations. Maintaining sufficient vitamin D status may reduce the risk of common infectious illness, which can negatively impact athletic training and performance. Further research is needed to determine whether vitamin D status influences risk for overtraining and inflammatory injury.

Funding support: None.

The authors thank the athletes who volunteered to participate in the study. They also thank Inge Harper at the National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, Phoenix Epidemiology and Clinical Research Branch, for assistance in interpreting the studies of Bannert et al. (2) and Spellerberg (30).

This work was partially supported by research funds from the Department of Family and Consumer Sciences.

Results of the present study do not constitute endorsement by the American College of Sports and Medicine.

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1. Aloia JF, Li-Ng M. Correspondence. Epidemiol Infect. 2007:1-4.
2. Bannert N, Starke I, Mohnike K, Frohner G. Parameters of mineral metabolism in children and adolescents in athletic training. Kinderarztl Prax. 1991;59(5):153-6.
3. Bergen-Cico DK, Short SH. Dietary intakes, energy expenditures, and anthropometric characteristics of adolescent female cross-country runners. J Am Diet Assoc. 1992;92(5):611-2.
4. Bischoff-Ferrari HA, Giovannucci E, Willett WC, Dietrich T, Dawson-Hughes B. Estimation of optimal serum concentrations of 25-hydroxyvitamin D for multiple health outcomes. Am J Clin Nutr. 2006;84(1):18-28.
5. Calvo MS, Whiting SJ, Barton CN. Vitamin D fortification in the United States and Canada: current status and data needs. Am J Clin Nutr. 2004;80(6 suppl):1710S-6S.
6. Cannell JJ, Hollis BW, Zasloff M, Heaney RP. Diagnosis and treatment of vitamin D deficiency. Expert Opin Pharmacother. 2008;9(1):107-18.
7. Cannell JJ, Vieth R, Umhau JC, et al. Epidemic influenza and vitamin D. Epidemiol Infect. 2006;134(6):1129-40.
8. Chen TC, Chimeh F, Lu Z, et al. Factors that influence the cutaneous synthesis and dietary sources of vitamin D. Arch Biochem Biophys. 2007;460(2):213-7.
9. Clark M, Reed DB, Crouse SF, Armstrong RB. Pre- and post-season dietary intake, body composition, and performance indices of NCAA division I female soccer players. Int J Sport Nutr Exerc Metab. 2003;13(3):303-19.
10. De Smet K, Contreras R. Human antimicrobial peptides: defensins, cathelicidins and histatins. Biotechnol Lett. 2005;27(18):1337-47.
11. Givon U, Friedman E, Reiner A, Vered I, Finestone A, Shemer J. Stress fractures in the Israeli defense forces from 1995 to 1996. Clin Orthop Relat Res. 2000;373:227-32.
12. Gombart AF, Borregaard N, Koeffler HP. Human cathelicidin antimicrobial peptide (CAMP) gene is a direct target of the vitamin D receptor and is strongly up-regulated in myeloid cells by 1,25-dihydroxyvitamin D3. FASEB J. 2005;19(9):1067-77.
13. Hamilton B, Tremblay C, Eirale C, Racinais S, Grantham J. Vitamin D deficiency in Middle Eastern sportsmen. Med Sci Sports Exerc. 2009;41(5 suppl):S405.
14. Heaney RP, Armas LA, Shary JR, Bell NH, Binkley N, Hollis BW. 25-Hydroxylation of vitamin D3: relation to circulating vitamin D3 under various input conditions. Am J Clin Nutr. 2008;87(6):1738-42.
15. Holick MF. Sunlight and vitamin D for bone health and prevention of autoimmune diseases, cancers, and cardiovascular disease. Am J Clin Nutr. 2004;80(6 suppl):1678S-88S.
16. Holick MF. Vitamin D deficiency. N Engl J Med. 2007;357(3):266-81.
17. Hollis BW. Circulating 25-hydroxyvitamin D levels indicative of vitamin D sufficiency: implications for establishing a new effective dietary intake recommendation for vitamin D. J Nutr. 2005;135(2):317-22.
18. Lappe J, Cullen D, Haynatzki G, Recker R, Ahlf R, Thompson K. Calcium and vitamin d supplementation decreases incidence of stress fractures in female navy recruits. J Bone Miner Res. 2008;23(5):741-9.
19. Lehtonen-Veromaa M, Mottonen T, Irjala K, et al. Vitamin D intake is low and hypovitaminosis D common in healthy 9- to 15-year-old Finnish girls. Eur J Clin Nutr. 1999;53(9):746-51.
20. Lovell G. Vitamin D status of females in an elite gymnastics program. Clin J Sport Med. 2008;18(2):159-61.
21. Maimoun L, Manetta J, Couret I, et al. The intensity level of physical exercise and the bone metabolism response. Int J Sports Med. 2006;27(2):105-11.
22. Matsuoka LY, Ide L, Wortsman J, MacLaughlin JA, Holick MF. Sunscreens suppress cutaneous vitamin D3 synthesis. J Clin Endocrinol Metab. 1987;64(6):1165-8.
23. Meyer C. Scientists probe role of vitamin D: deficiency a significant problem, experts say. JAMA. 2004;292(12):1416-8.
24. Muller K, Haahr PM, Diamant M, Rieneck K, Kharazmi A, Bendtzen K. 1,25-Dihydroxyvitamin D3 inhibits cytokine production by human blood monocytes at the post-transcriptional level. Cytokine. 1992;4(6):506-12.
25. Parikh SJ, Edelman M, Uwaifo GI, et al. The relationship between obesity and serum 1,25-dihydroxy vitamin D concentrations in healthy adults. J Clin Endocrinol Metab. 2004;89(3):1196-9.
26. Rankinen T, Lyytikainen S, Vanninen E, Penttila I, Rauramaa R, Uusitupa M. Nutritional status of the Finnish elite ski jumpers. Med Sci Sports Exerc. 1998;30(11):1592-7.
27. Ross AC, Taylor CL, Yaktine AL, and Del Valle HB, Editors. Dietary Reference Intakes for Calcium and Vitamin D. Washington, DC: Food and Nutrition Board, Institutes of Medicine; 2010. 483 p.
28. Ruohola JP, Laaksi I, Ylikomi T, et al. Association between serum 25(OH)D concentrations and bone stress fractures in Finnish young men. J Bone Miner Res. 2006;21(9):1483-8.
29. Snijder MB, van Dam RM, Visser M, et al. Adiposity in relation to vitamin D status and parathyroid hormone levels: a population-based study in older men and women. J Clin Endocrinol Metab. 2005;90(7):4119-23.
30. Spellerberg AE. Increase of athletic effectiveness by systematic ultraviolet irradiation. Strahlentherapie. 1952;88(3-4):567-70.
31. Sullivan SS, Cobb JL, Rosen CJ, et al. Assessment of sun exposure in adolescent girls using activity diaries. Nutr Res. 2003;23:631-44.
32. Tangpricha V, Turner A, Spina C, Decastro S, Chen TC, Holick MF. Tanning is associated with optimal vitamin D status (serum 25-hydroxyvitamin D concentration) and higher bone mineral density. Am J Clin Nutr. 2004;80(6):1645-9.
33. United States Department of Agriculture (USDA). Agriculture Research Service Web site [Internet]. Beltsville (MD): USDA National Nutrient Database for Standard Reference; [cited 2010 Jan 5]. Available from:
34. Valimaki VV, Alfthan H, Lehmuskallio E, et al. Vitamin D status as a determinant of peak bone mass in young Finnish men. J Clin Endocrinol Metab. 2004;89(1):76-80.
35. Valimaki VV, Alfthan H, Lehmuskallio E, et al. Risk factors for clinical stress fractures in male military recruits: a prospective cohort study. Bone. 2005;37(2):267-73.
36. Webb AR. Who, what, where and when-influences on cutaneous vitamin D synthesis. Prog Biophys Mol Biol. 2006;92(1):17-25.
37. Ziegler P, Nelson JA, Barratt-Fornell A, Fiveash L, Drewnowski A. Energy and macronutrient intakes of elite figure skaters. J Am Diet Assoc. 2001;101(3):319-25.
38. Zittermann A. Vitamin D in preventive medicine: are we ignoring the evidence? Br J Nutr. 2003;89(5):552-72.


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