Intense exercise is known to cause temporary impairments in immune function. Few studies, however, have investigated the effects of intense competitive exercise on immunoendocrine variables in elite team sport athletes. The aim of this study was to evaluate the time course of changes in selected immunoendocrine and inflammatory markers following an international rugby union game. Blood samples were taken from players (n = 10) on camp entry, the morning of the game (pre), immediately after (post) and 14 and 38 h into a passive recovery period. Players lost 1.4 +/- 0.2 kg of body mass during the game (ambient conditions, 11 degrees C, 45% RH). An acute phase inflammatory response was observed as reflected through immediate increases in serum cortisol and IL-6 (post) followed by delayed increases in serum creatine kinase (CK; 14 h) activity and C-reactive protein (CRP; 38 h); P < 0.05. Decreases in the number of circulating T lympocytes, NK cells and bacteria-stimulated neutrophil degranulation were also observed post-exercise (P < 0.05), indicative of decreased host immune protection. Following a large decrease in serum testosterone to cortisol (T/C) ratio immediately post and 14 h after exercise, T/C values then increased above those observed at camp entry 38 h into recovery (P < 0.05). This rebound anabolic stimulus may represent a physiological requirement for recovery following intense tissue damage resulting from game collisions. The findings also suggest that a game of international rugby elicits disturbances in host immunity, which last up 38 h into the recovery period.

Free radicals or oxidants are continuously produced in the body as a consequence of normal energy metabolism. The concentration of free radicals, together with lipid peroxidation, increases in some tissues as a physiological response to exercise - they have also been implicated in a variety of pathologies. The biochemical measurement of free radicals has relied in the main on the indirect assay of oxidative stress by-products. This study presents the first use of electron spin resonance (ESR) spectroscopy in conjunction with the spin-trapping technique, to measure directly the production of radical species in the venous blood of healthy human volunteers pre- and post-exhaustive aerobic exercise. Evidence is also presented of increased lipid peroxidation and total antioxidant capacity post-exercise.

Oxygen free radicals are highly reactive species that are produced in increased quantities during strenuous exercise and can damage critical biological targets such as membrane phospholipids. The present study examined the effect of acute ascorbic acid supplementation on exercise-induced free radical production in healthy subjects. Results demonstrate increases in the intensity of the alpha-phenyl-tert-butylnitrone adduct (0.05 +/- 0.02 preexercise vs. 0.19 +/- 0.03 postexercise, P = 0.002, arbitrary units) together with increased lipid hydroperoxides (1.14 +/- 0.06 micromol/l preexercise vs. 1.62 +/- 0.19 micromol/l postexercise, P = 0.005) and malondialdehyde (0.70 +/- 0.04 micromol/l preexercise vs. 0.80 +/- 0.04 micromol/l postexercise, P = 0.0152) in the control phase. After supplementation with ascorbic acid, there was no significant increase in the electron spin resonance signal intensity (0.02 +/- 0. 01 preexercise vs. 0.04 +/- 0.02 postexercise, arbitrary units), lipid hydroperoxides (1.12 +/- 0.21 micromol/l preexercise vs. 1.12 +/- 0.08 micromol/l postexercise), or malondialdehyde (0.63 +/- 0.07 micromol/l preexercise vs. 0.68 +/- 0.05 micromol/l postexercise). The results indicate that acute ascorbic acid supplementation prevented exercise-induced oxidative stress in these subjects.

Regular monitoring of s-IgA and s-Lys may be useful in the assessment of exercise stress and URI risk status in elite team sport athletes. A combination of alterations in training intensity and seasonal influence is a likely contributor to observed peaks in URI incidence. It is probable that stress-induced increases in cortisol release contribute to reductions in mucosal immunity, which, when lowered, predispose rugby players to increased risk of illness.

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