Q. A diagnosis of "Bilateral positive FABER test" indicates left and right hip/SIJ mobility dysfunction -
From a client: "Does this just mean I need to increase my hip mobility and range of motion?"
Yes, in general. The test tells us to look further into the hip and SIJ area. Together with the test below, the modified thomas test, which also tells us about the hip, we are led to try to improve whatever is limiting the hip from being mobile enough. In your case, your quads (and the tissue that wraps around it, the fascia) is pretty tight - it has adapted that way with your training and lifestyle. That contributes to tightness around the hip area. The hip joint ITSELF was compressed - meaning the subtle "accessory" glides were limited. Accessory glides are the small movements that you CAN NOT do yourself, such as glides and slides from anterior to posterior direction, medial to lateral direction and traction/compression. Accessory glides, when they are limited, will limit the "physiological" mobility. Physiological mobility is the range of motion that you CAN produce, ie hip flexion, extension, external and internal rotations. So, when your physiological range of motion is limited, as shown by these two tests, then.....hip mobility drills like stretching into the limited direction may not work......if they were going to work, they might have already (unless you don't stretch). So, regaining accessory slides and glides often restores physiological range of motion, or improves it at least - then the stretches work better. The thing about accessory glides and slides is that since you can't actively produce them, you need someone skilled to reset them by hand. And....often when the quads, hamstrings and glutes, with all their fascia, are tight also, regaining accessory glides needs help from soft tissue therapy and stretching to limit the negative effect of muscle-fascia tissue extensibility issues. In some individuals, being tight can be beneficial, but if you want to squat, lunge and deadlift fully, under load, being tight only limits the freedom of movement, limits your end-range positions, and can mess with your patterns and power. Think of the three P's - positions, patterns, power. Positions require mobility to at least minimum so you can get into the start position and end position. Patterns is the motor control required to move you between the start and end position. And power is the force production to express the pattern under load. Your strength training aims to increase more and more force production, but if you lack being able to get into the position, that alters motor control and your nervous system struggles to express power. Make sense?
So, the tib post tendon connects the tib post muscle, deep in the back of the lower leg, to the bottom of the foot.
It's like a long stiff spring. It absorbs shock, along with several other tendons/springs in the lower leg and foot.
For the tendon to absorb force and spring back, it needs the tib post muscle to contract at exactly the right time, contract/squeeze hard and give the tendon/spring something to anchor to. Two things there: it needs a healthy set of receptors in the foot to send a signal back that it's time to contract/squeeze the tib post muscle; and, it needs a healthy, strong tib post muscle.
In addition to healthy receptors and healthy tib post muscle, the tendon must have structure that tolerates forces that can be from 2 to 10 times your bodyweight.
This structure is like a series of strong cables (collagen fibres) held together by pliable glue (ground substance). Stationed along those cables, within the pliable glue, are tendon cells that are ready to rebuild when necessary.
What can go wrong? First, the health of the receptors is secondary to having mobility in the joints of the foot. When your foot hits the ground, the bones move, the ligaments, tendons and muscles that hold those bones together stretch. Inside the ligaments, tendons and muscles are special tissues that detect lengthening - they send a superfast signal back to the spinal cord that activates a nerve to send a signal back down the leg to the muscles attached to those tendons - they are activated to squeeze and pull back against the stretch of the tissue - this process relies on bones having the ability to subtly move so the movement can be detected. It also relies on not having pain that might interrupt the signal. It also relies on having a healthy nervous system up in the spinal cord, to send a signal back down, and it relies on having foot muscles that have the capacity to squeeze hard enough to counteract the stretching force of 2-10 times your bodyweight.
The difference in force, between 2 and 10 times your bodyweight is because some activities are low shock and others are high shock (like hopping down from a box).
When the muscles contract, it provides a strong anchor for the tendon at one end. At the other end is the bone that's moving - the tendon usually has the flexibility to elongate approximately 2% only of its resting length. So the tibialis posterior tendon is long, very long (from under the foot to up in the middle of the calf area). A 2% lengthening, at most, is not very much. Most of the stretch happens in the muscle attached to it. IF you get a lot of stretch, the whole muscle/tendon length gets longer - this looks like a foot and ankle collapsing forwards and inwards (dorsiflexion and eversion at the ankle and mid-foot). If you don't get a lot of stretch, the ankle collapses much less then springs back. The way to get not a lot of stretch is to have healthy foot receptors to send a signal and a strong tib post muscle to squeeze hard.
Progressively, as our bodyweight increases over our life, and we run and jump and hop, the muscles and tendons get strong and can tolerate those forces. Sometimes physiology gets in the way and it affects load tolerance. Some examples of what might affect it - increased bodyweight (more load than it's used to), periods of inactivity (the body loses some load tolerance), belly fat can affect tendon health, fatigue can affect muscle contraction ability to pre-tension the tendon.
When the body suffers a load that is higher than it cope with, the tendon cells wake up and get to work. Normally, the pliable glue that holds the tendons together contains a protein called Decorin. Most of the pliable glue, called ground substance, is called decorin. Tendon cells that suffer an acute overload might be signalled to produce a different protein called Aggrecans. Aggrecans is a key protein in cartilage and is hydrophilic, meaning it attracts water around it. In cartilage that is beneficial for "plumping" up the structural matrix that gives joint cartilage low friction and shock absorption characteristics. In tendons, a pliable glue/ground substance that has a protein spewed out by tendon cells that attracts water is not good - it causes the tendon to thicken - the ground susbtance thickens and the cable-like collagen fibres get pushed apart, losing connection with other and structural strength. The water that is attracted by aggrecans is not inflammatory fluid, just fluid. It doesn't have inflammatory cells in it. When the tendon suffers an acute overload and the tendon cells spew out aggrecans, the tendon thickens. The goal is to stop them spewing out aggrecans as soon as possible. There are some known substances that inhibit the tendon cells (known as tenocytes) from spewing out aggrecans - they are called tenocyte inhibitors and include three main ones - ibuprofen, green tea and doxycyclin. I think indocid might be another tenocyte inhibitor - I'd have to check that. These substances are primarily used for for other purposes, but interestingly they also inhibit tenocytes. So, ibuprofen is an anti-flammatory that works on tendon cells for a reason not related to inflammation. Green tea inhibits tendon cells from spewing aggrecans in a way that is unrelated to why most people drink green tea. I'm not sure if it's an anti-oxidant process or not. Doxycycline is an anti-biotic but it has an effect on tendon cells like the other two.
The window of opportunity for these three substances to effect the tenocyte is very small - as soon as you have an overload and notice tendon starting to thicken/swell, that's when you have to act. After it's already thickened it's too late. Interestingly, those who've taken these (especially green tea) after the tendon has already thickened tend to get good pain relief anyway so there's clearly some as yet unclear effect of it.
Now, we trust the body to re-model that tendon after the tenocyte has dumped aggrecans into its ground substance and pushed those collagen fibres apart. We trust it to do it, but it needs to happen under a minimum of good conditions. These conditions include not continuing to overload it and cause the tenocytes to keep spewing, and then applying some load to stimulate the collagen fibres to line back up straight. Tendons don't like being unloaded more than a couple of days - they need stimulus to remodel properly.
Now, there's another couple of points of consideration. Sometimes the ability of the tendon to remodel is limited, the damage is done. It can repair up to a point and will tolerate load up to a point. This can be helped by having foot joints that are supple and having a tib post muscle that is very strong.
The other point is that sometimes the tendon is less of a problem than the sheath that surrounds it - it can get irritated, by rubbing against bone and other tissues as the foot/ankle collapses. The irritation can cause the inner lining of the sheath (synovium) to react - this is what leads to sheath inflammation. So, you can have inflammation in the sheath (with inflammatory cells and fluid) and reactive processes inside the tendon itself with fluid that is not inflammatory. In the very early period after acute overload (first 1-2 days) an anti-inflammatory like ibuprofen might work on both the sheath and tendon. After a couple of days, the ibuprofen won't work on the tendon but might work on the sheath. Sheath inflammation is called tenosynovitis. Green tea can work on the tendon early on, and often after the damage is done - in the experience of my clients. A key element is revealing contributing factors - foot/ankle joint mobility dysfunction, tib post strength, and recognition of current state of reactivity of tendon and sheath, and subsequently load tolerance of the whole lower limb.
Why the dead bug bugs me.
There are exercises that have a use and become useless or less useful. It always depends - what did your evaluation reveal (screen, test or assess).
Here's why the dead bug bugs me.
The dead bug trains static stability of the trunk with other body parts moving. That might be necessary in individuals with motor control dysfunction in lumbo-pelvic control who need rudimentary static control... But wait....
Many individuals who have lumbo-pelvic dysfunction in the pillar (trunk-hips-shoulders) have unrecognised mobility problems, or pain, that negatively influence motor control - so, the motor control dysfunction is secondary in priority to revealing the presence, or not, of minimum mobility of the lower quarter, trunk and upper quarter, or pain.
For example, an individual whose Modified Thomas Test is positive, or whose FABER test is positive, is one who has demonstrable lower quarter mobility dysfunction - an inability to demonstrate minimum levels of hip extension, hip external rotation and/or sacroiliac/lumbar dysfunction of an as yet non-specific diagnoses. Or an individual who has dysfunctional lumbar-lock thoracic extension/rotation is one for whom further biomechanical testing is required to understand why the trunk is not behaving to minimum acceptable levels.
So, to take a person who has not enough thoracic extension/rotation, hip extension, external rotation and possible lumbo-sacral mobility dysfunction and train them to repetitively activate hip flexors is not to address the primary dysfunction - for when the individual who performs static trunk stability correctly, in supine, with repetitive hip flexion and shoulder movement within a tolerable range, then stands up and is required to use hip extension that they do not have, or hip external rotation that they do not have, in weightbearing, the lumbosacral spine will no longer retain static stability and the exercise will not have transfer....simply because the body will give up stability when it has limited mobility above or below the area of stability.
For that reason, diagnosing pain, mobility and motor control is priority. Then getting a referral for local biomechanical examination and understanding of whether the pain is nociceptive, chemical, central or neuropathic; understanding what movement directions do not have enough mobility - such as lower quarter extension/ER; or thoracic extension/rotation, then improving those and finally retraining the body how to access the new found mobility, which may THEN involve static trunk stability with limb movements.
Where the dead bug falls down, traditionally, as an exercise at THAT point, is that it biases hip flexion activity and not hip extension motor control. The number of individuals with undiagnosed thoracic and hip extension mobility dysfunction, ie below minimum levels of mobility, who are repeatedly activating hip flexion and wondering why they still don't have hip extension is astounding. That's because evaluation reveals what is necessary....the diagnosis before the intervention.
So, a better version is a mobility drill for thoracic extension/rotation, or for hip extension, followed by a motor control for hip extension and/or thoracic extension/rotation - such as prone to supine rolling, quadruped diagonals, half-kneeling lifting, or at lower levels still - the leg-lock bridge, or a core-activated single leg bridge, or if you want to do a dead bug, the lowering leg must finish the movement by actively extending all the way to neutral, and even to 10 degrees or more of hip extension - so a dead bug (if you must), to short-leg or straight-leg bridge.
Assess, don't guess. Don't give people your favourite exercise, give them what objective assessment reveals they need.
The sport of volleyball has a very high bias towards postures and activities that are associated with anterior tilt of the scapula, with or without protraction. This position is a rotator cuff killer. For example, the receiving pass position, the “pancake” (a protracted pass/dig with one hand).
Altered pitching patterns where early trunk rotation at foot contact has been seen to increase load on the shoulder (Sueyoshi et al, Aguinaldo et al, 2007). Further, delayed peak pelvic rotation and early upper torso rotation can lead to increased shoulder external rotation range (Oyama et al, 2014).
Many throws in handball are done similar to the ratchet-style hits of volleyball - where deceleration does not cross the midline and heavily biases the glenohumeral joint - this predisposes to local stress instead of shared stress.
Reduced total glenohumeral rotation has been identified as a risk factor among elite male handball players. (Clarsen et al, 2014).
Clarsen, B., Bahr, R., Andersson, S. H., Munk, R., & Myklebust, G. (2014). Reduced glenohumeral rotation, external rotation weakness and scapular dyskinesis are risk factors for shoulder injuries among elite male handball players: a prospective cohort study. Br J Sports Med, 48(17), 1327.
Tennis is an asymmetric sport with specific muscle-activation patterns, especially eccentrically in the supraspinatus, infraspinatus, and teres minor during the complex and rapid serving motion. In particular, the external rotators are highly loaded eccentrically during the deceleration phase by resisting shoulder internal rotation first, then sharing the deceleration of horizontal adduction at the glenohumeral joint with the rest of the body. A high percentage of athletes will have infraspinatus atrophy without apparent clinical significance. The external rotation strength deficits, whilst apparently not affecting tennis performance, has been reported as a risk factor for shoulder pain (Clarsen et al, 2014).
Clarsen, B., Bahr, R., Andersson, S. H., Munk, R., & Myklebust, G. (2014). Reduced glenohumeral rotation, external rotation weakness and scapular dyskinesis are risk factors for shoulder injuries among elite male handball players: a prospective cohort study. Br J Sports Med, 48(17), 1327. bjsm.bmj.com/content/48/17/1327.abstract
Our current and future generations are losing the ability to think without technology. There's a generalisation - I hate generalisations (I also understand the contradiction I just made). It seems if you want to begin a discussion, you need to start with a generalisation, then say it depends, of course. So, Our current and future generations are losing the ability to think without technology, except the ones who aren't. I'm seeing fewer of those in some parts of the world and more in others.
Let me give you an example: A young girl is at a boarding school. She must hand in her phone each night. She's caught with a second phone. The process of removing the second phone leaves her distraught. She's had a phone since she was six years old. Without a phone, literally, her brain works differently in a way she has anxiety about. What is her life experience without her phone? What language must she now use to communicate to the outside world if not in characters expressed through her fingertips? What are her memories that provide her with context about past decisions, or the development of values, attitudes and value of time? What is her ancestral program of beliefs if not those given her by her phone and internet connection?
Since our outputs are the sum of processing of our inputs, what will her outputs be like when she can not rely on her phone and internet connection to process? How will she handle inputs from a sensory world that isn't restricted to that coming from her phone?
I've come across many remarkable children in the current generation who stand out because they can....wait for it....look at you, smile, hold a conversation, listen and consider and reply accordingly. I would have thought that was a relatively normal occurrence in previous generations. I've come across exceptional clinicians and coaches with the same competency to think critically - it's exciting. And then there are those reliant on decision making based on what they can glean after referencing their phone...Trump-like.
I'm wondering whether there'll be a correlation with devolution of human intelligence as a stand-alone from technology, an evolution of human intelligence inseparable from technology or a revolution to excel with human critical thinking to make best use of technology. If you're in a position of service to a young generation - what are we up to, these days, Generation Alpha? - then think of this... who amongst them operates amongst others without their technology, and if you spot them, don't they stand out? Do you see how ridiculous that is? That standing up on your own two brains is the new standing out?
In Roman times, the populace was contained with entertainment in the great Colosseum. Since then, sport does the same. Be not a slave to it, though. The easier way to suppress critical thinking is to provide entertainment to the masses instantaneously, or drama, to have them unable to function properly until their next fix.....think gambling advertisement, Married At First Sight advertisements, The Bachelor advertisements....that is the de-volution of human intelligence as a stand-alone from technology and standards of critical thinking.
The teaching of courses in some parts of the world are challenging because without phones, students are unable to function. They take less in while recording on their phone (in case they ever want to watch or listen later, which they never do). If you insist that phones are put away, anxiety sets in and they take less in. And then we are back to the concept of education - from the latin, to educe, to bring out. It has been said by many, "Tell me and I'll forget. Show me and I may remember. Involve me and I learn."
Technology can involve people, no doubt. It is indeed telling and showing. I wonder, like anything, whether it can take over ones ability to think for yourself, to experience the great physical world we live in and I'm sure as hell it can't help you speak to someone in a normal way - 90% of the impression someone has of you occurs with your first words. It shouldn't be, "ok, google".
The "she'll be right" attitude that is necessary in survival circumstances does not belong in the first 6 weeks after joint injury. Let's get science-y on you. Fancy losing your cartilage FOREVER after a joint swelling when you ignore sound clinical care and guidelines? If you don't value your cartilage, ignore the following advice.
Here's the gist:
Should a person have a swelling in a joint, it is expected that the joint cartilage will NOT tolerate the same load as that experienced when they got injured, for at least 6 weeks. IF.....IF the person has another swelling, be very very careful, because if you have a 3rd setback within 6 weeks, expect an irreversible loss of articular cartilage. That's right - you will never again get joint cartilage to repair. Now you're set for osteoarthritis,
Pivotal research in rabbit articular cartilage has shown that synovitis induces a 20% loss of proteoglycans within 24 hours, and 30-60% within 5-7 days (Lowther and Gillard, 1976). The chondrocytes replaced the proteoglycans within 42 days, unless visible erosion was present and unless two repeat stimulus-led inflammations occurred, at which point chondrocytes were seen to be dead (Carmichael et al, 1977), visible erosion exists (Gillard and Lowther, 1976) and unable to replace lost proteoglycans (Lowther and Gillard, 1976; Carmichael et al, 1977). This is accompanied by a general decrease in metabolism in articular cartilage following an inflammatory response (Byers et al, 1985).
Lowther, D. A., & Gillard, G. C. (1976). Carrageenin-induced arthritis. I. The effect of intraarticular carrageenin on the chemical composition of articular cartilage. Arthritis Rheum, 19(4), 769-776.
Carmichael, D. J., Gillard, G. C., Lowther, D. A., Handley, C. J., & Santer, V. B. (1977). Carrageenin-induced arthritis. IV. Rate changes in cartilage matrix proteoglycan synthesis. Arthritis Rheum, 20(3), 834-840.
Gillard, G. C., & Lowther, D. A. (1976). Carrageenin-induced arthritis. II. Effect of intraarticular injection of carrageenin on the synthesis of proteoglycan in articular cartilage. Arthritis Rheum, 19(5), 918-922.
Byers, S., Handley, C. J., Lowther, D. A., & Sriratana, A. (1985). Carrageenin-induced arthritis. VI. Alterations in amino acid transport by articular cartilage in acute inflammatory arthritis. Ann Rheum Dis, 44(7), 477-484.
"significantly increased sustained attention"
"significantly lower cortisol level after training"
"significant decrease in negative affect after intervention"
Those are the summarised findings of an eight-week training program of diaphragmatic breathing, where participants were taught to breathe at 4 breaths/minute. Quite a drop from the typical adult who breathes at 12 breaths/minute.
Here's a link to the article.
And to kick start you to learn diaphragmatic breathing, try this facilitated breathing and facilitated breathing 2.
And here is Gray Cook's take on breathing.
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