Lowering weights in the gym, where muscles perform eccentric contractions, can lead to muscle soreness and weakness.

Credit: Vecteezy.com.

Oh, The Pain!

We've all been there: you crush a workout that felt great in the moment, only to wake up the next day (or worse, two days later) barely able to move, questioning your life choices.

That pain—the one that makes sitting down a strategic operation and has you walking like a robot for a few days—has a name: Delayed Onset Muscle Soreness, or DOMS.

It's particularly common after eccentric exercise—activities where your muscles lengthen while producing force. Think walking downhill, lowering weights, or even everyday activities like shovelling, swinging an axe, or sports involving running and jumping.

But why does this happen? Why does your body wait until 24-72 hours after exercise to remind you that you're not, in fact, a superhero?

The science behind DOMS is fascinating, and what's actually happening might surprise you…and even surprise some of the blog and medical web authors you’ve been following.

The Soreness Timeline: Why Pain Hits Later

Perhaps the most perplexing aspect of DOMS is its delayed nature. You finish a challenging workout feeling accomplished, maybe even great—then BAM!—a day or two later you're wincing with every movement.

This delay reflects the time it takes for the inflammatory process to develop fully. It's not the exercise itself that causes pain, but rather your body's response to it.

This response follows a predictable timeline:

0-2 hours post-exercise: Little to no pain, possibly some fatigue
12-24 hours: Mild soreness begins to develop
24-72 hours: Peak soreness (with the 48-hour mark often being the worst)
3-6 days: Gradual resolution of soreness

Soreness from exercise might not be felt at the time, but becomes prominent in the days after.
Credit: Alora Griffiths on Unsplash.

Debunking the Popular Myths

Let's clear up two persistent misconceptions:

Myth #1: Lactic Acid Causes Soreness

Contrary to popular belief, DOMS is not caused by lactic acid buildup. While both lactate and hydrogen ions (acid) can accumulate during intense exercise, only the hydrogen ions – which cause acidosis – tend to affect muscle function and contribute to a ‘burning’ or painful sensation during exercise. Lactate actually helps to minimise acidification and can be used to produce energy for muscle work. And both are cleared from the muscles within an hour after finishing your workout, so they can’t cause the pain you feel hours or days after exercise.

The lactic acid myth has been debunked for decades in scientific literature, yet it persists in fitness culture.

Myth #2: Torn Muscle Fibres Cause the Pain

The second common misconception is that the pain comes from torn muscle fibres. This dramatic image of ripped and shredded muscle tissue makes for good gym talk, but it's not what's actually happening…in most cases.

The severe muscle fibre damage, sometimes described in textbooks—with dramatic sarcomere disruption (damage to the microscopic building blocks of muscle fibres)—mostly occurs in laboratory settings using electrical stimulation of muscles rather than voluntary contractions. In real-world exercise, severe damage is rarer, and only seen in a small proportion of muscle fibres after extreme exercise like marathon running; these fibres undergo a longer and more complex repair process.

Severe muscle damage is highly unusual, although fibres can show signs of microdamage and a small proportion of fibres may show signs of necrosis after extreme exercise, like marathon running.

Credit: KJohansson, Wikicommons.

What's Really Happening Inside Your Muscles

So, if your muscle fibres aren't being torn apart during eccentric exercise, what's actually causing the weakness and subsequent pain? The first part of the process is a micro-level “damage” occurring in the fibres, triggering inflammation and contributing to muscle weakness.

1. The Calcium Connection

While there can be a small amount of direct damage due to muscle fibres being stretched while they produce high forces, the primary issue probably involves calcium regulation rather than major tears or severe structural damage:

During eccentric contractions, stretch-activated calcium channels in the muscle membrane open (and minor membrane damage may also allow calcium leak)
This allows extra calcium to enter the muscle fibres from outside, increasing the total calcium signal above normal
Channels inside muscle fibres that sense muscle activation and then release the calcium needed for muscle contraction also appear to ‘leak’ more calcium, and other channels that pump that calcium back into the calcium storage area (SERCA channels, which pump calcium into the sarcoplasmic reticulum), are reduced over the following days, contributing to increasing the total calcium signal above normal
This elevated calcium dose activates enzymes called calpains, increasing both their amount and their activity (i.e. the same calpain amount will do more work), and promotes local inflammation in the muscle
These calpains tag specific structural proteins for degradation and recycling, so important proteins in the muscles get cleaved off and recycled, affecting muscle contraction - the inflammation is important to drive blood flow and trigger the actions of important immune cells that help mop up the cleaved proteins and lay down new ones (inflammation can be beneficial!)
So, when we talk about ‘damage’, we should remember that most of what is seen in micrographs of ‘damaged’ muscle fibres is actually a disassembly of our proteins and rebuilding of them rather than a tearing or ripping of the fibres

Micrographs of a muscle fibre from the study of Crameri et al. (2007; The Journal of Physiology) show much less damage to sarcomeres after 210 maximal voluntary eccentric quadriceps contractions (A, top) than electrically-stimulated contractions (B, bottom).

This process is actually part of normal muscle maintenance. The muscle isn't being destroyed—it's being remodelled. But this process temporarily weakens the muscle.

The exact mechanisms that trigger the influx of calcium from outside the muscle fibre or cause leaks inside the fibre aren’t fully understood, but the shear forces created on the muscle fibre when an active muscle is stretched seems to be key - the greater the stretch (not necessarily the force), the greater the ‘damage’ and the force loss.

2. The Force Loss Phenomenon

While these processes occur, we become weaker. According to the current evidence, the calcium-triggered protein breakdown largely explains why you feel weaker, potentially during but mostly in the days after eccentric exercise:

Key connection proteins (e.g. desmin, dystrophin and others) that hold muscle sarcomeres in place and bind them to the muscle cell (fibre) membrane become disrupted, so forces aren’t transferred properly from sarcomeres to the tendons
Because these connection proteins are disassembled, some sarcomeres lose their normal structure and therefore also produce less force
The key force-producing proteins, actin and myosin, can then also be temporarily disassembled - without the need for calpains because the proteins become available for removal when the connection proteins are disassembled - further reducing muscle force capacity
Key proteins that sense muscle activation (e.g. dihydropyridine and ryanodine receptors) and then release the calcium required for muscle contraction may be degraded, reducing force production
Your nervous system also changes how it recruits muscles, partly because swelling and pain in the days after exercise reduce our ability to activate the muscles

Together, these factors create the weakness you feel.

Importantly, this doesn't mean your muscle fibres are dying. Muscle fibres don't regenerate through cell division, so if they became so damaged that they died then our muscles would waste away from over-exertion. We'd be in serious trouble! Luckily, this is exceptionally rare.

3. Where The Pain Really Comes From

But along with the weakness, we also feel pain when we move or press in on our muscles. But here's where things get really interesting: the pain you feel doesn't come from inside the “damaged” muscle fibres at all. Research using small electrodes inserted into different tissues shows:

When electrical current is applied inside muscle fibres: minimal to no pain is felt
When electrical current is applied to connective tissues: significant pain is felt
When no current (or other stimulus) is applied: no pain is felt

So, the muscle isn’t inherently painful but rather it appears that the connective tissues become more sensitive to painful stimuli, such as exercise or pressure on the muscle (or, in lab experiments, to an electrical current).

Pain receptors are predominantly located in the connective tissues surrounding muscles and within the fascia running through muscles—not in the muscle fibres themselves.

You might have heard something similar about our brain. Brain surgery can be done while we’re awake because the brain lacks pain receptors, and similarly, the inside of your muscle fibres isn’t the source of your post-workout agony.

So, what happens?

The eccentric exercise places strain on connective tissues, causing micro-level damage and triggering an inflammatory response in these tissues (as we talked about earlier).
In response, the muscle - including the connective tissues themselves - release protein messengers such as nerve growth factor (NGF; triggered by bradykinin release) and glial cell line-derived neurotrophic factor (GDNF) that sensitise the pain receptors.
This creates a “hyperalgesia”, or increase in pain sensitivity in the muscles, and particularly in the connective tissues.

The evidence for NGF playing an important role in DOMS is clearer at the present time. For example:

Injection of NGF into a muscle causes pain with a time course similar to DOMS, and specifically in the connective tissues (when injected into the fascia).
NGF causes a ‘central’, more global pain sensitivity, making it a prime candidate for DOMS pain.
The release of NGF has been found in human muscles after eccentric cycling exercise but not in the untrained control leg (increased GDNF was not detected).

Of potential importance is that swelling of local blood vessels can also trigger pain, although it’s less clear how important this source of pain is in the days after exercise.

Pain can be felt in your skin, blood vessels, and connective tissues, but there are very few pain receptors (nociceptors) inside the muscles. So your “muscle pain” isn’t exactly muscle pain.
Credit: Manu5, Wikicommons

The Remarkable Repeated Bout Effect

Perhaps the most fascinating aspect of eccentric exercise-induced soreness is how quickly your body adapts. This phenomenon, known as the "repeated bout effect," ensures that the same activity that leaves you hobbling the first time causes minimal soreness when repeated days or weeks later.

The protection provided by the repeated bout effect can last for months, to some degree, if the initial bout is painful enough.

What causes this protective effect? Recent research suggests it's largely about your connective tissues and maintaining optimum calcium levels:

Changes in the extracellular matrix surrounding muscle fibres
Remodelling of both collagenous and non-collagenous components
Strengthening of the structures that prevent excessive calcium entry
Increasing calcium uptake into the muscle’s mitochondria - the muscle’s energy powerhouses - and preventing the diminished re-uptake into the calcium storage site (SERCA-dependent uptake into the sarcoplasmic reticulum) to minimise the increase in calcium

These adaptations mean fewer calcium ions leak into the muscle fibres and any excess calcium can be effectively stored during future eccentric contractions, resulting in less protein breakdown and weakness. Simultaneously, the connective tissues become more resistant to damage, reducing inflammation and pain.

Our connective tissues, and our mitochondria, seem to save us!

But of course, other changes might also contribute. One would be a change in the nervous system, so we recruit our muscles in ways that might minimise damage (like, sharing forces better between muscles, or recruiting slower-twitch fibres that are less susceptible to damage). Another is a reduced inflammatory response after the exercise, which is really interesting.

So far, measures of inflammation show the opposite, with increases in many inflammatory molecules being observed in the blood and in the muscle 4 weeks after 300 eccentric knee extensor contractions. Although in one study, a decrease in an important pro-inflammatory signaller, NF-κB, was found in one leg 4 weeks after eccentric training of the opposite leg.

That’s right, eccentric training of one muscle can help to protect the same muscle on the other side of the body! The protection seems to be about half as strong as the protection on the trained muscle. And it seems changes in the muscles themselves might play at least some role. Future research should be interesting in this area…

Minimising Soreness: Practical Strategies

Understanding the true source of soreness leads to more effective prevention strategies:

Progressive overload: Gradually increase the intensity and volume of eccentric exercise over multiple sessions, or perform isometric contractions (where muscle length remains constant) at long muscle lengths in the days before performing eccentric contractions (long-length isometrics can cause a little damage and pain too, but also offers a bit of protection)
Start with minimal lengthening: Begin with small ranges of motion during eccentric movements and progressively increase (the amount of muscle lengthening is the biggest factor influencing damage and eventual pain)
Frequency matters: Regular exposure to eccentric exercise maintains the protective effect
Active recovery: Light movement increases blood flow to connective tissues, potentially speeding recovery
Proper nutrition: Adequate protein intake supports repair processes (some nutritional agents, including foods packed with antioxidants, show small beneficial effects so they’re worth exploring, but that’s a discussion for another time!)
Sleep: Quality sleep enhances recovery hormones and reduces inflammatory markers

The Bottom Line

The traditional narrative that muscle soreness comes from "torn muscle fibres" or from the build-up of lactic acid don’t match what science shows us. Instead, eccentric exercise triggers a complex series of events involving calcium regulation, protein turnover, and—most surprisingly—inflammation in connective tissues.

This understanding has practical implications:

Severe soreness isn't a badge of honour or necessary for progress—it's simply a sign your connective tissues are adapting to new demands
Gradually increasing eccentric exercise exposure is the most effective strategy to minimise weakness and soreness
The weakening effect of eccentric exercise is largely due to temporary protein disassembly and reduced ability to activate your muscles (both through reduced muscle activation and reduced calcium release when activated), not destruction or tearing of your muscle fibres
The pain comes from outside your muscle fibres, not inside them

It’s also important to remember that the concept of “no pain, no gain” isn’t backed up by science. We don’t need muscle damage and soreness for our muscles to grow - the loading provided to the muscle, even without detectible damage, is all you need. Rather, the soreness you feel just means your muscles haven’t been exposed to eccentric contractions (or long-length isometric contractions) lately. It’s perhaps a bit of a reminder to use your muscles more.

By understanding the science behind why your muscles hurt after exercise, you can train smarter, recover better, and build a sustainable relationship with fitness that doesn't require you to walk like a penguin after every workout.

Remember: the goal isn't to avoid soreness completely, but to manage it through intelligent training progression that allows your connective tissues and calcium regulation systems to adapt alongside your growing strength.

*Please feel free to republish this article online or in print for free provided the source is credited and no alterations are made. It is published under a Creative Commons — Attribution/No Derivatives license.

Why Your Muscles Hurt After Working Out: The Science of Soreness