1. An Updated Tendinopathy Protocol
Presented by Jonathan Hodges, PT, DPT

2. Tendinopathy Statistics
Tendon Injuries estimated at % of all sports injuries
50% among endurance athletes, 6% of sedentary individuals
Achilles Tendinopathy estimated at 55-65% of all Achilles’ tendon disorders
HSR image source:

3. Definitions and Terms Normal Tendon Abnormal Tendon
Regular Collagen Fibers
Inconspicuous ground substance
Spindle Shaped Tenocytes
Minimal vascularity/Nerves
Disorganized and altered collagen
Type III
Abundant ground substance
Activated cells and hypercellular
Increased vessels and nerves
Reference: Why and how exercise is the best treatment for tendinopathy J Cook La Trobe University, CSM 2016

4. The Science Behind Tendon Loading
Ref: From mechanical loading to collagen synthesis, structural changes and function in human tendon, M. Kj.r, H. Langberg, K. Heinemeier, M. L. Bayer, M. Hansen, L. Holm, S. Doessing, M. Kongsgaard, M. R. Krogsgaard, S. P. Magnusson

5. Brief Biochemistry!
Increased IGF-1, TGF-β-1 after exercise, leads to procollagen expression
Decreased in Females
Similar expression whether exercise was concentric, eccentric, or isometric
Suggests strain rather than stress/torque primary mechanism for growth
Chronic, habitual loading needed for tendon changes

6. Biochemistry (cont’d)
Increased tendon stiffness after resistance training
Must be “heavy”, no change in stiffness with light loading, even when matched for volume
“no great difference exists between beneficial loading…and tendon overloading”

7. Potential Mechanism for Collagen Synthesis
Integrin signaled when under strain, release of collagen mRNA and TGF- β-1 and (type I and III), new collagen synthesized.

8. LOADING Loading Cyclical: Bodyweight, jumping, running, cycling
Up-regulation of VEGF, IL-6, COX- 2
Elicits cell rounding
Mechanical: Weight training
Up-regulation of GH (collagen synthesis), endostatin, and increased fibril density
Image source:

9. Definitions and Terms
Excerpted from: Jill Cook, PT, Phd CSM presentation on “Why and How Exercise is the Best Treatment for Tendinopathy”, Feb 2016

10. Staging Tendinopathy Two clinically relevant stages
Reactive/Early Dysrepair: early disrepair, can be reversed
Late Dysrepair/Degenerative: Late disrepair, not reversible
• Remember that not ALL the tendon has pathology • Can have islands of pathology amongst normal tendon
Excerpted from: Jill Cook, PT, Phd CSM presentation on “Why and How Exercise is the Best Treatment for Tendinopathy”, Feb 2016

11. Reactive Tendinopathy
Non-inflammatory proliferative response in the cell and matrix
Occurs with acute tensile or compressive overload
Results in short term adaptive thickening of a portion of the tendon
Will either reduce stress (force/unit area) in increasing CSA or allow adaptation to compression
Results from acute overload (burst of unaccustomed physical activity)
Differs from normal tendon adaptation  tendon stiffening, little change in thickness
JL Cook, CR Pudham, Is Tendinopathy a Continuum? A Pathology Model to explain the Clinical Presentation of Load-Induced Tendinopathy.; Br Jr Sports Med 2009:43:

12. Tendon Dysrepair
Describes the attempt at tendon healing similar to reactive tendinopathy but with greater matrix breakdown
Chronic overload (months or years)
Increased number of cells results in marked increase in protein production
Results in separation of collagen and disorganization of the matrix
More focal and matrix changes more varied than in reactive stage
May have increase in vascularity and neuronal ingrowth
Some reversibility is possible with load management

13. Degenerative Tendinopathy
Areas of cell death due to apoptosis, trauma, or tenocyte exhaustion
Areas of acellularity, large areas of the matrix are disordered and filled with vessels, matrix breakdown, and little collagen
“islands” of degenerative pathology within other stages of tendon pathology and normal tendon
Little capacity for reversibility
Clinically  focal swelling and pain, repeated bouts of tendon pain
97% of tendons that rupture have degenerative change

14. Continuum Progression

15. Early Intervention

16. Protocol Progressions
Need to get Reactive Tendons calmed down!
Isometrics implemented until pain levels reduced (eccentrics often painful), dosed at 5x45 sec
Showed decreased pain 45 min after compared to no change with isotonics
Able to implement during season
Reactive Tendon
Leave them alone
Isometrics for analgesia
Use loads that are tolerated/helpful
Minimize aggravation (needles, frictions, eccentrics, etc)
Degenerative/Late Dysrepair
Strengthen healthy part of tendon
Strengthen Kinetic Chain

17. Heavy Slow Resistance Training
First establish irritability
Traditional Alfredson Protocol (3x15) used on untrained patients.
HSR: 3-5 second concentric and eccentric contraction
Decreased time compared to eccentric protocols
Progressive Loading
Beyer Protocol:
3x15 rep max (RM) week 1
3x12 RM weeks 2 and 3
4 x10 RM weeks 4 and 5
4x 8 RM weeks 6 to 8
4x6 RM weeks 9 to 12
2-3 min rest between sets
RPE of 8 on last 2 reps

18. Eccentrics vs HSR Eccentrics Heavy Slow Resistance
Increase in collagen production
78% training compliance (time?)
80% patient satisfaction (20 of 25) at 12 week f/u
76% patient satisfaction (19 of 25) at 52 week f/u
Increase in collagen production
92% training compliance
100% patient satisfaction (22 of 22) at 12 week f/u
96% patient satisfaction (21 of 22) at 52 week f/u

19. Final Thoughts Need to correctly stage tendon
Patient response primary measure
Mechanical loading needs to be matched to cyclic loading.
Rest turns tendons to mush!
HSR appears favorable to eccentrics for patient satisfaction.
Acute:Chronic loading needs to be established

20. Three Primary Considerations
Evaluation of Health Status
Clinical presentation
Evaluation of Participation Risk
Sport Risk
Decision Modification
Coaches/Season/Fear

21. Acute:Chronic Establish workload ratio
External Load (reps) x
Internal Load (time) x
Rate of Perceived Exertion
Acute (current week) Rate of 0.5 equals half of chronic (previous 4 weeks), 2.0 acute:chronic ratio equals double previous 4 week load
See injury rate increase at 1.5

22. Acute:Chronic Case Study Hamstring Strain
30 meters of sprints over 30 min workout (1.0m/min)
Week 2-3: 750 meters/30min (25m/min)
Re-Injured week 4

23. Risk Ratio

24. NVPT RTS Criteria
Single, Triple, and Crossover Hop Test, 90% of Uninvolved limb (UL) valgus fail sign
IKDC greater than 90%
T-test sub 11 sec
Side Plank Hip ABD greater than 90% of UL, No more than 1 DN (dysfunctional nonpainful) score on SFMA
Anterior Y-balance greater than 90%
Acute:Chronic ratio of sub 1.5 of normal in-season load

25. Questions??