Part 2: The research behind the technique

Part 3: What is P.A.I.L’s™ and how is it used in this system?

Part 4: Assessment techniques, and how the system sets itself apart

For more information on Functional Range Release and any of Dr. Spina’s other seminars, please visit Functional Anatomic Palpations Systems.

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• An inability to stabilize the pelvis while performing dynamic lower body movements (i.e. performing lunges in the weight room or skating in hockey) may result in shear forces sustained by the spine, creating a compensatory pattern of inefficient/lack of gluteal activation, muscle spasm, and undue stress on the hip joints and muscles.

Therefore, to minimize the risks to specific muscles that cross this joint, we must maximize the integrity of the slings that cross it. Four myofascial slings are involved here, and they include:

• Posterior oblique sling – located across the back from gluteus maximus, through the thoracodorsal fascia, and up to the latissimus dorsi.
• Anterior oblique sling – in the front of the body from the external oblique, through the anterior abdominal fascia, to the contralateral internal oblique and the adductor musculature
• Longitudinal sling – from the peroneii/fibularis group in the lateral lower leg, up the biceps femoris, the sacroiliac ligaments, through the deep thoracodorsal fascia, and up the erector musculature
• Lateral sling – containing the PRIMARY frontal plane stabilizers for the hip joint – the gluteus medius, tensor fascia lata, and the lateral stabilizers of thoracopelvic region (i.e. quadratus lumborum)

Therefore, to assess and correct one’s risk for hip and groin injuries, it would be prudent to test the integrity of these slings and their myofascial components through such testing procedures as the BUNKIE TEST.

One of the most important tenets in minimizing these injuries is the ability to CONTROL and STABILIZE this region while power is being generated. We want loads to be generated THROUGH THE JOINT and not to it!

Other considerations include ADDuctor to ABDuctor strength ratio, hip static and dynamic mobility, and joint centration.

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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

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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

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

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I’m not exactly talking about the wonders of the footballer for self-myofascial release, although I do think these are more effective than regular stretching in many cases. Nor am I speaking about multidirectional ankle mortise mobilizations. The external assistance that I speak of actually comes from a medial arch support.

A recent study published in JOSPT, examined the effect of Standing Wall Stretching on a number of variables in subjects with “neutral” foot alignment and in those with “flat” feet. The variables examined were:

• Displacement of the myotendinous junction (DMTJ) of the medial gastrocnemius
• Rearfoot angle
• Navicular height

The main finding of this study was that following the stretching protocol, the difference in DMTJ was significantly greater in those with flat feet (pes planus). Therefore, for those of you who recommend the Standing Wall Stretch to improve gastrocnemius length, it may be wise to use a medial arch support in those athletes presenting with Pes Planus.

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Tendinopathy? “Hmm…too vague. Get some diagnostic skills will ya?”

Tendinosis? “Now that’s more like it. Most tendon pathologies pass the inflammation stage and go directly to the degeneration stage…right?”

But do they?

Well maybe not! Franklyn-Miller et al recently published an editorial piece entitles “Fasciitis first before tendinopathy: does anatomy hold the key?” in the most recent issue of British Journal of Sports Medicine outlining the fact that most research articles have failed to mention the role of the enveloping fascia in tendon pathologies. Specifically, they state that in some conditions involving musculotendinous structures, inflammation of the fascia is actually present, similar to that of conditions such as plantar fasciitis (here we go again!)

Their argument stems from histological evidence of inflammatory infiltrates, the presence of a fascia-tendon interface, and the relatively high number of studies that make reference to the presence of a paratenon enveloping or overlying the Achilles tendon. In fact, this paratenon is actually the posterior fascia of the lower extremity! Note: this paratenon is frequently used as a landmark for guidance of therapeutic injections of the Achilles tendon.

Therefore, this posterior fascia or paratenon, may be  a source of pain and inflammation in very early stage “tendon” pathologies and adhesion of this structure to its underlying tendon may actually lead to abnormal tendon loads and subsequent tendinopathy.

Thus, keeping in line with one of the main outcomes of my post yesterday on Greater Trochanter Pain Syndrome, finding the root cause of pain local to a specific area is perhaps one of the most important, yet difficult, skills of a clinician. Therefore, it may be wise to occasionally ask ourselves do we really know what we think we know?

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This is quite a touchy subject and while you may THINK you have a good idea on whether to stretch or not, guess again! By now (2009), most of you think stretching is bad. Some on the other hand, still use “stretching” and “warming up” synonymously (these people probably tug really hard on a slab of meat to get it to medium-well). Now let me tell you what I think, but since I have a lot of info to cover, I’ll simply do so in point form.

What are we really doing?

• Viscoelasticity: when human tissue is held under tension for a long period of time, the force required to hold the tissue at this particular length decreases

• Neural mechanism: the increased range of motion (ROM) about a joint following a bout of stretching is actually an APPARENT increase. That is, no actual change in physical length, its actually an analgesic affect. This doesn’t apply to massage-based techniques either by hand or tool, just stretching

Pre-activity stretching

• Shrier and friends looked at acute stretching via a systematic review in 2004 and found some papers that showed negative effects, some showing conflicting effects, and one showing positive effects on performance measures.
• His review revealed NEGATIVE effects of pre-activity stretching on peak torque (Nelson et al, Evetovich et al, Cramer et al, Merek et al), strength endurance (Nelson et al), power output (Yamaguchi et al), balance, reaction, and movement times (Behm et al).
• Static stretching was found to increase (aka slow) 20m sprint time while dynamic stretching was found to improve 20m sprint time (Nelson et al).
• The one study showing positive effects in soccer players demonstrated dynamic stretching to IMPROVE the stationary 10m sprint, flying start 20m sprint, and agility (Little et al). This study also said static stretching did no harm.
• Running economy was also said to have improved with stretching
• NO EFFECTS were revealed for kicking foot speed (Young et al), tennis serve accuracy and power (Knudson et al), jump height (Woolstenhulme et al), and jump ability (Unick et al)
• Static stretching also has NO EFFECT on eccentric muscle contractions (Cramer et al)

Regular stretching

• A long-term, regular routine of stretching actually INCREASES the force production and velocity of contraction of muscle (Magnusson et al)

What about ballistic stretching?

• Mahieu et al examined both static and ballistic stretching about the ankle and found that while both improved joint ROM, passive resistive torque decreased with static stretching and passive stiffness (of the Achilles) decreased with ballistic work. See below for what I think about this.

But what does this all mean?

• “Generally” speaking, its ok to statically stretch at home and on a regular basis.
• “Generally” speaking, one should perform a dynamic warm up prior to competition

NOW THIS IS WHAT I THINK:

• Most of us are probably missing the boat and ignoring the neurophysiologic and contractile properties of the myofascia (more on this in a future post. just make sure you come back because this may completely change the way you look at muscles)
• Stretch only what needs to be stretched. If your athlete presents with an upper crossed-type syndrome, then he/she will likely need to work on their pectoralis minor. Stop cranking on their anterior capsule
• Wise cookies will not only look at muscles but also joints. Figure out what needs improved mobility through functional screening (Functional Movement Screens, Lyno Method, etc). Check out Ron Jones and Guy Voyer they’ve got some good stuff.
• Sometimes an athlete will need specific muscle work and other times they’ll need to address fascial restrictions. YOU NEED TO BE ABLE TO DISTINGUISH BETWEEN THE TWO!
• From a therapeutic perspective, first assess and compare single-joint vs multi-joint ROM. Address the single-joint issues first then follow with the multi-joint issues.
• Self-stretching of the lower extremity sucks and is very difficult to do effectively. Most of the time we end up stretching our tendons and ligaments (see ballistic stretching above) rather than stretching the muscle bellies or releasing fascial restrictions. Isolated stretching of the tendons and ligaments may actually be detrimental and decreasing their ability to store and release energy may put us at risk of injury. I don’t necessarily think ballistic work is bad, I just think it should be reserved for certain athletes and in certain instances. Releasing an adhesion at the muscle insertion is a different story (click here)
• In many cases, athletes should be using some type of external tool and or manual therapy to improve the length and pliability of a certain tissues. Its the mindless work that’s detrimental!
• Dynamic stretching should ONLY be performed in that ROM which is required for the particular sport participated in. That is, 5K clinic participants don’t need as much ROM as hurdlers and therefore, shouldn’t swing their hips like pendulum as high as hurdlers do.
• Proximal stability should precede distal mobility
• In many instances, its actually not the muscles that need stretching but the joints that need mobilizations. Think ankle mortise in squatting

And probably my #1 tip:

• Don’t be afraid to wear your Lulu Lemons! If athlete needs to improve their mobility around a particular joint for performance purposes (i.e. hurdler, high jumper), then let them. Just make sure they follow up their warm-up routine (in the sport-specific ROM) with a few exercises that address that muscle-joint complex’s stretch-shortening capabilities. What good is increased ROM when you’re become weak in that new ROM?

But here’s my little secret…

• Follow that up with a little vibration and BOOM..watch Usain go!

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Although the assessment and treatment of myofascial and kinetic chain dysfunction has been used for numerous years, its presence in therapy clinics and performance centres have increased tremendously in recent times.  Clinicians and strength coaches are well adept at developing the functional kinetic chain, however, very few understand importance of the fascial system. In order to adequately assess imbalance and dysfunction, a battery of tests must be performed.

An article by de Witt and Venter was published recently in the Journal of Bodywork and Movement Therapies and describes the “Bunkie” test for assessing functional strength. While “functional strength” encompases MUCH more than the myofascial system, let’s look at this testing procedure for assessing the fascial lines.

The Bunkie test has generally been used as the main assessment tool in the Lyno Method and is derived from the Afrikaans word ‘bankie’ for little bench. This testing procedure is comprised of 5 different tests for specific fascial lines.

Anterior power line

Medial stabilizing line

Lateral stabilizing line

Posterior stabilizing line

Posterior power line

The bench height should correspond with the length of the humerus (~ 25 -30cm)

Test position should be held for 20 – 40s (40s is preferred for endurance athletes)

While this testing procedure still warrants validation, it may be useful in challenging cases to reveal areas of “locked-long” fascia along the specific line examined.  A positive test for “locked-long” fascia is indicated by immediate pain upon testing, bodily rotation, and or inability to hold the correct position.

The assessment of “locked-short” fascia must also be performed but is not directly related to the “Bunkie” testing procedure. I will discuss the assessment of such fascia as well as treatment of “locked-long” fascia (weak) lines in a future post. But for now, I would like to know how many of you currently use this testing procedure and if so, what feedback you may have.

And while we’re talking about myofascial and kinetic chain dysfunction, here are two books/manuals that I’ve recently ordered and will be reviewing on this site sometime in the near future.

Photo sources: 1, 2, 3, 4

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