Fibrinogenolysis and fibrinolysis with strenuous exercise

Abstract

Twenty healthy young men were exercised on a treadmill according to the protocol of Balke and Ware. Mean duration of exercise was 24.9 +/- 5.7 min and mean maximum heart rate was 195 +/- 9. Fibrinolytic activity was markedly accelerated with euglobulin lysis times decreasing to 36% of control values and fibrinogen-fibrin degradation products increasing 109% after exercise. Assays for fibrin monomer were negative in all samples. In vivo fibrinogen A alpha-chin degradation was assessed by sodium dodecyl sulfate polyacrylamide gel electrophoresis of reduced samples of fibrin monomer isolated by clotting plasma samples in the presence of 0.1 M epsilon-aminocaproic acid and 1% disodium ethylenediaminetetraacetate. The A alpha-chain, the fibrinogen chain most susceptible to plasmin degeneration, showed no evidence of increased degeneration after exercise. Gel scans showed no decrease in the ratio of total alpha-chain to beta- and gamma-chains after exercise. The ratio of intact alpha 1 chain (alpha 1, 67,000 mol wt) to total alpha-chain was 0.66 +/- 0.13 before exercise, 0.64 +/- 0.14 immediately after exercise, and 0.65 +/- 0.13 1 h after exercise. The rate and extent of crosslinking of the alpha-chain of fibrin formed by clotting plasma samples was unaltered by exericse. These data suggest that physiologically significant fibrinogenolysis does not occur with strenuous exercise, even when fibrinolytic activity is markedly accelerated.

Blood Coagulation and Platelet Function following Maximal Exercise: Effects of Beta-Adrenoceptor Blockade

“…Despite the similar peak heart rates obtained following running, treadmill or bicycle exer cise the magnitude of rise in VIII:C is much greater following running exercises [11,26,27,30,31]. Thus we found a mean rise in VIII:C of only 23% at peak exercise (onestage assay).…”

“…Carteolol however did significantly modify the rise in VIII:C. The difference in the VIII:C response in the 13-blocker groups could indicate a possible role for PAA, possessed by carteolol, but it is more likely to be explained by differences in the intensity of (3-blockade which were pro duced in our study. The rise in VIIPRAg with exercise has been shown to be less than [25][26][27]34] or to parallel the rise in VIII:C [11,31,35,36], We have noted a slightly greater rise in VIII:RAg and have shown, for the first time, that the extent of the rise is smaller with propranolol (p < 0.01) and carteolol (NS: see fig. 1).…”

Effects of strenuous exercise on haemostasis: Table 1

“…[3][4][5] This is also reflected by a change in activated partial thromboplastin time, which measures the activity of the intrinsic and common pathways, after exercise such that it is reduced by 7-38%. [6][7][8][9][10][11][12][13][14][15][16][17][18] Studies of the effect of exercise on prothrombin time (a measure of the activity of extrinsic and common pathways) and thrombin time (a measure of common pathway activity) have given conflicting results. Most show no demonstrable effect on prothrombin time, [19][20][21][22] although some have shown a significant shortening of thrombin time.…”

Rapid purification of a high-affinity plasminogen activator from human blood plasma by specific adsorption on fibrin/Celite.

“…The possibility that plasminogen activator binding is mediated by trace amounts of plasminogen on the fibrin surface was excluded because purified plasminogen activator also binds to fibrin/Celite. It therefore may be postulated that the specificity of natural fibrinolysis, which restricts plasmin action to fibrin and protects fibrinogen from degradation (23)(24)(25) even in the absence of a2-antiplasmin (21), is mediated primarily by the unique affinity of the blood plasminogen activator for fibrin. The binding ofactivator to the clot activates adjacent plasminogen present in the ambient plasma or plasminogen adsorbed to fibrin.…”