진통제, 근합성에 영향을 주는가?

출처: Uniphysio

 

The evidence is mixed and age/dose-dependent, but chronic high-dose NSAID use in young adults appears to modestly blunt strength training adaptations, while occasional/low-dose use likely has little effect, and effects may even be favorable in older adults.

 

In young, healthy adults:

- High-dose ibuprofen (1200 mg/day) during 8 weeks of resistance training produced smaller quadriceps hypertrophy (3.7% vs 7.5%) and smaller strength gains compared with low-dose aspirin (75 mg/day). Follow-up mechanistic work from the same group found that established hypertrophy regulators (mTOR signaling, satellite cell content, myonuclear accretion, capillarization, ribosome biogenesis) were not differentially affected, so the mechanism for the blunted growth remains unclear.[1][2]

 

- Conversely, a 2025 trial using diclofenac 75 mg/day over 12 weeks of resistance training in trained men found greater quadriceps CSA/volume gains with NSAID versus placebo by week 84 (though without a corresponding strength advantage), suggesting NSAID effects may vary by drug, dose, and duration.[3]

 

- Lower/occasional doses appear largely inconsequential: 400 mg ibuprofen taken only on training days did not affect hypertrophy, strength, or soreness over 6 weeks. A single maximal dose of ibuprofen, celecoxib, or flurbiprofen before plyometric exercise did not alter muscle protein synthesis or degradation signaling.[4][5]

 

- Classic work from Trappe's group showed that acute high-intensity eccentric exercise increases muscle protein synthesis at 24 hours via prostaglandin (PGF2α) production, and this response was blocked by both ibuprofen and paracetamol (acetaminophen) at OTC doses, implicating COX-mediated prostaglandin signaling. However, local NSAID infusion (indomethacin) did not affect myofibrillar protein synthesis in another study, and results are inconsistent across studies.[4]

 

In older adults:

Several studies suggest NSAIDs (including ibuprofen) may actually enhance muscle mass and strength gains with resistance training, possibly due to a higher baseline inflammatory state in this population — the opposite direction of effect seen in young adults.[4][6]

 

Clinical takeaway

Occasional, low-dose NSAID use for pain relief around workouts is unlikely to meaningfully impair muscle growth in most patients. Regular, high-dose (near-maximal OTC, e.g., 1200 mg/day ibuprofen) use during a dedicated hypertrophy/strength program in young, otherwise healthy trainees carries a theoretical and some empirical signal for blunted gains, so patients focused on maximizing hypertrophy/strength could be advised to limit chronic high-dose NSAID use and favor acetaminophen or minimal-dose use only as needed, while overall evidence remains mixed and dose/agent-dependent.[2][3][7][4][1][6]

References

1. High Doses of Anti-Inflammatory Drugs Compromise Muscle Strength and Hypertrophic Adaptations to Resistance Training in Young Adults. Lilja M, Mandić M, Apró W, et al. Acta Physiologica (Oxford, England). 2018;222(2). doi:10.1111/apha.12948.
2. Limited Effect of Over-the-Counter Doses of Ibuprofen on Mechanisms Regulating Muscle Hypertrophy During Resistance Training in Young Adults. Lilja M, Moberg M, Apró W, et al. Journal of Applied Physiology (Bethesda, Md. : 1985). 2023;134(3):753-765. doi:10.1152/japplphysiol.00698.2022.
3. NSAID Ingestion Augments Training-Induced Muscle Hypertrophy and Differentially Affects Muscle mRNA Expression, but Not Strength Gains, in Trained Men. Mallinson JE, Taylor T, Constantin-Teodosiu D, et al. The Journal of Physiology. 2025;. doi:10.1113/JP289542.
4. Analgesic and anti‐inflammatory drugs in sports: Implications for exercise performance and training adaptations. Lundberg TR, Howatson G. Scandinavian Journal of Medicine & Science in Sports. 2018;28(11):2252-2262. doi:10.1111/sms.13275.
5. A Single, Maximal Dose of Celecoxib, Ibuprofen, or Flurbiprofen Does Not Reduce the Muscle Signalling Response to Plyometric Exercise in Young Healthy Adults. Roberts BM, Geddis AV, Sczuroski CE, et al. European Journal of Applied Physiology. 2024;124(12):3607-3617. doi:10.1007/s00421-024-05565-5.
6. Effects of Prostaglandins and COX-inhibiting Drugs on Skeletal Muscle Adaptations to Exercise. Trappe TA, Liu SZ. Journal of Applied Physiology (Bethesda, Md. : 1985). 2013;115(6):909-19. doi:10.1152/japplphysiol.00061.2013.
7. The Use of Nonsteroidal Anti-Inflammatory Drugs for Exercise-Induced Muscle Damage: Implications for Skeletal Muscle Development. Schoenfeld BJ. Sports Medicine (Auckland, N.Z.). 2012;42(12):1017-28. doi:10.2165/11635190-000000000-00000.

 

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Given the mixed evidence that both oral NSAIDs and acetaminophen can blunt acute muscle protein synthesis and adaptive signaling after resistance exercise, topical NSAIDs are likely the safest option for patients needing regular analgesia while strength training, since they achieve therapeutic local COX inhibition with minimal systemic drug exposure and avoid the systemic hepatic, renal, GI, and cardiovascular risks of oral agents.

 

Topical NSAIDs (preferred for localized musculoskeletal pain):

- Gel formulations of diclofenac and ketoprofen, along with ibuprofen gel and diclofenac patches, provide pain relief comparable to oral NSAIDs for acute musculoskeletal pain (sprains, strains, overuse injuries), per a Cochrane review.[1]

 

- Plasma concentrations after topical application are typically less than 5% of those from oral dosing, minimizing systemic COX inhibition and theoretically preserving more of the anabolic signaling that oral NSAIDs suppress, although this has not been directly tested for hypertrophy outcomes.[2][3]

- Adverse events are minimal, mainly mild local skin irritation, with no increased risk of GI upset compared with topical placebo.[1]

 

Oral options if systemic therapy is needed:

- Acetaminophen and oral NSAIDs are both reasonable first-line agents for nociceptive/inflammatory pain per American College of Sports Medicine/American Medical Society for Sports Medicine guidance, but as discussed previously, both have been shown to blunt early anabolic signaling (mTORC1 activity, MEK-ERK signaling, prostaglandin-mediated protein synthesis) after resistance exercise in mechanistic studies. A rodent study found low-dose acetaminophen did not affect chronic muscle mass or fiber-type adaptations despite acute AMPK/4E-BP1 signaling changes, suggesting occasional use is unlikely to meaningfully impair long-term hypertrophy.[4][5][6][7]

 

- If regular oral therapy is truly needed, intermittent or lowest-effective-dose use (rather than daily high-dose regimens) is preferable, with acetaminophen dosing capped below hepatotoxic thresholds (avoid >3–4 g/day, lower in patients with liver disease or heavy alcohol use).[8]

 

For chronic/persistent pain not resolving with initial measures:

- Nonpharmacologic strategies (exercise therapy itself, CBT, optimized sleep/nutrition) are foundational and preferred.[4][8]

- If pain has a neuropathic or nociplastic component, agents like duloxetine or gabapentinoids (gabapentin, pregabalin) are alternatives that avoid COX inhibition entirely and carry low misuse risk, though they don't have specific hypertrophy outcome data.[4][9]

- Opioids are not recommended as routine therapy given overdose risk and lack of benefit for musculoskeletal training-related pain.[8]

 

Practical takeaway

For localized post-workout muscle/joint pain, topical NSAIDs are a reasonable first choice given comparable efficacy with minimal systemic absorption and fewer theoretical concerns for muscle adaptation. Oral acetaminophen or NSAIDs remain acceptable for occasional use, but chronic daily high-dose oral regimens should be minimized in patients prioritizing hypertrophy/strength gains, with periodic reassessment of the underlying pain source.

References

1. Topical NSAIDs for Acute Musculoskeletal Pain in Adults. Derry S, Moore RA, Gaskell H, McIntyre M, Wiffen PJ. The Cochrane Database of Systematic Reviews. 2015;(6):CD007402. doi:10.1002/14651858.CD007402.pub3.
2. Efficacy of topical versus oral analgesic medication compared to a placebo in injured athletes: A systematic review with meta‐analysis. Nudo S, Jimenez-Garcia JA, Dover G. Scandinavian Journal of Medicine & Science in Sports. 2023;33(10):1884-1900. doi:10.1111/sms.14418.
3. Topical Analgesics for Acute and Chronic Pain in Adults - An Overview of Cochrane Reviews. Derry S, Wiffen PJ, Kalso EA, et al. The Cochrane Database of Systematic Reviews. 2017;5:CD008609. doi:10.1002/14651858.CD008609.pub2.
4. Select Issues in Pain Management for the Youth and Adolescent Athlete. Medicine and Science in Sports and Exercise. 2020;52(9):2037-2046. doi:10.1249/MSS.0000000000002333.
5. Prior Acetaminophen Consumption Impacts the Early Adaptive Cellular Response of Human Skeletal Muscle to Resistance Exercise. D'Lugos AC, Patel SH, Ormsby JC, et al. Journal of Applied Physiology (Bethesda, Md. : 1985). 2018;124(4):1012-1024. doi:10.1152/japplphysiol.00922.2017.
6. Analgesic and anti‐inflammatory drugs in sports: Implications for exercise performance and training adaptations. Lundberg TR, Howatson G. Scandinavian Journal of Medicine & Science in Sports. 2018;28(11):2252-2262. doi:10.1111/sms.13275.
7. Acetaminophen Influences Musculoskeletal Signaling but Not Adaptations to Endurance Exercise Training. Roberts BM, Geddis AV, Ciuciu A, et al. FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology. 2024;38(7):e23586. doi:10.1096/fj.202302642R.
8. CDC Guideline for Prescribing Opioids for Chronic Pain. Substance Abuse and Mental Health Services Administration (2016).
9. Nonopioid Pharmacologic Management of Chronic Noncancer Pain. Sokol R, Grossman E, Bourgery R. American Family Physician. 2025;112(2):187-196.