Effects of normal strength exercise on leukocyte accumulation were examined in 10 well-trained male subjects (27.2 +/- 2.7 yr). The workout, consisting of five maximal sets of three repetitions of leg press exercise and five maximal sets of six repetitions of knee extension exercise, was performed with the dominant leg, and the other leg served as control. Repeated maximal isokinetic knee extensions at 60 degrees /s were performed to evaluate neuromuscular fatigue and recovery after the workout. Accumulation of leukocytes was assessed with 99mTc-labeled cells, and repeated images of the thighs were taken 1-24 h after the workout. Maximal force-generating capacity in the exercised leg was reduced by 17 +/- 2% (P < 0.01) after the workout. The course of recovery followed a biphasic pattern characterized by halted recovery 10-23 h after exercise. The presence of leukocytes was approximately 10% higher in the exercised than in the control thigh 10 h after exercise (P < 0.05). This difference increased to approximately 15% at 20 h after exercise (P < 0.05). The retarded recovery of maximal force-generating capacity 10-20 h after exercise, together with a significant infiltration of leukocytes in exercised muscle during the same time interval, shows a temporal relation between leukocyte infiltration and impaired recovery.
Background: During infections, polymorphonuclear neutrophilic granulocytes (PMN) are mobilized from their bone marrow stores, travel with blood to the affected tissue, and kill invading microbes there. The signal(s) from the inflammatory site to the marrow are unknown, even though a number of humoral factors that can mobilize PMN, are well known. We have employed a standardized, non-infectious human model to elucidate relevant PMN mobilizers. Welltrained athletes performed a 60-min strenuous strength workout of leg muscles. Blood samples were drawn before, during and just after exercise, and then repeatedly during the following day. Cortisol, GH, ACTH, complement factors, high-sensitive CRP (muCRP), IL-6, G-CSF, IL-8 (CXCL8) and MIP-1β (CCL4) were measured in blood samples. PMN chemotaxins in test plasma was assessed with a micropore membrane technique.
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