Melatonin therapy for blunt trauma and strenuous exercise: A mechanism involving cytokines, NFκB, Akt, MAFBX and MURF-1

Gerald J. Maarman, Russel J. Reiter

Research output: Contribution to journalArticlepeer-review

6 Scopus citations


Muscle injury occurs due to trauma, strenuous exercise or sports activities; most people affected are athletes. Ineffectively treated muscle injury can negatively affect sports careers and quality of life after retirement from sports. Reports have indicated that the current therapeutic management of muscle injury, particularly anti-inflammatory drugs, are not necessarily effective. Therefore, better therapies are required. Accumulating evidence has demonstrated melatonin’s potent antioxidant and anti-inflammatory actions against muscle pathology in sarcopenia or atrophy in systemic disease. However, the underlying mechanisms for the protective effect of melatonin in the context of trauma/strenuous exercise are multifactorial and not well described. This paper reviews data on melatonin’s impact on muscle injury and findings that points toward the mechanisms through which melatonin achieves muscle protection. The general concept described in this review is that melatonin inhibits NFκB, reduces cytokine expression, increases Akt that downregulates the ratio of MAFBX and MURF-1 in order to limit the extent of muscle injury and promote muscle recovery post-injury. The work discussed in this review supports the notion that melatonin may be considered a possible therapy against trauma/sports related muscle injury. Inclusion of melatonin as a therapy in sports medicine could therefore provide a better treatment option for injured athletes and sports individuals.

Original languageEnglish (US)
Pages (from-to)1897-1901
Number of pages5
JournalJournal of Sports Sciences
Issue number16
StatePublished - Aug 18 2018


  • Melatonin
  • skeletal muscle injury
  • sports medicine

ASJC Scopus subject areas

  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation


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