Study Title: Return-to-Play in Sport: A Decision-Based Model
Authors: DW Creighton, I Shrier, R Shultz, WH Meeuwisse & GO Matheson
Journal: Clinical Journal of Sport Medicine
Date: September 2010

Summary:

• For those of you involved in sport medicine, here is an excellent example of scientific insight into the factors that may influence and determine Return to Play decision making.  This paper, authored by individuals at Stanford University, McGill University and the University of Calgary, details the all important, multifactorial decision making process of allowing an athlete to return to “full participation in sport without restriction”.  Through a literature synthesis, a model that included the Evaluation of Health Status, Evaluation of Participation Risk, and Decision Modification was proposed.  While the authors noted that the ability to quantify several decision elements may be limited, they suggested that decision modification must only be considered once participation risk is determined.

• Although seemingly short and straightforward, this paper provides comprehensive insight into the variables that must be considered by those in a priviledged position to determine whether or not an athlete is permitted, let alone mentally and/or physically capable of, returning to sport.

Complete resolution of symptoms "cannot be considered in isolation” when determining return to play

Creighton DW, Shrier I, Shultz R, Meeuwisse WH & Matheson GO. (2010). Return-to-play in sport: A decision-based model. Clinical Journal of Sport Medicine, 20(5); 379-385

This past week my most recent review was posted on Research Review Service, a site specifically for health care professionals of manual and rehabilitative therapy. The Influence of Reduced Hamstring Length on Patellofemoral Joint Stress During Squatting in Healthy Male Adults by Whyte et al was published earlier this year in Gait Posture.

Here's a brief summary of the study:

Study Purpose:

• To determine the presence of a relationship between hamstring length and PFJ stress at 3 specific knee joint angles of flexion.

Study Population:

• 16 recreationally active males divided into two groups based on knee joint angle-measured hamstring length.

Methodology:

• A biomechanical model incorporating knee joint angle, knee extensor moment, and PFJ contact area was used to quantify PFJ stress.
• MRI and 3D motion analyses were also utilized in this study.
• A one-way ANOVA to determine the variations in PFJ stress between the 2 groups (with and without reduced hamstring length) was used.

Main Findings:

• Patellofemoral Joint stresses differed significantly between the two groups at specific angles of knee flexion.
• No significant differences in hip angles between the two groups.

Clinical Application:

• This study demonstrated that subjects with reduced hamstring lengths have increased PFJ stress during various positions of the squatting movement.  As a result, such a decrease in length MAY contribute to the pathogenesis of various conditions relating to the knee.
• These results enable us to consider another factor when managing those with knee pathology.

For a complete and "evidence-informed" understanding of the study, check out my review. I have obviously left out specifics from this study in this post as Research Review Service is a paid membership site. However, if you would like more information, please do not hesitate to ask.

Here's a brief summary of an excellent paper by Boudreau et al from Manual Therapy. 

The purpose of this paper was to summarize several important aspects of motor-skill training for enhancing musculoskeletal rehabilitation.

Cortical Neuroplasticity: a dynamic feature of life that encompasses functional or morphological change in properties of neurons (connection strength, represenational patterns, neuron reorganization.

• Positive changes: improvements in motor performance
• Negative changes: decreases in performance, such as in the presence of chronic pain (low back pain resulting in decreased cortical spinal drive in lumbar musculature and subsequent shift in somatosensory representation)

It is hypothesized that motor-skill training can influence the direction of change in cortical neuroplasticity.

• That is, the representation of muscles affected by pain in the sensorimotor system.

Potential effects of motor-skill training:

• Improvements in task performance
• Improvements secondary to very short training intervals.
• Improvements occuring in two stages - 1) fast learning (following a single training session); 2) slower learning (across several sessions of practice)
• Improvements with activation of inhibited/delayed musculature via repeated voluntary contractions.

Methods of Optimizing Rehabilitation:

• Skilled training - skilled/precision tasks (vs strength training) should be performed to facilitate neuroplastic changes, and subsequently improvements in motor behaviour.
• Negative effects of the presence of pain during novel motor skill acquisition - since pain alters excitability of the primary motor cortex in a rapid manner, these responses are generally protective and counterintuitive in the motor-learning process. Negative effects are also demonstrated in the presence of low quality sleep, stress, and attention deficits. Therefore, motor-skill learning should be relatively pain free.
• Protective effect of motor-skill training - training prior to acute experimental pain may prevent unwanted cortical neuroplastic changes.
• Cognitive effort - the greater the complexity of a skilled task and its corresponding intent, results in greater cortical representation and changes.
• Quality - since no difference seems to exist with greater repetitions of within-session skill learning tasks, the primary focus of each rehabilitation session should be quality of performance.

The above information was derived from a multitude of studies and demonstrates that motor-skill training may positively influence cortical neuroplasticity in musculoskeletal rehabilitation
​

An article by Dr. S McGill compared the V-sit flexion endurance test vs the front plank test for endurance.

• The data from this study came from two sources (firefighters and kinesiology students).

• The main objective of this study was to assess the relationship between the V-sit test and the plank test for torso flexion endurance.

• The pearson correlation was r=0.34 (low correlation) as well as the r-squared value. It almost seems obvious that these two wouldn't correlate well as they are two totally different positions.

I think the main reason McGill did this study was because people were using the PLANK test in place of the V-SIT to test flexion endurance (which has plenty of data correlating poor endurance times with low back disorders).
​

• The moral of the story is to use the V-sit when doing your tests for flexion endurance.

• He also cautioned against "training the test" due to the high compressive loads.

DESTRUCTION PHASE:

Initial rupture and necrosis of myofibers

• However, 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 Remodeling Phases Are Concomitant – simultaneously supportive and competitive


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 the invading 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 

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

*The above review was a brief summary of Jarvinen's review on Muscle Injuries in the Americal Journal of Sports Medicine