  Fibrous networks are ideal functional materials since they provide mechanical
rigidity at low weight. Such structures are omnipresent in natural biomaterials
from cells to tissues, as well as in man-made materials from polymeric
composites to paper and textiles. Here, we demonstrate that fibrous networks of
the blood clotting protein fibrin undergo a strong and irreversible increase in
their mechanical rigidity in response to compression. This rigidification can
be precisely predetermined from the level of applied compressive strain,
providing a means to program the network rigidity without having to change its
composition. To identify the mechanism underlying this programmable
rigidification, we measure single fiber-fiber interactions using optical
tweezers. We further develop a minimal computational model of adhesive fiber
networks that shows that load-induced bond formation can explain the adaptation
of the fibrin networks to compressive loading. The model predicts that the
network stiffness after compressive programming obeys a universal power-law
dependence on the prestress built in by new bond formation, which we confirm
experimentally. The generality of this functional stiffening mechanism together
with our ability to quantitatively predict it provides a new powerful approach
to program the stiffness of fibrous materials and dynamically adapt them to
different loading conditions.
