Chemiluminescence response of granulocytes from elite athletes during recovery from one or two intense bouts of exercise.

In this study nine elite athletes each participated in three different 24- h trials, as follows: (1) complete bed rest (REST), (2) one bout of exercise at 1515 hours (ONE-EX), (3) two exercise bouts, one at 1100 hours and one at 1515 hours (TWO-EX-3 h), and (4) two exercise bouts, one at 0800 hours and one at 1515 hours (TWO-EX-6 h). Exercise was performed on a cycle ergometer with 10 min of warm-up and then 65 min at an exercise intensity of 75% of maximum oxygen uptake (VO(2max)). The polymorphonuclear neutrophil (PMN) counts increased consistently in response to exercise, and more in trial TWO-EX-3 h than in the two other exercise trials (P < 0.01). The respiratory burst of PMN was measured as chemiluminescence (CL), obtained with phorbol myristate (PMA) and serum-opsonised zymosan (SOZ) as stimulators. Exercise triggered the CL response for a defined number of PMN, significantly above baseline (REST) values (P < 0.05) for ONE-EX and TWO-EX-3 h, but not for TWO-EX-6 h. The strongest response was observed for TWO-EX-3 h, but the difference between exercise procedures was not significant. However, as a novel approach, a comparison was made using total oxidative potentials per litre of blood, as obtained by combining CL values and PMN numbers. TWO-EX-3 h yielded significantly higher values than the other experimental treatments. Thus, by this measure the total oxidative potential of PMN x l(-1) blood remains at a higher level with short intervals between exercise bouts (i.e. 3 h instead of 6 h), possibly due to a combined effect of cell number increase and the priming state of PMN. This may suggest that for intensive training twice a day, a recovery phase of 5-6 h is preferable. The elevation in cell number is best explained by a combined effect of catecholamines and cortisol. Growth hormone is one probable candidate as a stimulator of CL, but other molecular participants that respond to exercise may exert roles as either stimulators or inhibitors of CL.

Bioactive cytidine deaminase, an inhibitor of granulocyte-macrophage colony-forming cells, is massively released in fulminant meningococcal sepsis.

Cytidine deaminase (CDD) catalyzes the hydrolytic deamination of cytidine, which thereby is converted to uridine. CDD is found in serum and different tissues, with particularly high concentrations in polymorphonuclear neutrophils (PMN). We measured the CDD levels in plasma from patients with systemic meningococcal disease. Thirty-seven patients had significantly higher plasma levels of CDD than did 29 healthy control subjects (P=.0001). CDD levels in plasma or serum increased from a median of 96 ng/mL in healthy control subjects to medians of 168 ng/mL in patients without persistent shock (n=23; P=.001) and 422 ng/mL in patients with fulminant meningococcal septicemia (n=14; P=.0001). In most patients with fulminant septicemia, CDD levels in plasma increased during the first 3-53 h after the initiation of therapy (P=.003). CDD alone had no immediate harmful effect when injected into mice during a 4-day period. CDD may modulate the stimulatory effect of colony-stimulating factors on PMN in patients.