Blog
29
01
2019

Muscle Physiology Part 2

Last time we addressed some fundamental concepts in muscle physiology. If you haven’t read the article, I would recommend you read it HERE first, as we are going to get straight into it and the following will require some prerequisite knowledge.

As we discussed, fundamentally muscle grows because individual muscle cells increase in size. They may also increase in number, but this seems to be a very small effect if it does occur. For a cell to increase in size, it must synthesize more protein than it breaks down. Resistance training is the best-known method for stimulating this (yes, more so than eating more protein – so you can shut up about your 80% of results come from the kitchen bullsh*t).

What is it about resistance training that makes it such growth promoting activity? Why does it differ from other forms of exercise?

Good question. The answer is: Mechanical tension.

More specifically, it is the high degree of magnitude of tension experienced. Tension, which most importantly is experienced by the hard to recruit, but more easily grown, high threshold motor units.

What is this tension exactly? Mechanical tension is the loading that each individual fibre experiences through lengthening, shortening or isometric force production. While we experience some degree of tension at all times simply by resisting gravity, resistance training exaggerates the magnitude of tension experienced (and thus muscle size) to a greater degree than any other activity.

Mechanical tension elicits growth via its impact on mechanoreceptors. These sensory receptors are located on the membrane of muscle cells, and are sensitive to both the magnitude and duration of loading or distortion experienced by a muscle cell. The mechanoreceptors then take that information about how much and low long they were impacted by tension and they then transduce this into a biochemical response. This biochemical response activates certain anabolic pathways (mTOR, p70s6k), which then initiate an elevation in muscle protein synthesis lasting hours to days, depending on a few factors.

Muscle Tidbit: Tension is not limited to the longitudinal forces through the musculature. As fibres maintain a constant volume, any change in length, creates a change in diameter and thus produces lateral forces also. 

As we can see in the image above, when the muscle is elongated it becomes “thinner”. However, when we concentrically contract a muscle, pulling the two end points closer together, all the contents of the muscle are squashed together and that then forces them out sideways. This is the result on the right. We can see the muscle has become shorter, but wider. This widening force is a signal that the muscle needs to reinforce itself (hypertrophy) width ways, so that the muscle doesn’t “pop” when it is contracted. This is the process of increasing cross sectional area, or adding sarcomeres in parallel, as opposed to in-series.


So we know that generating tension is important for growing individual muscle fibres. This is where the foundational concepts that we touched on in Part 1 now begin to have a greater level of application.

Tension is the product of binding between the actin and myosin proteins, which slide past one another, as described by sliding filament theory. This binding is called cross bridging. Recruiting high threshold motor units will generate cross bridging in the most amount of muscle fibres possible, as described by the size principle. The force-velocity relationship then informs us that slower movements allow us to create the maximal amount of tension in all those fibres that have been activated (undergone cross-bridging). However, purposefully slow movement velocities due to conscious choice won’t recruit HTMU. Slow velocities must be achieved due to constraints of high force demand or high fatigue status.


A short tangent on working hard:

The above is a nice little reminder that if you’re not growing, maybe you’re not working as hard as what you think you are. Growth really only tends to be significant from training that tests you via sheer load or pain tolerance, and plenty of it.

With the rise in popularity of evidence-based fitness, RPE 7-8 has become the panacea of growth; you get good hypertrophy without diving headfirst off a recovery cliff. And the further you go down the evidence-based rabbit-hole, the more that applied scientific knowledge morphs into apparently common knowledge; “Everyone knows you can do more work over time if you don’t take everything to failure”.

While this is true, it should be noted that “work” isn’t synonymous with “growth” and there’s an assumption imbedded within in the utility of the RPE scale; namely, that you can accurately use it.

Consistently training at ~RPE 8 actually is very likely to be your best bet in regards to a stimulus vs. fatigue trade-off. However, both the research and a plethora of anecdotal evidence from coaches (myself included) demonstrates that just about everyone overestimates their RPE by about 1-3 reps. And if you don’t think you’re one of those people, think again.

Furthermore, if you’re one of those people that not only doesn’t overestimate their RPE, but claims to consistently underestimate it, then I have a potentially unwelcomed opinion for you also: most people I’ve seen who parade that claim around like it’s a badge of honor, also stop their sets short of a true RPE 10. Giving up and failing are certainly not the same thing, both in resistance training and life in general.

The type of person who claims to be so strong-willed that they go for another rep, convinced that they have more in the tank, then realizing half-way through that they don’t, is the same type of person I’ve seen who struggles to grind reps or push them out when the going gets hard. Quite simply, they voluntarily quit when it comes down to the pinch.

If you’re consistently taking yourself to “failure” unintentionally, I would recommend reassessing if that’s actually true failure that you’re hitting. There’s a good chance you’re just bailing on the set once it reaches the part that will actually make you grow.

I only mention this, as ensuring you’re pushing yourself during training will improve the results you get from training far more than any other training or programming variable you can manipulate. Programming is only important due to its impact on allowing you to work as hard as needed, as much and as often as possible, while still recovering. It is not a means to escape those things.

But, I’ve digressed long enough, let’s get back to the physiology again.

Now that we know tension is the primary driver of muscle growth, via its impact on mechanoreceptors, which then biochemically increases protein synthesis over breakdown. And we know to maximise the tension-based stimulus we must be moving something that is heavy or be fatigued (relatively close to failure).

Now, finally, we come to the more exciting, but equivocal mechanisms. This, is where contention begins to creep into the discussion.

For those of you who may be unfamiliar with the scientific literature in this area, in 2010 Brad Schoenfeld (one of, if not the leading researcher on muscle growth) published a massively influential paper. This paper was a brief review of the literature up until that point and discussed the three proposedmechanisms of training induced hypertrophy: Mechanical tension, metabolic stress and muscle damage.

We know about tension already, I won’t belabour that point anymore. However, Brad hypothesised, based on some empirical evidence, that the addition of metabolic by-products or muscle damage may enhance muscle anabolism following resistance training.  

And by all means it seems rather logical, and that assumption has pretty much become convention over the past 5+ years, but let’s examine things a little more closely before we just accept this as true.

Metabolic Stress:

This is the exercise-induced accumulation of metabolites, such as lactate, inorganic phosphate and hydrogen ions. This primarily occurs when anaerobic glycolysis is the primary source of energy production for exercise.

The proposed mechanisms for which metabolic stress causes hypertrophy are:

  • Increased fibre recruitment
  • Elevated hormonal response
  • Altered myokine production
  • Accumulation of ROS
  • Cell swelling

I think the biggest indication that the role of metabolic stress is not as established as some may lead you to believe, is that its proposed mechanisms commit bit of a logical no-no known as “kettle logic”.

Essentially, kettle logic is when you make multiple arguments, that can be conflicting or unrelated each other, in order to support a single point. When this is done, it is an indication that you are trying to find evidence to support your conclusion, rather than determining your conclusion based off of what the evidence actually indicates.

While we can’t completely dismiss metabolic stress due to uncertainty regarding its causative effects, it is something to be wary of. Science will always have elements of doubt and hypothesizing. So we can’t expect perfection. However, when it comes to interpreting science in the most effective manner possible, we must be careful that enticing and novel theories don’t impact our objective analysis of the data. How this applies to metabolic stress is rather simple: growth experienced through high rep, metabolite accumulating sets, still almost certainly occurs through WELL established pathways relating to mechanical tension. It is just that fatigue is required to lower activation thresholds of high threshold motor units, and with fatigue, comes an accumulation of metabolites. They are likely by-products of the process, not causative factors.

Deciding to dig a hole in the ground may result in you having both a hole in the ground and a sore back. But the sore back didn’t cause the hole in the ground. Correlation does not (always) equal causation.

When assessing the evidence in this way, which I contend is the correct way, there is little rationale for metabolic stress inducing growth. Personally speaking, I would be surprised if it didn’t contribute AT ALL – but again, if you want to be objective as possible, it is far from established.

What keeps me open minded about metabolic stress, is that the act of glycogen depletion through anaerobic glycolysis is likely to have some kind of signaling mechanisms to increase the size of the storage tank (muscle). However, the body functions in a complex and convoluted manner, so completely understanding these signaling pathways can be difficult, especially if the magnitude of their effect is small or very distal from the initial stimulus. What we can say confidently is if metabolic stress plays a role in hypertrophy; it is likely a very small effect.

With that said, there is certainly a place for metabolic stress/pump style work in a well-designed training program. However, that is beyond the scope of this article, where we will only be focusing on the physiological effects, not the practical implications.

Muscle Damage:


This is the exercise-induced destruction and deformation of muscle tissue and supporting structures. It can occur on the level of individual fibres, all the way up to large tears in the sarcolemma or cytoskeleton.
I stated in the first article, “for every gimme there’s a gotcha”. This is essentially Newton’s Third Law: For every action, there is an equal and opposite reaction. Using this line of reasoning, we could potentially make a claim that by creating damage, we elicit a response from the body that promotes growth.

BUT – What we must be careful of is presuming that the opposite action of damage is growth. In reality, the antonym of damage is repair. This semantic adjustment then transforms the question into something like: How does repair contribute to growth?

This is not a simple question to answer, even on a conceptual level, let alone when you’re studying the deep mechanistic processes. Early studies led to some erroneous conclusions when they observed there were higher muscle protein synthesis levels when greater amounts of damage were created. This greater level of synthesis did not mean it could be extrapolated into greater hypertrophy in the long term. The higher synthesis levels were a result of greater need for repair, and were also accompanied by higher levels of breakdown also, as dysfunctional muscle fibres had to be removed. All of which muddy the waters when trying to work out if damage leads to growth.

Repair (or recovery) seems fundamental to the growth process; it is what gets us back to baseline. But then that’s it. It doesn’t take us any further…. That’s the job of growth and adaptation.

Think about it like this:

You start with the number 10. You take 3 away. That’s damage. You’re now left with a total of 7. Through the process of repair, you get your 3 back. You’re at 10 again. Now, you add 2 more, that is growth. You end up with a total of 12.

Did the 3 you got back, when you went from 7 to 10, help in you achieving 12? Which was more than your original 10. Did it contribute to growth?

It seems like it did, because it moved us in the right direction… But only after it took us in the wrong direction initially…

What can be said however is that you definitely don’t want to be causing too much damage. While an optimal amount is still yet to be found, it can be said that more almost certainly isn’t better.

For example, rather than going from 10 to 7 back to 10, then onto 12. A scenario with greater damage may look something like: 10 to 6, back to 10, then onto 11. More damage means that a greater amount of adaptive resources are biased towards recovery, rather than adaptation.

However, there’s more! With too little damage, if we become way too afraid of it, say going from 10 to 9, this may only result in recovery and a return to 10 (or ever so slightly above, like 10.1). The disruption to the muscle likely wasn’t large enough to warrant the maximal adaptive response. If you don’t stress homeostasis, then the body will not have to adapt in order to try preserve it.

It is at this point that I want to close this discussion on damage. Quite simply, it should not be a focus of your training. Training hard, and therefore producing tension, will result in damage without purposely trying to generate it. If you do try to create exaggerated amounts of damage, then it is very likely you will reduce your muscle growth, by detracting from your adaptive resources and requiring a greater proportion of repair and rec0very than would have otherwise been needed.

This brings us to the end of Part 2 of our Muscle Physiology series. Things we covered today were:

– Mechanical tension is the reason that resistance training results in hypertrophic outcomes. Tension is detected by mechanoreceptors and transduced into a biochemical signal that alters the balance of muscle protein turnover to favour synthesis.

– Tension (and therefore muscle growth) is maximised when movement velocities are slow, while high threshold motor units are recruited. This typically requires heavy loads or high amounts of fatigue.

– Metabolic stress & muscle damage are likely small contributors to hypertrophy, if at all. This does not mean they should be actively avoided; they will both be present in a well-designed program. However, purposefully chasing them may lead to less than optimal results.

author: Lyndon Purcell

Lyndon is the Head Science Consultant of the JPS Health & Fitness team. Having completed his Bachelor of Exercise Science, Lyndon is a huge proponent of using science and evidence based methods to guide training and nutrition. Body composition (fat-loss and muscle growth) is his area of expertise.