MrRippedZilla
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The topic of injuries, specifically relating to joints & tendons, has gathered a decent amount of interest across the board to the point where it would be silly for me not to try and add something to the discussion. Building on the excellent work posted by Mythos here, I thought I'd share this amazing paper by Kjaer:
Role of Extracellular Matrix in Adaptation of Tendon and Skeletal Muscle to Mechanical Loading
This paper challenges some of the commonly accepted forms of recovery and coincides nicely with my experience helping clients work around/through injuries. It is 49 very technical pages so I think it's safe to say 99% of you will never read it but I'll do my best to provide a simplified overview here focusing on:
1) Why injuries happen
2) What can we do about them
A short physiology lesson
When a muscle contracts it has the same type of viscoelasticity (the ability to change its physical property based on length) as a rubber band. It's a stretchy, elastic material that when stretched out tightens and quickly snaps back into place when you let go of it.
Muscle can contract under its own power to cause active tension (shortening, rather than lengthening, the muscle). This active tension of the muscle pulls the bone along with it and causes movement around the joint. Simple biomechanics.
Now, our muscles & bones are exposed to extremely high forces from life in general. Something like going for a jog easily generates greater peak forces than anything you'll be doing in the gym. Even basic things that we did as kids like jumping/running around generates high, albeit brief, forces. So with all this force ging on it takes a lot of work to keep our muscles anchored to our bones.
Muscle tissue is surrounded by a network of collagen (making up 25% of the total protein in your body) & support cells known as an extracellular matrix (ECM). An ECM is basically a ladder for cells to to hold on to and produces growth factors along with a bunch of other cool stuff that helps keep these tissues together. So when muscle meets bone, the ECM thickens into a tough band of fibres known as a tendon.
It's down to our tendons to absorb & trasmit the forces of life and they have a pretty impressive range of strength & stretching ability in order to do this.
Tendon talk
In the past, people assumed that tendons and other connective tissues were just useless lumps of meat. The last few decades have taught us that they're actually active biological systems that are involved in signalling alongside hormones, growth factors, etc.
We all know that muscle responds to tension. It exists in a constant state of protein turnover with the damaged proteins being replaced with newly synthesized ones. Normally this is a balanced process but lifting sets off a cascade of chemical signals within the muscle fiber (in response to protein breakdown) that generates protein synthesis. This is how our muscles grow - a positive, rather than neutral, protein balance.
Why am I telling you all this? Well, our tendons respond in exactly the same way. A positive protein balance (collagen) to help make it better able to handle higher loads in the future.
This tendon adaptation is vital. I don't give a shit how much weight your muscles are capable of lifting if your tendons remain unchanged (zero adaptation), it is going to end very, very badly. If tendons along with other connective tissues grow & adapt alongside your muscles, could that alone explain the higher rate of injury that occurs with enhanced lifters? In other words, your muscles can now lift a lot heavier but if the tendons haven't adapted to this new high load...
Back when people thought tendons were useless, they were assumed to be avascular tissues (lacking blood supply). Now we know that they do receive blood but the amount is tiny compared to muscle. Kjaer mentions that, during exercise, a tendon gets only a fraction of the blood flow of nearby muscle:
"It has been possible to demonstrate in human models that blood flow within and around tendon connective tissue increases up to sevenfold during exercise, both in young, middle-aged, and elderly individuals...This increase is by far smaller than the 20-fold increase in adjacent skeletal muscle blood flow under similar exercise conditions."
The blood flow that reaches our tendons is regulated by an entirely different system (I'm not going into it) and our tendons have a relatively low metabolic activity so this tiny amount of blood flow is probably sufficient under normal circumstances but maybe not during training.
As we get older, collagen accumulates advanced glycation end products (AGEs, fascinating separate topic). These stiffer, "glycated" tendons can withstand higher stresses (good) but this comes with a price:
"...the accumulation of AGEs with aging thus indicates a stiffer and more load-resistant tendon and intramuscular ECM structure, but on the other hand reduces the ability to adapt to altered loading, as the turnover rate of collagen is markedly reduced."
Aging, and injuries to the tendons that accumulate AGEs, make your tendons stiffer/more resistant to higher loads but also reduces their ability to adapt to any damage. That is the issue here - the inability to adapt.
To make sure everyone is keeping up:
- Tendon adaptation is vital and may be compromised during AAS use due to muscle overtaking tendon in the rate of growth.
- Blood flow to our tendons is relatively poor, important point to address for recovery from injuries.
- Injuries increase with age due to reduced tendon adaptation and, as a result, reduced collagen turnover.
Overuse injuries
The harder you train, the more often you train hard, the higher the risk of injury. Tendons, like muscle, have a threshold for activity that once you go beyond it, you're risking tendinitis or a lot worse.
Kjaer mentions that though we use the word "overuse" to describe injuries from repetitive loading, we don't actually know if this is the cause. Some injuries occur due to changes in the collagen structure, tendon rubbing over bone and becoming worn out, etc. Overuse may be an issue but we don't know if loading per se is the cause.
He mentions other causes of overuse injuries like tissue inflammation and the regulation of blood flow & metabolism within the tissues that are worth exploring in greater detail.
Inflammation is a localized immune response involving chemical messengers, known as cytokines, that play a role in tendon pain & overuse injuries (also play a part in depression and other conditions). Two cytokines in particular, TNF-alpha & IL-1beta, directly act against collagen synthesis. Since heavy training, especially the kind you're unfamiliar with, elevates these cytokines, I think it's safe to assume that they may contribute to tendon injuries by hampering the process of tissue regeneration.
The inflammatory pathway COX-2 also negatively impacts tendon healing with data (mostly on rats) showing anti-inflammatory drugs to be helpful in this regard. We don't know if a solid dose of NSAIDs helps with overuse injuries but prostaglandins - inflammatory mediators made by COX-2 - seem to be bad for tendons. Kjaer thinks that anti-inflammatories, by blocking the synthesis of prostaglandins, might have a protective effect.
This is interesting since NSAIDs themselves may negatively impact protein synthesis in muscle depending on the data set in question. Whether this negative extends to actual hypertrophy is debatable with studies providing mixed results. Plus AAS use should negate this mostly. Hmm. My interpretation would be that at a normal dose, say below 1g, the positives of NSAIDs would outweigh the negative since being able to train pain free, even with the aid of NSAIDs, would be better for muscle growth than not being able to train at all.
Lack of blood flow is another common feature for tendon injuries. Hypoxia (lack of oxygen) triggers degenerative changes in tendons (think of the reduced capillary density you see in shoulder injuries, same type of thing). Less blood flow + decrease in muscle metabolic rate = broken down tendons. An obvious solution comes to mind here - mobility. By keeping things moving you'd be able to increase blood flow & the metabolic rate of muscle = higher collagen turnover.
Pain itself is cause by the release of nociceptive (pain causing) substances during both overuse & mechanical loading. Pain may actually have nothing to do with the injury (discussed a bit here) itself so something like tendonitis may not be an issue even if its aggravating. This too traces back to the inflammatory signals (COX-2 & prostaglandin in particular).
Another piece added to the puzzle:
- Tendon adaptation is vital and may be compromised during AAS use due to muscle overtaking tendon in the rate of growth.
- Blood flow to our tendons is relatively poor, important point to address for recovery from injuries.
- Injuries increase with age due to reduced tendon adaptation and, as a result, reduced collagen turnover.
- Inflammation plays a role but addressing it through pharmaceutical options may cause more problems than it solves.
Practical advice
Kjaer says:
"...several conservative treatments such as immobilization, physical therapy, stretching, and pharmacological treatment with NSAIDs as well as surgical procedures have by no means produced impressive results."
This goes hand in hand with my experience re the accepted treatments are only slightly better than nothing at all. The pain is eventually controlled but you never fix the issue. It can start all over again with the slightest aggravation and while the "if it hurts, don't do it" strategy is fine for some, for athletes, competitive bbers, etc it simply isn't an option.
Instead, Kjaer suggests trying out some alternatives.
Resistance training has been shown to improve overuse injuries in average folks (not us). Loading "of a certain magnitude" combined with stretching the area "induces increased reorganization of the collagen structures" which may strengthen the tendon. Eccentric loading does this a lot better than concentric and is an excellent method to adopt for certain forms of tendinitis. Plenty of studies available on this (as well as anecdotes) but one example was a case of tennis elbow a client had that went away with eccentric only work, 2-3xweek for a few weeks. Similar approach works for the knee.
The main point of this paper is this - keep the hurt area mobile irrespective of loading. Tendons get a terrible amount of blood at rest, which leads to a reduced metabolic rate and degenerative changes. Rest may feel good but does little to help the tendon. This extra blood flow may encourage healing through increased collagen synthesis.
The findings of this paper fit well with my experience re keeping active with regular loading to help with tendon injuries. The difference between, say, squatting 1-2xweek vs 5-6x week is pretty dramatic. The increased frequency leads to quicker healing, less chance of re-injury, etc - sounds counterintuitive but it's true.
Note that I'm not saying you should all start training with injuries under heavy weight every day. It's just to consider some type of loading as often as you can. Let the area feel a little stretch, some tension and pump a bit of blood in there. Even simple conditioning work like dragging a sled would do. As Kjaer says, healing from tendon overuse injuries "requires adjusted loading rather than absence of loading in the form of immobilization".
The anti-inflammatory suggestion is a controversial one. Ibuprofen at 800mg-1g does work for soft tissue pain and appears to possibly accelerate the process of healing but taking into account the big picture, I'm not sure if chronic use is a good idea. Especially at high doses. A moderate dose with occasional use is fine. I don't have much experience with other anti-inflammatories so cannot add much there.
So, if you've got a pain that won't leave you alone, it might be better to work through it rather than resting and making the problem worse
Speculating beyond this paper
The 4 key areas that this paper tells us to address in order to avoid/treat tendon injuries are 1) allowing time for tendon adaptation, 2) encouraging blood flow into the inflicted area, 3) increasing collagen synthesis and 4) controlling inflammation. Kjaer addressed 2 & 4 so I'll add my thoughts on 1 & 3.
1) - This is the main reason why we see an increase rate of injury among the enhanced population and, IMO, the best way to address it is with better programming when it comes to your training.
Everyone should know that going heavy all the time in the gym is a bad idea but we also know that higher frequency is good for our tendons. Therefore, a moderate intensity, high frequency approach with added eccentric only work during blasts/cycles makes a lot of sense to me if injury prevention is a major priority. You will still generate plenty of growth from the volume & AAS in your system and it allows you to save the high intensity work for the "off" periods where weight progression on the bar is going to be a lot slower anyway (therefore your tendons will have plenty of time to adapt).
3) I honestly don't think this should be the focus for enhanced lifters because the only way to noticeably increase collagen synthesis is through PEDs that most cannot access. Specifically, GH & IGF-1. Localized. Good luck with that.
The impact of AAS on collagen turnover is mixed with the data trending negative but honestly, I wouldn't be too focused on what specific AAS to use (some are better than others here but meh) since the common feature of them all is compromised endothelial function = worse off blood flow/more inflammation = bad for tendons anyway. Note that I'm talking about superphysiological doses, TRT is absolutely beneficial for injury prevention/recovery.
Then you have other pharmaceutical options that may/may not help that I won't go into too much detail on. Bupropion is an awesome fat loss aid and inhibits TNF-alpha, a key cytokine involved with inflammation, so that may be a cool addition in general. You have prostaglandin inhibitors and other more exotic options that will probably do more harm than good considering the end goal (get stronger, bigger, etc) so...TBC.
Excellent paper. Gives everyone plenty to think about.
Role of Extracellular Matrix in Adaptation of Tendon and Skeletal Muscle to Mechanical Loading
This paper challenges some of the commonly accepted forms of recovery and coincides nicely with my experience helping clients work around/through injuries. It is 49 very technical pages so I think it's safe to say 99% of you will never read it but I'll do my best to provide a simplified overview here focusing on:
1) Why injuries happen
2) What can we do about them
A short physiology lesson
When a muscle contracts it has the same type of viscoelasticity (the ability to change its physical property based on length) as a rubber band. It's a stretchy, elastic material that when stretched out tightens and quickly snaps back into place when you let go of it.
Muscle can contract under its own power to cause active tension (shortening, rather than lengthening, the muscle). This active tension of the muscle pulls the bone along with it and causes movement around the joint. Simple biomechanics.
Now, our muscles & bones are exposed to extremely high forces from life in general. Something like going for a jog easily generates greater peak forces than anything you'll be doing in the gym. Even basic things that we did as kids like jumping/running around generates high, albeit brief, forces. So with all this force ging on it takes a lot of work to keep our muscles anchored to our bones.
Muscle tissue is surrounded by a network of collagen (making up 25% of the total protein in your body) & support cells known as an extracellular matrix (ECM). An ECM is basically a ladder for cells to to hold on to and produces growth factors along with a bunch of other cool stuff that helps keep these tissues together. So when muscle meets bone, the ECM thickens into a tough band of fibres known as a tendon.
It's down to our tendons to absorb & trasmit the forces of life and they have a pretty impressive range of strength & stretching ability in order to do this.
Tendon talk
In the past, people assumed that tendons and other connective tissues were just useless lumps of meat. The last few decades have taught us that they're actually active biological systems that are involved in signalling alongside hormones, growth factors, etc.
We all know that muscle responds to tension. It exists in a constant state of protein turnover with the damaged proteins being replaced with newly synthesized ones. Normally this is a balanced process but lifting sets off a cascade of chemical signals within the muscle fiber (in response to protein breakdown) that generates protein synthesis. This is how our muscles grow - a positive, rather than neutral, protein balance.
Why am I telling you all this? Well, our tendons respond in exactly the same way. A positive protein balance (collagen) to help make it better able to handle higher loads in the future.
This tendon adaptation is vital. I don't give a shit how much weight your muscles are capable of lifting if your tendons remain unchanged (zero adaptation), it is going to end very, very badly. If tendons along with other connective tissues grow & adapt alongside your muscles, could that alone explain the higher rate of injury that occurs with enhanced lifters? In other words, your muscles can now lift a lot heavier but if the tendons haven't adapted to this new high load...
Back when people thought tendons were useless, they were assumed to be avascular tissues (lacking blood supply). Now we know that they do receive blood but the amount is tiny compared to muscle. Kjaer mentions that, during exercise, a tendon gets only a fraction of the blood flow of nearby muscle:
"It has been possible to demonstrate in human models that blood flow within and around tendon connective tissue increases up to sevenfold during exercise, both in young, middle-aged, and elderly individuals...This increase is by far smaller than the 20-fold increase in adjacent skeletal muscle blood flow under similar exercise conditions."
The blood flow that reaches our tendons is regulated by an entirely different system (I'm not going into it) and our tendons have a relatively low metabolic activity so this tiny amount of blood flow is probably sufficient under normal circumstances but maybe not during training.
As we get older, collagen accumulates advanced glycation end products (AGEs, fascinating separate topic). These stiffer, "glycated" tendons can withstand higher stresses (good) but this comes with a price:
"...the accumulation of AGEs with aging thus indicates a stiffer and more load-resistant tendon and intramuscular ECM structure, but on the other hand reduces the ability to adapt to altered loading, as the turnover rate of collagen is markedly reduced."
Aging, and injuries to the tendons that accumulate AGEs, make your tendons stiffer/more resistant to higher loads but also reduces their ability to adapt to any damage. That is the issue here - the inability to adapt.
To make sure everyone is keeping up:
- Tendon adaptation is vital and may be compromised during AAS use due to muscle overtaking tendon in the rate of growth.
- Blood flow to our tendons is relatively poor, important point to address for recovery from injuries.
- Injuries increase with age due to reduced tendon adaptation and, as a result, reduced collagen turnover.
Overuse injuries
The harder you train, the more often you train hard, the higher the risk of injury. Tendons, like muscle, have a threshold for activity that once you go beyond it, you're risking tendinitis or a lot worse.
Kjaer mentions that though we use the word "overuse" to describe injuries from repetitive loading, we don't actually know if this is the cause. Some injuries occur due to changes in the collagen structure, tendon rubbing over bone and becoming worn out, etc. Overuse may be an issue but we don't know if loading per se is the cause.
He mentions other causes of overuse injuries like tissue inflammation and the regulation of blood flow & metabolism within the tissues that are worth exploring in greater detail.
Inflammation is a localized immune response involving chemical messengers, known as cytokines, that play a role in tendon pain & overuse injuries (also play a part in depression and other conditions). Two cytokines in particular, TNF-alpha & IL-1beta, directly act against collagen synthesis. Since heavy training, especially the kind you're unfamiliar with, elevates these cytokines, I think it's safe to assume that they may contribute to tendon injuries by hampering the process of tissue regeneration.
The inflammatory pathway COX-2 also negatively impacts tendon healing with data (mostly on rats) showing anti-inflammatory drugs to be helpful in this regard. We don't know if a solid dose of NSAIDs helps with overuse injuries but prostaglandins - inflammatory mediators made by COX-2 - seem to be bad for tendons. Kjaer thinks that anti-inflammatories, by blocking the synthesis of prostaglandins, might have a protective effect.
This is interesting since NSAIDs themselves may negatively impact protein synthesis in muscle depending on the data set in question. Whether this negative extends to actual hypertrophy is debatable with studies providing mixed results. Plus AAS use should negate this mostly. Hmm. My interpretation would be that at a normal dose, say below 1g, the positives of NSAIDs would outweigh the negative since being able to train pain free, even with the aid of NSAIDs, would be better for muscle growth than not being able to train at all.
Lack of blood flow is another common feature for tendon injuries. Hypoxia (lack of oxygen) triggers degenerative changes in tendons (think of the reduced capillary density you see in shoulder injuries, same type of thing). Less blood flow + decrease in muscle metabolic rate = broken down tendons. An obvious solution comes to mind here - mobility. By keeping things moving you'd be able to increase blood flow & the metabolic rate of muscle = higher collagen turnover.
Pain itself is cause by the release of nociceptive (pain causing) substances during both overuse & mechanical loading. Pain may actually have nothing to do with the injury (discussed a bit here) itself so something like tendonitis may not be an issue even if its aggravating. This too traces back to the inflammatory signals (COX-2 & prostaglandin in particular).
Another piece added to the puzzle:
- Tendon adaptation is vital and may be compromised during AAS use due to muscle overtaking tendon in the rate of growth.
- Blood flow to our tendons is relatively poor, important point to address for recovery from injuries.
- Injuries increase with age due to reduced tendon adaptation and, as a result, reduced collagen turnover.
- Inflammation plays a role but addressing it through pharmaceutical options may cause more problems than it solves.
Practical advice
Kjaer says:
"...several conservative treatments such as immobilization, physical therapy, stretching, and pharmacological treatment with NSAIDs as well as surgical procedures have by no means produced impressive results."
This goes hand in hand with my experience re the accepted treatments are only slightly better than nothing at all. The pain is eventually controlled but you never fix the issue. It can start all over again with the slightest aggravation and while the "if it hurts, don't do it" strategy is fine for some, for athletes, competitive bbers, etc it simply isn't an option.
Instead, Kjaer suggests trying out some alternatives.
Resistance training has been shown to improve overuse injuries in average folks (not us). Loading "of a certain magnitude" combined with stretching the area "induces increased reorganization of the collagen structures" which may strengthen the tendon. Eccentric loading does this a lot better than concentric and is an excellent method to adopt for certain forms of tendinitis. Plenty of studies available on this (as well as anecdotes) but one example was a case of tennis elbow a client had that went away with eccentric only work, 2-3xweek for a few weeks. Similar approach works for the knee.
The main point of this paper is this - keep the hurt area mobile irrespective of loading. Tendons get a terrible amount of blood at rest, which leads to a reduced metabolic rate and degenerative changes. Rest may feel good but does little to help the tendon. This extra blood flow may encourage healing through increased collagen synthesis.
The findings of this paper fit well with my experience re keeping active with regular loading to help with tendon injuries. The difference between, say, squatting 1-2xweek vs 5-6x week is pretty dramatic. The increased frequency leads to quicker healing, less chance of re-injury, etc - sounds counterintuitive but it's true.
Note that I'm not saying you should all start training with injuries under heavy weight every day. It's just to consider some type of loading as often as you can. Let the area feel a little stretch, some tension and pump a bit of blood in there. Even simple conditioning work like dragging a sled would do. As Kjaer says, healing from tendon overuse injuries "requires adjusted loading rather than absence of loading in the form of immobilization".
The anti-inflammatory suggestion is a controversial one. Ibuprofen at 800mg-1g does work for soft tissue pain and appears to possibly accelerate the process of healing but taking into account the big picture, I'm not sure if chronic use is a good idea. Especially at high doses. A moderate dose with occasional use is fine. I don't have much experience with other anti-inflammatories so cannot add much there.
So, if you've got a pain that won't leave you alone, it might be better to work through it rather than resting and making the problem worse
Speculating beyond this paper
The 4 key areas that this paper tells us to address in order to avoid/treat tendon injuries are 1) allowing time for tendon adaptation, 2) encouraging blood flow into the inflicted area, 3) increasing collagen synthesis and 4) controlling inflammation. Kjaer addressed 2 & 4 so I'll add my thoughts on 1 & 3.
1) - This is the main reason why we see an increase rate of injury among the enhanced population and, IMO, the best way to address it is with better programming when it comes to your training.
Everyone should know that going heavy all the time in the gym is a bad idea but we also know that higher frequency is good for our tendons. Therefore, a moderate intensity, high frequency approach with added eccentric only work during blasts/cycles makes a lot of sense to me if injury prevention is a major priority. You will still generate plenty of growth from the volume & AAS in your system and it allows you to save the high intensity work for the "off" periods where weight progression on the bar is going to be a lot slower anyway (therefore your tendons will have plenty of time to adapt).
3) I honestly don't think this should be the focus for enhanced lifters because the only way to noticeably increase collagen synthesis is through PEDs that most cannot access. Specifically, GH & IGF-1. Localized. Good luck with that.
The impact of AAS on collagen turnover is mixed with the data trending negative but honestly, I wouldn't be too focused on what specific AAS to use (some are better than others here but meh) since the common feature of them all is compromised endothelial function = worse off blood flow/more inflammation = bad for tendons anyway. Note that I'm talking about superphysiological doses, TRT is absolutely beneficial for injury prevention/recovery.
Then you have other pharmaceutical options that may/may not help that I won't go into too much detail on. Bupropion is an awesome fat loss aid and inhibits TNF-alpha, a key cytokine involved with inflammation, so that may be a cool addition in general. You have prostaglandin inhibitors and other more exotic options that will probably do more harm than good considering the end goal (get stronger, bigger, etc) so...TBC.
Excellent paper. Gives everyone plenty to think about.
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