Neutralisation of muscle tumour necrosis factor alpha does not attenuate exercise-induced muscle pain but does improve muscle strength in healthy male volunteers.
OBJECTIVE
Inflammatory mediators, such as tumour necrosis factor alpha (TNFalpha), may contribute to delayed-onset muscle soreness. The effect of neutralising TNFalpha with etanercept, a soluble TNFalpha receptor, on delayed-onset muscle soreness (DOMS) induced in the quadriceps muscle was analysed.


METHODS
On two separate occasions at least 6 weeks apart, etanercept 25 mg or vehicle was given subcutaneously 1 hour before unaccustomed exercise to 12 healthy men in a randomised double-blind cross-over format. To induce DOMS, subjects completed 4 sets of 15 repetitions at 80% of their one-repetition maximum (1RM), using a 45 degrees inclined leg press. Muscle soreness was assessed using a 100-mm visual analogue scale (VAS), and pressure pain threshold (PPT) on the thigh before and 24, 48 and 72 hours after exercise. Changes in the subject's muscle strength were detected by reassessing the subject's 1RM 24, 48 and 72 hours after exercise.


RESULTS
Muscle strength decreased 24 and 48 hours after exercise regardless of agent administered (analysis of variance, p<0.001). At 72 hours after exercise, muscle strength was significantly greater (p<0.01) after etanercept than after placebo. The exercise protocol induced significant DOMS for up to 72 hours, as reflected by reduced PPT and increased VAS scores (p<0.001). Etanercept had no effect on PPT or VAS.


CONCLUSIONS
TNFalpha does not affect muscle soreness associated with unaccustomed exercise, but may improve the recovery of muscle function.
Rice
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Brain Function Research Unit, School of Physiology, University of the Witwatersrand, Johannesburg, South Africa.
Chantler
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Loram
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D000328:Adult; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D003402:Creatine Kinase / Q000097:blood; D018592:Cross-Over Studies; D004311:Double-Blind Method; D000068800:Etanercept; D015444:Exercise / Q000502:physiology*; D006801:Humans; D007074:Immunoglobulin G / Q000494:pharmacology*; D008297:Male; D053580:Muscle Strength / Q000502:physiology*; D018482:Muscle, Skeletal / Q000502:physiology*; D010146:Pain / Q000209:etiology / Q000517:prevention & control; D010147:Pain Measurement; D018124:Receptors, Tumor Necrosis Factor; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
D000894:Anti-Inflammatory Agents, Non-Steroidal; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D003402:Creatine Kinase; D000068800:Etanercept