Three Phases of Muscle Injury and Applied Healing

In 2010, I summarized the three phases of muscle injury & healing as described by Jarvinen (2005) in AJSM.

Now, a number of years have passed and a number of journal articles have been published since then but indeed, the science still remains relatively the same.

Recent and relevant articles published:

• Regeneration of injured skeletal muscle after injury by Jarvinen et al
• The inflammatory response to skeletal muscle injury: illuminating complexities by Smith et al
• Basic science and clinical studies coincide: active approach treatment is needed after sports injury by Kannus et al
• Muscle injuries: optimizing recovery by Jarvinen et al

Since my thought processes and clinical experiences have evolved over the years, what I would like to do below, is provide a brief summary of practical "healing method" applications (that have worked for me) to the phases as an update to my original post. My updates will be in red.
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Destruction Phase:

Initial rupture and necrosis of myofibers

• Note, within hours the propagation of necrosis is halted to a local process (similar to a “fire door” mechanism)

Hematoma formation occurs between the ruptured stumps of the myofibers

Blood vessels tear and release inflammatory cells

• Later, inflammation is amplified as “wound hormones” are released by satellite cells and necrotized myofibers – these act as chemotactants, signaling for further inflammation

*Note: Repair and Remodelling Phases Are Concomitant – simultaneously supportive and competitive

In this phase, my primary objective is to protect. For protection, I want to ensure that the hematoma between the ruptured stumps do indeed form so that the two "detached ends" can reconnect if you will. The simplest method is protect from further damage. In most cases, this occurs naturally (i.e. athlete voluntarily or involuntarily removes self from competition or training). In some cases, the athlete will continue but once the activity is completed, protection should be the first priority. Additionally, it is important to incorporate lateralizations and regressions in training to minimize deconditioning and facilitate positive humoral and hormonal responses.

Relevant resources on training during injury:

• Training = Rehab 2 by Weingroff (coming soon)
• Val Nasedkin interview on SportsRehabExpert.com

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Repair Phase:

Phagocytosis of necrotized tissue

• Initially, polymorphonuclear leukocytes are the most abundant cells but within the first day, these are replaced by monocytes/macrophages which proteolyse and phagocytose the necrotic tissue

Regeneration of myofibers

• Pool of satellite cells beneath the basal lamina (present since fetal development) proliferate in response to injury, differentiate into myoblasts, and join together to form multinucleated myotubes (these myotubes then fuse with the injured myofiber that survived the trauma)
• Undifferentiated stem cells which are extralaminally within the connective tissue give rise to determined myoblasts and differentiate to myotubes
• Regeneration of intramuscular nerves is also necessary as a lack of reinnervation of the myofiber results in atrophy

Production of a connective tissue scar

• Initial injury results in a hematoma but within the first day, the hematoma is invaded by inflammatory cells (including phagocytes)
• Blood-derived fibrin and fibronectin cross-link to form a scaffold and anchorage site for theinvading fibroblasts
• Fibroblasts then start synthesizing the proteins and proteoglycans of the ECM to restore the integrity of the connective tissue framework
• Fibronectin is followed by Type III collagen. (Type I collagen production is initiated days later).
• The initially large granulation tissue (scar) eventually condenses into a small mass made up mostly of Type I
• The scar is initially the weakest point but infusion of TYPE I collagen (and the cross-link formation with maturation) makes it stronger (tensile strength) than the adjacent myofibers by day 10 post-injury. Therefore, reinjury ISN’T simply the “breaking up of scar tissue”

Capillary in-growth into injured area

• Vascularization is the first sign of regeneration and required for subsequent recovery process
• New capillaries have only a moderate capacity for aerobic metabolism and, therefore, rely on anaerobic means
• BUT during the final stages of regeneration, aerobic metabolism is needed (principle energy pathway) for the regeneration of myofibers - Regeneration does not progress beyond the newly formed thin myotube stage unless a sufficient capillary in-growth has ensured the required supply of oxygen for the aerobic metabolism

My next goal is to preserve. For preservation, my goal is to initiate the healing process as soon as possible and NOT prevent inflammation from actually occurring. Traditionally, we have been trained to think that inflammation is bad yet in order for step 2 (repair) to occur, inflammation is necessary. But more specifically, what we want is "good in, bad out". Only now are we gaining insight into the negative effects of rest, icing and cryotherapy on tissue healing rates and sooner or later we'll be enlightened with the negative effects of compression as well. Those who are well read already know the value of muscle contraction on lymphatic circulation and hormonal responses post-injury. My current approach is to promote as frequent muscle contractions as possible, in as safe and protective manner as possible. Whether via simple distal extremity ABCs, digit contractions, bicycle riding, or non-fatiguing electrical stimulation, my goal is to initiate the healing process rather than delaying it (by ice and/or compression).

Recent and relevant resources on the role of inflammation on tissue healing:

• Iced! The illusionary treatment option by Reinl
• "Anti" Inflammatory by Reinl et al 

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Remodeling Phase:

Maturation of the regenerated myofibers

Contraction and reorganization of the scar tissue

• Myofibers that survived form branches as well as try to pierce through the scar on either side. The branches adhere to the connective tissue (scar) to form mini-Muscle Tendon Junctions. As mentioned above, the scar, therefore becomes stronger than its adjacent myofibers, rendering the myofibers more susceptible to injury if reaggravated
• Reinforced lateral adhesions (branches) also form to reduce the movement of the stumps and reduce the pull on the fragile scar. These lateral adhesions are formed as a result of intentional mechanical stress (free/forced mobilizations)
• Overtime the scar progressively diminishes bringing the stumps closer together – until the myofibers become interlaced (though likely not reunited)

Recovery of the functional capacity of the muscle

• Depends on severity of injury and nature of hematoma (intra vs inter muscular hematoma) of the injured muscle

Last, but not least, my objective here is to promote remodelling. Thanks to my friend and colleague, Dr. Andreo Spina, I have gained a better appreciation for role manual methods in influencing tissue remodelling.  Research tells us that cells turn over but respond secondary to stimuli. This is common knowledge. However, from a manual therapy standpoint, applied and controlled forces applied to tissue lead to chemical signalling, interaction and communication. So whether it be via force application with our hands or progressive angular isometric loading (or other), tissues are influenced and remodelled along the lines of applied stresses. Remodelling certainly does not end with manual therapy or isometric loading but from my recent experiences, I believe it should start there. What transpires next should be left up to the discretion of the rehab clinician and/or strength coach and based on the particular athlete at hand. 

Relevant resources on therapeutic application for tissue remodelling:

• What is PAILs (progressive angular isometric loading)? by Spina
• Functional Anatomy Blog by Spina
• Massage and Acute Injuries by Ward​