The mechanical properties of a blood clot are of crucial importance for its ability to stem the flow of blood at a site of vascular injury. These properties are largely determined by the underlying structural scaffold which forms during blood coagulation, a branched network of the biopolymer fibrin. Alterations in the structure of this network, such as changes in fiber density, fiber thickness or branching probability, strongly affect the mechanics of the network.The relationship between network architecture and bulk-level mechanics is commonly investigated using in vitro fibrin networks polymerized under static conditions. However, in the body, blood clots form under a highly dynamic mechanical environment: Nascent fibrin fibers are constantly exposed to the pulsatile shear flow of blood and the concurrent oscillatory dilation of the vessel walls. However, the effects of mechanical perturbations during polymerization on clot structure and the resultant mechanical properties remain unknown.Here, we polymerize fibrin networks while applying continuous oscillatory shear perturbations of varying strain amplitude. Despite these mechanical perturbations, fibrin can form rigid clots which exhibit a significantly later onset of the non-linear strain-stiffening response, a postponed rupture strain, and a lowered linear modulus compared to clots formed without perturbations. Up to perturbation amplitudes of 45% shear strain, the typical non-linear stiffness of these clots as well as their rupture stresses are of similar magnitude to those formed without perturbation. We show by confocal microscopy that these changes in the mechanical properties result from a formation of two architecturally distinct layers within the clot: one layer shows a highly bundled structure, while the other layer is virtually unaltered. This architectural adjustment may serve as a means for adapting blood clots to the mechanical loading conditions of the environment in which they form.