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.

The effect of strenuous exercise, calorie deficiency and sleep deprivation on white blood cells, plasma immunoglobulins and cytokines.

Moderate exercise appears to stimulate the immune system, but there is good evidence that intense exercise can cause immune deficiency. In the present study the authors examined the effect of continuous physical exercise (35% of VO2 max), calorie deficiency and sleep deprivation on the immune system of young men participating in a 5-7 days military training course. There was a two-three fold increase of neutrophils from day 1, the values remained high and decreased slightly at the end of the course. Monocyte counts also increased with a pattern similar to that of neutrophils. Eosinophils decreased to 30% of control and lymphocyte numbers decreased by 30-40%. All the major subgroups (CD4 T cells, CD8 T cells, B cells, NK cells) were reduced. Neutrophil function, as tested by measuring chemotaxis, was significantly stimulated during the first days of the course, in particular in the group with the lowest calorie intake. The mitogenic response of lymphocytes to PHA and Con A was variable, ranging from stimulation during one course to no effect in another course. Serum levels of immunoglobulins decreased significantly during the course. IgG was reduced by 6-7%, IgA by 10-20% and IgM by 20-35%. The authors found no changes of interleukin 1, 2 and 4 during the course, but a (12-20%) reduction (P less than 0.01) of interleukin 6, and an increase (P less than 0.01) of granulocyte-macrophage colony stimulating factor. Altogether the results from the ranger course present a mixed-up picture. The non-specific phagocyte-related immunity was enhanced. On the other hand, the data indicate that even a moderate physical activity, around the clock, caused significant suppression of a number of parameters reflecting the status of the specific, lymphocyte-related immunity. It is noteworthy, however, that there was no significantly increased infection rate during the course or in the first 4-5 weeks thereafter.

Effect of in vivo corticosterone and acute food deprivation on rat resident peritoneal cell chemiluminescence after activation ex vivo.

Adrenoglucocorticoid regulation of rat peritoneal monocyte/macrophage function was studied by exposing rats to corticosterone (CS) in the drinking water, and to fast (48 h). Production of reactive oxygen metabolites was measured by luminol amplified chemiluminescence (CL) in preparations of peritoneal cells activated by serum treated zymosan (STZ). Administration of CS which led to an increase in plasma CS from 31 (controls) to 46 ng mL-1, reduced CL (per cell) by 31%. Fast, which did not change plasma CS or ACTH, also had an inhibitory effect on CL (-25%), while the combination of CS administration and fast strongly inhibited the CL (-89%), indicating that plasma CS and fast reduced CL in a synergistic way. Similar effects on cell number were observed: CS-administration, fast and the combination reduced macrophage numbers (-13, -19.7 and -55%), while no significant effect was observed on the number of monocytes. The effect of adrenalectomy (adx) was studied in another series of experiments; adx induced no significant change in peritoneal leucocyte number or composition, while cells from adx animals had significantly higher chemiluminescence reaction than cells from sham operated animals. CS substitution in adx animals reduced CL by 30% while sham operated animals had 49% lower CL in adx. The data from adx animals also suggest that endogenous levels of CS are inhibitory for CL, but the results are not conclusive for the effect of very low doses of CS since other mechanisms than elimination of CS could prime the chemiluminescence reaction after adx. In conclusion, a moderate elevation of CS after systemic administration in vivo reduced the total number of mononuclear phagocytes in rat peritoneum, reduced the relative number of macrophages compared with monocytes, and suppressed the function of monocytes/macrophages by reducing the production of reactive oxygen molecules in activated cells. Furthermore, the effect of corticosterone was also dependent on the physiological situation, since the effects of fast and corticosterone were synergistic.

Adrenaline stimulated cyclic adenosine monophosphate response in leucocytes is reduced after prolonged physical activity combined with sleep and energy deprivation.

The mechanism for adrenergic desensitisation during physical stress was studied by measuring [125I] cyanopindolol ([125I]CYP) binding sites and the adrenaline stimulated cyclic adenosine monophosphate (cAMP) responses in peripheral blood leucocytes from ten male cadets during a 5-day military training course. The cadets had physical activities around the clock corresponding to a daily energy consumption of about 40,000 kJ but with an intake of only 2,000 kJ, and only 1-3 h of sleep in the 5 days. During the course, the maximal cAMP response to adrenaline stimulation was reduced to about 45% in granulocytes and to 52% in mononuclear cells, and the half maximal response was obtained only at 5-10 times higher adrenaline concentrations than in the control experiment. The binding sites for [125I]-CYP in mononuclear cells increased during the course. However, [125I]-CYP measured not only surface receptors but also intracellular receptors and might even have represented other binding sites. In conclusion, this study showed that decreased cAMP response to adrenergic stimulation would seem to be one of the mechanisms behind adrenergic desensitisation during stress.

Atrial natriuretic peptide in plasma after prolonged physical strain, energy deficiency and sleep deprivation.

Plasma concentrations of atrial natriuretic peptide (ANP) were investigated daily in 16 male cadets during a 6-day military training course with continuous heavy physical activities, sleep and energy deficiency (course I). At the end of another similar course (course II) 15 cadets were studied during 30-min cycle exercise at 50% maximal oxygen uptake with and without glucose infusion. A small, but not significant increase was found in the plasma concentrations of ANP during course I from 9.6 (SEM 1.1) pmol.l-1 in the control experiment to 11.1 (SEM 0.5) pmol.l-1 on day 5. During course II a small but significant increase was found from 7.8 (SEM 0.5) pmol.l-1 in the control experiment to 9.1 (SEM 0.5) pmol.l-1 at the end of the course. Plasma osmolality and chloride concentration decreased during the course. During the exercise test a significant increase was seen in ANP concentration from 8.2 (SEM 0.8) to 13.1 (SEM 2.0) pmol.l-1 in the control experiment and from 9.4 (SEM 0.7) to 13.5 (SEM 1.2) pmol.l-1 during the course. This response was attenuated by glucose infusion, an effect which may have been due to an exercise induced increase in plasma chloride concentration being abolished. In contrast, the potassium concentration response to exercise was increased during the course but unaffected by glucose infusion. In conclusion, the large increases in endogenous plasma catecholamine concentration shown to take place during previous courses were not reflected in the plasma concentrations of ANP, indicating only a moderate cardiac stress or no cardiac work overload during such courses.

Effect of VIP on the respiratory burst in human monocytes ex vivo during prolonged strain and energy deficiency.

VIP-stimulated cyclic AMP production and VIP effect on the production of reactive oxygen compounds in human monocytes activated by serum opsonized zymosan (respiratory burst) were studied during a ranger training course lasting for five days with almost continuous physical activity, and deficiency of sleep and energy. Respiratory burst was inhibited and cyclic AMP production was stimulated by VIP on all days. Maximum cyclic AMP production stimulated by VIP (0.1 microM) on the day of control was 148.6% of basal, and 255.3%, 213.8%, 218.9% and 198.7% on Days 1, 2, 3 and 5. Maximum inhibition was observed 20 min after addition of the peptide on the day of control, after 5 min on Days 1, 2 and 3, and after 10 min on Day 5. Inhibition at the 5-min time point was 33.1% on the day of control, and 34.7%, 53.6%, 53.3% and 36.2% on the different days during the training course. The observed increment in VIP effect adds to prior reported data about increased VIP secretion during the training course, and may indicate enhanced physiological significance of VIP during stress.