Sunlight, Red Light and Your Skin: What Different Wavelengths Do to Collagen and Mitochondria

Mycena Skin: Ingredient Science Series · Deep Dive: Light Biology

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Light isn't one thing, and this article covers two sources of it: natural sunlight, and artificial red light from LED panels, face masks and other devices.

Sunlight is a mix of wavelengths, and each band does something different once it reaches your skin. Red-light devices take just two of those bands, red and near-infrared, and deliver them in a concentrated, measured dose. Used well, both can be good for skin.

We cover what sunlight is made of and what it does for you, how deep each band travels, where too much UV works against collagen, how red-light devices are thought to act on skin mitochondria, why dose matters so much, and a simple routine that pairs early morning sun with brief red-light sessions on the face.

Part 1: What sunlight is made of

At ground level on a clear day, sunlight is roughly:

• About 5% ultraviolet (UV). Of that, about 95% is UVA (315–400 nm) and about 5% is UVB (280–315 nm).
• About 40–45% visible light (400–700 nm), from violet and blue through to red.
• About 50% infrared, mostly near-infrared (700–1,400 nm).

The mix shifts through the day. UVB has to travel through more atmosphere when the sun is low, so it drops off sharply in the early morning and late afternoon, while red and near-infrared light stay comparatively strong. At midday, UVB peaks.

How deep each band goes

Longer wavelengths generally travel deeper into skin, up to the point where water absorbs them.

• UVB is mostly absorbed in the epidermis, the outer layer. It's the band that causes sunburn and the one skin uses to make vitamin D.
• UVA reaches into the dermis, where collagen and fibroblasts live.
• Blue light reaches about as far as UVA, into the upper dermis.
• Red light (about 630–670 nm) reaches into the dermis.
• Near-infrared (about 800–850 nm) travels deepest, several millimeters, into the lower dermis and beyond.

Exact depths depend on skin type, pigment, thickness and blood flow, so treat these as a guide rather than fixed numbers. The pattern is what matters: the bands that reach the collagen layer include UVA, which drives sun-related aging when exposure is heavy, and red and near-infrared, the bands used in red-light therapy.

Part 2: What sunlight does for you

Human skin evolved under the sun, and regular daylight does a lot of good.

• Vitamin D. UVB is how skin makes vitamin D, which the body needs for bones, muscles and immune function. UVB is strongest from late morning to mid-afternoon, so short sessions then make the most of it.
• Nitric oxide. UVA releases nitric oxide stored in the skin, which relaxes blood vessels. In one study, UVA exposure lowered blood pressure slightly (Liu et al., 2014).
• Your body clock. Bright morning light reaching the eyes sets the body's master clock, which shapes sleep, mood and hormone rhythms. Skin cells run their own daily clocks too.
• Free red and near-infrared. About half of sunlight's energy is infrared. Early and late-day light is rich in red and near-infrared while carrying little UVB: the same bands used in red-light therapy.
• Natural adaptation. With gradual, regular exposure, skin adapts. It thickens its outer layer and builds melanin, its own light filter.
• The big picture. A Swedish study that followed about 30,000 women for 20 years found that those who avoided the sun had higher death rates from all causes than those who got more of it (Lindqvist et al., 2014). It's observational, but it's a reminder that avoiding the sun has costs too.

When UV outpaces repair

The downside of sunlight is about dose. Skin handles everyday light well. Trouble builds when UV repeatedly outpaces skin's ability to repair, especially with burns and long midday exposure. Dermatologists call this photoaging, and one widely cited study estimated that sun exposure accounts for most of the visible aging on the face. The biology was mapped out largely by Gary Fisher, John Voorhees and colleagues at the University of Michigan in the 1990s.

At high doses, two things happen at once:

• Breakdown speeds up. UV generates reactive oxygen species in skin cells, which activate a switch called AP-1. That turns on matrix metalloproteinases (MMPs), the enzymes that cut collagen.
• Building slows down. The same signals interfere with TGF-β, the pathway that tells fibroblasts to make new collagen.

Heavy UV also damages mitochondrial DNA. One well-studied marker, the "common deletion", builds up in skin that's had years of intense sun, and mitochondria carrying it make less energy.

The takeaway isn't to avoid the sun. It's to get it the way skin handles best: often, early in the day, and without burning.

Part 3: How red and near-infrared light are thought to work

Red-light devices, from LED panels and face masks to handheld wands, deliver concentrated red and near-infrared light. Using them on skin is called photobiomodulation (PBM). It has been studied since the late 1960s, when Endre Mester noticed that low-power laser light sped up hair regrowth and wound healing in mice.

The mitochondrial target

The leading explanation centers on cytochrome c oxidase, the last enzyme in the mitochondrial electron transport chain (Complex IV). Work by Tiina Karu and others showed that this enzyme absorbs light in specific red and near-infrared bands. Its absorption peaks sit roughly around 620, 680, 760 and 820 nm.

The proposed sequence:

1. Red or near-infrared photons are absorbed by cytochrome c oxidase.
2. That appears to release nitric oxide, which can sit in the enzyme's active site and block oxygen.
3. With the block cleared, electron transport and oxygen use pick up, and the cell makes more ATP.
4. A brief, small rise in reactive oxygen species acts as a signal rather than as damage, switching on genes involved in repair and growth.

This isn't settled. Other explanations, including effects on water near the mitochondrial membrane and on light-sensitive ion channels, are also being studied. But the cytochrome c oxidase model is the most widely cited, and it explains why the useful wavelengths cluster in red and near-infrared.

What happens to collagen

In fibroblast studies, red light has increased cell proliferation and procollagen production and lowered MMP activity. That's the opposite of what UV does. Human studies are smaller, but they point the same way:

• Lee and colleagues (2007) treated one side of the face in 76 people with 633 nm, 830 nm or combined LED light, against a sham light, twice a week for four weeks. Wrinkles and elasticity improved, and biopsies showed more collagen and elastic fibers.
• Barolet and colleagues (2009) used pulsed 660 nm LED light. In the lab it raised procollagen and lowered MMP-1 in fibroblasts. In a small clinical study it improved skin texture and wrinkle depth.
• Wunsch and Matuschka (2014) ran a randomized, controlled trial with 136 volunteers, using red or broader red-to-near-infrared light (about 9 J/cm² per session) twice a week for 30 sessions. Participants reported better complexion and skin feel, and ultrasound showed increased collagen density compared with controls.

These studies are promising but small, and the devices, wavelengths and doses vary widely. Red light is a reasonable, low-risk tool, and it works best alongside sensible sun habits.

Part 4: Dose is everything

Photobiomodulation follows a biphasic dose response. Too little light does nothing. A moderate dose stimulates. Too much can switch the benefit off or even start to cause harm. Michael Hamblin and colleagues have described this as the light-therapy version of the Arndt–Schulz rule.

How dose is measured

Light dose (fluence) is measured in joules per square centimeter:

Dose (J/cm²) = irradiance (W/cm²) × time (seconds)

A device delivering 50 mW/cm² for 100 seconds gives 5 J/cm². The same device held twice as far away delivers much less, because irradiance falls off quickly with distance. That's why a device's stated power means little unless you know its irradiance at the distance you actually use it.

When near-infrared turns against you

Dose matters for sunlight too. Jean Krutmann's group showed that high doses of infrared-A, like those in strong midday sun, can raise MMP-1 through mitochondrial signaling. Heat does something similar: warming skin to around 40–43°C raises collagen-degrading enzymes. So the same near-infrared band that looks helpful at controlled doses can add to photoaging when it comes with intense sun and heat.

There's also early lab evidence pointing the other way. Near-infrared pre-exposure has made fibroblasts more resistant to UV damage in cell studies. Some researchers see that as one reason morning light, rich in red and near-infrared and low in UVB, may be the gentlest part of the day for skin. That idea is interesting but not proven in people.

Part 5: Putting it into practice

A practical way to think about it is band by band:

• UVB and UVA: get them often and briefly. Early and late-day light is gentle, a short midday session makes vitamin D, and the rule that matters most is never to burn.
• Blue light: a minor factor for most people compared with UV. There's some evidence it deepens pigmentation in darker skin tones.
• Red and near-infrared: a deliberate, dosed tool. If you use a device, look for stated wavelengths in the 630–670 nm and 810–850 nm ranges, a stated irradiance, and a consistent routine several times a week. Protect your eyes from bright near-infrared, which is hard to see.
• Heat: avoid cooking your skin. Long sessions that leave skin hot defeat the purpose.
• Daylight: enjoy it, especially early and late in the day, when the UV share is low.

A suggested daily light routine

Here's a simple routine that puts this together. Treat it as a starting point rather than a prescription.

• Early morning sun, every day (10–20 minutes). Get outside within an hour or two of sunrise, when the UV index is low and red and near-infrared make up a larger share of the light. Leave your face uncovered, but don't look at the sun.
• Red light on the face, 3–5 times a week (about 5–10 minutes). Use a device with stated wavelengths in the red (630–670 nm) and near-infrared (810–850 nm) ranges, at the distance and time its maker specifies. The largest trial above used about 9 J/cm² per session, twice a week. Wear the eye protection supplied and stop if your skin feels hot.
• Before and after. Start with clean, dry skin so nothing blocks the light, and apply your serum afterward.
• Midday: short and never burned. A brief stretch of midday sun is when skin makes the most vitamin D. Keep it short enough that you never burn, then move to shade.
• Rest days. Take two days a week off red light. More isn't better.

Part 6: Putting it together

Light affects skin through the same two levers as everything else in this series: the signal to build and the rate of breakdown. Too much UV pushes both the wrong way at once. It turns on the enzymes that cut collagen, turns down new collagen production and wears out the mitochondria that power repair. Red and near-infrared light, at the right dose, appear to do roughly the opposite, giving fibroblast mitochondria a small push that shows up as more collagen and less breakdown.

The practical message is simple. Get sunlight the way skin handles best, often, early and never burned, and treat red light as a measured tool rather than more-is-better.

Where Mycena fits

Our serums are built for the other side of this story, the daily care that sits alongside good light habits. Copper Theory pairs 2% GHK-Cu with tremella and sodium hyaluronate for skin that looks firmer and more hydrated. Vital Theory combines cordyceps extract, niacinamide and adenosine for skin that looks brighter and more rested. Both fit easily into the routine above: apply them after your morning red-light session.

References

• Fisher GJ, et al. Molecular basis of sun-induced premature skin ageing and retinoid antagonism. Nature, 1996.
• Fisher GJ, et al. Pathophysiology of premature skin aging induced by ultraviolet light. New England Journal of Medicine, 1997.
• Berneburg M, et al. Induction of the photoaging-associated mitochondrial common deletion in vivo in normal human skin. Journal of Investigative Dermatology, 2004.
• Liu D, Fernandez BO, Hamilton A, et al. UVA irradiation of human skin vasodilates arterial vasculature and lowers blood pressure independently of nitric oxide synthase. Journal of Investigative Dermatology, 2014.
• Lindqvist PG, Epstein E, Landin-Olsson M, et al. Avoidance of sun exposure is a risk factor for all-cause mortality: results from the Melanoma in Southern Sweden cohort. Journal of Internal Medicine, 2014.
• Karu T. Primary and secondary mechanisms of action of visible to near-IR radiation on cells. Journal of Photochemistry and Photobiology B, 1999.
• Huang YY, Chen AC, Carroll JD, Hamblin MR. Biphasic dose response in low level light therapy. Dose-Response, 2009.
• Lee SY, et al. A prospective, randomized, placebo-controlled, double-blinded, and split-face clinical study on LED phototherapy for skin rejuvenation. Journal of Photochemistry and Photobiology B, 2007.
• Barolet D, Roberge CJ, Auger FA, Boucher A, Germain L. Regulation of skin collagen metabolism in vitro using a pulsed 660 nm LED light source. Journal of Investigative Dermatology, 2009.
• Wunsch A, Matuschka K. A controlled trial to determine the efficacy of red and near-infrared light treatment in patient satisfaction, reduction of fine lines, wrinkles, skin roughness, and intradermal collagen density increase. Photomedicine and Laser Surgery, 2014.
• Schroeder P, et al. Infrared radiation-induced matrix metalloproteinase in human skin: implications for protection. Journal of Investigative Dermatology, 2008.
• Flament F, et al. Effect of the sun on visible clinical signs of aging in Caucasian skin. Clinical, Cosmetic and Investigational Dermatology, 2013.

This article is for educational purposes and isn't medical advice. Talk with a dermatologist before starting light therapy, especially if you take photosensitizing medications or have a history of skin cancer.

These statements have not been evaluated by the Food and Drug Administration. Mycena Skin products are cosmetics and are not intended to diagnose, treat, cure, or prevent any disease. Ingredient research is provided for education and describes the ingredients, not claims about finished-product performance.