Eccentric training in patients with chronic Achilles tendinosis

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Time to abandon the "tendinitis" myth
Painful, overuse tendon conditions have a non-inflammatory pathology

    Tendinitis such as that of the Achilles, lateral elbow, and rotator cuff tendons is a common presentation to family practitioners and various medical specialists. Most currently practising general practitioners were taught, and many still believe, that patients who present with overuse tendinitis have a largely inflammatory condition and will benefit from anti-inflammatory medication. Unfortunately this dogma is deeply entrenched. Ten of 11 readily available sports medicine texts specifically recommend non-steroidal anti-inflammatory drugs for treating painful conditions like Achilles and patellar tendinitis despite the lack of a biological rationale or clinical evidence for this approach.
    Instead of adhering to the myths above, physicians should acknowledge that painful overuse tendon conditions have a non-inflammatory pathology. Light microscopy of patients operated on for tendon pain reveals collagen separation-thin, frayed, and fragile tendon fibrils, separated from each other lengthwise and disrupted in cross section. There is an apparent increase in tenocytes with myofibroblastic differentiation (tendon repair cells) and classic inflammatory cells are usually absent. This is tendinosis and it was first described 25 years ago, but this fundamental of musculoskeletal medicine has not yet replaced the tendinitis myth. Tendinosis is not merely a long term corollary of short term tendinitis. Animal studies show that within two to three weeks of tendon insult tendinosis is present and inflammatory cells are absent.
    A critical review of the role of various anti-inflammatory medications in soft tissue conditions found limited evidence of short term pain relief and no evidence of their effectiveness in providing even medium term clinical resolution of clearly diagnosed tendon disorders. Laboratory studies have not shown a therapeutic role for these medications. Corticosteroid injections provide mixed results in relieving the pain of tendinopathy.

    If general practitioners, orthopaedic surgeons, and other members of the healthcare professions treating tendon disorders made a quantum shift from previous flawed teaching about overuse tendinitis and adopted these data there would be immediate ramifications. Nomenclature for the clinical presentation of tendon disorders would reflect the true histopathological basis underlying clinical presentation. The term tendinitis would rarely cross doctors' lips. Numerous authorities recommend the term tendinopathy (for example, Achilles tendinopathy) as this acknowledges that the condition is not tendinitis. We favour this term for clinical diagnosis. Most importantly, we must acknowledge, at least till contrary data appear, that anti-inflammatory pharmacotherapy does not provide significant long term benefit in tendinopathy. Nevertheless, high quality randomised controlled trials are urgently needed to examine the long term effects of these medications on tendinopathy. 

    If general practitioners treating musculoskeletal conditions embraced the tendinopathy paradigm, it would provide patients with an accurate description of their condition. It would avoid inappropriate pharmacotherapy with its attendant costs and comorbidity. Furthermore, by accepting need to allow time for collagen turnover and remodelling inherent in the pathology of tendinosis, doctors would be free to provide patients with a realistic prognosis that better reflects the finding of prospective clinical studies. These conditions take months rather than weeks to resolve. 

    Some pockets of the sports medicine, orthopaedics, and rheumatology specialties have adopted this paradigm, but it must no longer remain within that cabal. It is time for medical educators to accept the irrefutable evidence that the term tendonitis must be abandoned to highlight a new perspective on tendon disorders. Adopting the tendinopathy paradigm is essential if general practitioners are to practise evidence based medicine. However, there remain many unanswered questions, particularly with respect to treatment.

Gymboss Timers

FROM: British Medical Journal: 324:626-627

Eccentric training in patients with chronic Achilles tendinosis: normalised tendon structure and decreased thickness at follow up

British Journal of Sports Medicine: 2004;38:8-11

L Öhberg1, R Lorentzon2 and H Alfredson2: 1Department of Radiation Sciences, Diagnostic Radiology, Umeå University, Umeå, Sweden; 2Department of Surgical and Perioperative Science, Sports Medicine and National Institute for Working Life, University of Umeå


Objective: To prospectively investigate tendon thickness and tendon structure by ultrasonography in patients treated with eccentric calf muscle training for painful chronic Achilles tendinosis located at the 2–6 cm level in the tendon.

Methods: The patients were examined with grey scale ultrasonography before and 3.8 years (mean) after the 12 week eccentric training regimen. At follow up, a questionnaire assessed present activity level and satisfaction with treatment.

Results: Twenty six tendons in twenty five patients (19 men and six women) with a mean age of 50 years were followed for a mean of 3.8 years (range 1.6–7.75). All patients had a long duration of painful symptoms (mean 17.1 months) from chronic Achilles tendinosis before treatment. At follow up, 22 of 25 patients were satisfied with treatment and active in Achilles tendon loading activities at the desired level. Ultrasonography showed that tendon thickness (at the widest part) had decreased significantly (p<0.005) after treatment (7.6 (2.3) v 8.8 (3) mm; mean (SD)). In untreated normal tendons, there was no significant difference in thickness after treatment (5.3 (1.3) mm before and 5.9 (0.8) mm after). All tendons with tendinosis had structural abnormalities (hypoechoic areas and irregular structure) before the start of treatment. After treatment, the structure was normal in 19 of the 26 tendons. Six of the seven patients with remaining structural abnormalities experienced pain in the tendon during loading.

Conclusions: Ultrasonographic follow up of patients with mid-portion painful chronic Achilles tendinosis treated with eccentric calf muscle training showed a localised decrease in tendon thickness and a normalised tendon structure in most patients. Remaining structural tendon abnormalities seemed to be associated with residual pain in the tendon. 


Note: Eccentric stretching does work. By doing it, I went from not being able to run because of the acute pain to where I now run in flats with no pain. RKD


Abuse of androgenic-anabolic steroids and adverse effects in athletes
By Fumihiro Yamasawa


    Androgenic-anabolic steroids (AASs) have been a major element in doping in sports for 50 years and they are the most abused substances in athletics. While it is true that AASs can contribute to improved performance in several sports, there are numerous reports of negative side effects, especially in the cardiovascular, hepatobiliary, reproductive and psychiatric systems. This article includes overviews of the abuse of AASs in sport and the techniques used in the practice as well as a detailed explanation of how AASs work on users. Its main focus, however, is on a long list of reported negative side effects, some of which can be fatal. The author concludes by stressing the importance of the fight against doping and the need to educate athletes and those around them, stressing the dangers involved AAS abuse.


    Androgenic-anabolic steroids (AASs) are, variants of the endogenous androgen testosterone, many of which have been synthesised since the 1950's. While AASs have been prescribed ethically for delayed puberty, hematological disorders, catabolic diseases and some kinds of cancer, athletes have, unfortunately, misused them to try to improve their performances. In fact, AASs have been a major element of doping in sports for about 50 years. The history of AAS abuse is practically the history of doping, and sports or competitions where AAS abuse seems prevalent are sometimes referred to as 'Chemical Games:
    According to the annual reports of the IOC Medical Commission, AASs have been the substances most abused by athletes. Over the past 20 years, the IAAF has conducted more than 33,000 doping tests and 37% of the approximately 1,200 positive cases were for AASs. Perhaps the most notorious recent scandal in sports involved many top performers in athletics and several other sports in the United States who illegally used tetra hydrogestrinone (THG), an AAS distributed by the BALCO company that was designed to avoid detection in ordinary doping control tests.
    The World Anti-Doping Code and its associated international standards, including the 'Prohibited List' and the 'Therapeutic Use Exemption; have been in effect since 1 January 2004. Together, these will harmonise and promote the worldwide fight against doping. The 2004 Olympic Games in Athens were the first held under the code and many measures were taken before and during the Games both inside and outside of the competition areas. Unfortunately, Athens has been called 'the Doping Olympics' because the number of positive cases was the highest in the history of the Games. Twenty-four athletes, including seven medallists, tested positive for prohibited substances. AASs were detected in several, including one gold medallist.
    Abuse of AASs is not limited to top athletes. They are well known across a range of sports. It has been reported that many weightlifters have used 20 to 100 times the amount of a normal therapeutic prescription of AAS. AAS use is also known to be a common practice of many amateur and even young sportsmen and sportswomen. Moreover, many of the people who use one or more of the commercially available dietary supplements may unwittingly be taking AASs or precursors of testosterone as some of these products have been intentionally or unintentionally contaminated.
    It is well known that sportsmen and sportswomen abusing AASs indicate disturbances of their mental and physical status. As an extreme example, an increased incidence of premature mortality among power-lifters has been shown. However, the adverse effects cannot be determined scientifically for all cases because many are only described in individual case reports. Moreover, the critical dose of any AAS that causes health troubles has yet to be identified and it may depend on the individual taking the drug.
    Though randomised, double blind, placebo controlled studies are scientifically preferable for the investigation of the effects of any drug, there are ethical considerations when working with sportsmen and sportswomen. It is hardly acceptable to expose healthy young athletes to potentially hazardous drugs in supra-physiological dosages to determine whether these drugs improve performance or to confirm the adverse effects that may occur. Accepting these limitations in investigations, this article will, after introductory explanations of how AASs are used in doping practice and the nature and mechanism of action of naturally occurring testosterone and synthetic AASs, focus on the adverse effects on the health of AAS abuser-athletes.
    The author fully supports current anti-doping regulations. It is the hoped that the provision of the information contained in this article will help athletes, coaches and medical personnel to make morally and ethically sound decisions and that it will contribute to the greater efforts ensure that sport on all levels is both fair and safe.

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In the following sections current knowledge of the health risks associated with AAS abuse are summarised:

1. Cardiovascular disorders
    The occurrence of serious cardiovascular events in healthy young athletes is associated with the abuse of AASs. These events include coronary artery disease, acute myocardial infarction, atrial fibrillation, QT dispersion, development of cardiomyopathy, cerebro-vascular accident, systemic thrombosis and cardiac sudden death. However, it is quite difficult to prove the relation between AAS abuse and these events.
    It is certain that AASs strongly affect the risk factors of cardiovascular diseases. Serum cholesterol metabolism is affected by AAS use. High-density lipoprotein (HDL)-cholesterol is an independent risk factor for the occurrence of cardiovascular disease. There is strong evidence that HDL-cholesterol level is suppressed remarkably by AAS use. This suppression is more than 50% dependent on the steroids used and dosage. The reduction can be observed within a few days of AAS administration. On the other hand, low-density lipoprotein (LDL)-cholesterol levels generally increase with AAS administration. LDL-cholesterol is an independent risk factor for generalised arteriosclerosis, which is characterised by the thickening of arterial walls and narrowing of arterial internal diameters. Most AASs cause water and electrolytes storage in the muscles. Several studies have shown an elevation of systolic or diastolic pressure results from high doses of AAS. High blood pressure is related to water and sodium retention in the body. Edema may occur when large doses of AASs are used. Elevated blood pressure normalises within six to eight weeks of abstinence from AAS.
    Use of AAS may lead to structural changes in the heart. Some echocardiography studies report mild hypertrophy of the left ventricle and thickening of the left ventricular posterior wall and interventricular septum in AAS abusing bodybuilders. However, the reports of structural changes relating to AAS abuse are still controversial, and are based upon the results of published prospective studies.
    In summary, AAS abusers who take large doses for longer periods will have serious disturbances of lipoprotein metabolism and high blood pressure, which are strong risk factors for generalised arteriosclerosis. These can lead to coronary artery diseases, cerebro-vascular disease and peripheral arterial occlusions in AAS abusers. Hence, AAS can present significant cardiovascular risks to the users.

2. Hepatic side effects
    Hepatic side effects due to AAS abuse are hazardous and have been a great concern for athletes. As the 17-alpha alkylated AASs are taken orally, they are absorbed in the small intestine and catabolised by the liver. Alkylation of androgens at the 17-alpha position markedly retards their hepatic metabolism and can cause hepatotixicity. Hepatic side effects include intra-hepatic cholestasis, peliosis hepatis and hepatocellular carcinoma. Fluoxymesterone, methyltestosterone, methandrostenolone, oxandrolone, stanozolol and oxymetholone are substances of the 17-alpha alkylated AAS group. Parenterally administered AASs seem to have less serious side effects on the liver.
    Cholestatic hepatitis has been reported developing after two to five months of 17alpha AAS use. The initial symptoms are prominent jaundice and itch. Increases in plasma activity of liver enzymes such as aspartate aminotransferase (AST), alanine aminotransferase (ALT) , alkaline phosphatase (ALP) and gamma glutamyl transpeptidase (GGT) are often associated with hyperbilirubinemia. Peliosis hepatis is a hemorrhagic cystic degeneration of the liver, which may lead to fibrosis and portal hypertension, Intra-abdominal hemorrhage and rupture of the cyst may lead to fatal bleeding. Recent studies suggest that individuals with abnormal liver functions before AAS use appear to be at risk for liver diseases. Persons who have used large amounts of a 17-alpha alkylated AAS for prolonged periods may develop hepatocellular carcinoma'6, but AAS associated liver cancers have been reported in only a few athletes.

3. Adverse effects on female reproductive system and female athletes
    Daily production and plasma concentration of testosterone is less than 10% in females compared males. Therefore, intra-cellular androgen receptors are not saturated with testosterone in females and exogenous AASs can have strong effects both anabolic and androgenic when used in females. Female AAS abusers may show male muscularity and masculine facial characteristics.
    AASs affect the hypothalamic-pituitarygonadal axis. An increase of plasma androgens will inhibit the production and release of LH and follicular stimulating hormone (FSH) from the anterior pituitary lobe, a process that is known as the endogenous negative feed back mechanism. This results in a decline in serum levels of oestrogen and progesterone. These changes of female hormones inhibit follicle formation and ovulation and thus lead to irregularities of the menstrual cycle. However, there exists an interindividual difference in response to AASs.
    Other side effects of AAS abuse in female athletes are acne, coarsening of the skin, hair loss, recession of the frontal hairline, deepening of the voice, increased facial hair growth, increased sexual desire, breast atrophy and hypertrophy of the clitoris. The breast atrophy, lowering of the voice and hypertrophy of the clitoris are generally irreversible. The severity of the side effects, which occur in female AAS abusers, is related to the type of AAS, dosage and duration of use.

4. Feminising side effects and other adverse effects on male athletes
    AAS administered to healthy males work as 'relatively weak' androgens because plasma concentrations of testosterone are already at a naturally high level. As the androgen-receptor proteins are almost saturated with testosterone and DHT. exogenous AAS cannot have as strong an effect on peripheral cells. So, AASs can work as relatively weak androgens and large anabolic effects may not be obtained in muscle cells even if the athletes use doses of AASs that are 20-100 times larger than the therapeutic dose. In fact, the administration of supra-physiological doses of AASs may not result in any more growth of muscle than is afforded by the normal concentrations of testosterone. Further, much of the AAS will be converted to estrogens in peripheral tissues (aromatisation) and so the administration of testosterone esters causes an increase in plasma concentration of oestrogen. The androgen/oestrogen imbalance will result in gynecomastia, fat deposit, water retention and erectile dysfunction. There is a great deal of difference in what percentage of each AAS will be aromatised to oestrogen. For example, it is reported that 20% of methandrostenolone and 40% of oxymetholone will be aromatised.
    LH and FSH are responsible for regulating spermatogenesis and steroidogenesis in the testis. When AAS is administered to male athletes, the production and secretion of LH and FSH will be reduced within 24 hours in the same manner as in the female athletes, and then testosterone secretion will be decreased. The decline of plasma concentration of LH, FSH and testosterone will result in oligospermia, azoospermia and shrinkage of the testicles. The practice of 'stacking' will strongly suppress the male gonadal function for a long period. The recovery of the male gonadal function will take from several months to one year after interruption of AAS abuse.
    One of the most well known side effects of AAS abuse is gynecomastia in male athletes. Gynecomastia is the abnormal enlargement of one or both breasts, an effect sometimes referred to as 'bitch tits'. It is a great concern for some athletes because of the cosmetic problem. They may experience swelling of the breasts and painful nodular tissues. Gynecomastia in males is caused by increased levels of plasma oestrogens, which are formed byaromatisation and conversion of large amounts of AAS in peripheral tissues. Gynecomastia is generally irreversible and some athletes have to have surgical procedures to remove the soft tissues.
    Some AAS abusing athletes use human chorionic gonadotropin (HCG), anti-oestrogens (clomiphen citrate, tamoxifen) and aromatase inhibitors (testolactone) at the same time to stimulate steroidogenesis in the testis and overcome increased oestrogen activities. These processes are thought to be effective in preventing the formation of gynecomastia. This seems to be theoretically true, but the response is different in each individual. In fact, some cases have shown a worsening of the gynecomastia with these preventive processes. The best treatment for gynecomastia is to quit AAS use completely.
    Additionally, long-term AAS use may result in prostate cancer in males.

5. Psychological effects
AAS abuse (generally with high doses) can cause adverse psychological effects. These include irritability, hostility, aggression, euphoria, increased anxiety, and increased sexual desireD.31. With prolonged high dosage, abusers come to have a dependency on AASs and develop extremely aggressive behaviour. This mental state results in inability to control behaviour, loss of friendship and depression, sometimes with suicide. Other side effects are schizophrenic and manic-depressive disturbances, pathological anxiety, sleep disturbances and acute neurosis, such as hallucinations and paranoia. The occurrence and seriousness of AAS associated mood disturbances are thought to be dose dependent.

6. Infectious complications
    As AASs are often obtained on the black market, contamination can be a serious problem, especially in cases where they are administered parenterally. Skin infections and dermal abscesses at injection sites have been reported. Abusers can also develop infective endocarditis. Human immunodeficiency virus (HIV) and hepatitis Band C virus infections have also been reported among people who shared contaminated needles to inject AASs.

7. Adverse effects in musculo-skeletal system

    Idiopathic ruptures of the tendons are strongly related to AAS abuse. Though AASs may cause hypertrophy of muscles, they will not strength-en the tendons and may even cause tendon degeneration. Tendons, therefore, may be damaged by the contraction of hypertrophied muscles and the risk of tendon rupture will be increased. It may be reasonable to assume that tendon injuries are mostly associated with high doses of AAS abuse over a long period.

8. Adverse effects in pre-pubertal boys

    When androgens and AASs are given in pre-pubertal boys, the effect will be precocious sexual development; penis enlargement and increased frequency of penile erections. AASs will cause the premature closure of the growth plates in the long bones and result in a decrease in the total height achieved.


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