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If You're Not Sore, It Still Worked

Walk out of leg day barely able to lower yourself onto a chair, and it feels like proof. You worked. The next morning's staircase confirms it. Then a week rolls around where you're not sore at all, and the doubt creeps in — has the program gone soft? Am I not training hard enough?

For most lifters, soreness is the scorecard. Sore means a good session. Not sore means a wasted one. It's one of the most durable beliefs in training, and both halves of it are wrong.

Soreness — delayed-onset muscle soreness, DOMS — is real. But it doesn't measure what people think it measures. It tracks how unfamiliar the work was, not how productive it was. You can build muscle with almost none of it, and you can be wrecked for three days by a session that grew nothing in particular.

Where "no pain, no gain" comes from

The logic seems airtight. Hard training damages muscle fibres. The body repairs that damage and overshoots, building back bigger. Soreness is the felt edge of that damage. So more soreness should mean more damage, more repair, more growth.

The belief is so embedded that surveys of lifters find many treat DOMS as one of their primary gauges of whether a workout was effective.[1] The trouble is that every link in that chain is weaker than it sounds — and the last link, damage-to-growth, mostly doesn't hold at all.

The study that tested it head-on

In 2011, Kyle Flann and colleagues built an experiment to test the "no pain, no gain" premise directly.[2] They put two groups through eight weeks of identical, work-matched training. One group — the naïve group — jumped straight in and got the full damaging, sore response. The other — pre-trained — spent three extra weeks ramping up gradually, specifically so they'd reach the same training without the soreness or detectable damage.

Same work. One group sore, one group not. The result: both groups gained the same muscle size and the same strength.

The soreness was optional. The gains weren't tied to it.

Soreness isn't what you think it is

Part of the confusion is that most people are wrong about what DOMS even is. It isn't lactic acid — that clears within an hour of training and was never the cause. The current mechanistic picture is that DOMS is a nerve-sensitisation phenomenon: unaccustomed mechanical loading triggers the release of factors like nerve growth factor that leave the muscle's pain receptors hypersensitive for a day or two.[3]

The key word is unaccustomed. Soreness is fundamentally a novelty signal. It spikes when you do something new — a new exercise, a new range of motion, a lot of lengthening (eccentric) work, or your first session back after a layoff — and it fades fast as the movement becomes familiar. This is the repeated-bout effect: the session that destroyed you in week one barely registers by week three, even though you're lifting the same or more. Nothing about your training got less effective. Your nervous system just stopped sounding the alarm.

Damage isn't the engine

If damage drove growth, the early, high-damage phase of a program should be where most of the building happens. It isn't.

Felipe Damas and colleagues tracked muscle protein synthesis and muscle damage across ten weeks of training.[4] In the first week — peak damage, peak soreness — the protein-synthesis response was large, but much of it was going toward repairing damage, not building new muscle. Only later, once damage had subsided and the repeated-bout effect had kicked in, did the protein-synthesis response actually start tracking real hypertrophy. Their conclusion was blunt: muscle damage is not the process that drives growth.

This fits a broader finding that the acute signals people lean on as proxies — the burn, the pump, the next-day soreness, even the protein-synthesis spike after a single session — don't predict who actually builds muscle over months.[5]

Soreness tracks novelty, not progress. You can build muscle and strength with almost none of it — and being wrecked for three days proves only that the work was unfamiliar.

So what actually drives growth

If not damage, then what? The same three levers that show up in every honest account of hypertrophy: total weekly volume, proximity to failure, and progressive overload. Soreness isn't on the list. It's a downstream side effect that correlates loosely with hard training, not a cause of anything.

That has a practical consequence most apps get wrong: you can't read your training off your soreness. A familiar lift you're progressing on will stop making you sore long before it stops building muscle. Judge the session by whether your reps and load are moving and whether you're training close enough to failure — not by how you feel on the stairs tomorrow. (It's also why how you count volume matters far more than how sore a session leaves you.)

The part that should change your recovery

Here's the twist that catches people out. If soreness doesn't matter, you might as well crush it with whatever feels good — ice baths, cold showers, anti-inflammatories. Except that blunting the very response you're trying to provoke can blunt the adaptation along with it.

When researchers had trained lifters do regular post-workout cold-water immersion through a resistance program, the cold group built less muscle than the group that simply let recovery happen — with the molecular signals for growth measurably suppressed.[6] Maximal strength held up better than size, but the message for anyone training for muscle is clear: routinely icing away your soreness can cost you some of what you trained for. Reserve aggressive cold recovery for when in-season performance matters more than adaptation. (The evidence on anti-inflammatories points the same direction, though it's more mixed.)

The honest caveats

The evidence here is strong on direction but worth keeping in proportion. The Flann study was small and used eccentric cycling, not free weights. The damage-versus-growth work is mostly in younger, less-trained lifters. Individual variability in soreness is enormous — two people doing identical work can have opposite responses, so soreness tells you even less at the individual level than the averages suggest. And some early damage-linked signalling probably does contribute a little to growth; the claim is that damage isn't necessary or proportional, not that it's irrelevant.

One distinction that isn't a caveat but a hard rule: muscle soreness is not joint or tendon pain. Diffuse, achy, both-sides tenderness that peaks a day or two after a new stimulus is normal. Sharp, localised pain, pain inside a joint, or pain during a movement is an injury signal — never something to train through. And in the rare case of severe, disproportionate pain with heavy swelling and dark urine after extreme unaccustomed work, that's a medical issue, not a badge.

How JSON.fit handles this

JSON.fit builds your programs around the levers that actually drive growth — total volume, proximity to failure, and progressive overload — not around soreness. It never treats soreness as a target to chase, and it never reads the absence of soreness as a reason to pile on more volume. Soreness is something to expect when a program or an exercise is new, and to read as novelty rather than a verdict on the session. Joint or connective pain is a different thing entirely — an injury signal, never something to train through.

The full research breakdown and citations are at json.fit/soreness-references.md.

The honest summary

Soreness is real, but it's a novelty alarm, not a progress meter. You can build muscle and strength with little or none of it, the damage it reflects isn't the engine of growth, and the single most actionable finding runs opposite to intuition: aggressively erasing soreness with cold-water immersion can erase some of your gains along with it. Train for volume, effort, and progression, and let soreness be a side effect you neither chase nor fear. If the only way you can tell a workout "worked" is whether you're sore the next day, you're measuring the wrong thing.

Training built on what drives growth — not on how sore it leaves you.

Download JSON.fit — free on the App Store

References

  1. Schoenfeld, B.J., & Contreras, B. (2013). Is postexercise muscle soreness a valid indicator of muscular adaptations? Strength and Conditioning Journal, 35(5), 16–21. journals.lww.com/nsca-scj
  2. Flann, K.L., LaStayo, P.C., McClain, D.A., Hazel, M., & Lindstedt, S.L. (2011). Muscle damage and muscle remodeling: no pain, no gain? Journal of Experimental Biology, 214(4), 674–679. pubmed.ncbi.nlm.nih.gov/21270317
  3. Mizumura, K., & Taguchi, T. (2024). Neurochemical mechanism of muscular pain: insight from the study on delayed onset muscle soreness. Journal of Physiological Sciences, 74(1), 4. pubmed.ncbi.nlm.nih.gov/38267849
  4. Damas, F., Phillips, S.M., Libardi, C.A., et al. (2016). Resistance training-induced changes in integrated myofibrillar protein synthesis are related to hypertrophy only after attenuation of muscle damage. Journal of Physiology, 594(18), 5209–5222. pubmed.ncbi.nlm.nih.gov/27219125
  5. Mitchell, C.J., Churchward-Venne, T.A., Parise, G., Bellamy, L., Baker, S.K., Smith, K., et al. (2014). Acute post-exercise myofibrillar protein synthesis is not correlated with resistance training-induced muscle hypertrophy in young men. PLOS ONE, 9(2), e89431. journals.plos.org
  6. Fyfe, J.J., et al. (2019). Cold water immersion attenuates anabolic signaling and skeletal muscle fiber hypertrophy, but not strength gain, following whole-body resistance training. Journal of Applied Physiology. pubmed.ncbi.nlm.nih.gov/31513450