Resistance exercise and naproxen sodium: effects on a stable PGF2α metabolite and morphological adaptations of the upper body appendicular skeleton.
BACKGROUND
Exercise-induced inflammation has been shown to be necessary for successful skeletal muscle regeneration post-injury. Accordingly, numerous investigations have demonstrated consequences of COX-inhibitors, anti-inflammatory drugs which prevent prostaglandin formation. In addition to its roles in inflammation, prostaglandin F2α (PGF2α) also mediates vital regenerative processes The majority of research to report consequences of suppressing inflammation has utilized acute injury models in combination with acute COX-inhibitor administration. To address the limited research investigating regular consumption of COX-inhibitors over time in exercising humans, the purpose of this study was to determine effects of a non-selective COX-inhibitor on a PGF2α metabolite and morphological adaptations of the upper body appendicular skeleton during periodized resistance training. Twenty-three (N = 23) recreationally trained college-aged males were randomly assigned to receive placebo (n = 11) or naproxen sodium (n = 12). Treatments were prophylactically administered in double-blind fashion with supervised upper body resistance exercise performed twice per week for 6 weeks. Venous blood was sampled pre- and post-exercise and analyzed for 13, 14-dihydro-15-keto PGF2α using enzyme immunoassay. Factorial mixed-design repeated-measures ANOVAs were utilized to examine relative changes in the plasma PGF2α metabolite and upper body appendicular morphology over the training period.


RESULTS
Naproxen sodium significantly reduced the acute PGF2α metabolite response to exercise (p = 0.013); however, this effect diminished over time (p = 0.02), and both treatment groups exhibited significant increases in dominant arm skeletal muscle tissue (p = 0.037).


CONCLUSIONS
Despite acute inhibition of the PGF2α metabolite at early time points, naproxen sodium did not hinder positive morphological adaptations of the upper body in response to resistance training.
Physical Education, Health, and Recreation, Eastern Washington University, 200 Physical Education Building, Cheney, WA, 99004, USA. cbrewer7@ewu.edu.
Christi B
CB
Brewer
Department of Pharmacy Administration, School of Pharmacy, University of Mississippi, Oxford, MS, USA. phjpb@olemiss.edu.
John P
JP
Bentley
Department of Biology, University of Mississippi, Oxford, MS, USA. lainyday@olemiss.edu.
Lainy B
LB
Day
Department of Electrical Engineering, University of Mississippi, 308 Anderson Hall, Oxford, MS, USA. waddell@olemiss.edu.
Dwight E
DE
Waddell
D000222:Adaptation, Physiological / Q000187:drug effects* / Q000502:physiology*; D000328:Adult; D001133:Bones of Upper Extremity / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology*; D016861:Cyclooxygenase Inhibitors / Q000627:therapeutic use; D015237:Dinoprost / Q000378:metabolism*; D004311:Double-Blind Method; D015444:Exercise / Q000502:physiology*; D006801:Humans; D007249:Inflammation / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D009288:Naproxen / Q000627:therapeutic use*; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D055070:Resistance Training / Q000379:methods; D055815:Young Adult
D016861:Cyclooxygenase Inhibitors; D009288:Naproxen; D015237:Dinoprost; D011451:Prostaglandin-Endoperoxide Synthases
COX-inhibitor; Inflammation; Naproxen sodium; Non-steroidal anti-inflammatory drug (NSAID); Prostaglandin F2α; Resistance exercise