You ride outside more than almost anyone you know. Four, five, six days a week on the road. Hours in the sun. And you would be entirely reasonable to assume your vitamin D levels are fine.
They are probably not.
When Graeme Close and his team at Liverpool John Moores University started testing elite athletes across a range of outdoor sports, they found something that surprised even them. More than half the athletes tested — people who trained outdoors for a living — had vitamin D levels below the threshold for adequacy. Not borderline. Below it. Footballers, rugby players, jockeys, athletes whose entire working life is spent outside in daylight.
Cyclists are not exempt. If anything, the combination of covered skin, sunscreen, early-morning or late-evening training times, and northern latitudes puts serious riders at particular risk. The fact that you train outdoors does not protect you the way you think it does.
And this matters. Because vitamin D is not a minor player in athletic performance. It is a hormone that governs muscle function, bone metabolism, and immune regulation — three systems that sit at the centre of everything a cyclist cares about. It is also one of the most commonly missed elements of cycling nutrition.
Vitamin D is not a vitamin
This is where most people's understanding falls apart before it even starts. Vitamin D was misclassified when it was discovered in the 1920s, and the name stuck. It is not a vitamin. It is a secosteroid hormone — your body manufactures it when UVB radiation from sunlight hits the skin and converts 7-dehydrocholesterol into cholecalciferol (vitamin D3). That molecule then travels to the liver, where it becomes 25-hydroxyvitamin D, and then to the kidneys, where it becomes the active hormone calcitriol.
Why does the classification matter? Because hormones do not just plug a nutritional gap. They regulate entire biological systems through receptor binding. Vitamin D receptors — VDRs — are expressed in skeletal muscle, cardiac muscle, bone tissue, immune cells, the gut, the brain, and the pancreas. When your vitamin D levels drop, you are not just missing a nutrient. You are running a hormonal system below operating capacity.
Close's research group has been particularly clear on this point. VDR expression in muscle tissue means vitamin D directly influences muscle protein synthesis, muscle fibre composition, and the calcium handling that drives contraction. It is not a downstream effect. It is direct regulation.
Why cyclists are particularly vulnerable
The assumption is simple enough: outdoor sport equals sun exposure equals adequate vitamin D. The reality is more complicated, and the reasons are layered.
Latitude. UVB radiation — the specific wavelength that triggers vitamin D synthesis — only reaches the earth's surface at meaningful intensity when the sun is above approximately 45 degrees in the sky. In the UK and Ireland, that window runs from roughly April to September. During winter months, the sun never climbs high enough for your skin to produce any meaningful vitamin D, regardless of how long you spend outside. If you live above 35 degrees north — which covers all of the UK, Ireland, northern Europe, most of Canada, and a significant portion of the northern United States — you have zero cutaneous vitamin D production for four to six months of the year.
Sun angle and training times. Even during summer, most amateur cyclists ride before 9am or after 5pm. Commute rides are dawn or dusk. Club spins often leave at 8am. The UVB window is roughly 10am to 3pm in northern latitudes. You can ride four hours on a Saturday morning and get almost no vitamin D production because you started at 7am and finished at 11am — with most of the ride completed before the sun was high enough to matter.
Covered skin. Cycling kit covers a lot of surface area. Arm warmers, leg warmers, gilets, base layers, full-finger gloves — for half the year or more, the only exposed skin is your face and the back of your hands. Vitamin D synthesis requires direct UVB exposure to uncovered skin, and the amount produced is proportional to the surface area exposed. A face and two hands is not enough.
Sunscreen. SPF 30 blocks approximately 97% of UVB radiation. Cyclists riding in summer are rightly protecting their skin — particularly the face, neck, and arms that take hours of direct exposure. But effective sun protection effectively eliminates vitamin D production from the protected areas. This is not an argument against sunscreen. It is an argument for supplementation.
Body composition. Vitamin D is fat-soluble and gets sequestered in adipose tissue. Cyclists who carry more body fat need higher circulating levels to achieve the same tissue availability as leaner riders. This is a genuine physiological variable, not a judgement call.
Indoor training. Zwift, the turbo trainer, the indoor season. Any time you spend training indoors is time spent producing zero vitamin D. For riders who do 30-50% of their training volume indoors — and in northern climates that is common from October to March — the cumulative deficit grows rapidly.
The net effect is that a cyclist living in London, Dublin, or Manchester who trains 10-12 hours a week can easily go from October to April with negligible vitamin D production. Six months. That is enough time for levels to drop well below the adequacy threshold, even if they entered autumn with good stores.
Testing: the only way to know
Guessing your vitamin D status is a waste of time. Symptoms of deficiency are vague — fatigue, muscle weakness, bone pain, low mood, frequent illness — and overlap with half a dozen other conditions including overtraining, iron deficiency, and simple under-fuelling. The only way to know your actual status is a blood test.
The test you want. Serum 25-hydroxyvitamin D, written as 25(OH)D. This is the circulating form of vitamin D and the standard biomarker used by every sports medicine and endocrinology lab in the world. It reflects your vitamin D status over the previous two to three weeks. Do not accept a test for 1,25-dihydroxyvitamin D — that is the active hormonal form, and it is tightly regulated by the kidneys, which means it can appear normal even when your stores are depleted.
What the numbers mean:
- Below 25 nmol/L (10 ng/mL) — severely deficient. Associated with rickets, osteomalacia, significant immune compromise, and measurable muscle weakness. Requires medical intervention.
- 25-50 nmol/L (10-20 ng/mL) — deficient. Performance impairment likely. Immune function compromised. Bone metabolism disrupted. Needs corrective supplementation.
- 50-75 nmol/L (20-30 ng/mL) — insufficient. You are not clinically deficient, but you are below the level most sports medicine researchers consider adequate for athletes. Many riders sit here and assume they are fine.
- 75-125 nmol/L (30-50 ng/mL) — adequate. This is where you want to be. The Endocrine Society, most sports medicine guidelines, and researchers like Close and Owens converge on this range as the target for athletic populations.
- Above 125 nmol/L (50 ng/mL) — no additional benefit demonstrated, and levels above 250 nmol/L (100 ng/mL) enter the territory where toxicity becomes a concern.
When to test. Twice a year is the minimum for serious cyclists. Once at the end of winter (February or March) to catch the seasonal nadir, and once at the end of summer (September or October) to confirm your stores are topped up before the dark months. If you are correcting a deficiency, retest 12 weeks after starting supplementation to check the dose is working.
What it costs. In the UK, a vitamin D test through your GP is free if they agree to run it — and most will if you present symptoms or explain you are an endurance athlete. Private testing through services like Medichecks or Thriva runs roughly $30-50. In the US, most insurance covers it, or you can order it directly through services like InsideTracker for a similar price. The cost is trivial relative to what most cyclists spend on tyres.
The performance connection — what the evidence actually supports
This is where you need to be careful. Vitamin D is a genuine physiological player in athletic performance, but it is not a magic supplement that will add watts to your FTP. The evidence base is mixed, and being honest about what it supports and what it does not is more useful than hype.
What the evidence supports strongly:
Immune function. This is the most robust finding in the vitamin D and athlete literature. Owens, Close, and Morton at Liverpool John Moores published a series of studies showing that athletes with vitamin D levels above 75 nmol/L had significantly fewer upper respiratory tract infections (URTIs) during winter training blocks than athletes below that threshold. URTIs are the primary reason amateur cyclists miss training days. Losing a week to a cold in January does more damage to your February fitness than a marginal supplement ever compensates for. The immune connection alone justifies monitoring your levels.
Vitamin D modulates both the innate and adaptive immune systems. It enhances the antimicrobial action of macrophages and monocytes — your first line of defence — while also regulating T-cell function to prevent the kind of excessive inflammatory response that turns a minor infection into a week-long chest cold. During heavy training blocks, when the immune system is already suppressed from training load, adequate vitamin D provides a buffer.
Muscle function and recovery. VDR expression in skeletal muscle is well established. Close et al. demonstrated that correcting vitamin D deficiency in athletes improved muscle recovery markers — specifically, participants who corrected from deficient to adequate levels showed faster recovery of peak torque after damaging exercise. The caveat is important: correcting a deficiency improves function. There is much weaker evidence that supplementing above adequate levels improves function further. If you are already at 90 nmol/L, taking more vitamin D will not make your muscles recover faster.
Barker et al. published similar findings showing that higher vitamin D levels were associated with faster strength recovery following intense exercise. The mechanism is thought to involve vitamin D's role in calcium signalling within the muscle cell and its influence on the inflammatory-repair cascade that follows training damage.
What the evidence is mixed on:
VO2max and aerobic performance. Several observational studies have found correlations between vitamin D levels and VO2max. Koundourakis et al. found that professional footballers with higher vitamin D levels had better VO2max scores. But observational data cannot prove causation — fitter athletes may spend more time outdoors, or their better overall health habits may drive both the higher vitamin D and the higher VO2max. The interventional studies — where researchers give vitamin D supplements and measure whether VO2max actually improves — are inconsistent. Some show modest improvements. Others show nothing. The current honest assessment is that correcting a deficiency probably removes a limiter, but supplementation in already-adequate individuals does not reliably improve aerobic capacity.
Power output. Same story. A few small studies suggest improvements in strength and power output after correcting deficiency. But the results are not consistent enough to make strong claims, and many of the positive studies have small sample sizes. Close has been careful to note that the performance benefits of vitamin D are most likely about removing a deficit, not about supercharging a system that is already working properly.
Bone density: the quiet crisis for cyclists
This deserves its own section because it is arguably the most important long-term health consideration for serious cyclists, and vitamin D sits at the centre of it.
Cycling is a non-weight-bearing sport. Your skeleton does not receive the mechanical loading stimulus that runners, footballers, or even tennis players get. Without that stimulus, bone mineral density does not maintain itself the way it should. Barry and Kohrt's research at the University of Colorado demonstrated that competitive male cyclists had significantly lower bone mineral density at the hip and spine compared to age-matched controls — not sedentary people, but people who were physically active in weight-bearing activities.
This is not a minor academic finding. It means that a dedicated cyclist who rides 10-15 hours a week for two decades without any weight-bearing cross-training is accumulating genuine osteoporotic risk. And the risk compounds with age. Masters cyclists — the 40-55 demographic who make up the majority of serious amateur riders — are already experiencing age-related bone density decline. Cycling does nothing to counteract it and may contribute to it through the cortisol and energy expenditure profile of long endurance sessions.
Vitamin D and calcium form the primary regulatory axis for bone mineral metabolism. Vitamin D promotes calcium absorption in the gut — without adequate vitamin D, you absorb only 10-15% of dietary calcium. With adequate levels, absorption jumps to 30-40%. It also regulates parathyroid hormone (PTH), which drives bone resorption when calcium levels drop. Chronically low vitamin D means chronically elevated PTH, which means your body steadily pulls calcium from your bones to maintain blood calcium levels.
If you are a cyclist over 40, you should be thinking about vitamin D and bone density as a single linked system. Supplement vitamin D to improve calcium absorption. Ensure adequate dietary calcium — 1,000-1,200mg per day from food sources. And add some form of weight-bearing or impact exercise to your weekly routine, even if it is just 20 minutes of skipping or body-weight exercises twice a week. The bone density guide covers this in detail.
Dosing and timing: getting the details right
The good news is that vitamin D supplementation is cheap, safe at appropriate doses, and effective. The bad news is that most people get the details wrong in small ways that reduce how much benefit they actually get.
D3, not D2. Vitamin D3 (cholecalciferol) is the form your skin produces and the form that most effectively raises and maintains serum 25(OH)D levels. Heaney and colleagues at Creighton University demonstrated that D3 is approximately 87% more potent than D2 (ergocalciferol) in raising blood levels. D2 has a shorter half-life and is cleared from the body faster. Unless you need a plant-derived source (D3 is typically from lanolin; vegan D3 derived from lichen is available), always choose D3.
Dose ranges. For most cyclists:
- Maintenance (levels already 75-125 nmol/L): 1,000-2,000 IU daily, primarily through winter months.
- Correction (levels 50-75 nmol/L): 2,000-4,000 IU daily for 12 weeks, then retest and drop to maintenance.
- Deficiency (levels below 50 nmol/L): 4,000-6,000 IU daily for 8-12 weeks under guidance, then retest. Some practitioners prescribe a single large loading dose (e.g., 300,000 IU), but evidence suggests daily dosing is more physiologically stable.
Take it with fat. This is the detail most people miss. Vitamin D is fat-soluble. It requires dietary fat for absorption in the gut. Dawson-Hughes and colleagues showed that taking vitamin D with a fat-containing meal increased serum levels by approximately 50% compared to taking it on an empty stomach or with a fat-free meal. Take your vitamin D with breakfast or dinner — whichever meal contains the most fat. With eggs. With avocado. With peanut butter. Not with a black coffee and nothing else.
Seasonal adjustment. If you live above 35 degrees north, you are producing meaningful vitamin D from sunlight only between April and September. Many riders need supplementation year-round but at different doses — higher through October to March, lower through April to September when sun exposure contributes. Some riders in northern latitudes find they need to supplement even in summer, particularly if they train early or late and use sunscreen diligently.
Toxicity. Vitamin D toxicity (hypervitaminosis D) is real but requires sustained doses above 10,000 IU per day for months. It causes hypercalcaemia — elevated blood calcium — leading to nausea, vomiting, weakness, and potential kidney damage. The European Food Safety Authority's tolerable upper intake is 4,000 IU per day for long-term use. Staying within the ranges above and testing twice a year eliminates any meaningful risk.
Cofactors. Vitamin D works in concert with other nutrients. Vitamin K2 directs calcium into bones rather than soft tissues — supplementing K2 alongside D3 is sensible, particularly for cyclists concerned about bone density. Magnesium is also involved in vitamin D metabolism — the body needs magnesium to convert vitamin D into its active form. If your magnesium is low, your vitamin D supplementation is less effective. The magnesium guide covers this relationship.
Food sources: limited but worth knowing
You cannot reliably meet your vitamin D needs through food alone. The amounts in most foods are simply too small. But dietary sources contribute, and they are worth incorporating.
- Oily fish. The best dietary source by a wide margin. A 100g serving of wild salmon provides roughly 600-1,000 IU of vitamin D. Mackerel, sardines, and herring are similarly rich. Tinned sardines on toast is one of the most vitamin D-dense meals you can eat.
- Egg yolks. Around 40 IU per yolk, so you would need 25-50 eggs a day to meet your needs from eggs alone. Useful as a contributor, not a solution.
- Fortified foods. Fortified milk, fortified orange juice, fortified cereals, and fortified plant milks typically provide 100-150 IU per serving. In countries like Finland and Sweden, aggressive fortification policies have measurably improved population vitamin D status.
- Mushrooms exposed to UV light. Certain mushrooms — particularly maitake and UV-treated button mushrooms — contain meaningful vitamin D2 (not D3). The amounts vary enormously depending on growing conditions. A useful addition for plant-based cyclists but not a reliable primary source.
- Cod liver oil. A single tablespoon provides approximately 1,360 IU. It was the original vitamin D supplement before isolation of the molecule. Still works. Still tastes like cod liver oil.
The practical takeaway is that oily fish two to three times a week, eggs regularly, and fortified foods where available will give you a useful baseline. Supplementation fills the gap between what food provides and what your body needs.
The practical protocol
If you have read this far, here is the order of operations. Simple. No guesswork.
- Get tested. Serum 25(OH)D. Do it now if you have never checked it. If it is winter, expect your levels to be lower than you think.
- Read the number. Below 50 nmol/L is deficient. Between 50 and 75 is insufficient. You are aiming for 75-125 nmol/L.
- Start supplementation based on your result. Deficient: 4,000-6,000 IU D3 daily. Insufficient: 2,000-4,000 IU daily. Adequate: 1,000-2,000 IU daily through winter.
- Take it with food. A meal containing fat. Every time. This is non-negotiable if you want to absorb what you are paying for.
- Add K2 and ensure magnesium is covered. Vitamin K2 (MK-7 form, 100-200 mcg) alongside D3. Magnesium glycinate 200-400mg in the evening.
- Retest at 12 weeks. If you are correcting a deficiency, you need to confirm the dose is working. A single test tells you where you are. Two tests tell you which direction you are heading.
- Build it into your annual rhythm. Test in February/March and September/October. Adjust supplementation by season. Make it as routine as checking your chain wear.
This is not complicated. A bottle of vitamin D3 costs less than a single energy gel. The test costs less than a new inner tube. And the consequences of ignoring it — weakened bones, suppressed immunity, impaired recovery — are real, measurable, and entirely avoidable.
If you are working through questions like this alongside your training — what to test, how to dose, how the different supplements interact — that is exactly the kind of thing the Roadman Cycling community on Skool exists for. Real riders asking real questions, not marketing dressed up as science.