There is much speculation AAS induce deleterious changes in tendon leading to greater rupture potential, especially amongst the medical community..
Research at first suggests that hypothesis could be correct, looking closer at the evidence, most studies on collagen biosynthesis are done on animals, what human studies are done might suggest alternative hypothesis..
We know tendon deteriorates with age, and disuse, which can be mitigated at least in part by resistance exercise..
Some AAS but not all can reduce extracellular water, which could impact tendon stiffness and flexibility..
Users of AAS are more likely to lift heavier weights than non users..
A brief overview of research on tendon structure and physiology:
A muscle is attached to its tendon at the end of the fibers, where the different collagen types of muscle tissue fuse or interdigitate with collagen fibrils of the tendon.? Collagen is known to adapt to different levels of physical activity, and its biosynthesis is coupled to muscular growth.
Davison PF: Tendon, in Weiss B, Jayson MIV (eds): Collagen in Health and Disease. Edinburgh, Churchill Livingstone, 1982, pp 498-505
Tendons consist almost entirely of type I collagen,? whereas in muscle, types I and III are the major Types II and types IV and V are also found.
Light N, Champion AE: Characterization of muscle epimysium, perimysium and endomysium collagens. Biochem J 219: 1017-1026, 1984.
In vitro studies have shown that older tendon tissue displays:
(1) an increase in collagen cross-linking;
(2) a reduction in collagen fibril crimp angle;
(3) an increase in elastin content;
(4) a reduction in extracellular water and mucopolysacharide content; and
(5) an increase in type V collagen.
Kjaer M (2004). Role of extracellular matrix in adaptation of tendon and skeletal muscle to mechanical loading. Physiol Rev 84, 649?698.
Despite the reduction in tendon stiffness with ageing, resistive loading has been shown to significantly reverse/mitigate these alterations
Resistive loading exercise has also been found to counteract the decrease in tendon stiffness induced by prolonged inactivity (bed rest)
Tendon properties are worsened by chronic disuse and ageing, but training can partly mitigate these changes highlighting the plasticity of tendons to variations in mechanical loading.
Reeves ND, Maganaris CN & Narici MV (2003a). Effect of strength training on human patella tendon mechanical properties of older individuals. J Physiol 548, 971?981.
Reeves ND, Maganaris CN & Narici MV (2005b). Plasticity of dynamic muscle performance with strength training in elderly humans. Muscle Nerve 31, 355?364
Research on AAS induced damage:
It was originally suggested by Michna and Stang-Voss that anabolic steroids could cause a predisposition to tendon ruptures. Clinical reports also seem to confirm this. In his later studies, Michna has shown that anabolic steroid treatment causes alterations in collagen fibril architecture in tendons by increasing the number of dysplastic collagen fibrils.
Michna H: Organisation of collagen fibrils in tendon: Changes induced by an anabolic steroid I and II. A morphometric and stereologic analysis. Virchows Arch 52: 87-98, 1986.
Wood et al. found biomechanical changes in tendons after treatment that might also predispose the tendon to injuries, suggesting that anabolic steroids might have adverse effects on the biosynthesis of collagen in tendon.
Wood TO, Cooke PH, Goodship AE: The effect of exercise and anabolic steroids on the mechanical properties and crimp morphology of the rat tendon. Am J Sports Med 16: 153-158, 1988
Some possibilities:
The causes of AAS-associated tendon rupture are still incompletely understood. Two alternative (and not mutually exclusive) hypotheses should be considered:
One possibility is that AAS use has little or no deleterious effect on tendons themselves but merely causes massive hypertrophy of muscles without causing any corresponding strengthening of the associated tendons. Thus, the muscle may simply become too strong for its tendon, increasing the possibility of rupture in response to a sudden stress.
Alternatively, it is possible that high doses of AAS, perhaps in conjunction with intense muscular exercise, may damage the structure of the tendons themselves, making them more vulnerable to rupture even in the absence of excessive stress.
Evidence favoring the latter hypothesis comes from various animal studies, which have typically found that AAS exposure, usually in conjunction with exercise, led to collagen dysplasia, causing tendons to become stiffer and less flexible, with an increased crimp angle and earlier liability to failure..
Inhofe PD, Grana WA, Egle D, Min KW, Tomasek J. The effects of anabolic steroids on rat tendon: an ultrastructural, biomechanical, and biochemical analysis. Am J Sports Med. 1995;23(2):227-232.
Karpakka JA, Pesola MK, Takala TE. The effects of anabolic steroids on collagen synthesis in rat skeletal muscle and tendon: a preliminary report. Am J Sports Med. 1992;20(3):262-266.
Marqueti RC, Parizotto NA, Chriguer RS, Perez SE, Selistre-de-Araujo HS. Androgenic-anabolic steroids associated with mechanical loading inhibit matrix metallopeptidase activity and affect the remodelling of the Achilles tendon in rats. Am J Sports Med. 2006;34(8):1274-1280
Michna H. Appearance and ultrastructure of intranuclear crystalloids in tendon fibroblasts induced by an anabolic steroid hormone in the mouse. Acta Anat (Basel). 1988;133(3):247-250.
Tsitsilonis S, Panayiotis CE, Athanasios MS, et al. Anabolic androgenic steroids reverse the beneficial effect of exercise on tendon biomechanics: an experimental study. Foot Ankle Surg. 2014;20(2):94-99.
However, one human study using electron microscopy found no evidence of collagen fibril ultrastructural abnormalities in the ruptured tendons of 2 AAS users compared with 2 non?AAS using controls.
Evans NA, Bowrey DJ, Newman GR. Ultrastructural analysis of ruptured tendon from anabolic steroid users. Injury. 1998;29(10):769-773.
Something I found in my files:
Inflammation & repair
Connective tissues have very poor blood flow compared to their adjacent muscles. A tendon gets something like 1-3% of the blood moving through a nearby muscle while at rest, and that only increases by around seven times during activity -- whereas a muscle will see around 20 times the flow as at rest.
When you lift something heavy, the muscles are transmitting force through the skeleton through all those tendon attachments, and they're stimulated to grow the same way as muscles. Mechanical tension and stretch signals remodelling and protein synthesis, only in tendons it's collagen turnover that's stimulated.
As we age, our tendons get stiffer, which is good in that they're more resistant to blow-out, but bad in that collagen turnover is way down -- so wear-and-tear can add up as healing is slowed.
What's all this mean? A tendon which isn't moving isn't getting blood, and it's not being stimulated to rebuild any worn-out collagen. All these aches and pains need to be kept moving -- moving them gets blood going, which stimulates collagen turnover -- and preferably kept under as much loading as possible. Obviously you don't want to add to the wear-and-tear, but keeping the aches under some kind of resistance adds to the collagen turnover.
I'm thinking that a lot of the injuries we rack up are happening because the muscles get trained and heal up just fine -- but the tendons are only getting one or two or three exposures to increased blood flow and loading each week (and only that many opportunities to heal and grow) so they gradually wear down. One of the papers I found even suggested that resting was exactly the wrong strategy. You want "adjusted loading rather than absence of loading in the form of immobilization" as he put it.
That doesn't necessarily mean you should be squatting or pressing or whatever every day, but it does give a lot more credibility to the idea of active rest, whether that's going for a walk, doing some push-ups, band work, spending 20 minutes on the cycle or rower, what have you. Keep it moving, and keep it as resisted as possible.
Squatting to a max every day is one of the more extreme solutions but it's got precedent.. I'm still not sure what to make of all the anti-inflamm research.
Inflammation does play at least some role in repairing damage to tissues, but a lot of tissue remodelling processes aren't "damage" and aren't treated like damage.
At least two of the papers I can think of showed that a dose of NSAIDs blocked the COX pathway (which is crucial in the early stages of inflammation) and that this blocked protein synthesis in skeletal muscle after training -- but another study tested the actual strength and size gains over I think 8 weeks and found no effect.
The question to me is how much of the actual tissue damage, which needs the inflammatory response, is key to training? Some of it at least, otherwise MPS wouldn't be inhibited by a COX blockade (and there are other hints that later inflammatory products work some voodoo on satellite cells, but that's a whole different conversation) -- but how much can that matter if the NSAID doses aren't affecting real gains? Real life always has to be the measuring stick.
To me that says something else is going on, and we're missing a big part of the picture. One possibility: they say "protein synthesis" is down, but we don't know what proteins are being synthesized. It could well be that the decrease is because cytokines and prostaglandins and whatever else aren't being synthesized, rather than the fractions we'd need for myofibril turnover.
I would try limiting ibuprofen intake as much as possible, but trying not to sweat it if you really need it. The way I figure, if it's keeping you mobile and training, that's worth whatever biochemical trade-offs we might be taking. And honestly when I'm feeling beat up after a hard week, hitting 800mg of ibuprofen takes the edge off and lets most people sleep like a baby. I think that's worth more than any negatives.
One other thing that's worth a look is topical ibuprofen. You won't get that system-wide crackdown on sickness behavior, but you can apply a dose directly on a joint or tendon that's acting up. Since it won't be in circulation, you don't have to worry about all the negative effects.
During exercise, blood flow increase in both tendinous and peritendinous tissue is reduced by 40%, mainly through cyclooxygenase-2 (COX-2)-specific pathways (Langberg et al. 2003). Because PGs play a nociceptive role and act in concert with other substances during inflammatory processes, and play a role in regulating blood flow, the question arises as to whether it is beneficial to inhibit PG release with non-steroidal anti-inflammatory drugs (or even to block blood flow by sclerosing the peritendinous vessels) in situations where individuals suffer from tendinopathy or peritendinitis.
So COX-2 -> PG (an inflammatory pathway) leads to a pretty sharp reduction in blood flow during exercise...and nuking COX-2 with a dose of ibuprofen might help prevent that reduction.
Research at first suggests that hypothesis could be correct, looking closer at the evidence, most studies on collagen biosynthesis are done on animals, what human studies are done might suggest alternative hypothesis..
We know tendon deteriorates with age, and disuse, which can be mitigated at least in part by resistance exercise..
Some AAS but not all can reduce extracellular water, which could impact tendon stiffness and flexibility..
Users of AAS are more likely to lift heavier weights than non users..
A brief overview of research on tendon structure and physiology:
A muscle is attached to its tendon at the end of the fibers, where the different collagen types of muscle tissue fuse or interdigitate with collagen fibrils of the tendon.? Collagen is known to adapt to different levels of physical activity, and its biosynthesis is coupled to muscular growth.
Davison PF: Tendon, in Weiss B, Jayson MIV (eds): Collagen in Health and Disease. Edinburgh, Churchill Livingstone, 1982, pp 498-505
Tendons consist almost entirely of type I collagen,? whereas in muscle, types I and III are the major Types II and types IV and V are also found.
Light N, Champion AE: Characterization of muscle epimysium, perimysium and endomysium collagens. Biochem J 219: 1017-1026, 1984.
In vitro studies have shown that older tendon tissue displays:
(1) an increase in collagen cross-linking;
(2) a reduction in collagen fibril crimp angle;
(3) an increase in elastin content;
(4) a reduction in extracellular water and mucopolysacharide content; and
(5) an increase in type V collagen.
Kjaer M (2004). Role of extracellular matrix in adaptation of tendon and skeletal muscle to mechanical loading. Physiol Rev 84, 649?698.
Despite the reduction in tendon stiffness with ageing, resistive loading has been shown to significantly reverse/mitigate these alterations
Resistive loading exercise has also been found to counteract the decrease in tendon stiffness induced by prolonged inactivity (bed rest)
Tendon properties are worsened by chronic disuse and ageing, but training can partly mitigate these changes highlighting the plasticity of tendons to variations in mechanical loading.
Reeves ND, Maganaris CN & Narici MV (2003a). Effect of strength training on human patella tendon mechanical properties of older individuals. J Physiol 548, 971?981.
Reeves ND, Maganaris CN & Narici MV (2005b). Plasticity of dynamic muscle performance with strength training in elderly humans. Muscle Nerve 31, 355?364
Research on AAS induced damage:
It was originally suggested by Michna and Stang-Voss that anabolic steroids could cause a predisposition to tendon ruptures. Clinical reports also seem to confirm this. In his later studies, Michna has shown that anabolic steroid treatment causes alterations in collagen fibril architecture in tendons by increasing the number of dysplastic collagen fibrils.
Michna H: Organisation of collagen fibrils in tendon: Changes induced by an anabolic steroid I and II. A morphometric and stereologic analysis. Virchows Arch 52: 87-98, 1986.
Wood et al. found biomechanical changes in tendons after treatment that might also predispose the tendon to injuries, suggesting that anabolic steroids might have adverse effects on the biosynthesis of collagen in tendon.
Wood TO, Cooke PH, Goodship AE: The effect of exercise and anabolic steroids on the mechanical properties and crimp morphology of the rat tendon. Am J Sports Med 16: 153-158, 1988
Some possibilities:
The causes of AAS-associated tendon rupture are still incompletely understood. Two alternative (and not mutually exclusive) hypotheses should be considered:
One possibility is that AAS use has little or no deleterious effect on tendons themselves but merely causes massive hypertrophy of muscles without causing any corresponding strengthening of the associated tendons. Thus, the muscle may simply become too strong for its tendon, increasing the possibility of rupture in response to a sudden stress.
Alternatively, it is possible that high doses of AAS, perhaps in conjunction with intense muscular exercise, may damage the structure of the tendons themselves, making them more vulnerable to rupture even in the absence of excessive stress.
Evidence favoring the latter hypothesis comes from various animal studies, which have typically found that AAS exposure, usually in conjunction with exercise, led to collagen dysplasia, causing tendons to become stiffer and less flexible, with an increased crimp angle and earlier liability to failure..
Inhofe PD, Grana WA, Egle D, Min KW, Tomasek J. The effects of anabolic steroids on rat tendon: an ultrastructural, biomechanical, and biochemical analysis. Am J Sports Med. 1995;23(2):227-232.
Karpakka JA, Pesola MK, Takala TE. The effects of anabolic steroids on collagen synthesis in rat skeletal muscle and tendon: a preliminary report. Am J Sports Med. 1992;20(3):262-266.
Marqueti RC, Parizotto NA, Chriguer RS, Perez SE, Selistre-de-Araujo HS. Androgenic-anabolic steroids associated with mechanical loading inhibit matrix metallopeptidase activity and affect the remodelling of the Achilles tendon in rats. Am J Sports Med. 2006;34(8):1274-1280
Michna H. Appearance and ultrastructure of intranuclear crystalloids in tendon fibroblasts induced by an anabolic steroid hormone in the mouse. Acta Anat (Basel). 1988;133(3):247-250.
Tsitsilonis S, Panayiotis CE, Athanasios MS, et al. Anabolic androgenic steroids reverse the beneficial effect of exercise on tendon biomechanics: an experimental study. Foot Ankle Surg. 2014;20(2):94-99.
However, one human study using electron microscopy found no evidence of collagen fibril ultrastructural abnormalities in the ruptured tendons of 2 AAS users compared with 2 non?AAS using controls.
Evans NA, Bowrey DJ, Newman GR. Ultrastructural analysis of ruptured tendon from anabolic steroid users. Injury. 1998;29(10):769-773.
Something I found in my files:
Inflammation & repair
Connective tissues have very poor blood flow compared to their adjacent muscles. A tendon gets something like 1-3% of the blood moving through a nearby muscle while at rest, and that only increases by around seven times during activity -- whereas a muscle will see around 20 times the flow as at rest.
When you lift something heavy, the muscles are transmitting force through the skeleton through all those tendon attachments, and they're stimulated to grow the same way as muscles. Mechanical tension and stretch signals remodelling and protein synthesis, only in tendons it's collagen turnover that's stimulated.
As we age, our tendons get stiffer, which is good in that they're more resistant to blow-out, but bad in that collagen turnover is way down -- so wear-and-tear can add up as healing is slowed.
What's all this mean? A tendon which isn't moving isn't getting blood, and it's not being stimulated to rebuild any worn-out collagen. All these aches and pains need to be kept moving -- moving them gets blood going, which stimulates collagen turnover -- and preferably kept under as much loading as possible. Obviously you don't want to add to the wear-and-tear, but keeping the aches under some kind of resistance adds to the collagen turnover.
I'm thinking that a lot of the injuries we rack up are happening because the muscles get trained and heal up just fine -- but the tendons are only getting one or two or three exposures to increased blood flow and loading each week (and only that many opportunities to heal and grow) so they gradually wear down. One of the papers I found even suggested that resting was exactly the wrong strategy. You want "adjusted loading rather than absence of loading in the form of immobilization" as he put it.
That doesn't necessarily mean you should be squatting or pressing or whatever every day, but it does give a lot more credibility to the idea of active rest, whether that's going for a walk, doing some push-ups, band work, spending 20 minutes on the cycle or rower, what have you. Keep it moving, and keep it as resisted as possible.
Squatting to a max every day is one of the more extreme solutions but it's got precedent.. I'm still not sure what to make of all the anti-inflamm research.
Inflammation does play at least some role in repairing damage to tissues, but a lot of tissue remodelling processes aren't "damage" and aren't treated like damage.
At least two of the papers I can think of showed that a dose of NSAIDs blocked the COX pathway (which is crucial in the early stages of inflammation) and that this blocked protein synthesis in skeletal muscle after training -- but another study tested the actual strength and size gains over I think 8 weeks and found no effect.
The question to me is how much of the actual tissue damage, which needs the inflammatory response, is key to training? Some of it at least, otherwise MPS wouldn't be inhibited by a COX blockade (and there are other hints that later inflammatory products work some voodoo on satellite cells, but that's a whole different conversation) -- but how much can that matter if the NSAID doses aren't affecting real gains? Real life always has to be the measuring stick.
To me that says something else is going on, and we're missing a big part of the picture. One possibility: they say "protein synthesis" is down, but we don't know what proteins are being synthesized. It could well be that the decrease is because cytokines and prostaglandins and whatever else aren't being synthesized, rather than the fractions we'd need for myofibril turnover.
I would try limiting ibuprofen intake as much as possible, but trying not to sweat it if you really need it. The way I figure, if it's keeping you mobile and training, that's worth whatever biochemical trade-offs we might be taking. And honestly when I'm feeling beat up after a hard week, hitting 800mg of ibuprofen takes the edge off and lets most people sleep like a baby. I think that's worth more than any negatives.
One other thing that's worth a look is topical ibuprofen. You won't get that system-wide crackdown on sickness behavior, but you can apply a dose directly on a joint or tendon that's acting up. Since it won't be in circulation, you don't have to worry about all the negative effects.
During exercise, blood flow increase in both tendinous and peritendinous tissue is reduced by 40%, mainly through cyclooxygenase-2 (COX-2)-specific pathways (Langberg et al. 2003). Because PGs play a nociceptive role and act in concert with other substances during inflammatory processes, and play a role in regulating blood flow, the question arises as to whether it is beneficial to inhibit PG release with non-steroidal anti-inflammatory drugs (or even to block blood flow by sclerosing the peritendinous vessels) in situations where individuals suffer from tendinopathy or peritendinitis.
So COX-2 -> PG (an inflammatory pathway) leads to a pretty sharp reduction in blood flow during exercise...and nuking COX-2 with a dose of ibuprofen might help prevent that reduction.
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The sports surgeon could've fixed it but the "fixing" would have been 3 metal hooks pulling the tendon and muscle back to its original spot. He said it would prob tear again if I went back to BB-type training and when I dieted down,the hooks would be very ugly and right on the surface. I believe being on and off gear for 20 yrs could have damaged my tendons resulting in a tear. I tore it doing my second set of 315lbs on the flat bench- fully warmed up.