Preventing seasonal declines in vitamin D with exercise

With autumn and winter approaching, those of us in the northern hemisphere can reliably count on certain seasonal changes: lower temperatures, shorter days, and with the reduced sunlight, a decline in our levels of circulating vitamin D. Vitamin D is utilized by nearly every tissue in the body, exerting essential effects for various processes such as maintaining bone and immune health. But despite the importance of this molecule, many people have insufficient levels, especially in winter. While some may turn to sun lamps or vitamin D supplements to combat deficiency, researchers Perkin et al. recently examined whether a different intervention—namely, cardiorespiratory exercise—might help to prevent the decline in vitamin D levels typically seen in winter months.¹

Vitamin D: the role of sunlight and fat mass

Those who have listened to our previous AMA on sun exposure will know that ultraviolet (UV) rays from the sun provide a powerful source of vitamin D, as they stimulate the skin to convert a vitamin D precursor (7-dehydrocholesterol) into D3, which is subsequently converted through additional steps to the active form of vitamin D: 1,25-(OH)₂D.² Indeed, UV light is such a strong stimulator of vitamin D production that those with lighter skin tones only need about nine minutes of sunlight over about one third of the body’s surface area to meet their daily vitamin D requirements—at least in the summer months, when sunlight to the northern hemisphere is most direct.³ In the winter months, however, weaker and shorter periods of sunlight, combined with added layers of clothing reducing skin exposure to sunlight, can lead to a D3 deficiency, particularly for those living at higher latitudes.

The situation is typically even worse for those with excess fat mass. Since vitamin D is a fat soluble vitamin, circulating vitamin D tends to become sequestered in adipose tissue, such that individuals with excess adiposity have even less vitamin D available for use throughout the body. This has been reported to translate to a nearly 75% higher risk of vitamin D deficiency among individuals with obesity relative to those with normal BMIs,⁴ and even supplementation has been shown to have a blunted effect in those with more adipose tissue.⁵ 

But what if we could mobilize more vitamin D out of those fat stores? Exercise—even when it doesn’t result in net weight loss—is known to stimulate lipolysis (i.e., the breakdown of fat), and thus, Perkin et al. hypothesized that the lipolysis achieved with exercise could release more vitamin D into circulation.¹

What they did

To isolate the impact of exercise on vitamin D levels, the authors conducted a randomized trial in which sedentary participants with overweight or obesity were assigned to either an exercise group (n=21) or a control group (n=20) for 10 weeks. The exercise intervention involved four cardiovascular exercise sessions per week at an indoor gym: two treadmill walking sessions and two exercise bike sessions, one at steady state and one composed of low-volume high intensity intervals. The intensity and duration of the exercise was tailored to individual fitness levels and adjusted throughout the study, with each of the exercises designed to meet a pre-determined energy expenditure per session (12 kJ/kg progressing to 15 kJ/kg). By contrast, the control group was instructed to make no changes to their baseline lifestyle (thus, any changes in vitamin D would presumably be due to seasonal declines).

The study took place during winter months in the UK, and all participants were prohibited from taking vitamin D supplements during the study period and were required to maintain their baseline body weight. (This was achieved through increased caloric intake to match the added energy expenditure, but diet was monitored via food diary to ensure vitamin D intake did not increase from baseline.) Together, these parameters were intended to isolate the effect of exercise itself, without additional impacts from any changes in body weight, diet, or sun exposure. 

What they found

At baseline, both groups exhibited comparable levels of both the bioactive form of vitamin D, 1,25-(OH)₂D₃, and an intermediate form, 25-(OH)D (found in adipose tissue and the primary form in circulation). Specifically, baseline levels of the active form were around 100 pmol/L on average between groups, while 25-(OH)D levels averaged just over 50 nmol/L. While the bioactive form does not have defined ranges or thresholds for deficiency, it’s worth noting that the average baseline 25-(OH)D level was just above the threshold for insufficiency (defined as <50 nmol/L) and roughly double the threshold for outright deficiency (defined as <25 nmol/L), meaning that nearly half of all participants met criteria for vitamin D insufficiency or deficiency at the start of the study.

By the end of the study—that is, after 10 weeks of winter in the UK—the control group had experienced a 15% decline in circulating bioactive vitamin D, while the exercise group maintained baseline levels. The average difference between the two groups at the end of the study period was 14.4 pmol/L (95% CI: 0.5–26.8 pmol/L), which translates to a moderate effect size (though the effect was quite variable between individuals). Meanwhile, levels of the intermediate form of vitamin D also dropped significantly from baseline in the control group but not the exercise group, though the between-group difference in this case was just shy of reaching statistical significance (P=0.07). (Any changes in the concentration of other forms of vitamin D, including various metabolites of vitamin D, were not significantly different between groups.)

These findings suggest that exercise can blunt the seasonal decline in vitamin D status, particularly for the active form of the molecule that has the greatest influence on cellular function.

What questions remain open?

While these results add to the mountain of evidence supporting the many benefits of exercise, several important questions with respect to the scope and implications of these findings remain unanswered.

We must keep in mind that the study population was limited to individuals with overweight and obesity, many of whom already met the criteria for vitamin D insufficiency at baseline. Given that vitamin D sequesters in fat tissue and that individuals with obesity often exhibit adipose tissue dysfunction,⁶ it’s possible that lean individuals would experience greater or lesser effects than those with obesity. The relationship between adiposity and vitamin D metabolism is complex, and thus extrapolating these findings to different body composition profiles requires caution.

Additionally, this study was unable to show clear evidence of their hypothesized mechanism—i.e., that exercise enhanced vitamin D release from fat stores. While previous studies have shown transient increases in serum vitamin D after exercise,⁷ in the present 10-week study, both groups showed decreases in vitamin D in subcutaneous adipose tissue, with no significant differences between exercise and control interventions (though the exercise group trended toward greater losses). Exercise has numerous physiological effects, so it’s possible that other mechanisms might also be at play (e.g., changes in the conversion rate of the storage form of vitamin D to the active form), which in turn might inform the best strategies for utilizing exercise to combat seasonal vitamin D decline. (This study focused exclusively on moderate cardio exercise, but it’s possible that the metabolic adaptations associated with resistance training or higher- or lower-intensity cardio training might offer additional benefits.)

What does this leave us with? Despite the lack of change from baseline in the bioactive form of vitamin D, those in the exercise group still exhibited some losses in other vitamin D forms and metabolites over the course of the study, suggesting that exercise is unlikely to prevent the seasonal decline in vitamin D alone. However, it may be an important adjunct to vitamin D supplementation and dietary sources, especially for those who are at higher risk for deficiency, such as those with excess adiposity or darker skin tones. (Melanin naturally reduces the amount of vitamin D produced from UV exposure, making winter vitamin D maintenance more challenging for these populations.)

The bottom line

These data don’t negate the importance of vitamin D supplementation, particularly for those with documented deficiency or insufficiency. (While the “optimal range” of vitamin D is still debated—see the scrutinizing supplements AMA—generally speaking, you will want to shoot for around 50 ng/mL, with anything above 80 ng/mL considered excessive.) Instead, this research suggests that exercise could serve as a valuable complementary strategy, and may even be sufficient on its own to prevent seasonal declines among those who are at relatively low risk—such as those with fairer skin or at lower latitudes, where sunlight isn’t in such short supply in winter.

But in a larger sense, this simply adds yet another compelling reason to maintain regular exercise during winter months. Beyond the well-established benefits for cardiovascular health, metabolic function, and mental well-being, exercise may also help preserve vitamin D, providing yet another reason to prioritize physical activity year-round.

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References

1. Perkin OJ, Davies SE, Hewison M, et al. Exercise without weight loss prevents seasonal decline in vitamin D metabolites: The VitaDEx randomized controlled trial. Adv Sci (Weinh). 2025;12(22):e2416312. doi:10.1002/advs.202416312
2. Bikle DD. Vitamin D metabolism, mechanism of action, and clinical applications. Chem Biol. 2014;21(3):319-329. doi:10.1016/j.chembiol.2013.12.016
3. Webb AR, Kazantzidis A, Kift RC, Farrar MD, Wilkinson J, Rhodes LE. Meeting vitamin D requirements in white Caucasians at UK latitudes: Providing a choice. Nutrients. 2018;10(4):497. doi:10.3390/nu10040497
4. Lin LY, Smeeth L, Langan S, Warren-Gash C. Distribution of vitamin D status in the UK: a cross-sectional analysis of UK Biobank. BMJ Open. 2021;11(1):e038503. doi:10.1136/bmjopen-2020-038503
5. de Oliveira LF, de Azevedo LG, da Mota Santana J, de Sales LPC, Pereira-Santos M. Obesity and overweight decreases the effect of vitamin D supplementation in adults: systematic review and meta-analysis of randomized controlled trials. Rev Endocr Metab Disord. 2020;21(1):67-76. doi:10.1007/s11154-019-09527-7
6. Reyes-Farias M, Fos-Domenech J, Serra D, Herrero L, Sánchez-Infantes D. White adipose tissue dysfunction in obesity and aging. Biochem Pharmacol. 2021;192(114723):114723. doi:10.1016/j.bcp.2021.114723
7. Sun X, Cao ZB, Taniguchi H, Tanisawa K, Higuchi M. Effect of an acute bout of endurance exercise on serum 25(OH)D concentrations in young adults. J Clin Endocrinol Metab. 2017;102(11):3937-3944. doi:10.1210/jc.2017-00146