Acute exercise transiently alters the balance of the haemostatic system. To what extent exercise intensity influences coagulation potential and its clinical significance (sig.) is debatable. A new functional biomarker of haemostasis has been developed that quantifies clot microstructure (fractal dimension, df) and its mechanical properties (elasticity/storage modulus, G’GP) at the gel point (GP) of coagulating blood (1)(2). In this study, GP measurements were compared to standard coagulation markers during and following recovery from an incremental exercise test to volitional exhaustion. Twenty four healthy human subjects (3 females, age = 26 ± 1 years, Mean ± SEM) performed an incremental exercise test to exhaustion on a recumbent bicycle ergometer. Venous blood was drawn without stasis at: rest, 5 min into low intensity exercise (5 Watts; LowEx), at the point of volitional exhaustion (269 ± 10 Watts, MaxEx), 45 min (Rec45) & 60 min (Rec60) into passive recovery. 7 ml of unadulterated blood was transferred to a double gap concentric cylinder geometry of a DHR-2 rheometer (TA Instruments) with gel time kinetics (TGP, seconds, s), df and G’GP (pascal) calculated as previously described (1). In isolated plasma, prothrombin time (PT, s), activated partial thromboplastin time (aPTT, s) and fibrinogen (FBG, g/L) were measured. 1-way ANOVA compared mean difference followed by post hoc Bonferroni paired samples t-test (p< 0.05). MaxEx sig. increased df (1.719 ± 0.011 vs. 1.794 ± 0.011, n = 18-23; Figure 1A) and G’GP (0.047 ± 0.003 vs. 0.072 ± 0.004, n = 18-23), returning to baseline at 45 min recovery (df: 1.732 ± 0.015; G’GP: 0.050 ± 0.004). TGP (Figure 1B) was sig. shortened by MaxEx when compared to LowEx, (112 ± 9 vs. 85 ± 5, n = 18-23), returning to baseline values at 60 min recovery (117 ± 9). Compared to rest, MaxEx sig. shortened aPTT (33 ± 2 vs. 28 ± 1, n = 18-22; Figure 1C) and remained shortened 60 min after exercise cessation. There was no sig. alterations in PT or FBG. Maximal exercise has a marked effect on the developing clot microstructure of coagulating blood (df and G’GP), as well as its kinetics (TGP and aPTT). Interestingly, maximal exercise transiently increased df to levels observed in vascular hypercoagulable diseased states (3). After exercise, clot structure (df and G’GP) is first to recover to pre-exercise values, followed by clot kinetics in whole blood, with kinetic markers in plasma remaining active for longer. An increase in df was not mirrored by a change in FBG concentration or standard kinetic markers. This gives new information on the effect of MaxEx on haemostasis and clot formation. Further studies are required to determine the effect of age related exercise, especially those with associated comorbidities.