Two tablets against a light warm background: on the left, a red-orange aspirin tablet with a warm glow and the inscription "restores", and on the right, a white oval ibuprofen tablet with a cold shadow and the inscription "inhibits"."

Aspirin after injury repairs muscles. Ibuprofen inhibits.

After a tough workout, my hand automatically reaches for ibuprofen. It's almost a reflex – my shoulder aches, my quad aches, I swallow a pill, and forget about it. A recent study on bioRxiv shows that this isn't a neutral habit for muscle recovery. And that a penny's worth of aspirin does the opposite in the same circumstances.

What have [they/you] done

Researchers from Canada and the US (Lu et al., April 2026) compared aspirin and non-aspirin NSAIDs — indomethacin, celecoxib, SC-236 — at two levels.

In vitro myoblast precursor cells (C2C12), which would have fused into muscle fibres. Indomethacin and celecoxib at usual therapeutic concentrations notably inhibited myogenesis – fibre formation. Aspirin only inhibited it at unrealistically high concentrations.

In vivo Mice were subjected to acute muscle injury induced by barium chloride and then treated with either 3 mg/kg/day indomethacin or aspirin. Indomethacin:

  • Reduced the cross-sectional area of the regenerating fibres
  • Resuming strength recovery

Aspirin in the same dosage:

  • Did not slow regeneration
  • Accelerated resolution of inflammation
  • Helped restore strength

A separate experiment on transgenic mice lacking 12/15-LOX (the enzyme that synthesises lipoxins and resolvins) showed that such animals exhibit an excessive and prolonged inflammatory response, confirming that the pro-resolving pathway is indeed important.

Why do two similar NSAIDs work differently

All NSAIDs block COX-2, the enzyme that produces inflammatory prostaglandins. This is what they're taught in med school. But aspirin does this in a special way.

Aspirin acetylates COX-2 irreversibly. Acetylated COX-2 does not die; it switches to a different job. Instead of prostaglandins, it starts to produce precursors for a class of molecules called aspirin-triggered specialised pro-resolving mediators (AT-SPMs) – aspirin-triggered lipoxins and resolvins.

These aren't “anti-inflammatory” molecules in the usual sense. They are molecules Resolution Inflammation - they don't suppress it, they actively end it and initiate the recovery phase:

  • They stop the influx of neutrophils
  • Activates macrophages, which clear away dead cells
  • Signal muscle stem cells to initiate regeneration

Other NSAIDs – ibuprofen, indomethacin, celecoxib – simply block COX-2 completely. Inflammation is suppressed, but along with it, the resolution pathway is also suppressed. The body has fewer signals to finish the job.

What does this imply for training?

This study is on mice. A dose of 3 mg/kg for a 70 kg human is approximately 210 mg of aspirin, which is half a standard tablet. This is below the typical analgesic dose (500 mg) and significantly above the cardiac dose (81 mg). It is too early to translate directly to humans.

But the direction is clear — and it aligns with what sports medicine already knows:

Ibuprofen after weight training is a bad idea. Roberts et al. (2017), Lilja et al. (2018) — separately showed that maximum doses of ibuprofen (1200 mg/day) inhibit hypertrophy in humans. The same mechanism: blocking COX-2 = a weaker signal for adaptation.

Aspirin is another beast. Through acetylated COX-2, it doesn't switch off the signal. At low doses (≤200 mg), it may even help.

Paracetamol is neutral. It is not an NSAID, it does not block COX-2 in peripheral tissues. If an analgesic is needed on recovery days, paracetamol is the safest choice from an adaptation perspective.

When NSAIDs are actually needed

This is not an argument against ibuprofen in general. In three situations, it remains useful:

  1. Sharp pain that prevents movement — short course 1–3 days.
  2. Systemic inflammation — arthritis, post-operation.
  3. An injury with swelling where pressure needs to be mechanically reduced — for example, a serious sprain.

What you shouldn't do is take ibuprofen preventatively “so it doesn't hurt tomorrow” or “so you don't get DOMS”. This reduces the adaptation signal without any real benefit.

What to do today

A simple protocol based on what we know:

  • My head hurts after a heavy session. — wait 24 hours. DOMS is a normal part of adaptation, it does not require treatment.
  • You still need a painkiller. — paracetamol, or 200 mg of aspirin.
  • Sharp pain that prevents sleeping/walking — ibuprofen short course, as usual.
  • You chronically swallow ibuprofen after every workout. — this is a signal that the load is inadequate, not that ibuprofen is needed.

Restrictions

Again, research in mice. A direct clinical translation would require RCTs in humans, which likely nobody will fund (aspirin is an unpatented drug, so the pharma industry's interest is minimal). Therefore, we will likely be dealing with mechanistic confirmation from animal models plus indirect data from people who have taken aspirin for other reasons.

Aspirin has its side effects: gastrointestinal risks, anticoagulation. Before you take it regularly, you need to weigh this up. This particularly applies to people taking cardio-aspirin – extra doses are not necessary.

The most practical conclusion: The default post-workout painkiller is not ibuprofen. Better nothing. If anything, paracetamol.

Source: Lu X, Rehman H, Sercu AS, et al. Aspirin hastens resolution of skeletal muscle inflammation and promotes recovery of muscle strength following acute injury. bioRxiv 2026. DOI: 10.64898/2026.04.21.719989

Additional context: Lilja M et al., Acta Physiol 2018; Schoenfeld BJ. Sports Med 2012 (review of NSAIDs and hypertrophy).

Similar articles