Effects of time of day and acute resistance exercise on platelet activation and function
Department of Sport and Exercise Physiology, Faculty of Sport Sciences, Shahid Beheshti University G.C., Tehran, Iran. Clinical hemorheology and microcirculation
(Impact Factor: 2.24).
01/2010; 45(2-4):391-9. DOI: 10.3233/CH-2010-1321
The present study was designed to ascertain the interaction between time of day and resistance exercise on platelet activation and function. Ten healthy male subjects (age, 29.3 +/- 4.5 yr) undertook identical bouts of resistance exercise on two separate occasions. Tests were randomised and performed at two different time of day (08:00 and 20:00 h). Subjects performed 3 sets of 7 repetitions of six exercises at 80% of 1RM, which was followed by 30 min recovery. Beta-thromboglobulin (B-TG) and platelet indices were measured at rest, post-exercise and at the completion of recovery. Platelet aggregation was determined in platelet rich plasma using collagen and three different concentrations of adenosine-5'-diphosphate. Platelet aggregations induced by different aggregating agents at rest were significantly higher in the morning (p < 0.05). Although platelet aggregations induced by collagen and ADP did not change in response to resistance exercise, significant differences between the results in the morning and evening trials were observed (p < 0.01). These differences emulated the differences observed at rest. A significant (P < 0.05) increase in B-TG was found following exercise with no difference between morning and evening trials. It was concluded that resistance exercise induces significant changes in platelet activation, irrespective of time of day, as assessed by beta-thromboglobulin.
Available from: Frederico Ribeiro Neto
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ABSTRACT: Physical inactivity is considered a risk factor for cardiovascular disease and is strongly associated with changes in arterial structure. Regular physical activity and exercise contributes to the prevention of coronary artery disease. Therefore, cardiovascular and resistance training improve hemostatic parameters and promote a less thrombotic blood profile. This review highlights the studies, mechanisms, and outcomes relating to the effectiveness of resistance training on the process of hemostasis. The Pubmed, Scopus, Medline, Scielo, Lilacs, Ibecs, and Cochrane databases were used to locate the original articles. Seventeen studies were found during the research process. Of these, ten articles were excluded. Those protocols using a high volume of training for young adults showed a greater fibrinolytic response, and training protocols with intensities above 80% of 1 maximum repetition showed an increased platelet activity. In subjects with coronary artery disease, just one session of resistance training resulted in improvement in the fibrinolytic system (tissue plasminogen activator) without raising potential thrombotic markers.
International Journal of General Medicine 03/2012; 5:249-54. DOI:10.2147/IJGM.S29197
Available from: Lisa A Fortier
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ABSTRACT: Platelet concentrates such as platelet-rich plasma (PRP) have gained popularity in sports medicine and orthopaedics to promote accelerated physiologic healing and return to function. Each PRP product varies depending on patient factors and the system used to generate it. Blood from some patients may fail to make PRP, and most clinicians use PRP without performing cell counts on either the blood or the preparation to confirm that the solution is truly PRP. Components in this milieu have bioactive functions that affect musculoskeletal tissue regeneration and healing. Platelets are activated by collagen or other molecules and release growth factors from alpha granules. Additional substances are released from dense bodies and lysosomes. Soluble proteins also present in PRP function in hemostasis, whereas others serve as biomarkers of musculoskeletal injury. Electrolytes and soluble plasma hormones are required for cellular signaling and regulation. Leukocytes and erythrocytes are present in PRP and function in inflammation, immunity, and additional cellular signaling pathways. This article supports the emerging paradigm that more than just platelets are playing a role in clinical responses to PRP. Depending on the specific constituents of a PRP preparation, the clinical use can theoretically be matched to the pathology being treated in an effort to improve clinical efficacy.
Arthroscopy The Journal of Arthroscopic and Related Surgery 03/2012; 28(3):429-39. DOI:10.1016/j.arthro.2011.10.018 · 3.21 Impact Factor
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ABSTRACT: Fibrinogen constitutes an important plasma glycoprotein involved in hemostasis and in inflammation. Previously, we have shown that at physiological concentrations, soluble fibrinogen is able to modulate the pattern of neutrophil activation. This led us to propose that under these conditions, fibrinogen could as well interfere with the adhesive behaviour of circulating neutrophils which is of utmost importance in their recruitment to the vascular wall during inflammatory processes. To address our working hypothesis, in vitro adhesion assays were here performed in a flow chamber by using primary cultures of human umbilical vein endothelial cells (HUVEC) and neutrophils isolated from peripheral venous blood of healthy human donors. In the presence of a physiological concentration of soluble fibrinogen (300 mg/dL), we observed that despite the number of neutrophils rolling on an activated endothelium was not affected, their rolling velocity was increased in comparison to that of non-activated neutrophils. Consequently as expected, the number of fibrinogen-treated neutrophils adhering to activated HUVEC monolayers was significantly diminished. Overall, we have here demonstrated that at least in vitro, soluble fibrinogen under physiological concentrations is able to modulate the interaction of neutrophils with the vascular endothelium. In vivo studies will enable us in the future to study the physiological relevance of these findings and further to understand the mechanisms underlying this function.
Clinical hemorheology and microcirculation 12/2012; 56(1). DOI:10.3233/CH-121662 · 2.24 Impact Factor
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