Tendinopathy (Jill Cook workshop)

Questions for Jill Cook

- I understand you have said tendinopathy is almost always due to overloading. 
What is your definition of overloading in this context?
what is not overloadng for several months of stable lifestyle and training.....

Ultrasound-Guided Percutaneous Tenotomy
platelet rich plasma
prolotherapy (dextrose la)
dry needling fenestration.
glyceryl trinitrate patches
dietary interventions i.e. low carb and weight loss

ultrasound, iontophoresis and low-level laser therapy.
Current data support the use of eccentric strengthening protocols, sclerotherapy, and nitric oxide patches
 Preliminary work with growth factors and stem cells is promising, but further study is required in these fields.


I ask because in my experience, overload is not a discrete phenomenon. Rather it has many variables we are yet to understand the relative contribution of.
an athlete's workload may not overload in one month, but may in the next month, due to changes in compromised emotional state, sleep, hydration, nutrition.
If we don't understand the relative contribution of inputs, this makes progressing a rehab workload more art than science.

It seems to me overloading in this context means any workload/stress, that results in compromised tendon recovery.

- have you a protocol or recommendations for avoiding overload and tendinopathy?

- obesity, diabetes 2, post menopausal, adolescent load, ulcerative colitis, seronegative factors.

- Have you liaised with veterinarians from the horse racing industry, in which tendinopathy is a significant pathology?

nitrate patches?

Peter Malliaras 2006 a
Patella and Achilles Tendons Risk Factors
Diabetes T2, insulin resistance, higher total and ldl and lower hdl Cholesterol, waist circumference,

 advanced glycation end-products
Diabetes has a significant impact on the function of tendons due to the accumulation of advanced glycation end-products in the load-bearing collagen. In addition, tendon vascularity and healing may be reduced due to diabetes-induced changes in the peripheral vascular system, and impaired synthesis of collagen and glycosaminoglycan.

The cause of these marrow edema patterns remains unclear—it may be related to marrow hyperemia and related to overlying tendon friction or it may be a result of hyperemia of the overlying tendon sheath. We excluded patients who had symptoms for less than 1 month, so this process is not likely to represent edema from an acute traumatic event, nor is it likely to represent edema-type signal caused by trabecular reorganization in response to stress, as reported for other locations in the foot and ankle [4, 5]. Subtendinous bone marrow edema has a high association with location of symptoms and overlying tendon abnormality, and when present, may be a reliable indicator of true disease. Bone proliferation was observed on MR images of two ankles in the region of subtendinous bone marrow edema, supporting the hypothesis proposed in previous studies that nonarticular spurring may be associated with tendinopathy.

The overexpression of AGEs may explain the fibroblastic proliferation and deposition of collagen matrix in idiopathic frozen shoulder.

In diabetics who have an increased production of an AGE, kidney damage reduces the subsequent urinary removal of AGEs, forming a positive feedback loop that increases the rate of damage. In a 1997 study, diabetic and healthy subjects were given a single meal of egg white (56 g protein), cooked with or without 100 g of fructose; there was a greater than 200-fold increase in AGE immunoreactivity from the meal with fructose.[29]

During long standing hyperglycaemic state in diabetes mellitus, glucose forms covalent adducts with the plasma proteins through a non-enzymatic process known as glycation. Protein glycation and formation of advanced glycation end products (AGEs) play an important role in the pathogenesis of diabetic complications like retinopathy, nephropathy, neuropathy, cardiomyopathy along with some other diseases such as rheumatoid arthritis, osteoporosis and aging. Glycation of proteins interferes with their normal functions by disrupting molecular conformation, altering enzymatic activity, and interfering with receptor functioning. AGEs form intra- and extracellular cross linking not only with proteins, but with some other endogenous key molecules including lipids and nucleic acids to contribute in the development of diabetic complications. Recent studies suggest that AGEs interact with plasma membrane localized receptors for AGEs (RAGE) to alter intracellular signaling, gene expression, release of pro-inflammatory molecules and free radicals. The present review discusses the glycation of plasma proteins such as albumin, fibrinogen, globulins and collagen to form different types of AGEs. Furthermore, the role of AGEs in the pathogenesis of diabetic complications including retinopathy, cataract, neuropathy, nephropathy and cardiomyopathy is also discussed.

In heterozygous familial hypercholesterolaemia, most patients develop Achilles xanthomatosis, a marker of high risk for cardiovascular disease caused by cholesterol deposition in the tendons. Tendon degeneration has also been observed in non-familial hypercholesterolaemia. Monosodium urate crystal deposition in soft tissues is a hallmark of chronic gouty arthritis. In this group of diseases, the mobilization of cholesterol and uric acid crystals is presumably followed by low-grade inflammation, which is responsible for tendon degeneration. Adiposity may contribute to tendon disorders via two different mechanisms: increased weight on the load-bearing tendons and systemic dysmetabolic factors that trigger subclinical persistent inflammation. Finally, tendon abnormalities have been observed in some rare congenital metabolism disorders such as alkaptonuria.

Table 1.

Systemic diseases affecting tendon
Disease     Structural defect or effect on tendon
Inherited disorders    
    Ochronosis (homocystinuria)     Deficient collagen and elastin cross-linking
    Aspartylglycosaminuria (AGU)     Abnormal collagen/deficient cross-linking?
    Haemochromatosis     Accumulation of iron in matrix
    Menkes kinky hair syndrome     Defect in collagen and elastin cross-linking
    Mucopolysaccharidoses     Abnormal collagen fibrils, increased GAG
    Marfan syndrome     Abnormal fibril structure
    Ehlers–Danlos syndromes     Various defects in collagen processing and structure
    Osteogenesis imperfecta     Genetic defects in type I collagen
    Lipid storage diseases     Xanthomas: slow growing lipid deposits
    Myopathies and dystrophies     Abnormal fibril structure
Endocrine and metabolic diseases    
    Diabetes mellitus     Increased glycation and cross-linking of collagen
    Adrenal disorders     Altered collagen metabolism
    Thyroid disorders     Calcification and accumulation of deposits
    Amyloidosis     Accumulation of deposits between fibrils
    Renal disease     Elastosis, destruction of collagen fibres
Rheumatological diseases    
    Rheumatoid arthritis     Destruction of collagen: inflammatory infiltrate
    Spondylarthropathies     Inflammation at insertion, fibrosis and calcification
    Reactive arthritis     Inflammation at insertion
    Reiter's syndrome     Inflammation at insertion
    Gout     Urate crystal deposits and inflammation
    Pseudogout     Calcium pyrophosphate deposits and inflammation

 Because healthy tendons can withstand very high tensile loads—much higher than required for their normal function—these conditions are rarely truly spontaneous and are associated with at least some degree of matrix degeneration [10, 11]. The precise nature of the degenerative process is still the matter of debate. There are a variety of degenerative features associated with tendinopathy, including glycosaminoglycan (GAG) accumulation, calcification and lipid accumulation. However, many of these features are found in normal tendons and are not necessarily pathological [5, 6, 12–14]

Reducing sugars such as pentose derived from the circulation bind irreversibly to long-lived proteins in the matrix [59, 65]. There are no enzymes involved, and sugars attach throughout the length of the collagen molecule. Over time, Amadori rearrangement results in the formation of irreversible cross-links between adjacent sugars, creating Maillard browning products, perhaps better known as advanced glycation end-products (AGEs). AGEs are responsible for many of the altered physical and chemical properties of ageing tissues, such as the reduction in elasticity and decreased solubility. They also have an effect on cell–matrix interactions in the tissue, a possible cause of some of the altered cell activities seen in diseases of ageing, such as osteoarthritis [66, 67]. Although there are a variety of AGEs, the best characterized is the naturally fluorescent cross-link known as pentosidine [68]. Because the turnover of matrix proteins such as collagen is generally very low, AGEs such as pentosidine accumulate gradually on collagen molecules with age. Consequently, the pentosidine content serves as a marker of the molecular age of the tissue, and this property has been exploited in recent studies of the tendon matrix [61]


Objective To produce a best evidence synthesis of the clinical effects of topical glyceryl trinitrate (GTN) in the treatment of tendinopathies.

Design A systematic review of published randomised controlled trials (RCTs) of the use of GTN in patients with tendinopathy.

Data sources MEDLINE, Embase, Scopus and CINAHL from database inception to January 2018.

Methods We examined RCTs comparing the effects of topical GTN with either placebo or other treatments on tendinopathy. Overall quality of each eligible study was determined based on a combined assessment of internal validity, external validity and precision. The level of evidence for each assessed parameter was rated based on the system by van Tulder et al.

Results A total of 10 eligible RCTs were identified including patients with tendinopathy of the rotator cuff (n=4), wrist extensors (n=3), Achilles (n=2) and patellar (n=1) tendons. For all tendinopathies, improvements in pain were significant when comparing GTN versus placebo in the short term (<8 weeks; poor evidence). Significant improvements in midterm outcomes for treatment with GTN versus placebo included the following: patient satisfaction (strong evidence); chances of being asymptomatic with activities of daily living (strong evidence); range of movement (moderate evidence); strength (moderate evidence); pain (at night and with activity; poor evidence) and local tenderness (poor evidence). Patients treated with topical GTN reported a higher incidence of headaches than those who received placebo (moderate evidence).

Conclusions and relevance Treatment of tendinopathies with topical GTN for up to 6 months appears to be superior to placebo and may therefore be a useful adjunct to the treating healthcare professions.

load response test : monitor 24 hour hop pain after strength session (delayed pain post rehab)
build strength before loading rate
2x/week as with horses with tendinopathy

based on Training Impulse developed by Roger Banister first man to break 4 minute mile in 1954
Roger had a 60 year medical career focusing on diseases of the autonomic nervous system.

training peaks software
acute vs chronic training load
ATL = exp. weighted av. of TSS for last 7 days (or 14 days) = today's fatigue
CTL = today's fitness = 42 day exp. weighted av. of trainging over last 3 mths.

TSS  = training stress score = each workout's duration * intensity as % of threshold power/speed
FORM = training stress balance  =  race readiness = yesterday's Fitness-Fatigue  = performance state, am I likely to perform at my best?  negative form means you are likely carrying a lot of fatigue, so have compromised form.

How common is prediabetes?

More than 84 million people ages 18 and older have prediabetes in the United States.1 That’s about 1 out of every 3 adults.


REVIEW ARTICLEPathogenesis and management of tendinopathies in sportsmedicineM. P. Mead1|J. P. Gumucio1,2|T. M. Awan1|C. L. Mendias1,2|K. B. Sugg1,2,3