Youth Wrestling




Healing Process - Successful Rehabilitation & The Healing Process


Once a tissue becomes injured the healing process begins immediately. Successful rehabilitation programs are based on the understanding of the healing process. The body will heal in a sequence of various phases. The rehabilitation program will be based on recognition and timing of these various healing phases. The healing response depends on the following three phases:1


. Inflammatory Response Phase

. Fibroblastic Repair Phase

. Maturation Remodeling Phase


Inflammatory Response Phase 

Destruction of a tissue produces a direct injury to the cells of the tissues and this will result in an altered cellular metabolism. In addition, substances that initiate the inflammatory response are released. These substances cause characteristic swelling, redness, tenderness, and increased temperature.1

Inflammation is the process by which leukocytes, phagocytic cells, and exudates are delivered to the injured tissue. The purpose of this process is to localize or dispose of injury by-products such as blood and damaged cells. This is achieved by phagocytosis and sets the stage for repair.1

There is a change in hemodynamics which involves vascular spasm, formation of a platelet plug, blood coagulation, and growth of fibrous tissue. There is a vasoconstriction around the injury site for the first 5-10 minutes post injury, and soon after there is rapid hyperemia of the area due to vessel dilation.1

There are three chemical mediators that will limit the amount of exudate and swelling after injury. The chemical mediators are histamine, leukotaxin, and necrosin. Histamine is released from the injured mast cells. Histamine causes vasodilatation and increased cell permeability. This adds to the swelling effect. Leukotaxin is responsible for the lining up of leukocytes along the cell walls and also increases cell permeability. This affects the passage of the fluid and white blood cells through the cell walls (diapedesis) to form exudates. Therefore changes in hemodynamics are important for exudates formation and supplying leukocytes to the injured area. Necrosin is responsible for phagocytic activity. The amount of swelling that occurs is related to the extent of vessel damage.1

Thromboplastin causes prothrombin to be changed into thrombin. This causes the conversion of fibrinogen into a sticky fibrin clot that shuts off blood supply to the injured area. Clot formation begins approximately 12 hours after injury and ends 48 hours after injury. As a result the injured area becomes walled off and the leukocytes phagocytize most of the foreign debris. This sets up the stage for the fibroblastic repair phase and ends the 2-4 day long inflammatory response.1

Note: Chronic Inflammation occurs when the acute inflammatory phase does not eliminate the injuring agent and restore tissues to their normal physiological state.

Fibroblastic Repair Phase

The fibroblastic phase generates activity leading to scar formation and repair of the injured tissue. Fibroplasia (scar formation) begins within the first few hours after injury and may last for as long as 4-6 weeks. With the onset of the new phase, signs and symptoms of the inflammatory response phase start to subside. The athlete will still be tender and any stress to the injured structure will still cause pain. When scar formation progresses and the tissues become stronger, tenderness and pain will begin to heal.1 

During this phase there is a lack of oxygen to the affected area. To compensate the body forms capillary buds which grow into the wound. Now the wound can heal aerobically and with increased oxygen delivery, comes increased blood flow, which delivers nutrients essential for tissue generation in the area.1 

The fibrin clot will begin to breakdown, and the breakdown will cause the formation of granulation tissue (a connective tissue). Granulation tissue consists of fibroblast, collagen, and capillaries. It appears as a reddish mass of connective tissue that fills in gaps during the healing process. 1

When capillaries grow into the wound, fibroblast accumulate at the injury site arranging themselves parallel to the capillaries. Fibroblastic cells begin to synthesize an extra cellular matrix. The matrix consists of collagen, elastin, ground substance, glycosaminoglycans, and fluid. On day six or seven, fibroblast begin producing collagen fibers that are deposited in a random fashion throughout the forming scar. The collagen begins to proliferate and the tensile strength of the wound rapidly increases in proportion to the rate of collagen synthesis. When the tensile strength increases, the number of fibroblast diminishes to signal the beginning of the maturation phase.1 

Maturation Remodeling Phase

The maturation-remodeling phase is a long process that involves the realignment or remodeling of the collagen fibers that make up scar tissue. The realignment will depend on the tensile forces to which the scar tissue is subjected. As stress and strain are applied to the collagen fibers, the fibers realign in a position of maximum efficiency parallel to the lines of tension. The tissue will then gradually become normal in appearance and function. Usually within three weeks, a firm scar will exist. However, the maturation phase may take as long as several years to complete.1

. Factors that Slow Down Healing

. Edema

. Hemorrhage

. Tissue Separation

. Muscle Spasm

. Vascular Supply

. Atrophy

. Corticosteroids

. Infections

. Humidity, Climate, and Oxygen Tension

. Scars and Keloids

. Health, Age, and Nutrition 

By: Craig Angle - ME.d, ME.d, ATC, CSCS

Author of the book: How to Raise a Successful Athlete

Former CEO: The Athlete Project


1.       Prentice , William. Rehabilitation Techniques in Sports Medicine. Mosby:

2nd Ed. Missouri; 1995.

2.       Starkey, Chad. Therapeutic Modalities for Athletic Trainers. F.A. Davis

Company; 1993

3.       Merrick, M. A., Jutte, L.S., Smith, M. E. Cold modalities with different

thermodynamic properties produce different surface and intramuscular temperatures.

J of Athletic Training Research. 2003, 38: 28-33

4.       Knight, K.L. Cryrotherapy in Sport Injury Management. Champaign, IL: Human

Kinetics; 1995.

5.       Arnhiem, D. D., Prentice, W. E., Principles of Athletic Training. McGraw-Hill:

9th Ed. Boston; 1997

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