Introduction to Measuring Flexibility Transcript

Introduction & Learning Objectives

In this lesson we start to look at the process of measuring flexibility. Knowing how to measure
flexibility accurately is an important part of a flexibility coach’s role because it is the main way that we
can tell if the programme we gave to the client is actually working or if they are just wasting their time
and energy. The aim of this course is to make you a great flexibility coach, and that means teaching
you how to write programmes that are effective and efficient. Effective means they work and efficient
means they work with the least expense of time and energy. Therefore, by the end of this lesson, you
will know how total range of motion is divided into different components. You will know the difference
between active and passive insufficiency. You will know how arthrokinematic motions affect flexibility,
including why range of motion is not a great way to diagnose hypermobility. You will know the
different types of end-feel and what they mean, as well as how to recognise capsular and non-
capsular patterns of restriction. And finally, you will learn about different devices that are used to
measure flexibility.

Components of Range of Motion

You learned very early on in the course that flexibility and range of motion are not exactly the same
thing. Flexibility is the motor ability that determines the capacity of your joints to change position, and
range of motion is the way we primarily measure a change in position. However, for all intents and
purposes, we tend to say that flexibility is range of motion. Researchers and physicians have been
using range of motion to quantify joint flexibility for at least one hundred years. For example, Hoffman
1905 wrote about range of motion differences between people who were barefoot and people who
wore shoes. These days it is common practice to measure range of motion using a goniometer, which
is a type of handheld tool designed to accurately measure angles. We will look at other tools which
can be used, but the earliest incarnations of goniometers date back to the 16th century. But
goniometers have not always been used, and there has been much debate about whether using a
handheld instrument or just using visual approximation is more accurate for quantifying joint angles.
One of the first authors to make the claim that using sight is as accurate as a goniometer was
Cleveland in 1918, and Rowe 1964 wrote that visually estimating joint angle is as good as, if not better
than, using a goniometer, and it is especially useful when common bony landmarks are difficult to spot
or palpate, such as when large amount of muscles or adipose tissue are present. The way a
goniometer works is that an examiner will look or feel for parts of the skeleton that are common to
everyone, such as the anterior superior iliac spine or ASIS at the front of the pelvis, or the greater
trochanter on the outside of the upper thigh, and the examiner will use those as a guide to try and
make the joint angle assessment as accurate and as objective as possible. However, other authors,
such as Moore 1949 and Salter 1955 reported that using a goniometer is more reliable than guessing
by sight. Rose and colleagues 2002 wrote that, although visual accuracy improves with experience, it
is still an inaccurate technique and they therefore recommended that goniometers should be used for
measuring angles. In 2019, Lang and Milosavljevic found that the accuracy of visual estimation varied
depending upon the plane of motion, for example, shoulder extension was underestimated while
shoulder internal rotation was overestimated, and they reported that using visual estimation to
evaluate shoulder movements resulted in a wide range of error, and therefore more objective
measures should be used. The question has been raised about whether it is the tool itself or the
person using the tool which lacks reliability. We refer to these as inter-rater reliability and intra-rater
reliability. Remember, reliability is about how consistent a test is at measuring a particular thing. The
word “rater” refers to the person doing the test. Inter-rater reliability is about how consistently a test
can be performed by different raters, i.e., by different people. Intra-rater reliability is about how
consistently a test can be performed by one rater, i.e., the same person doing the test again and
again. In a 2001 study by Hayes and colleagues, the authors reported that little difference existed
between visual inspection and using a goniometer, and that the people who performed the tests were
not very accurate, regardless of whether they used their eyes or a goniometer. Based upon that
article, it would seem that the reliability of measuring joint angle depends more upon the person than
the method being used. However, in a systematic review by Van de Pol and colleagues in 2010, the
authors reported that, in general, measuring range of motion using instruments, be that goniometers

© Flexibility Research Ltd. All rights reserved.

or inclinometers, results in higher reliability than using vision. Overall, the current body of research
suggests that instrument-assisted measurement is more objective than visual examination, and so that
is the stance that this course will take. You will often see in the literature that researchers will measure
two components of total range of motion, 1) joint range of motion and 2) muscle length. Joint range of
motion is, of course, the motion available at any single joint, and it is primarily influenced the structure
of bones and the geometry of joints, as well as the physiological characteristics of the connective
tissues which surround the joint and make up the capsule. A human joint can be described in basic
terms as the point at which two bones meet, and there is typically a gap or a space between the ends
of the bones. We call this the joint cavity. It is the joint cavity that allows the articular surfaces, or the
ends of the bones covered in articular cartilage, to move relative to one another. If that space or that
cavity did not exist, the joint could not move. Conditions in which joint space narrowing occurs, such
as osteoarthritis, where this gap between the ends of the bones gets smaller, is often accompanied by
reductions in the joint’s ability to move. The joint capsule looks like a sac-like envelope which forms a
type of sleeve around a synovial joint, and it encloses the joint cavity. The capsule is made up of
dense, fibrous connective tissues that attach to the bones via specialised attachment zones at the end
of each involved bone. The capsule seals the joint space and provides passive stability by limiting
movements, it contributes to active stability via its proprioceptive nerve endings, and it may even form
part of the articular surfaces for the joint. The thickness of the capsule varies according to the stresses
which are placed on it, and it may also incorporate tendons at their attachment points, meaning that
muscles merge into tendons and tendons merge into the joint capsule. Believe it or not, there are
some authors who actually doubt the existence of the joint capsule as a defined structure, since they
argue that it should actually be regarded as a basketwork of the surrounding ligaments and tendons
that just appear to form a fibrous capsule around the joint space. If we go back to earlier in the course
when I said that nothing in the body is isolated and many of the divisions and separations that we give
names to are just there to aid in our understanding, then what those authors say makes sense.
However, it is easier to think about the joint capsule as being separate and so in this course we will
treat it as an individual structure separate from the muscle and its tendons, but always keep in the
back of your mind that everything is connected and everything is just part of everything else. We will
look at the joint capsule and its contributions to flexibility in more detail later in the course. The second
component of total range of motion that I mentioned was muscle length. According to White 2014
maximal muscle length is the greatest extensibility of a muscle-tendon unit. You will also see the
muscle-tendon unit described in the literature as the musculotendinous unit, or MTU, so that is just
something to be mindful of. Muscle length is the maximal distance that can be reached between the
proximal and distal attachment points of a muscle. How far a muscle can extend or lengthen will
dictate the amount of range of motion available to a given joint or series of joints to quite a large
degree. According to Gajdosik and colleagues 1993 and Gajdosik, in practical terms, muscle length is
not measured directly. Instead, it is measured indirectly by determining the maximal static passive
range of motion of the joint or joints which the muscle crosses. Remember however that even though
we say we are measuring muscle length, the range of motion at a joint is affected by the integrity of
the joint surfaces and the extensibility of the capsule tissues, the ligaments, fascia, and even the skin.
But if we test joint range of motion, whether we are using visual estimation or a handheld instrument
like a goniometer, why then do we need to test muscle length too? Well, the purpose of testing muscle
length is because doing so allows us to ascertain whether a lack of flexibility is caused by the length of
the inactive antagonist muscle or by some other structure. When we are able to get a better idea of
knowing which structures are involved, we are better able to choose more specific and more effective
exercises for training. Generally speaking, we can categorise muscles by the number of joints they
cross from their proximal to their distal attachments. An attachment is simply the thing that joins a
muscle to a bone. In most cases, the attachment will be a strip of connective tissue which we call a
tendon. However, it can sometimes be a sheet of connective tissue which we call an aponeurosis,
such as the thoracolumbar fascia in the low back. When muscles cross one joint and therefore
influence the motion of only one joint, we can them monoarticular muscles. Or “one joint muscles” if
you prefer. Two-joint muscles, as you probably guessed, cross and influence the motion of two joints.
We can also call those biarticular muscles if we want to be a bit more formal. Multi-joint muscles, as
the name suggests, cross and influence multiple joints. According to Kendall and colleagues 1993, for
one-joint muscles, range of motion and muscle length will measure the same. This means there will be
no difference between the length of a one-joint or monoarticular muscle and the measurement of joint
range of motion in the direction opposite to the muscle’s direction of shortening. If a one-joint muscle

© Flexibility Research Ltd. All rights reserved.

is shorter than normal, either because of neurological guarding owing to a heightened stretch reflex or
because the tissues are physically short, which we call mechanical tightness, then range of motion will
be decreased and the end-feel will be firm, owing to the muscle being stretched. I first talked about
end-feel in lesson 7.1 when we looked at the relationship between flexibility and sex, hormones, and
genetics. End-feel is generally how we measure the quality of mobility in a joint, i.e., the intra-articular
motions. I said there are three normal types of end-feel, 1) bony, 2) firm, and 3) soft. The second type,
firm end-feel, is caused by the stretch of the muscle and its associated connective tissue elements,
the epimysium, perimysium, and endomysium. Both the resistance you feel when you try to passively
move a joint to its limit of range of motion will be firm and the muscle itself will be firm to the touch
when you palpate it. This firmness is caused primarily by a rise in passive tension within the
connective tissue elements of muscle. Many trainers and therapists believe that during a passive
stretch, either a dynamic passive or static passive stretch, there is no muscle activation. This belief is
owing in part to a 2000 study by Fowles, Sale, and MacDougall which demonstrated no EMG activity
was seen during passive stretching, the implication being that there was no stretch reflex response.
However, it is important to remember that the nervous system is never completely silent, and that
includes during passive stretching. At some point along the muscle’s length during a passive stretch,
the stretch reflex will still occur, even if it is only by a small amount. The stretch reflex has two
components, a dynamic part and a static part. They are often considered to be two separate stretch
reflexes because they each have their own reflex arcs. Latash 2013 wrote that when muscle length is
short, it shows no signs of activation. A very slow stretch of the muscle will lead to a relatively small
increase in its force due to the elasticity of the peripheral tissues, which is the passive tension I was
talking about a few moments ago. At some point along the muscle’s length, the muscle will start to
show signs of activation. Continuing to stretch will lead to an increase in muscle force accompanied
by an increase in the level of activation. We call this mechanism which leads to changes in muscle
activation and force in response to a slow stretch the static stretch reflex, and in some corners of the
literature it is also called the tonic stretch reflex. It is very important to understand that the static
stretch reflex is an involuntary mechanism. You cannot stop it from occurring. So, if you are currently
thinking, “If the stretch reflex causes the muscles to activate at some point along their length, then it
can’t be a passive stretch,” understand that when we talk about active stretching, we are referring
primarily to voluntary activation, i.e., you are willingly contracting the muscles. It is also important to
remember that at some point along the muscle’s length, usually towards the outer limits of range of
motion, there will not be enough overlap between the sarcomeres, or the parts of the muscle that
contract, and so the muscle cannot physically contract even though it may still be receiving
instructions from the nervous system telling it to contract. So, active tension will eventually drop off.
This is one of the reasons why static passive flexibility will always be greater than dynamic active and
static active, because we can always stretch the tissues past the point at which the muscles can
activate. And at that point, the contribution to total tension in the muscle is entirely from the passive
tension that arises in the connective tissue elements. So, for all intents and purposes, despite a rise in
involuntary active tension at some point along the muscle’s length, we can still call the exercise a
passive stretch for 2 main reasons. 1) The amount of active tension will not be anywhere near the
same level of active tension that can be produced during a voluntary contraction, and 2) the stretch
will start as a passive stretch and, if the stretch is continued past the point at which the sarcomeres
can no longer contract, either voluntarily or involuntarily, it becomes a passive stretch again. Going
back to the subject of end-feel, a client might complain of pain in the region of the tight muscle and
tendon. The presence of a firm end-feel accompanied by pain where the muscle is tight is typically
used by clinicians to confirm muscle shortness as the cause of a joint’s movement limitation. If a one-
joint muscle is abnormally lax, meaning that it offers no passive resistance to stretch, then passive
tension in the joint capsule and ligaments may initially help to maintain normal range of motion.
However, over time, these structures often get lengthened as well, and overall passive range of
motion in the joint will increase. Because the indirect measurement of the length of one-joint muscles
is the same as the measurement of passive joint range of motion, there are not specific muscle length
tests for one-joint muscles. In contrast to one-joint muscles, the length of two-joint, or biarticular,
muscles, and multi-joint muscles, is not usually sufficient enough to allow full range of motion to occur
simultaneously at all joints crossed by these muscles. This inability of a muscle to lengthen and allow
simultaneous full range of motion at all of the joints it crosses is called passive insufficiency. In simple
terms, the muscle does not have enough length to fully extend across all joints at the same time. To
give you an example, consider the hamstrings. When the knee is fully extended, the hip has a harder
time flexing. Similarly, when the hip is fully flexed, the knee has a harder time extending. When the
hamstring group is short or tight, there is simply not enough length in it to permit both full hip flexion

© Flexibility Research Ltd. All rights reserved.

and knee extension at the same time. Another example that you can try for yourself right now is to flex
your wrist so that you bring the palm of your hand as close as possible to the anterior aspect of your
forearm. Now watch what happens when you try to make a tight fist with that hand. If you have normal
tissue extensibility in the wrist extensors on the posterior aspect of the forearm, then one of two things
is likely to happen. 1) You cannot make a properly tight fist, or 2) you have to flex your wrist slightly to
move your hand away from the anterior aspect of your forearm to be able to make the fist. This is
because there is usually not enough length in the wrist and finger extensors to be able to make a fist
while the wrist is in full anatomical flexion. Now, if you had thought that there might also such a thing
as active insufficiency, then you would be correct. When a two-joint or multi-joint muscle shortens
over two or more joints at the same time, then there is not enough overlap between the sarcomeres to
create sufficient tension. In other words, the muscle is shortened and there is so much slack that the
myofilaments, or the actin and myosin proteins, run out of binding sites and so they cannot contract
enough to create tension. For a sarcomere to contract, it has to shorten. But it cannot shorten if it is
already maximally shortened. So, if we go back to the wrist example, if you flex your wrist so that the
wrist flexors on the anterior aspect of the forearm are already shortened, you will see that when you
try to make a fist, you have relatively little grip strength in that position compared to when your wrist is
in a neutral position, because when your wrist is flexed, the muscle which are responsible for
clenching your fist were already in a shortened position. So, that is passive and active insufficiency.
Now, something else which I need to talk about here is that people often use the terms active
insufficiency and passive insufficiency incorrectly, at least according to how those terms were
originally defined. The original usage of those terms was as I just explained to you, active
insufficiency is when a biarticular or multi-joint muscle shortens over all of its joints at the same time
and there is so much slack that it cannot effectively contract to produce tension, and passive
insufficiency is when a biarticular or multi-joint muscle lengthens over all of its joints at the same time
and there is not enough length to permit full range of motion to be displayed at all of those joints
simultaneously. However, often, especially in the health and fitness industry and on social media,
people will use the term active insufficiency to describe a lack of strength in the agonists and they will
use the term passive insufficiency to describe a lack of extensibility in the antagonists. While true
active insufficiency is caused by an inability of the muscle to contract and produce force, it is not
necessarily because of a lack of strength. It is simply a characteristic of human anatomy and the
placement of its attachment sites relative to its length. Similarly, people use the term passive
insufficiency to describe an inability of muscles to lengthen in all types of muscles, including
monoarticular or one-joint muscles, when in reality, the term passive insufficiency is reserved only for
two-joint or multi-joint muscles. Again, passive insufficiency, like active insufficiency, is an anatomical
characteristic more so than a physiological one. It would be more accurate to use terms like strength
insufficiency and extensibility insufficiency to describe what most people are talking about in the
health and fitness industry. Remember, true active insufficiency is caused by the muscle being in a
shortened position rather than true physiological weakness. And true passive insufficiency is caused
by the muscle being in a lengthened position rather than true physiological tightness. Now, with
training, we can improve both active insufficiency and passive insufficiency. When we perform
strengthening exercises in either a shortened or lengthened position, as we do in agonist and
antagonist static active stretching respectively, we can change the active length-tension relationship
so that the curve extends in both directions as you see on screen. When the curve extends to the left,
or it experiences what is often described in the literature as a left-shift, we improve our ability to exert
strength in a shortened position. When that happens, we tend to see things like cramping and spasm
disappear, which are common features of contracting a muscle in a very shortened position especially
amongst beginner trainees. When the curve extends to the right, or it experiences what we call a
right-shift, we improve our ability to exert strength in a lengthened position. That happens because of
a concomitant increase in tissue length, i.e., sarcomerogenesis, which is the laying down of new
sarcomeres or contractile units in a longitudinal direction. That helps to address a lot of the
extensibility issues that people will experience. In one-joint muscles, the lack of extensibility, or what
people erroneously call passive insufficiency, is not caused by the muscle already being in a
lengthened position, it’s usually caused by neurological tightness. The nervous system is stopping
you from fully extending that muscle via the stretch reflex, either because you lack experience in that
position, or you experienced a previous injury to those tissues and the nervous system is trying to
protect you, etc. You have enough physical length in the muscle. If we were to anaesthetise you and
therefore bypass the nervous system, we would be able to extend that muscle to its full length. But
when you are awake, you have to spend time in that position by stretching. When you stretch, you
improve your tolerance to the discomfort of stretching and it doesn’t hurt as much, and you
recondition the stretch reflex to fire later and later into the range of motion. In essence, you convince

© Flexibility Research Ltd. All rights reserved.

the nervous system that the new range of motion is not a danger and so it does not need to protect
the muscle so aggressively. In addition to neurological tightness, there may also be genuine
mechanical shortening of the tissues, where the tissues have gotten physically shorter, usually
through immobilisation after injury or because of sedentary lifestyle habits. Now, it may be that a two-
joint muscle may not be in a fully shortened position but it still struggles to exert enough force to move
all of the joints. For example, you take your hip partially into flexion, so the rectus femoris is now in a
partially-shortened position, and then you try to extend your knee, but you struggle to do so because
you lack strength. What then are we dealing with? Are we dealing with active insufficiency or a lack of
strength? In truth, it’s probably a bit of both. What term should we use, then? The terms that I prefer
to use which covers both active and passive insufficiency as they were originally intended to be used
in reference to two-joint or multi-joint muscles, and which covers a lack of strength and a lack of
extensibility in one-joint muscles, is agonist insufficiency and antagonist insufficiency. So, in the
example of flexing your hip part of the way, and then extending your knee, in which you are
demonstrating both active insufficiency and strength insufficiency, we can simply use the term agonist
insufficiency and cover all the bases. The same applies to antagonist insufficiency. Whether the
inability of a muscle to lengthen is because it is a two-joint muscle demonstrating passive insufficiency
in the original definition of that phrase, or because there is neurological or mechanical tightness, we
can cover all of those things by calling it antagonist insufficiency. Remember, agonists are the
muscles which shorten and which are usually primarily responsible for moving the joint, and the
antagonists are the muscles which lengthen. When we use the terms agonist insufficiency and
antagonist insufficiency, we are using simpler terms to address all of the things that might be limiting
motion or the generation of force in a given position. When a muscle is displaying agonist
insufficiency, it cannot contract to produce force, either because it is already in a shortened position
and/or because it is weak. When a muscle is displaying antagonist insufficiency, it cannot lengthen
and thus limits range of motion, either because it is already in a lengthened position or because there
is so neurological or mechanical issue limiting extensibility of the tissues. And we can use this
understanding of agonist and antagonist insufficiency to come up with better ways for assessing
range of motion. For example, if a two-joint or multi-joint muscle crosses a joint that you want to
examine for range of motion, then the client must be positioned so that the antagonist does not limit
the joint’s range of motion. To allow full range of motion at the joint you are trying to examine and to
ensure sufficient length in the muscle, the muscle must be put on slack at all of the joints the muscle
crosses which are not being assessed. We can take the triceps as an example, which is a two-joint
muscle that extends the elbow and shoulder. The triceps displays antagonist insufficiency during full
shoulder flexion and full elbow flexion. When you assess elbow flexion range of motion, you need to
put the shoulder in a neutral position so that there is sufficient length in the triceps to allow full flexion
at the elbow. If you want to assess the length of a two-joint muscle, you need to position the client so
that the muscle is lengthened over the proximal and distal joints that the muscle crosses. One joint is
held in a full range of motion position while attempts are made to further lengthen the muscle by
moving the second joint through its full range of motion. If we take the triceps as an example, we
would start with the arm in a neutral position, we would then move the elbow through its full flexion
range of motion, and then we would flex the shoulder through its full range of motion. The end-feel
you should feel in this situation would be firm, owing to the development of passive tension in the
stretched muscle, i.e., the triceps. The length of a two-joint muscle is indirectly assessed by
measuring the static passive range of motion in the direction opposition to the muscle’s action at the
second joint. In this example, the length of the triceps is indirectly assessed by measuring the static
passive range of motion of the shoulder in the direction of flexion. The length of a multi-joint muscle is
assessed in a similar manner to the way we assess the length of two-joint muscles. However, the
client is positioned in such a way so that the muscle is lengthened over all of the joints that the muscle
crosses, except for one last joint. You would then attempt to further lengthen the muscle by moving
that last joint through its full range of motion. Again, just like for two-joint muscles, the end-feel should
be firm because of the passive tension which has built up in the stretched muscle. An example of a
multi-joint muscle test is the Thomas Test, which involves muscles that cross the vertebrae in the
spine, the hip joint, and the knee joint. You will be shown how to perform the Thomas Test and other
ways to measure range of motion and muscle length as the course progresses. I said in previous
lessons that there really is no such thing as normal range of motion, just averages taken from a
sample of the population. However, in the literature, these averages are called normative values,
which is a bit misleading in my opinion, because it can fool people into thinking that there exists a so-
called normal level of range of motion that we must possess at each joint, and if we don’t have it, then
we are somehow dysfunctional, which is not true at all. But, the normative values on joint angles at

© Flexibility Research Ltd. All rights reserved.

the end of each muscle length test, as well as information on the reliability and validity of each test,
will be given to you when you are shown how to do each test.

Arthrokinematics

Motion at a joint occurs because one joint surface moves relative to another joint surface. I have said
in previous lessons that the word we use to describe such motions is arthrokinematics. The arthro
comes from the Greek arthron, meaning a joint. The word kinematics comes from physics and it is
used to describe the motion of an object without regard to the forces that cause motion.
Arthrokinematics are the internal movements that occur inside the joint capsule. We cannot see, feel,
or control them ourselves. They are completely passive. They are also called accessory motions or
relative motions. The movements we can see, feel and control ourselves are referred to as
osteokinematics. The word osteo comes from the Greek osteon meaning bone. So, osteokinematics
are the movements we create with the shafts of bones that protrude out from the joints. Although
motion occurs around the axis which we call a joint, in truth, it is the osteokinematic motions which we
measure during assessment of range of motion, so measuring flexibility is actually a measurement of
osteokinematic motion. Osteokinematics are also sometimes called physiological movements or real
movements because they are the tangible movements we can control and see. Although we will
mostly be interested in osteokinematics during flexibility assessment and training, for now we are
going to focus our attention on arthrokinematics, because if there is a fault with the internal mechanics
of the joint then the ostoekinematic movements will also be affected. We have to know how to address
arthrokinematic issues if they exist, but before we can do that, we first need to understand exactly
what are arthrokinematics. When we are talking about the human body, kinematics describes the
motion of bones including the type, direction, and magnitude of motion, the location of the bone in
three-dimensional space, and the rate of change or the velocity of the bone. A bone will do one of
three types of movement. 1) Translation, which is also called linear displacement. 2) Rotation, which is
also referred to as angular displacement. And 3) a combination of translation and rotation, which tends
to occur most often. In translation, or translatory motion, all points on the bone move in the same
direction at the same time. In rotation, or rotary motion, the bone spins around a fixed point. When we
are talking about the movements of joint surfaces, i.e., arthrokinematics, there are three types of
movement which can occur. They are called glides, spins, and rolls. Sometimes you will see a
movement called a slide, but it is exactly the same thing as a glide. So, the words glide and slide are
used interchangeably and which one you decide to use is entirely up to you. A glide is a translatory
motion, and it involves the gliding, or sliding, of one joint surface over another, like when a braked
wheel skids on ice. A spin is a rotary motion, just like the spinning top from Inception. All points on the
moving joint surface rotate around a fixed axis of motion. A roll is also a rotary motion, which is similar
to the rolling of the bottom of a rocking chair on the floor or the rolling of a tyre on the road. In the
image on screen, you can also see how all three movements are represented by the actions of a car
tyre. In the human body, glides, spins, and rolls usually occur in a combination with one another and
result in angular movements of the shafts of the bones. According to Kisner and Colby 2007, the
combination of gliding and rolling is often referred to as roll-gliding, or sometimes roll-sliding, and it
allows for increased motion at the joint by postponing the joint compression and separation that would
occur at either side of the joint during a pure roll. The direction of the rolling and gliding components
of a roll-glide will vary depending upon the shape of the moving joint surface. The articular surfaces of
joints tend to be either concave or convex. The simplest way to remember the difference is that a
cave goes inwards in a mountain, and so a concave surface bends inwards. Convex is simply the
opposite, the surface bends outwards. An example is the hip joint. The acetabulum, or hip socket, is
the concave surface because it bends or curves inwards. The head of the femur is the convex surface
because it bends or curves outwards. These two surfaces come together to form the familiar ball-and-
socket joint, which is more formally known as the coxo-femoral joint. If a concave joint surface is
moving, the concave surface will roll and slide in the same direction as the angular motion of the shaft
of the bone. If we continue to use the hip joint as an example, if the femur remains stationary and the
pelvis moves, the acetabulum will slide in the same direction as the angular motion of the pelvis. If a
convex surface is moving, the convex surface will roll in the same direction as the shaft of the bone
but it will glide in the opposite direction. Again, looking at the hip, if the femur rotates towards the
plane of abduction, towards the outside of the body, then the joint surface, in this case the head of the
femur, will glide or slide in the opposite direction, towards the median plane, which divides the body

© Flexibility Research Ltd. All rights reserved.

into left and right halves. Arthrokinematic motions are what most authors are referring to when they
utilise the term joint mobility. This is why techniques which are designed to improve the
arthrokinematics of a joint are called mobilisations. When we talk about hypermobility, especially in the
absence of connective tissue disorders, we are discussing shapes of bones and structures of joints
that permit a large amplitude of arthrokinematic motion, which in turn facilitates a larger than average
amplitude of physiological or osteokinematic motion. However, for the sake of clarity, I will try to avoid
using the term “joint mobility” throughout this course, and I will instead reserve the word mobility for
discussions of moving with a mobile base of support. According to White 2014, we can examine
arthrokinematic motions to check for the amount of movement, tissue resistance at the end of the
motion, and the effect on a person’s symptoms if they have any. The ranges of arthrokinematic motion
are very small and they cannot be measured with a goniometer or a ruler. Instead, arthrokinematic
motions are subjectively compared with the same motion on the contralateral side of the body.
Contralateral just means the opposite side of the body. So, you would test the affected joint on one
side of the body, then you would compare it to the unaffected joint on the opposite side of the body. If
you have some experience doing joint play assessments, then you can compare the arthrokinematic
motion with how it felt to test people of a similar age and sex as the person you are currently testing.
According to Kaltenborn 1999, we can use an ordinal grading scale that goes from 0 to 6, as you can
see on screen, and we use these to assign a description depending upon the amount of
arthrokinematic motion present. As I said earlier, arthrokinematic motions are also called accessory or
joint play motions. When there is absolutely zero play within the joint, meaning it does not move at all,
then we assign it a grade of zero and we say that the status of the joint is ankylosed. According to
Wharton and Morgan 1970, an ankylosed joint, often referred to as just ankylosis, is an abnormally stiff
joint which is often caused by some kind of pathology, such as arthritis-related inflammation and
narrowing of the joint space, or the deposition of fibrotic tissues in the joint capsule, or bursitis, etc.
When there is barely any movement, we assign it a grade of 1 and we say there is considerably
hypomobility present. Again, the term mobility in the context of joints is used most often to describe
these passive, accessory, internal joint motions. As you probably guessed, since a hypermobile joint is
one in which there is a large amount of joint play, a hypomobile joint is one in which there is not much
joint play at all. In hypomobility, range of motion is restricted and the end-feel occurs early in the
range of motion and may be different in quality to what would normally be expected. The limitation can
be caused by a number of issues, including abnormalities in the joint surfaces, shortening of the joint
capsules, ligaments, muscles, fascia, or skin, and inflammation in any of these structures. According to
Steultjens and colleagues 2000, hypomobility in healthy joints is rare, and it is commonly associated
with orthopaedic conditions like osteoarthritis, spine disorders, and according to Rao and colleagues
2006 and Sauseng and colleagues 2002, in metabolic disorders like diabetes. Decreased joint play,
and subsequently decreased flexibility, is also a common consequence of immobilising a joint after
fracture and scar development after burns. Neurological conditions such as stroke, head trauma,
cerebral palsy, and complex regional pain syndrome, or CRPS, which is a condition that I am currently
living with, can result in hypomobility owing to loss of voluntary movement, increased muscle tone,
immobilisation, and pain. If there is only slight hypomobility or loss of normal joint play, we assign a
grade of 2 and we say that slight hypomobility is present. If the joint feels normal, we give it a grade of
3 and we say there is normal joint play. If there is slightly more joint play than we would expect, we
give it a grade of 4 and we say there is sight hypermobility present. I discussed hypermobility at length
in the lesson on sex, hormones, and genetics, so I am not going to get into it too much here, but I will
talk about it briefly just as a bit of a refresher for you. Hypermobility is often considered to be the
ability to move one or more joints actively or passively beyond so-called normal limits given the
person’s age and biological sex. You might be thinking that this sounds a lot like being flexible.
Flexibility is just the range of motion at any given joint. A joint can have low flexibility or high flexibility.
All flexible people are not hypermobile but all hypermobile people are flexible. The difference between
flexibility and hypermobility is that hypermobility is caused by a shape and structure of joints which
allows for a lot of joint play, and when there is more joint play, i.e., more passive, accessory motion,
then there will be greater osteokinematic or physiological motion. Hypermobility is also caused by the
laxity of soft tissue structures such as ligaments, capsules, and muscles that would otherwise normally
prevent excessive motion at a joint. I have talked previously about how the first stage in diagnosing
hypermobility is the Beighton Hypermobility Score, which is also called the Beighton score and the
Beighton criteria, and this table on screen was adapted from Beighton and colleagues 1973. Again,
there are significant issues with the Beighton score because it does not measure all joints in the body.

© Flexibility Research Ltd. All rights reserved.

A person could have hypermobile joints in the cervical spine which have considerable joint play and
therefore permit an abnormally large range of motion, yet they would not be considered hypermobile
because the Beighton score does not check for that. We also looked at elbow hyperextension in the
lesson on sex, hormones, and genetics, and how the presence of a supratrochlear foramen in females
can permit a larger than normal range of motion. Although it is the structure of the surrounding bones
which is permitting a large range of motion, the intrinsic mechanics of the elbow joint and the laxity of
the capsule, ligaments, and so forth, could all be relatively normal, meaning that there is normal joint
play in the joint itself and therefore we would not necessarily classify it as a hypermobile joint.
Furthermore, being able to place the palms on the floor by flexing the trunk and keeping the knees
straight should not be used to diagnose hypermobility because a person with average joint structure
and average tissue stiffness can achieve that position quite easily just with rational training. There are
ample examples on social media of people being able to do a forward fold, also called a pike in the
gymnastics and callisthenics communities, because they did such things as Romanian deadlifts,
Jefferson curls, and isometric stretches, yet if we tested their joints, they would have normal joint play,
and so they would not be considered hypermobile. There have been recommendations over the years
to update and amend the Beighton score. For example, Grahame 2001 recommended that we should
also be considering measurement of shoulder external rotation greater than 90°, cervical spine flexion
greater than 60°, and distal interphalangeal joint hyperextension, i.e., the third knuckle of the fingers,
greater than 60°, among others. A 2013 systematic review and meta-analysis by Smith and colleagues
also recommended that we should include tests of proprioception when screening for hypermobility
because people with hypermobility syndromes have significantly poor joint position sense compared
to non-hypermobile people. Why do they have poor joint position sense? Hypermobile joints are more
susceptible to abnormal postures and therefore abnormal weight-bearing on the articular surfaces,
which leads to what is called chondral damage. The word chondro refers to cartilage. So,
hypermobility can lead to damage of articular cartilage. Articular cartilage is a highly specialised
connective tissue that covers the ends of the long bones of load bearing, diarthrodial joints such as
the knee, hip, shoulder, and ankle. Its job is to provide for a smooth, lubricated surface to allow a low-
friction joint movement and to promote efficient load transmission. According to Korhonen and
colleagues 2002, its ability to deform under dynamic compressive loading is critical for reducing stress
to the underlying bone and for effective mechanotransduction. Articular cartilage is avascular,
meaning it gets no direct blood supply, it is aneural, meaning it has no direct innervation from the
nervous system, and it is alymphatic, meaning that it has no means to remove waste byproduct build-
up, which results in a tissue which is intrinsically difficult to repair if damaged. As such, according to
Wilusz and colleagues 2014, the immediate periarticular environment of the chondrocytes appears to
play a critical role in regulating cell activity. Articular chondrocytes are cells that make up the cartilage
and their metabolism is stimulated by mechanical loads. Mechanical loads like compression induce
the biosynthesis of molecules that preserve integrity and maintain a state of catabolic and anabolic
processes, keeping the tissue in balance. The nature of this response to mechanical loads is
dependent upon things like the history of loading, the amount of loading, and the frequency of loading.
When loads are too great, they fail to enhance extracellular matrix synthesis, and static or low-
frequency loads inhibit matrix synthesis, whereas dynamic compression, i.e., movement, can markedly
stimulate matrix production. The cell’s response to load occurs through the process of
mechanotransduction whereby compression of the tissue results in matrix and cellular deformation,
the development of hydrostatic and osmotic pressures, fluid flow, and changes in ion concentrations,
fixed charge density, and water content. Primary cilia, which are finger-like organelles that extend
dynamically from cell surfaces, detect these changes that, along with other mechanosensors on the
cell surface such as integrins and ion channels, initiate intercellular signalling pathways resulting in
tissue remodelling processes. Other mechanoreceptors in and around the joint that detect these
changes in the cartilage too. For example, according to Zimny 1988, in the menisci, more commonly
called knee cartilage, nerves penetrate the outer and middle one-third of the body and horns of the
perimeniscal tissue, with a greater concentration at the horns. These nerves feed the information
about the deformation of the cartilage tissues from compressive loads to the central nervous system,
which contributes to the person’s ability to maintain appropriate joint positions. When the cartilage
tissue is damaged by abnormal weight-bearing, which is very common in hypermobile joints, the
afferent process of relaying information from the joint to the nervous system gets interfered with and
so the person is less able to adequately control the position of that joint. So, there is a lot to think
about when considering a diagnosis of hypermobility and simply having somebody perform a handful

© Flexibility Research Ltd. All rights reserved.

of postures like we ask people to do when filling out the Beighton score is simply not enough to say if
somebody is genuinely hypermobile or not. A larger-than-normal amplitude of range of motion is a
side effect of abnormal arthrokinematics, but the only way to tell if the larger-than-normal range of
motion is caused by abnormal arthrokinematics is to test those arthrokinematic motions by doing joint
play assessments. So, in my opinion, we should do away with range of motion assessments for
diagnosing hypermobility for two reasons, 1) it eliminates confusion of people linking range of motion
with the term hypermobility, which may be why some people mistakenly believe joint mobility is
measured by range of motion. Joint mobility, aka arthrokinematics, is not measured by range of
motion, it is measured by testing joint play. And 2) like I have already said, flexibility alone is not
indicative of hypermobility. The only way to know if somebody has a hypermobile joint is to test the
accessory motions by doing joint play tests. The only way to do that is to put your hands on that joint
and put an amount of force into the joint and see how the joint physically responds. Going back to the
arthrokinematic or accessory motion grades, if we do a joint play test and there is a substantial
amount of internal motion in the joint, we assign it a grade of 5 and we say there is considerable
hypermobility present. And if we do a test and the joint is basically flopping all over the place inside
the joint capsule, we assign it a grade of 6 and we call it an unstable joint because there is simply no
stability present within the joint.

End-Feel

An important aspect of testing arthrokinematics is end-feel. I’ve talked about end-feel a lot in this
lesson and a little bit in the lesson on sex, hormones and genetics, but what exactly is end-feel? The
amount of arthrokinematic motion in a joint is determined by the unique structure of that joint. Some
joints are structured so that the joint capsules limit the motion in a particular direction, whereas other
joints are structured so that it is ligaments which limit the motion. The type of structure that limits
motion has a characteristic feel that can be detected by a person who is testing static passive range of
motion when slight overpressure is applied at the end of the motion. This feeling, which is experienced
by the person testing the joint as a barrier to further motion, is called the end-feel. Developing the
ability to determine the character of the end-feel requires practice and sensitivity of touch. Remember
that arthrokinematic motions are very small, so the determination of the end-feel has to be carried out
slowly and carefully to be able to detect the limit of motion and to be able to distinguish among the
various normal and abnormal end-feels. The ability to distinguish between the various end-feels helps
the person testing the joint to identify the type of limiting structure. Different people have described a
variety of normal and abnormal end-feels. Some of those people, whose names you will probably
encounter at various points throughout the literature, include James Cyriax, a British doctor who is
commonly referred to as the father of orthopaedic medicine, and Freddy Kaltenborn, a Norwegian
manual therapist who apprenticed with Cyriax. I briefly described the different types of end-feel in
lesson 7.1, but I will expand upon them here. The table on screen shows you normal end-feels. You
can see the name of the end-feel, its description, and an example for each. Soft end-feel is attributed
to the approximation of soft tissue. The phrase “soft tissue approximation” simply means that soft
tissues came into contact with each other and blocked further motion. A prime example is flexing the
knee, the calf makes contact with the hamstring. If there is a large amount of lean muscle or adipose
tissue, and adipose tissue is just another way of saying fatty tissue, then motion will be limited. The
myths around people like bodybuilders being inflexible because they are muscle-bound is probably
partly attributable to large amounts of muscle stopping further motion, in addition to bodybuilders
lifting weights through a less than full range of motion. Firm end-feel is caused by muscular stretch,
and I talked about firm end-feel in more detail earlier in the lesson. It can be attributable to muscular
stretch, capsular stretch, or ligamentous stretch. An example of muscular stretch is hip flexion with the
knee straight, which would be a demonstration of passive tension of the hamstring muscles. An
example of capsular stretch is extending the metacarpophalangeal joints of the fingers, which would
be felt as tension in the anterior capsule. An example of ligamentous stretch is supination of the
forearm, in which you would feel tension in the palmar radioulnar ligament of the inferior radioulnar
joint at the wrist, the interosseous membrane, and the oblique cord. And hard end-feel is caused bone
one bone surface contacting with another bone surface, with the most common example being
extension at the elbow where the olecranon process of the ulna makes contact with the olecranon
fossa of the humerus. The new table on screen gives you similar information about abnormal end-
feels. Abnormal end-feels are also called pathological end-feels. Soft end-feel occurs sooner or later in

© Flexibility Research Ltd. All rights reserved.

the range of motion than is usual or it occurs in a joint that normally has a firm or hard end-feel. It can
feel boggy, which means it has a mushy quality to it. This is typically caused by an oedema, or
swelling, in the soft tissues, or inflammation in the synovial membrane called synovitis. A firm end-feel
that is pathological occurs sooner or later in the range of motion than usual or in a joint which normally
has a soft or hard end-feel. It is most often caused by increased muscle tone, which is also called
neurological guarding, and it frequently occurs when a person is in a chronic sympathetic state. We
will look at the sympathetic and parasympathetic nervous systems later in the course, but being in a
chronic sympathetic state means that you are constantly in the so-called fight or flight state. An
abnormal firm end-feel can also be called by mechanical shortening of the joint capsule, muscles,
ligaments, and fascia. An abnormal hard end-feel occurs sooner or later in the range of motion than is
usual or in a joint that normally has a soft or firm end-feel. The person testing the joint can feel a bony
grating or a bony block. Some example conditions in which this can occur includes chondromalacia,
osteoarthritis, loose bony fragments or bits of cartilage in the joint, myositis ossificans, and fractures.
And an empty end-feel occurs when there is no real end-feel because pain prevents the person
testing the joint being able to take the joint to the end of range of motion, and no resistance is felt
except for the client’s individual’s protective muscle spasm which acts as a kind of split against further
motion. This can be caused by acute joint inflammation, bursitis, abscess, fracture, or a psychogenic
disorder in which the central nervous system is preventing that joint being moved further for some
psychological reason or another. Although end-feel testing has been used by clinicians for decades,
there continues to be a lot of debate between researchers about its reliability and validity. Kawamura
and colleagues 2020 reported that reliability and validity tend to improve over time because more
years of clinical experience relates to improved ability to discriminate between the types of end-feel.
So, it seems that testing arthrokinematic motions can be a useful tool for diagnosing abnormal intrinsic
joint movements, but that it requires a fair bit of practice and experience to be able to use it
accurately. Here is an exercise you can try with a friend or family member to help you practice
developing the ability to determine the end of range of motion and to differentiate among the three
normal end-feels, which are soft, firm, and hard. There are three tests in the exercise, one for each
end-feel. The first is to test elbow flexion so you can get a feel for soft end-feel. Step one pick
somebody with whom you can practice the technique. Step two position your practice partner supine
with their arm placed close to the side of their body. You should place a rolled-up towel under the
distal end of the humerus to allow space for full elbow extension. Their forearm is placed in full
supination with the palm of their hand facing the ceiling. Step three stabilise the distal end of your
practice partner’s humerus, i.e., the proximal joint segment, with one of your hands to prevent flexion
of the shoulder. Step four with your other hand, slowly move your practice partner’s forearm through
their full range of motion of elbow flexion until you feel resistance limiting the motion. Step five very
gently push against the resistance until not further flexion can be achieved. Carefully note the quality
of the resistance. You should feel a soft end-feel, which is caused by compression of the muscle bulk
of the anterior forearm with the bulk of the anterior upper arm. You can compare this soft end-feel
with the soft end-feel found in the knee. The second test is to get an idea for firm end-feel. Step one
place your practice partner in a sitting position so that their lower leg is over the edge of the
supporting surface and the knee is flexed at least 30 degrees. Step two with one hand, stabilise the
distal end of the tibia and fibula to prevent knee extension and hip motions. Step three with your other
hand on the plantar surface of the metatarsals, slowly move your practice partner’s foot through the
full dorsiflexion range of motion until you feel resistance limiting the motion. Step four push against the
resistance until no further dorsiflexion can be achieved. Again, carefully note the quality of the
resistance. You should feel a firm end-feel, which is caused by tension in the Achilles tendon from the
soleus muscle, the posterior portion of the deltoid ligament, the posterior talofibular ligament, the
calcaneofibular ligament, the posterior joint capsule, and the wedging of the talus into the mortise
formed by the tibia and fibula. You can compare this sensation with the firm end-feel which we get
during metacarpophalangeal extension of the fingers. The third test is to get an appreciation for hard
end-feel. Step one place your practice partner in the supine position with their arm placed close to the
side of their body. Place a small, rolled-up towel under the distal end of their humerus to allow full
elbow extension. Their forearm should be in full supination, again, the palm of the hand is facing the
ceiling. The easiest way to remember the difference between supination and pronation is that
supination is like holding a soup bowl in the palm of your hand. Supination, palm up. Pronation, palm
down. Rest one of your hands on the towel and hold the posterior, distal end of your practice partner’s
humerus in order to stabilise the segment and prevent extension of the shoulder. With your other

© Flexibility Research Ltd. All rights reserved.

hand, slowly move your partner’s forearm through their full range of elbow extension until you feel
resistance which is limiting the motion. Gently push against the resistance until no further extension
can be achieved. Again, note the quality of the resistance. You will notice that hard end-feel has no
give to it. Like I said earlier, hard end-feel in elbow extension is caused by contact between the
olecranon process of the ulna and the olecranon fossa of the humerus. You can compare this hard
end-feel with the hard end-feel usually felt in radial deviation of the wrist.

Capsular Patterns of Restriction

In addition to types of end-feel, James Cyriax came up with the idea that pathological conditions
involving the entire joint capsule cause a particular pattern of restriction involving all or most of the
motions of the joint. We call these patterns of restriction capsular patterns. The restrictions do not
involve a fixed number of degrees for each motion but rather a fixed proportion of one motion relative
to another motion. For example, the capsular pattern of limitation for the elbow is a greater limitation
of flexion than of extension. The elbow joint can normally achieve a static passive range of motion
from 0 to 150 degrees. If there is mild capsular restriction, the final 15 degrees of flexion and the final
5 degrees of extension might be limited so that the range of motion is actually 5 to 135 degrees. If the
capsular restriction is more severe, the final 30 degrees of flexion and the final 10 degrees of
extension might be restricted so that the range of motion is 10 to 120 degrees. The table on screen is
adapted from Dyrek 1994 and it shows you the established capsular patterns of the peripheral joints. I
will briefly talk about some of them. In the glenohumeral joint, when the joint capsule is affected, we
tend to see greatest loss of lateral rotation, a moderate loss of abduction, and a minimal loss of medial
rotation. The last part about medial rotation, or internal rotation, is interesting because in the health
and fitness industry a lot of people tend to say that internal rotation is the joint action that tends to get
affected, but that is not necessarily the case. In the elbow, which is a combination of the humeroulnar,
humeroradial, and proximal radioulnar joints, more range is lost in flexion than in extension, and
rotation tends to be full and painless except in advanced cases of disease. In the forearm, or the
proximal and distal radioulnar joints, we tend to see an equal loss of supination and pronation, but it
only occurs if the elbow has marked restrictions of flexion and extension. In the wrist, i.e., the
radiocarpal and midcarpal joints, there is a bit of contention in the literature and between the different
manual therapy systems. James Cyriax said that there is equal loss of flexion and extension, with slight
loss of ulnar and radial deviation, whereas Freddy Kaltenborn said there is equal loss of all motions.
When the hip capsule is restricted, Cyriax wrote that we will see greatest loss of motion in internal
rotation and flexion, we will see some loss of abduction, and slight loss of extension. There will be little
to no loss and adduction and external rotation. Kaltenborn did not differ too much in his teachings. He
agreed with Cyriax that greatest loss of motion is experienced in internal rotation, but he said there
would be less restriction of extension, abduction, flexion, and external rotation. Although opinions
about the validity and reliability of capsular patterns differ, the findings of the majority of the research
seems to support the concept of capsular patterns of restriction. Hertling and Kessler 2005 stated that
the concept of capsular patterns can be further classified into two general categories, 1) conditions in
which there is considerable joint effusion or synovial inflammation, and 2) conditions in which there is
relative capsular fibrosis. Joint effusion and synovial inflammation accompany pathologies like
traumatic arthritis, infectious arthritis, acute rheumatoid arthritis, and gout. In conditions like those, the
joint capsule gets distended, meaning it swells up, because the capsule fills with excessive intra-
articular synovial fluid, and that causes the joint to maintain a position that allows the greatest intra-
articular joint volume. Further movement is inhibited by pain triggered by stretching the capsule and
muscle spasms designed to protect the capsule, and therefore a capsular pattern emerges. Relative
capsular fibrosis often occurs during chronic low-level capsular inflammation, immobilisation of a joint,
and following acute capsular inflammation. These conditions can increase the relative proportion of
collagen compared with the amount of a group of complex polysaccharides called
mucopolysaccharides in the joint capsule, or they can even change the structure of the collagen. This
results in a significant decrease in the extensibility of the entire capsule and thus causes a capsular
pattern of restriction. There are noncapsular patterns of restriction, too. A noncapsular pattern is a
limitation of motion that is not proportioned similarly to a capsular pattern. A noncapsular pattern is
usually caused by a condition involving structures other than the entire joint capsule, and they are
typically caused by ligament shortening, muscle strains, and muscle contractures. Noncapsular
patterns usually involve only one or two motions of a joint, whereas capsular patterns involve all or

© Flexibility Research Ltd. All rights reserved.

most motions of a joint. For example, a biceps muscle strain can result in pain and restriction of
motion at the end of the elbow extension range. Elbow extension is affected but elbow flexion is not
affected. That is an example of noncapsular patterns of restriction. Being able to identify capsular and
noncapsular patterns of restriction helps to provide information about what may or may not be the
cause of a person’s inflexibility.

Positional Fault Hypothesis

A common narrative that accompanies many manual therapy techniques designed to treat
arthrokinematic motions, like mobilisations, is that the application of force into the joint capsule will
correct a fault in the position of the ends of the bones or some minor incongruency between the
bones which might be a source of the client’s problem, be that pain, stiffness or whatever. The idea is
that by using force to change the profile of the glide, spin, or roll, we can create substantial changes in
the arthrokinematic motions. A famous physical therapist called Brian Mulligan came up with the
theory for this mechanism, and he called it the positional fault hypothesis. Again, it is based upon the
assumption that there are minor incongruencies in bone alignment at the joints. The issue with this
hypothesis, however, is that these minor bony faults are difficult to measure in practice, and there is
nothing to say that these minor position faults are not still present after the pain has disappeared and
movement has been restored. There has been some support in the literature for the presence of
positional faults using diagnostic medical imaging like X-ray in the ankle, knee, and shoulder, but no
studies have yet evaluated the restoration of positional faults using manual therapy techniques. Even if
the positional fault hypothesis is valid, it is likely that there are a number of other mechanisms
responsible for the resolution of a person’s symptoms which have nothing to do with correcting bone
alignment. The most probablr mechanism is that the application of non-painful manual contact and the
input of force into the joint stimulates large diameter afferent nerve fibres, and over many repetitions
of the technique, we can facilitate the re-learning of previous pain-free motor memories. Regardless of
what the actual underlying mechanism might be, arthrokinematic manual therapy techniques like
mobilisations do have a rich history in the literature of reducing pain and restoring motion in the joint.
For example, Meyer and colleagues 2020 demonstrated that a technique called mobilisation with
movement, where a traction force is applied to the joint, either with the hands or using some type of
resistance band or a physical therapy belt, is combined with active, voluntary movement at the joint,
and it significantly improves acute range of motion in people with limited ankle flexibility after only a
couple of sets. Because most insurance providers will not cover you to perform hands-on manual
therapy techniques without training, and it is almost impossible to teach you how to do these
techniques without live, in-person training, this course can only show you how to teach clients to
perform these techniques on themselves. But that is a good thing. Getting clients to do the techniques
themselves will limit dependency upon these techniques, which is something we want to try and avoid.

Measurement Devices

We are going to finish this introductory lesson to measuring flexibility by looking at some of the
instruments and devices which are often used by clinicians, researchers, and trainers. So, I said
earlier that angle-measuring devices have been used for centuries, and, according to Smith 1982, the
universal goniometer that most people use to measure range of motion today is based upon devices
that first appeared in France in the first few years of the 20th century. Indeed, the first publications to
discuss the use of goniometers are in the French medical literature, and despite there now being
thousands and thousands of English-language articles covering goniometers, the goniometer was not
described in the British or American literature until at least 1914. According to Moore 1949, the world
wars spurred the interest in and use of goniometers, and although there have been many variations
developed over the years, the goniometer that clinicians use today has remained relatively unchanged
from the design that first appeared over 100 years ago. It was William Arthur Clark in 1920 who first
described a standardised starting position for measurement that was identical to the anatomical
position currently used, with the exception of the ankle, which he described as fully plantarflexed. He
was also one of the first researcher to give us values for normal range of motion of the spine and
peripheral joints. Today, there are three notation systems used to define range of motion, and they are
the 0- to 180-degree system, the 180- to 0-degree system, and the 360-degree system. In the 0- to
180-degree system, the upper and lower extremity joints are at 0 degrees for flexion-extension and

© Flexibility Research Ltd. All rights reserved.

abduction-adduction when the body is in the anatomical position, and at 0 degrees for rotation when
the body is in the neutral position. The image on screen shows you the difference between the
anatomical position and the neutral position. The anatomical position is on the left and the neutral
position is on the right. In the anatomical position, the forearm is supinated so that the palms of the
hands face anteriorly, i.e., to the front. In the neutral position, and we call it neutral with respect to
rotation, the palm of the hand faces the side of the body. However, it is important to remember that in
many systems, textbooks, and research papers, the anatomical position is often referred to as
anatomical neutral or anatomical zero, because in that position, all of the joints are considered to be at
zero degrees in their range of motion, with the exception of course for upper extremity rotation. In the
anatomical position, the hips are in 0 degrees of rotation, so the neutral position that is on the right of
the screen is reserved exclusively for the arms. Normally, a given range of motion begins at 0 degrees
and proceeds in an arc towards 180 degrees. This 0- to 180-degree system is also called the neutral
zero method, meaning that each joint begins at zero degrees of motion in the anatomical position. It
was given to us by an American doctor from Pittsburgh called David Silver in 1923 ] and it has
become the most widely used system throughout the world, recommended by both the American
Academy of Orthopaedic Surgeons and the American Medical. To give you an example, the range of
motion for shoulder flexion, where the shoulder begins at 0 degrees in the anatomical position, and it
ends with the arm raised directly overhead at 180 degrees in what is called full flexion, is expressed in
the neutral zero method as 0 to 180 degrees. The range of motion for extension, which starts in full
flexion with the arm raised overhead and ends by bringing the arm back to the anatomical position, is
not usually measured because this range of motion represents the same path of motion that was
measured during shoulder flexion. Shoulder extension is measured from 0 degrees to the maximum
point that the arm can move behind the body. Just like we do not measure extension from the maximal
point of flexion back to anatomical zero, we also do not measure flexion from the maximal point of
extension back to anatomical zero. So, range of motion assessments will ignore extension from 180
degrees of flexion to zero and they will also ignore flexion from the maximal point of extension to zero,
which are the arcs of motion you can see represented by the red arrows on screen. Most clinicians
and researchers ignore those paths because they are simply the reverse of the paths of motion that
we just measured. And this is true for all joints in the body. However, even though they tend to be
ignored during assessment, the action of bringing the arm back from full flexion to zero is still called
extension. Some authors will also refer to taking the arm from zero to behind the body as
hyperextension, but really it is still part of the path of motion we call extension. You can call it
extension or hyperextension, it’s up to you. In the other two systems I mentioned, the 180- to 0-degree
system and the 360-degree system, are rarely used in the literature and in clinical practice because
they are hard to use and interpret. For that reason I am not going to explain them here because that
will probably just confuse you. However, be mindful that if you are reading a research paper and the
authors have defined the anatomical position as 180 degrees, instead of 0 degrees as most other
people do, then they are using either the 180- to 0-degree system or the 360-degree system. But in
most of the literature authors will use the 0- to 180-degree system that I described in the example of
shoulder flexion and extension, in which the anatomical position is defined as 0 degrees. Over the
next several weeks you are going to be shown specific ways to measure range of motion using a
universal goniometer because that tends to be the simplest, fastest, and cheapest way of quantifying
flexibility. However, here I will briefly talk about other tools that some clinicians and researchers use
just so that you at least have an awareness of them, because you might decide that you would rather
use one of those instead. First up is the inclinometer which, as the name suggests, is a device used for
measuring the incline, tilt, or slope of an object relative to the direction of gravity. One of the earliest
reports of using an inclinometer was given by Fox and Van Breeman in 1934 in which they used a
circular scale with a weighted pointer attached at one end that they called the pendulum goniometer.
Then, in the 1950s, JR Leighton gave us the Leighton Flexometer, which consists of a 360-degree dial
and a weighted gravity needle and a strap which attaches to the limb. You can now get inclinometer
apps for your smartphone, which are proving very popular as an accessible way for measuring range
of motion, and they are a lot cheaper than other digital inclinometers which can get quite expensive.
They are proving very reliable, too. For example, Shin and colleagues 2012 reported that smartphone
inclinometers generally have excellent intra-rater reliability, meaning that the same person will be
accurate with most movements using one. The great thing about smartphone inclinometer apps is that
their convenience, cost-effectiveness, and general ease of use means that you can instruct a client
and their partner or one of their friends to do range of motion measurements at home if you are

© Flexibility Research Ltd. All rights reserved.

coaching them virtually. Still photography has been used to measure joint range of motion since at
least 1945 and it remains a popular method even today. While measuring range of motion using still
photography can take a little bit more time and effort than doing a hands-on assessment in a clinic
setting, still photography assessment has been shown to be more accurate, for example, Fish and
Wingate 1985 reported that accuracy of joint angle measurement at the angle using photography was
greater than standard, hands-on goniometry. The rise in the use of smartphones has produced a
number of apps which feature the ability to measure joint angle from a photograph for you. As virtual
coaching, which is sometimes referred to as “telehealth,” becomes more popular, it is highly likely that
this is something you will use with your clients. Detailed instructions on how to measure angles for
each joint in the body using both a goniometer and still photography will be given in upcoming
lessons. And finally, radiography is considered the gold standard against which all other techniques
for measuring joint range of motion are compared against. However, given the health risks associated
with repeatedly blasting your clients with high-powered X-rays, as well as the prohibitive costs and
impracticality of using radiographic equipment, this course will not teach you how to operate an X-ray
machine. When it comes to measuring muscle length, there are generally two methods used, 1)
composite tests and 2) direct measurement. Composite tests consist of measuring motion across
more than one muscle or more than one joint, for example, the famous but flawed sit-and-reach test,
the fingertip to floor test, and Apley’s scratch test. Direct measurement consists of looking at the
excursion between adjacent segments of one joint. Despite the popularity of composite tests like the
sit-and-reach test, it is important to remember that flexibility does not exist as a general characteristic.
Although the sympathetic and parasympathetic nervous systems can have an inhibitory and
facilitatory effect on range of motion through the whole body, the effect is not that significant when
compared to joint-specific flexibility training. In other words, although there can be a global effect on
rage of motion depending upon which autonomic state we are in, a person who can do the splits very
easily will still be able to do the splits when in a highly sympathetic state, i.e., when they are in a high
fight or flight state, it will just take them longer to get into the splits because of the increase in muscle
tone. A person cannot hope to achieve the splits just by doing breathing exercises and a mindfulness
practice. Margaret Harris wrote in 1969 that there is no evidence that flexibility exists as a single
characteristic of the human body. Thus, no one composite test or no one joint action measure can
give a satisfactory index of the flexibility characteristics of an individual. Furthermore, Cheryl Hubley-
Kozey, currently professor at the Schools of Physiotherapy and of Biomedical Engineering at
Dalhousie University in Canada, stated that composite tests do not provide accurate measurements of
flexibility because these tests assess combinations of movements across several joints and involving
several muscles. She said that composite tests are of questionable accuracy owing to difficulty in
determining which muscles are being examined and which are actually contributing to the movement,
and composite tests at best serve as gross approximations for flexibility. Therefore, in the subsequent
lessons in this course in which you will be given practical instructions on how to measure flexibility,
you will be shown mostly direct measurement methods for the various joints of the body.

Summary

To summarise, total range of motion is often divided into two sub-components, 1) joint range of
motion, which is the distance the joint and its bony shaft can travel, and 2) muscle length, which is the
amount that the muscle or muscles crossing the joint can extend or lengthen. Using an instrument like
a goniometer tends to be more accurate than using visual estimation, and using still photography is
even more accurate than using a goniometer. A one-joint or monoarticular muscle is a muscle which
crosses one joint only, and in such cases, range of motion and muscle length are considered to be the
same. In two-joint or biarticular muscles, and multi-joint muscles, are muscles which cross two or
more joints. Generally speaking, two-joint muscles do not have enough length in them to allow all
joints to express their full range of motion at the same time. We refer to this as passive insufficiency.
To measure joint range of motion at joints which are crossed by two-joint or multi-joint muscles, the
muscle must be placed in a shortened position at the joints which are not being measured in order to
facilitate full range of motion at the joint which is being measured. The opposite of passive
insufficiency is called active insufficiency, and this is where two-joint or multi-joint muscles are placed
in such a shortened position that they are unable to generate sufficient active tension. It is important to
remember that passive and active insufficiency, as they are defined in this way, are characteristics of
anatomy. Passive insufficiency is not the same as poor extensibility. Likewise, a lack of strength is not

© Flexibility Research Ltd. All rights reserved.

the same as active insufficiency. However, people in the health and fitness industry are using those
definitions with increasing frequency. Because true passive and active insufficiency and poor
extensibility and lack of strength can often occur at the same time to some degree, the terms agonist
insufficiency and antagonist insufficiency are useful terms that describe both true, anatomical active
and passive insufficiency, as well as a lack of strength and a lack of muscle extensibility.
Arthrokinematic motions consist of rolls, spins, and glides or slides, and most human movements
consist of a combination of these intrinsic joint motions. In the majority of the literature, the term “joint
mobility” is used to refer to these motions, and when a person has poor joint mobility it is because
there is some arthrokinematic dysfunction present, i.e., the joint surfaces cannot move relative to one
another like they normally should be able to. It has been proposed that dysfunctional arthrokinematics
might be caused by a position fault between the bones, however, this theory, called the positional fault
hypothesis, remains to be proven. The state of a joint’s internal health can be detected by doing
hands-on assessments called joint play tests, which provide a specific type of end-feel depending
upon the structures which are involved and the presence of any pathologies. When the internal,
accessory movement of the joint is limited, we call it a hypomobile joint. When the internal, accessory
movement of the joint is excessive, we call it a hypermobile joint. Range of motion is not a useful
indication of true joint hypermobility, in which the structure of the joints is such that excessive motion
is not limited by physical restraints that would otherwise be present in normal joints, like limited
extensibility in the capsule and ligaments, because a person can train to have a high level of flexibility
but have perfectly normal, non-hypermobile joints. When the joint capsule is a cause of limited range
of motion, the joint will usually present familiar patterns of restriction, which we call capsular patterns.
When it is something else besides the entire joint capsule causing the limited range of motion, we call
those noncapsular patterns of restriction. And finally, many different devices exist to measure range of
motion, the universal, two-armed goniometer being the most common, however, you may find using
digital inclinometers or still photography apps on your smartphone the most convenient to use for
your particular circumstances.

© Flexibility Research Ltd. All rights reserved.