The 'open window' theory is characterised by short term suppression of the immune system following an acute bout of endurance exercise. This window of opportunity may allow for an increase in susceptibility to upper respiratory illness (URI). Many studies have indicated a decrease in immune function in response to exercise. However, many studies do not indicate changes in immune function past 2 hours after the completion of exercise, consequently failing to determine whether these immune cells numbers, or importantly their function, return to resting levels before the start of another bout of exercise. 2 Ten male 'A' grade cyclists (age 24.2 ± 5.3 years; body mass 73.8 ± 6.5 kg; VO2max 65.9 ± 7.1 mL.kg -1 .min -1 ) exercised for two hours at 90% of their second ventilatory threshold. Blood samples were collected pre-, immediately post-, 2 hours, 4 hours, 6 hours, 8 hours, and 24 hours post-exercise. Immune variables examined included total leukocyte counts, neutrophil function (oxidative burst and phagocytic function), lymphocyte subset counts (CD4 + , CD8 + , and CD16 + /56 + ), natural killer cell activity (NKCA), and NK phenotypes (CD56 dim CD16 + , and CD56 bright CD16 -).There was a significant increase in total lymphocyte numbers from pre-, to immediately postexercise (p<0.01), followed by a significant decrease at 2 hours post-exercise (p<0.001). CD4 + T-cell counts significantly increased from pre-exercise, to 4 hours post-(p<0.05), and 6 hours post-exercise (p<0.01). However, NK (CD16 + /56 + ) cell numbers decreased significantly from pre-exercise to 4 h post-exercise (p<0.05), to 6 h post-exercise (p<0.05), and to 8 h post-exercise (p<0.01). In contrast, CD56 bright CD16 -NK cell counts significantly increased from pre-exercise to immediately post-exercise (p<0.01). Neutrophil oxidative burst activity did not significantly change in response to exercise, while neutrophil cell counts significantly increased from preexercise, to immediately post-exercise (p<0.05), and 2 hours post-exercise (p<0.01), and remained significantly above pre-exercise levels to 8 hours post-exercise (p<0.01). Neutrophil phagocytic function significantly decreased from 2 hours post-exercise, to 6 hours post-(p<0.05), and 24 hours post-exercise (p<0.05). Finally, eosinophil cell counts significantly increased from 2 hours post to 6 hours post-(p<0.05), and 8 hours post-exercise (p<0.05).This is the first study to show changes in immunological variables up to 8 hours post-exercise, including significant NK cell suppression, NK cell phenotype changes, a significant increase in total lymphocyte counts, and a significant increase in eosinophil cell counts all at 8 hours postexercise. Suppression of total lymphocyte counts, NK cell counts and neutrophil phagocytic function following exercise may be important in the increased rate of URI in response to regular intense endurance training.
This study investigated the effect of 10 W*min(-1) (Slow ramp, SR), 30 W*min(-1) (Medium ramp, MR) and 50 W*min(-1) (Fast ramp, FR) exercise protocols on assessments of the first (VT1) and second (VT2) ventilation thresholds and peak oxygen uptake (VO(2)peak) in 12 highly-trained male cyclists (mean +/- SD age = 26 +/- 6 yr). Expired gas sampled from a mixing chamber was analyzed on-line and VT1 and VT2 were defined as two break-points in 20-s-average plots of pulmonary ventilation (V(E)), ventilatory equivalents for O(2) (V(E)/VO(2)) and CO(2) (V(E)/VCO(2)), and fractions of expired O(2) (F(E)O(2)) and CO(2) (F(E)CO(2)). Arterialized-venous blood samples were analyzed for blood-gas and acid-base status. VO(2)peak was significantly lower (p < 0.05) for SR (4.65 +/- 0.53 l small middle dot min(-1)) compared to MR (4.89 +/- 0.56 l *min(-1)) and FR (4.88 +/- 0.57 l *min(-1)) protocols. CO(2) output and blood PCO(2) were lower (p < 0.05), and V(E)/VCO(2) was higher (p < 0.05), above VT1 for SR compared to MR and FR protocols. No significant differences were observed among the protocols for VO(2), % VO(2)peak, V(E), plasma lactate ([La(-)]) and blood hydrogen ion concentration ([H(+)]), and heart rate (HR) values at VT1 or VT2. The work rate (WR) measured at VT1, VT2 and VO(2)peak increased (p < 0.05) with steeper ramp slopes. It was concluded that, in highly-trained cyclists, assessments of VT1 and VT2 are independent of ramp rate (10, 30, 50 W*min(-1)) when expressed as VO(2), % VO(2)peak, V(E), plasma [La(-)], blood [H(+)] and HR values, whereas VO(2)peak is lower during 10 W*min(-1) compared to 30 and 50 W*min(-1) ramp protocols. In addition, the WR measured at VT1, VT2 and VO(2)peak varies with the ramp slope and should be utilized cautiously when prescribing training or evaluating performance.
We investigated how moderate exercise affects neutrophil microbicidal activity and whether exercise-induced responses are associated with changes in growth hormone (GH) secretion. Biological fluctuations were controlled for and GH secretion was manipulated by glucose ingestion. In eight men, 1 h of moderate exercise increased intracellular H2O2 generation in response to phorbol 12-myristate 13-acetate stimulation by threefold (P = 0.025) and complement receptor expression by 20% (P = 0.045). These responses were accompanied by a twofold increase in the plasma concentration of elastase, a marker of neutrophil activation in vivo. The plasma concentration of GH increased 10-fold after exercise, but this was reduced to 3-fold by glucose ingestion (P < 0.001), which also blunted elastase release (P < 0.001). Although the magnitude of H2O2 generation increased in proportion to the increase in plasma GH concentration, it declined progressively once this exceeded 20 ng/ml. The net response of neutrophils to exercise may represent a balance between the individual responses of subpopulations that are unaffected, primed, or fully activated by circulating mediators that respond to exercise and to dietary glucose intake.
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