“…Although considered to be a major factor, activation of the HPA axis alone cannot wholly account for changes in the neutrophil function (Laing et al, 2008), as some of the noted inhibitory effects of cortisol on receptor mediated responses (e.g., fMLP) would not explain decreased responses to stimulants that activate neutrophils independent of surface receptors (e.g., PMA) (O'Flaherty et al, 1991;Tomchek et al, 1991;Peake, 2002). Thus other mechanisms have also been suggested to be involved in neutrophil dysfunction, where elevations in catecholamines, cyclic adenosine monophosphate, complement proteins (C5a), direct cellular oxidative damage and growth hormone may occur with the inflammatory response to prolonged exercise and have been shown to interfere with calcium signaling or other intermediates of intracellular pathways (Henson et al, 1978;Hack et al, 1994;Suzuki et al, 1999;Thibault et al, 2000;Tintinger et al, 2001;Robson et al, 2003;Laing et al, 2008).…”