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

Tendinopathy Statistics Tendon Injuries estimated at 30-50% 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: http://www.visionquestcoaching.com/2012/12/11/achilles-tendinopathy/

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

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

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

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”

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.

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: http://breakingmuscle.com/endurance-sports/athlete-journal-andrew-read-entry-41-im-an-ironman

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

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

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 2009:43:409-416

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

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

Continuum Progression

Early Intervention

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

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

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

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

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

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

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

Risk Ratio

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

Questions??