During this stage there is vasodilation (a widening of the blood vessels) and an increase in blood viscosity to the injured area. This is then followed by a brief period of vasoconstriction (narrowing of the blood vessels) which is bought about by the release of histamine and prostaglandin cascades from the injury site. Due to this increase in hydrostatic pressure in the blood vessels and chemotactic processes, there is also vasopermability.  This causes leakage of protein rich plasma and fluid into the initial tissue spaces, creating an exudate that envelopes the injury site and helps contain infection.

Platelets are able to clot the damaged areas. Leukocytes migrate, and endothelial cells swell. Neutrophils initially debride the wound, followed by the macrophages and other phagocytic cells. The end result is an injury site increased vasodilation, vasopermability, phagocytis and a weak fibrin clot, that is the first structure in the repair process. This stage lasts from the bleeding stage to 2-3 days after injury.

If there are cardinal signs of inflammation (redness, heat, pain, loss of function) then strengthening techniques must not be instigated as the tensile strength of the tissue is weak. However, modalities such as cryotherapy (ice) may be used to prevent prolonged inflammation and reduce excessive scar tissue formation and fibrosis. Premature exercise will result in increases oedema (swelling) from the breaking of the fibrin mesh that has formed.

This stage is approximately 2-3 days – 3 weeks + post injury. During this stage the fibrin mesh is replaced with highly vascular granulation tissue containing collagen, elastin and components of the extracellular matrix (GAGs).  Fibroblasts migrate to the injury site from the surrounding tissues and are responsible for laying down collagen productions and fibroblastic activities 2-3 weeks post injury, termed fibroplasia. There is also increased local circulation to the injury site through anaglgenesis as capillaries grow towards the wound.

Tensile strength of the tissue is still weak at this stage but tensile loading through stretching and manual therapy can be used to manipulate the collagen deposition. Type III collagen is initially laid down in a haphazard manner with less cross links so tensile loading helps align the fibres in a parallel fashion.  Compression techniques can also be used to influence fluid flow and viscoelastic properties of the tissue.

This stage starts as early as 1-2 weeks post injury and lasts up to 18 months. The type III collagen is replaced with stronger, longer standard type I collagen which contains more cross links. Granulation tissue is replaced with mature scar tissue with increased tensile strength. Myofibroblasts commence wound contraction and therefore ROM activities are still important to produce a functional scar.

Strength exercises can now be used, especially in the eccentric contraction range which will help to increase the tensile strength of the non-contractile elements (scar tissue).  At this stage there is a devascularisation of the wound and therefore less potential to influence healing in this stage.  If safe, resume strengthening exercises and reverse the effects of immobilisation. Immobilisation will result in the proliferation of connective tissue in the muscle and loss of ground substance as well as poorly orientated collagen cross links. Thus, early mobilisation is vital but must not be too aggressive to exceed the tensile strength of the tissue.