“…Further support for the role of AL is evidence that high intensity exercise increases PL‐PGE 2 in equine (Lindinger, MacNicol, Karrow, & Pearson, ) and human athletes under acute exercise conditions (Capó, Martorell, Sureda, Riera et al., ; Capó, Martorell, Sureda, Tur, & Pons, ); an effect that may be augmented, at least in part, by increased production of PGE 2 by polymorphonuclear cells taken from trained vs untrained individuals (Capó, Martorell, Sureda, Riera et al., ). PGE 2 is an important contributor to adaptation to and/or recovery from exercise by inducing vasodilation (Capó, Martorell, Sureda, Riera et al., ), muscle hypertrophy (Burd et al., ) and resolution of inflammation (Serhan, ). While the precise nature of the interaction between PGE 2 and exercise has not been defined, it is known that blockade of exercise‐induced PGE 2 production in athletes by administration of non‐steroidal anti‐inflammatory drugs increases oxidative stress associated with the exercise bout (McAnulty et al., ), and inhibits exercise‐induced muscle protein synthesis (Trappe, White, Lambert, Hellerstein, & Evans, ).…”