JANUARY 14, 2017 BY JASON EURE

Squatting with Patellar Tendinopathy

Trying to squat with achy knees can be tricky – you don’t want to lose too much strength, but you want to
the problem to go away. Here’s what you need to do

Training with tendon injuries can be a frustrating endeavor. Within a

session, focus shifts from performance cues to the sensation of pain and
impending anxiety regarding what this means for long-term health and
training capacity. As a former strength and conditioning coach, as well as
someone who has been training consistently for the majority of my life, I
have a strong appreciation for the pursuit of strength, and I intimately
understand the innate drive to train despite facing injury. Fortunately, I
have been able to merge my passion with my knowledge as a Physical
Therapist to assist many individuals within this realm. Through practice, I
have been able to provide value on an individual level, and I hope to use this
platform to offer perspective on a wider scale.

Mandatory disclaimer: This is not meant to be a replacement for a consult

with a medical professional. If you are experiencing pain beyond what is
deemed normal aches and pains associated with training, you should seek
help. A physical therapist can serve an invaluable role in restoring your
ability to train following musculoskeletal injuries. However, knowledge and
treatment paradigms vary widely between professionals, and tendinopathy
management is rapidly evolving with our growing understanding of the
disorder, requiring deliberate effort to keep up to date. The best advice I
can offer is to do your homework to ensure your therapist is aware of the
demands of your chosen sport, remains current in his or her knowledge of
tendon rehabilitation, and offers more than passive modalities for “healing.”

This article is going to start from the ground up, going over tendon
structure, function, and adaptive capacity, as well as theories of pathology,
rehabilitation principles, and ways to maintain a training stimulus while
addressing the problem. While I obviously think this is important to gain
insight into the “whys” behind the process, I acknowledge not everyone
wants to go back to physiology 101. Feel free to skip ahead to the practical
recommendations if you want; I did my best to make it a self-contained
section. If you’re feeling particularly rushed, you can even jump straight to
the summary below and use the remainder of the article as a reference (no
judgment).

Anatomy and Biomechanics:

In the simplest sense, tendons are soft, fibrous tissues that connect muscle
to bone and function to transmit force to facilitate movement around a joint
and absorb external force to limit muscle damage (1, 2). Tendons are
predominantly composed of water (approximately 55-70% of total weight)
with the remaining dry weight being comprised primarily of collagen (60-
85%). Collagen is a stiff structural protein which comes in many variants
within humans; however, for our purposes today, we’ll limit the discussion
to the two main types found in tendons, Type I and Type III collagen (90%
and up to 10% respectively)3. These molecules are organized in a precise,
hierarchical fashion parallel to the long axis of the tendon; thus affording
the high tensile strength required for their role in transmitting uniaxial
forces (2).

Source: http://jbjs.org/content/87/1/187
Interestingly, the mechanical behavior of a tendon is dependent upon the
type of stress applied (4, 5, 40). When exposed to stresses, their ability to
stretch and recoil serves a protective role for the attaching musculature,
allowing for the delay and reduction of total force (5). Previous studies have
demonstrated that under most conditions, stretching of the tendon is out of
phase with the adjoining muscle fibers. During eccentric contractions,
lengthening of the muscle-tendon unit (MTU) is initially accommodated for
almost exclusively by the tendon while the muscle fibers remain the same
length (or even shorten). Subsequently, the tendon then recoils as it releases
the absorbed energy to skeletal muscle, causing elongation of the contractile
fibers. Importantly, the rate at which energy is stored in the tendon is
significantly greater than the rate of energy release to the muscle – sparing
musculature from high power stressors while prolonging the muscle’s
ability to maintain optimal length-tension relationships required for force
expression or dissipation.

Additionally, these dynamics change based upon the intensity and rate of
the applied load due to a tendon’s viscoelastic characteristics. Like viscous
materials, tendons display time-dependent mechanical characteristics in
which they become stiffer as the rate of loading increases. This enables the
tendon to tolerate a wide bandwidth of velocities with relatively small
changes in length between conditions. Like elastic structures, tendons also
display time-independent characteristics in which the intensity of the stress
drives length changes regardless of the application rate, allowing for greater
muscular power (and subsequent movement economy) upon recoil. These
two seemingly distinct qualities are present within the same structure in
varying proportions based upon the specific task constraints. During the
early eccentric contraction, fluid is forcefully pushed out of the tendon,
resulting in high viscous resistance. Constant tension (and tissue
compression) does not allow for the return of fluid prior to concentric
muscular action, leaving the elastic qualities of the tendon to predominate
during the concentric phase (4, 40). In totality, this introduces the complex
behavior tendons display. Their adaptability is vital to our success as a
species, as the ability to buffer stressors of varying magnitude and rate
allow for amazing variability in human movement without major adverse
responses (4, 5, 6, 40).
The primary focus of this article is going to be the patellar tendon, due to its
propensity for injury within the sport of powerlifting. The patellar tendon
attaches to the inferior pole of the patella (knee cap) and the tibial
tuberosity (bony protrusion at the top of your shin). Although the majority
of the patellar tendon fibers do not directly attach to the quadriceps
musculature, they act functionally as a tendon in conjunction with the
quadriceps tendon. In this role, the patellar tendon serves to facilitate action
of the knee extensors to allow for optimal pull on the tibia during dynamic
movement (7).

Source: https://en.wikipedia.org/wiki/Patellar_ligament#/media/File:Gray345.png
Scientists estimate that the patellar tendon can
withstand between 10,000 to 15,000 N of force, which
equates to approximately 13-19x body weight for an
80-kg individual (8). To provide context, Nisell and
Ekholm conducted a study where they mathematically
estimated patellar tendon loads during the barbell
squat (250 kg squat performed by a 110 kg lifter). They
demonstrated peak forces only reached 6,000 N – far
below the expected failure threshold (9).

Not all tendons serve the same functional role. Tendons are classified into
two distinct categories: positional tendons, which act to predominantly
position limbs, or energy-storing tendons, which act more as springs to
allow for more efficient movement. The patellar tendon is an energy-storing
tendon due to its specific functional role and altered physiological
properties. In order to effectively store and return energy efficiently, the
patellar tendon has higher elastin content, lower absolute levels of collagen,
and a higher relative proportion of Type III collagen versus Type I (Type III
has lower stiffness, allowing for improved extensibility and recoil) when
compared to positional tendons (2). Additionally, energy-storing tendons
display significantly lower levels of collagen turnover, resulting in a half-life
of approximately 200 years (important concept for rehabilitation purposes
to be discussed later).
Adaptability:

Now that some background information has been presented, we can get to
the important part: if and how we can alter the physical properties of
tendons. Central to this premise is the concept of
mechanotransduction. Mechanotransduction, by definition, is the
mechanism by which cells convert mechanical stimuli into cellular
responses (10). Cells are sensitive to forces such as shear, tension, and
compression, and they respond accordingly through cellular proliferation,
migration, tissue repair, altered metabolism, and even stem cell
differentiation and maturation (10). Thus, in essence, stress is the language
our cells speak, serving to stimulate both positive and negative change.
Tendon cells are no exception, sensing and responding to stressors in their
surrounding environment. Load is a primary stressor which our tendons
detect and functions as a vehicle to drive rehabilitative efforts.

The inner portion of a tendon is formed during years of peak growth (during
time of puberty) and is essentially not renewed thereafter. Therefore, when
exposed to sufficient load, the subsequent changes observed in tendon
structure are almost exclusive to the outer periphery of tendons (13).

Source: Kjaer M, Bayer ML, Eliasson P, Heinemeier KM. What is the impact of
inflammation on the critical interplay between mechanical signaling and biochemical
changes in tendon matrix?. J Appl Physiol. 2013;115(6):879-83
The non-homogenous response to loading contributes to a lower absolute
ceiling of adaptability in tendons when compared to musculature.
Additionally, in the metabolically active segments of tendons, the tissues
also display lower relative adaptive capacity than skeletal muscle due in part
to oxygen consumption levels calculated to be approximately 7.5x lower
(15). This may paint a bleak picture for our ability to modify tendon
structure an appreciable amount, but several recent systematic reviews
demonstrate meaningful effects of loading on tendon structure. Primarily,
three key features of tendons have been studied in response to acute and
chronic loading: tendon mechanical (stiffness), material (Young’s Modulus),
and morphological (cross-sectional area, level of molecular cross-linking)
properties (11,12). Stiffness refers to the ability to resist deformation, and
Young’s modulus refers to stiffness when tendon dimensions are taken into
account (12). Alterations in material properties are believed to be the acute
response to tendon loading, with significant increases noted within the first
several months of training (increased stiffness reportedly ranging from 26%
to 85%), and changes in morphological qualities are believed to be the
chronic adaptation after years of training (increased cross-sectional area
reportedly ranging from 1.5% to 36%) (12).

Tendinopathy
Classically, tendon pathologies were separated into two discrete conditions
referred to as tendinitis and tendinosis. Both were considered “overuse”
injuries with the former representing an acute, inflammatory condition and
the latter representing a degenerative condition. Inflammation’s role in the
disorder has been questioned recently, with evidence suggesting that while
there are an increased number of inflammatory cells present in pathological
tendons, the response observed is not in line with a traditional
inflammatory response and the presence of inflammatory markers does not
necessarily support inflammation as the primary event or key driver of
tendon pathology (16, 17). This revelation, in conjunction with the totality of
evidence, led away from the belief that these conditions are mutually
exclusive. Therefore, the more generic term “tendinopathy” is preferred over
the aforementioned terminology.

Additionally, the causative mechanism of “overuse” is antiquated and

perpetuates an inaccurate notion of how biological organisms respond to
stress. The amount of stress required to evoke a mal-adaptive tendon
response is constantly changing based upon fluctuating individual
constraints. For example, an athlete may be able to tolerate a very high
workload if they deliberately condition themselves to withstand that level of
stress over an appreciable amount of time. That very same athlete may
experience negative consequences while performing a fraction of that
volume if they are coming off a period of detraining due to the plasticity of
various structural, hormonal, and enzymatic qualities which are mediated
by habitual loading (3, 10). Hence, we should instead view the triggering
event as a ratio instead of an absolute – that the applied loads
(magnitude/frequency/rate) exceeded our body’s ability to adequately
respond in specific contexts.

Dr. Jill Cook, a leading researcher in the field, proposed that tendinitis and
tendinosis are different aspects of the same complex continuum and has
organized tendinopathy into three distinct phases: 1) reactive tendinopathy,
2) tendon dysrepair, and 3) degenerative tendinopathy (16, 20). A reactive
tendinopathy is believed to be an acute, reversible process brought about by
a rapid increase in mechanical loading. The tendon swells due to an increase
in water retention and is proposed to be a protective response to reduce
stress along involved collagen fibers (20, 21). Tendon dysrepair is suggested
to follow if loading exceeds tendon capacity for a substantial period of time.
Here, we continue to see increased fiber diameter, but the tendon matrix
begins to breakdown and there is evidence of neural and vascular ingrowth.
Finally, a tendon reaches a degenerative state, characterized by further
collagen disorganization, advanced matrix breakdown, and increased fiber
thickness.
Source
In clinical findings, the hallmark features of patellar tendinopathy across all
three stages include pain localized to the inferior pole of the patella and
load related pain that increases with the demand on the knee extensors. To
differentiate a tendon disorder from other sources of similar symptoms, it
should be noted that there is rarely pain in resting states and we typically
see a dose-dependency of pain, with increased intensity or rate of loading
associated with increased reports of pain (18). Again, I am not condoning
self-diagnosis of the disorder. If your condition aligns with these symptoms,
or there is any pain beyond normal aches associated with training, I would
seek a medical provider.

Practical Implications
Tendon Rehab

The most important concept to understand with tendon rehabilitation is

that there is very little evidence to suggest there is any reversibility noted
within affected regions of degenerative tendons – with minimal
physiological adaptations noted following rehabilitative efforts (16, 21, 22).
At first, this would appear to contradict the adaptive process detailed above.
But, once the extracellular matrix is disrupted beyond a certain threshold,
the involved region loses its ability to transmit load; thus, there is no
mechanical stimulus to force change (22). However, because there is enough
redundancy within tendons, we do not need this to occur specifically at the
site of degeneration. A recent ultrasound study demonstrated that
pathological tendons have an increased mean cross-sectional area and an
increased anterior to posterior diameter compared to non-pathological
tendons. And while there is a reduced relative percentage of aligned fibrillar
structures (and a coinciding increase in the percentage of disorganized
tissues), in absolute terms, these tendons contain increased amounts of
load-bearing tissues comparatively. Therefore, while our efforts may not
impact areas of disorganization within an involved tendon, we can evoke
desired changes within the plentiful areas of aligned collagen. This idea can
be adequately visualized by the metaphor “treat the donut, not the hole”
where the “donut” refers to the viable collagen structures and the “hole”
refers to the degenerative and/or disorganized fibers (16).

First and foremost, we are concerned with optimal tissue loading to

facilitate the desired response. There is a pervasive notion that more is
better. However, as mentioned above, loading beyond our ability to adapt
will have detrimental consequences and will only serve to perpetuate our
cycle of frustration. Dr. Scott Dye proposed a tissue homeostasis model
which included a concept known as the “envelope of function,” serving to
demarcate the boundaries for the safe range of load acceptance and
transference within a given period of time (23). To force positive
adaptations, we must find the sweet spot within the envelope of function
where the total stress is enough to disrupt tissue homeostasis and create an
impetus for change without diminishing structural integrity.
Image from Scot Morrison’s blog, an excellent read for clinicians looking for more on
the dose-response relationship in rehab.
So the important question is how do we know how much is right? Research
groups studying tendon rehabilitation have adopted a system based on
subjective feedback regarding pain within training and over a 24-hour
window immediately following (18).

Important tangent: Pain is a widely misunderstood phenomenon, with many

misinterpreting pain as a direct indication of tissue damage. While pain
neuroscience is beyond the scope of this article, it is imperative to
understand that pain is a protective mechanism of the body and not simply
a reflection of the tissue state. While pain does indeed strongly correlate to
tissue damage in acute traumatic events, this association is diminished over
time, and tissue physiology does not predict pain response in chronic
conditions. Therefore, do not panic if you experience low levels of pain, you
are (probably) not doing significant harm and you are (probably) not
experiencing a major setback. (For more on the topic of pain, please read
thisfree full text from Lorimer Moseley)

Typically, you will be able to determine tissue tolerance to load based

upon a simple self-assessment within a specific movement pattern. (This
will look familiar to those of you who are aware of David
Dellanave’s Biofeedback training. Similar concept utilized for rehab
purposes.)
  Find a movement that you can perform consistently to stress the
patellar tendon. In research, this is often a single leg squat performed
on a decline board; however, all that matters is that you choose a task
which directly stresses the tendon and can be performed in a consistent
manner on a daily basis.
 Note your level of pain within this task on a 0-10 scale and use this as
your reference point.
 Perform your training session while modifying stress (through any of
the variables to be discussed soon) as to maintain, at most, low-
intensity pain. The threshold is variable depending on the individual,
but I typically stop patients between 3-4 out of 10.
 Check your chosen pattern at the same time of day, every day, and log
your level of discomfort. If your pain is below or remains the same as
your initial assessment: You are probably tolerating the current level of
stress well and can maintain or increase the training demands. If your
pain increases compared to your initial assessment: The total stress
may be too much and you may need to alter your training strategy.

Training Considerations:
Each of the upcoming variables impact total stress upon the involved
tendon in varying capacities. Finding the right balance while ensuring you
are addressing qualities you wish to develop is a difficult process. The best I
can offer is education on several factors believed to be important. I will
leave the nuts and bolts of programming up to you on an individual basis.

In order to improve load-bearing capacity of the viable structures within

pathological tendons, we need to ensure net synthesis of collagen. Following
resistance training, there is an increase in collagen turnover, both synthesis
and degradation. Initially, enzymatic activity leads to a net protein loss, with
a net gain not observed until approximately 36 hours after exercise (see
figure below). Therefore, it is believed that for positive adaptations to be
observed, a certain restitution period is beneficial. Without adequate
recovery time, it is likely there will be a net loss of collagen, rendering the
tendon vulnerable to excessive loading (3). Considering these findings, it is
best to space training sessions out by at least 36-48 hours to facilitate
desired outcomes. Although I make this recommendation, there are many
studies which have used daily low-volume loading programs successfully
(39). These outcomes mean there is likely a threshold effect for the collagen
turnover rates discussed and the extended periods of reduced loading may
not be required for positive results. But for practical purposes, the
suggested training frequency is sufficient and convenient for most.

Training Volume

The careful administration of training volume is critical to providing

optimal levels of stress. Greg has done an excellent job of discussing the
merits of different volume metrics here, but for our purposes, any method
which can be performed consistently will suffice. We must find and
implement a training volume within our envelope of function, somewhere
between the minimum effective dosage and our maximum recoverable
volume (MRV). While it may sound appealing to jump to our MRV, this
presents several challenges in the rehabilitative process.

The stress applied to tendons is not isolated within the four walls of the
gym and this concept demands particular consideration for tendons of the
lower body, such as the patellar tendon, which are required for locomotion.
Stresses associated with daily demands typically represent a small absolute
value of our tendon’s capacity. However, in pathological tendons, these
same stressors represent a significantly higher relative percentage of that
capacity and may have a critical impact upon your ability to train. The daily
fluctuation in additional load is hard to quantify and account for, rendering
it difficult to walk the fine line of your MRV within session. Additionally, the
magnitude of difference in adaptations observed between performing the
MRV and those seen using a more conservative volume is speculatively not
large enough to overcome the detriment of overshooting your tendon’s
current capabilities.

This leads to the notion that it is much more reasonable to underestimate

yourself at first, ensure you are tolerating the current load well (using the
24-hour symptom response noted above), and gradually build volume
accordingly.

Exercise Selection and Order

To this point, an unmentioned consideration is the impact a condition such

as tendinopathy has on neural regulation of force expression. Paradoxically,
individuals with tendinopathy display both elevated corticospinal
excitability as well as cortical inhibition of the quadriceps musculature (24,
25, 26). It is believed there is greater pre-activation and enhanced
excitability of the quadriceps in order to increase muscular stiffness to
accommodate for the greater compliance of pathological tendons, with
increased cortical inhibition postulated to limit total force capacity (24, 25,
32). While these neural abnormalities may be inefficient (likened to a novice
driver controlling the speed of their car with one foot on the brake and one
on the accelerator) they are protective in nature, serving to reduce
mechanical loading of the vulnerable tissues (26). Obviously, this regulatory
strategy may impact our ability to load the involved musculotendinous unit
as desired, and is clearly not ideal for anyone wishing to maximize muscular
hypertrophy or improve their powerlifting total. The fortunate news is that
recent investigations have indicated we may be able to significantly alter the
aforementioned abnormalities through relatively simple means. Rio et al.
conducted a study on patients with patellar tendinopathy where they
compared the influence of isometric contractions to isotonic contractions
on pain, quadriceps strength (measured in terms of maximum voluntary
isometric contractions (MVIC)) and measures of corticospinal inhibition (25).
Performing five 45 second isometric knee extensions (60 degrees of knee
flexion) with 70% 1RM had significantly greater impact on all three variables
than the isotonic exercise. More specifically, the reduced inhibition achieved
through isometric loading led to an average MVIC increase of 18.7%
immediately following the intervention, with sustained improvements noted
for at least 45 minutes. Note: This does not imply you will squat 20% more
during your training. It does, however, provide preliminary data to support
the use of moderate-to-high intensity isometric loading to start your
training session. This will assist in normalizing the neuromuscular control
of the involved lower extremity and potentially improve load tolerance and
force expression for the duration of your routine.

(The Spanish Squat is a commonly substituted exercise if you don’t have a

leg extension machine available to you).

Following a warm-up period which includes isometric loading, it is time to

choose a primary squat pattern. Greg has extensively written in regards to
the difference between squat techniques when it comes to probable
muscular effort and development. And while the discrepancies in muscular
demands are likely small, the movement pattern chosen can have significant
impact on the stress placed upon the patellar tendon. Mathematical models
have demonstrated patellar tendon force (through a combination of tensile
and compressive stress) is directly proportional to knee flexion angle during
the squat (8). Stress is maximized at angles of deep knee flexion (reaching
approximately 6000 N at 130 degrees) and slowly decreases to 2000 N by 30
degrees. Therefore, particularly during early stages of rehabilitative
efforts, it is wise to limit loading in significant knee flexion (18, 27, 28).
Practically, this leads to choosing options where your movement is
constrained biomechanically rather than consciously adjusting your depth
or effort. A great starting point would be a box squat. Within this pattern,
you are able to sit back an unnatural amount to increase the hip flexion
moment (thus increasing hip extension demands) while maintaining a
shallow, vertical tibia. Additionally, a box affords you the specific control
over knee angles which allows you to train at or below your chosen low-
intensity pain threshold. Over time (weeks to months), a simple progression
would be to move to a low-bar back squat, followed by high-bar back
squat, and finally front squat (if so desired) as tissue tolerance allows.

Note the
different biomechanical positions of the knee at the bottom of each squat variation.
Photo from: http://www.thebarbellphysio.com/squat-assessment-checklist/
Great resource for clinicians working with athletic populations.
In conjunction with modifying your squat selection, the benefit of
accommodating resistance should be intuitive. The ability to progressively
load the squat as you rise from the bottom position can be useful to
maximize the training effect without excessively loading tendons in their
most susceptible position. It should be noted that bands and chains are not
equal in this respect. When controlling for other variables (such as intensity
and velocity), it has been demonstrated that forces on the patellar tendon
during the eccentric portion of a squat are 15-35% greater than the
concentric (8). Thus, using a traditional band-resisted setup may be
counterproductive because this accentuates the downward pull during the
lowering phase. Chains or a reverse-band configuration are probably the
superior option here for altering the resistance throughout the
movement.
Finally, it is commonly hypothesized that solely performing compound
movements may not adequately stress the involved tendon due to conscious
or subconscious compensatory strategies (18). This may be as blatant as a
deviated movement pattern to shield sensitized tissues or could be as
insidious as the neural protective adaptations outlined above. Therefore, it
is probably best to include some form of isolated leg extension towards
the end of your training session to ensure adequate loading of the
involved musculotendinous unit. Be sure to account for this when
determining your appropriate training volume

Training Intensity

Traditionally, eccentric contractions were thought to be the vital component

of tendon rehab and were used extensively to address the pathological
condition. However, Bohm et al. recently conducted a systematic review
where they examined the influence of different loading conditions and types
on adaptive response. They found that type of contraction used is irrelevant
(with one notable exception to be mentioned later), and the primary
difference in outcomes was attributable to the intensity of exercise used
(11). So, the natural question is what is the optimal intensity to drive tendon
adaptations? To clarify, by intensity, I do not mean effort. In this context,
intensity implies percentage of your one repetition maximum. While skeletal
muscle is extremely responsive to a wide variety of stimuli, with positive
adaptations noted in a multitude of training conditions, tendons require
more specific loading parameters11,29,30. When controlling for effort,
muscular adaptations have been demonstrated between low and high load
conditions (between 30-90% 1RM), whereas tendons do not express
significant mechanical, material, or morphological adaptations when loaded
below 70% 1RM (11, 29). Higher intensity contractions are hypothesized to
induce greater strain on the involved tendon, leading to a loss of normal
collagen crimp, increased fiber recruitment, and greater cell deformation – a
necessary stimulus to evoke the intended consequences (11). Therefore, it is
important to perform your targeted exercises at or above 70% 1RM to
elicit desired changes.
(70% 1RM usually correlates to your 10-15 rep max; however, this number is
highly variable between individuals and can differ from exercise to exercise.
It is best to estimate your 1RM by performing a rep max test with the
highest intensity you can without experiencing pain).

Training Velocity

The exception to the irrelevance of contraction type on tissue adaptation is

plyometric contractions. Load duration appears to be an important
consideration when determining exercise selection. The incorporation of
heavy, slow resistance training has grown in popularity due to the positive
outcomes achieved, whereas rehab efforts solely using high velocity,
plyometric contractions have failed to consistently produce significant
tendon adaptations (11).

Speculatively, high loading rates have also commonly been viewed as a risk
factor for tendon damage and have been proposed to be an important
modifiable variable to consider when performing resistance training (7, 8,
18). Fortunately, Earp et al. conducted a study using barbell back squats to
gain insight on tendon dynamics (and subsequent stress) when velocity
demands are changed. They had participants perform back squats using 60%
1RM either using a deliberate tempo (2 s eccentric, 1 s pause, 2 s
concentric), a self-selected pace without a pause, or perform a maximum-
speed jump squat. Viscous qualities of the tendon unit allowed for very little
difference in tendon lengthening early in the eccentric contraction despite
large fluctuations in speed. However, rate of tendon loading was greater in
the high-velocity conditions during this period – leading to greater force
through the tendon during the late eccentric phase and early concentric
phase comparatively (40). This knee angle, as noted above, is the most
mechanically vulnerable position for the tendon and high levels of stress
within this specific posture pose a substantial concern for overloading a
pathological tendon. Based on this knowledge, it may initially seem
appealing to remove all high-velocity training from your program. However;
this should come as a tough pill to swallow, considering recent
evidence suggests training at your maximum velocity is a valuable stimulus
for improved muscular strength and hypertrophy. Luckily, a closer look
provides room for optimism.

An important distinction is the difference between intent to move at

maximum velocity versus actually moving at a high velocity. It has been
proposed that intention to move at maximum speed, rather than the
specifics of the movement itself, is the critical factor to the muscular
adaptations discussed above (33). And while this concept is far from
unequivocally accepted, there is enough evidence to suggest effort is a
major contributor in this response through neurophysiological mechanisms.
Unlike muscle tissue, the discrepancies in stress to the tendons appear
highly specific to the velocities rather than intent. Thus, if we choose the
right parameters for exercise (primarily heavy enough load), we can
constrain the absolute velocity of the squat (to limit tendon stress) while
still providing maximal effort to move as quickly as possible (to elicit
muscular adaptations). Additionally, even if we were to train at higher
movement speeds, the stress experienced within the tendon changes
throughout the squat. In Earp’s research, once participants initiated
concentric contractions, rate of force development through the tendon
drops to a fraction of the values obtained during the late eccentric phase.
Furthermore, the absolute values of tendon force were significantly lower
during the concentric portion of the lift compared to eccentric at all
velocities measured (40). This finding indicates that velocity’s contribution
to stress is amplified during the eccentric phase of the squat and mitigated
during the concentric.

Earp’s research, taken together with literature concerning intent’s role in

muscular adaptations, provides evidence to the notion that modifying
velocity during the eccentric portion of the squat is beneficial to limit total
stress, while it is probably unnecessary, and potentially suboptimal, during
the concentric aspect. Therefore, it is recommended to use a slow,
deliberate tempo during the lowering phase (typically 3-4
second) followed by maximum effort concentrically.
You can simply perform a self-timed descent, or you can implement an
external pacing device such as a metronome. The choice may matter, as
preliminary data has revealed an interesting observation from performing
tempo training with auditory cueing. Imaging studies have shown that there
are different activation patterns in the brain, with broad cortical and
subcortical activation seen in self-paced movements compared to highly
localized cortical activation when performing metronome-paced movement
(34). This brain activity manifests as changes in excitatory and inhibitory
neural activity similar to that observed following prolonged isometric
contractions, leading to the common adoption of metronome training to
address tendinopathies (24, 34). However, it is important to note that this
data is in its infancy: The neural response has not been investigated within
the specific context of patellar tendinopathies, the movements studied are
typically simple, single-joint contractions, and it is yet to be determined if
there is an additive effect when combined with isometric loading. The
changes observed may simply be due to an external focus during the
movement task and there is probably nothing specific regarding metronome
training that is vital to obtaining this result. Pragmatically, however, the
effort required to use an external pacing device is small, leaving you with a
favorable risk-reward ratio regardless of the true effectiveness.
Rehab Duration

The final consideration is the duration of time you should be actively

attempting to modify training stress to accommodate for the injured tissue.
In short, you probably always want to monitor total training load to some
extent when considering the known injury risk when acute workload
drastically differs from chronic levels (35). However, the most important
time frame for careful monitoring is within the first 8 to 12 weeks from the
start of rehabilitation efforts. The literary consensus is that improvements
in tendon pain and function are not correlated to changes in tendon
structure (36). Pain, as alluded to earlier, is a complex phenomenon that
relays information regarding more than simply the state of the peripheral
tissue. The noxious sensation associated with tendinopathies is usually
reduced significantly within the first several weeks after introducing
therapeutic interventions; however, this does not mean your time rehabbing
your injury has concluded. While there may a drastic reduction in
sensitivity, tendon material properties are relatively unchanged until
approximately the 8-12 week mark and morphological adaptations likely
take much longer (currently, no definite time-course for adaptation has been
agreed upon but consistent findings appear after years of training) (11, 12).
Prospective studies have demonstrated that underlying structural pathology
increases the risk of developing symptoms; thus, the patellar tendon is
particularly susceptible within the crucial period of time where most
athletes feel pain-free despite the persistence of structural insufficiencies
(16).

Additionally, the potential risks are amplified when considering the

mismatch between muscle and tendon development. Muscular adaptations
are noted as early as 3-7 weeks, and muscular force generation capacity is
largely influenced by neural mechanisms early in resistance training
programs. In contrast, tendons rely predominantly on structural factors for
their strength and their physical capacity is minimally influenced until
anatomical adaptations occur (37, 38). Thus, within the first several months
of rehab, the pathological tendon may be subjected to significantly greater
levels of stress from the quadriceps musculature than it is capable of
tolerating (31). The allure of lifting at your previous level is hard to
suppress, especially when under the guise of full-health due to a pain-free
state. Fight the urge and trust the process. Patience is a virtue when
returning from an injury, and even if you do everything right, you can’t rush
physiology. Therefore, deliberate efforts should be made to account for
total stress within the first three months independent of the presence of
pain, and progress should be made in conservative increments.
In Summary:
 If there is pain, it is advised you seek medical consult. Even if you hold an adequate
knowledge of tendon rehabilitation, there are many additional considerations which
need to be addressed. Mobility and strength deficits above and below the knee are
commonly observed following prolonged patellar tendinopathy, and many display
maladaptive compensatory loading strategies which can contribute to future
ailments. Expert evaluation is warranted in most situations.
 Stress is the language our tendons speak. We must stress the involved structures
(through deliberate loading) within our individual envelope of function to facilitate
desired adaptations.
 The degenerative portion of tendons display little to no adaptations following
progressive loading…and this is ok. Pathological tendons compensate for areas of
disorganization by increasing the absolute amount of aligned collagen fibers (those
capable of transmitting force), and this should be the focus of rehab efforts. “Treat
the donut, not the hole”
 Use a within-session and post-session subjective monitoring system to ensure load
tolerance. Keep within-session discomfort to at or below 3-4/10 and ensure daily
testing remains at or below the initial level.
 Begin training sessions with moderate to high intensity isometric contractions to
desensitize the involved tissues and reduce cortical inhibition (typically 5×45
seconds, 70% 1RM leg extension performed between 30-60 degrees of knee flexion).
 Initially avoid loading into deep knee flexion angles. Progress from box squats to
low-bar back squats, to high-bar back squats, to front squats (if wanted). The use of
accommodating resistance can be beneficial to reduce absolute loads in the bottom
position of a squat.
 Finish training sessions with isolated leg extensions (machine or Spanish squat) to
address potential stress shielding of the involved tendon.
 Volume must be consistently tracked. Err on the conservative side, staying closer to
your minimal effective dose rather than your maximum recoverable volume, and
gradually build session and weekly volume as tolerance allows.
 Include high-intensity exercises, at or above 70% 1RM, to adequately drive the
remodeling of collagen structures.
 Perform all major lifts with a slow, deliberate eccentric (preferably with an external
auditory cue) and maximum effort concentric.
 Ideally, allow 36-48 hours between training sessions to optimize net collagen
synthesis.
 Rehab efforts must be consistent for at least 8-12 weeks. Tendon metabolic rate is
slower and the response is generally smaller when compared to activity seen in the
adjoining musculature. One must account for this for several months while
the tendon is still in a vulnerable state.

For anyone looking to keep up to date with tendon rehab, I highly

recommend following Peter Malliaras’ blog
onhttp://tendinopathyrehab.com/. Many of his posts were valuable
resources for this article.