Platelet activity, sensitivity to agonist, and platelet-leukocyte conjugate formation after long-term exercise

Abstract

For rehabilitation training it is recommended that the intensity of exercise should be distinctly below the individual anaerobic threshold (IAT). We investigated platelet activity, reactivity and platelet-leukocyte conjugate formation following a stardardized treadmill (TR) ergometer test at 90% IAT for 60-120 min. Seventeen healthy male non-smokers underwent TR. Blood samples were taken after a 30-min rest, immediately after exercise, and 2 h after exercise completion. Platelets were detected flow cytometrically by CD41 in whole blood, activated platelets by CD62P. In addition, stimulation of platelets in vitro with 7.5 microM TRAP-6 was performed. For testing platelet-leukocyte conjugates, antibodies against CD45 and CD41 were used. After TR the percent of non-stimulated CD62P-positive platelets (%PC) remained unchanged (1.65 +/- 0.56 to 1.73 +/- 0.79%PC) (mean +/- SD). In contrast, an increase (P<0.05) from 31.9 +/- 13.5 to 37.4 +/- 15.0 %PC in CD62P, TRAP-6 stimulated and enhanced (P<0.01) platelet-leukocyte conjugates (11.7 +/- 3.7 to 16.1 +/- 6.9, CD41-%PC) after TR were observed. Both changes were independent of thrombin generation measured by F1+2 and TAT, and reversible after 2 h. Long-term exercise (90% IAT) on a treadmill ergometer only leads to a moderate increase of platelet reactivity and platelet-leukocyte conjugates. The determination of platelet-leukocyte conjugates may offer the possibility to detect an early activation stage of platelets in vivo.

Physical stress as a model to study variations in ADAMTS‐13 activity, von Willebrand factor level and platelet activation

“…It has previously been shown that intense exercise increases the plasma level of von Willebrand factor (VWF) [2]. Platelet aggregation associated with an enhanced expression of adhesion molecules on platelets such as P-selectin (CD62P) and glycoprotein (GP) IIb/IIIa is also increased after the prolonged exercise [3]. However, the underlying mechanisms of exercise-induced changes on platelet aggregability remain unclear.…”

“…The Pro 33 isoform has received a great deal of attention since it was first reported to be associated with acute coronary artery syndromes [1]. A correlation between the Pro 33 polymorphism of integrin a IIb b 3 and increased platelet activation [2] and aggregation [3] has also been reported. However, the few other studies that have evaluated platelet functional differences based on the Pro 33 polymorphism have observed inconsistent and, in several cases, possibly conflicting results [4,5] /Pro 33 subjects were pooled and a IIb b 3 purified as described by Shock et al [6].…”

A Study on Affect of Severity of Exercise on Platelet Function

“…Growing evidences indicate that benefit of physical activity on cardiovascular disease may result to some extent from effects on hemostasis. [4][5][6] The intensity of exercise should be below the individual anaerobic threshold. It is to be investigated whether a strenuous aerobic exercise might counterbalance these advantageous modifications and very little data is available on the influence of physical exercise on primary hemostasis.…”

The effects of antiplatelet agents on platelet–leukocyte aggregations in patients with acute cerebral infarction

“…Flow cytometry was used to measure the level of PLA in the whole blood [12,14]. The procedure was as follows: À Take 20 ll anticoagulated blood containing 3.8% natrium citricum into the tube that contained 100 ml mixed liquor of monoclonal antibodies of CD45 labeled with phycoerythrin (PE) and CD42a labeled with fluorescein isothiocyanate (Exaipha Biologicals company, USA), incubate the mixed liquid for 20 min in a dark room after fully mixed;`Add 4% paraformaldehyde (with final concentration 1%) to the tubes to fix for 10 min;´Take 500 ll lysate for erythrocyte (used for flow cytometry) into the tube for 5-8 min (eBioscience company, USA);Ĉ entrifuge the mixed liquid at 500 r/min, remove the supernatant liquid, then take 500 ll phosphate buffered solution containing 1%paraformaldehyde, succuss softly to make the cell suspension again;˜The samples were analyzed by flow cytometry (FACS Calibur type, Becton Dickinson company) for 4 h to classify lymphocytes, monocytes and neutrophils and distinguish leukocytes combined the platelets from which were not combined at the same time; Þ 10,000 leukocytes were analyzed in every sample, both CD45 and CD42a positive particles represented that the percentage of PLA in the leukocytes was calculated; þ The percentages of PLA, PLyA, PMA, PNA were calculated, respectively.…”

“…The activated platelets often combine leucocytes and form PLA in patients with acute cerebral ischaemia. In recent years, research on PLA has shown that PLA is a sensitive marker of platelet activation [8][9][10][11][12]. In addition, McCabe et al [4] reported PMA formation increased in the acute phase (n = 79) and convalescent phase (n = 70) of patients after ischaemic stroke or transient ischaemic attack.…”