The following is a guest blog by Jasper De Coninck, one of our PT Course graduates. If you’re a science nerd interested in the mechanistic side of how the nervous system adapts to strength training, this is for you. There’s a lot of information in this article, but if you’re just looking for practical tips, this may be a bit of a dense read.
A couple of years ago, I stumbled upon a forum Q&A thread with legendary weightlifting coach John Broz. The thread was 18 pages of pure pleasure. What really stuck with me was Broz posting about his lifters easily benching a small cow without actually training the movement. When asked for a reason, Broz answered, kind of dry but to the point:
If you never benched before in your life, and squatted 2000 pounds, do you think you could bench 500? When you are a monster…enough said.
For me, this just knocked the ball out of the park. Even without ever deliberately practicing a movement pattern, they were just amongst the very elite. Could it be that heavy jerking has such a carry-over to the bench? Of course, these athletes were closing in on their genetic muscular potential. The amount of muscle mass they carry is definitely a piece to the puzzle. Maybe they were even “above their natty max”. But that’s not the point… The point is they all had trained their nervous system for multiple years which could result in a more long-term and permanent adaptation of this system. Strength depends partly on the hypertrophy of the muscle and partly on the ability of the nervous system to contract these muscles. The adaptive changes that happen within the nervous system in response to strength training are called neural adaptations (23).
We’ve all seen those plots displaying gains over time. Initially, the neurological graph maxes out quite rapidly and hypertrophy lags behind. However, this doesn’t mean that a newbie trainee doesn’t have a meaningful hypertrophic response and that all his gains are just the result of neural adaptations. In fact, there are plenty of articles stating the contrary (24,25). These graphs do imply that from the intermediate stage onwards, hypertrophy becomes the main and only driver of progress. They also imply that from then on, neural adaptations are just close to nada… The most well-known example is provided below.
Figure from Sale et al (23)
The short term adaptations of the nervous system
Even in our modern era, where total knowledge doubles roughly every year, we only skim the surface of what’s known in certain areas. Our nervous system is one of those domains. In strength training, the nervous system is viewed as a plastic piece of software that can be altered in a matter of weeks to months. When you start training, you get a meet-and-greet with the lovely newbie gains. These initial gains come fast (and go fast if you stop training the movement pattern). In the past, these strength gains were attributed to (26):
- The increased recruitment and synchronization of the motor units.
- The muscular and muscle fiber contractions getting more coordinated. The sequence changes in which you recruit muscles and muscle fibers. This in turn, results in a smoother movement pattern. In the literature, this is referred to as intra- and intermuscular coordination.
- An increase in the rate of firing of your nerves, resulting in a higher muscular tension. This is called rate coding or neural drive.
- Your technique getting better.
Disclaimer: The following section can be a bit of a dense read with me nerding away. If you’re not interested in geeking out, feel free to skip it.
The model of increased motor unit activation and synchronization, intra- and intermuscular coordination, rate coding and technique is terribly redundant. Increased neural drive stands without a doubt as a contributor. Although motor units can be fired independently, the notion of intramuscular coordination seems less plausible. The impact of a change in force production on such a ‘micro level’ will be negligible. This means that the order in which you recruit adjacent motor units will only have the potential to change strength output to a tiny degree. In the literature, motor units seem to be synchronized and recruited mainly by an increase in neural drive (19).
Inter-muscular coordination stands as a second contributor. The nervous system has a lot of possibilities in the way it recruits muscles. Each muscle (region) has different relative strength levels to one-another. Moreover, these strength levels are dynamic in nature and depend on factors such as your gains or fatigue. This gives a lot of possibilities to make movement patterns more efficient. The dynamic systems theory states that when your movement pattern advances and leans closer and closer to perfection on a ‘macroscopic level’, its variability on a ‘micro level’ increases. You get all jolly and frisky by the sight of an expert squatting. From the outside, each repetition is just an exact copy of the previous one. If you were to open up the hood and take a look underneath at the nervous system, you would see the exact opposite. The expert has a wide range of options to adapt his pattern to different internal or external influences. The last neural factor to strength, technique, is just a redundancy of intermuscular coordination on a more ‘macroscopic level’.
The plastic nervous system can be even more adaptable by making you stronger within a single session. The same goes for being weaker, but discussing the effect of fatigue would be just too obvious. Post activation potentiation (PAP) is a short term improvement in force production due to a previous contraction. Most of the time, PAP is done coupling a strength exercise to increase performance in a consequent explosive exercise. Some of the research behind PAP is still quite hypothetical (11,35). On a muscular level, there could be slight changes in muscle architecture. The oblique line of pull of the muscle fibers, called the pennation angle, could decrease. Therefore, force transmission would be more direct to the line of pull. Explosive exercise could also have an impact on muscle/tendon stiffness. In theory, increased stiffness could improve your performance in the following strength exercise. In practice, this doesn’t add up since tendon stiffness is either unchanged or decreases after exercise. However, there is some hard science available (34). Some proteins within a muscle fiber (the myosin regulatory light chains) become more sensitive to calcium which makes it easier for them to contract. Even connective tissue, like fascia, can adapt to make consequent contractions easier. This white web crawls between all other tissue in the body and gives it its distinct shape. Recently, Schleip et al (27) have shown that it is able to contract. On a nervous system level, there is an increased transmission of the excitation potential of the synapses. As a consequence, signals are conducted faster to the muscles and it becomes easier to recruit higher order motor units. In a nutshell, PAP is the first window where the sum of fitness and fatigue is higher than at the start of a training bout. The positive difference between the two makes you perform better. The second window is obviously after a longer period of rest. By then, you have hopefully supercompensated before a subsequent training bout.
The short term adaptations of the nervous system have been researched the shit out of them thoroughly. These adaptations seem to be functional in nature by optimizing efficiency. Long term adaptations are more structural in nature and mean you’re actually changing the tissue on a cellular level. These are the adaptations that come slowly and are there to stay. We all want them… now. To date, any long term adaptations have been attributed to more structural factors on a muscular level. It seems quite illogical that all other systems of the human body can have a meaningful impact on strength by adapting both functionally, in the short term, and structurally, in the long term, except for the nervous system… Did we fall prey to the sucker effect?
“A Sucker Effect is a magic routine in which the audience is led to believe that they have detected or been told the method of the trick, but the magician double crosses them leading to a surprise ending.”
In training, load should always be within the confines of the capacity of the system. The load should be high enough to stress the tissues slightly above their current tolerance level to create a positive adaptation. Essentially, training induced damage and injury should be viewed on a continuum and should differ only in magnitude and outcome from one another. When load exceeds the capacity of the system, it results in injury. To put it in the form of some primary school math equations:
Load < Capacity = waste of time
Capacity <= Load = training
Capacity < Load = injury
Whether the damage is a consequence of internal force production of the muscle fibers themselves or external force from a trauma, is irrelevant to the body’s reaction. It seems to be the same. The main pathway responsible for hypertrophy, mTOR, is activated in rats after pressure trauma to their muscle (28). The central nervous system (CNS) is comprised of the brain and the spinal cord. After injury or disease in either of them (29,30), mTOR regulates both neuroprotective and neuroregenerative functions. If you look at the speed of regeneration of different tissues to trauma, you can get an idea how quickly they adapt to training. In the literature, the easiest way to get an objective view at this is to take a look at the regeneration time of the tissue at hand. Let us dive into the system regeneration time of muscle, connective and neural tissue.
In a study by Ekstrand (10), they studied the time it took for football players to return to play after a thigh muscle injury: “Median lay-off time of functional disorders was 5-8 days without significant differences between a minor/moderate partial tear or a complete tear.” Being able to return to play doesn’t mean complete structural healing of the tissue at hand. The injury has simply healed enough to be able to do the activity functionally. Mendiguchia (say it 10 times quickly) et al (31) showed that soccer players returning from a hamstrings injury had substantial lower sprinting speed performance. It took approximately 2 months of regular soccer training for performance to return to pre-injury levels. Another study (12) analyzed 255 hamstrings injuries and classified them as grade I or II injuries. Grade I injuries meant an abstinence of 18+-15 days, grade II 21 to 26 days. The conclusion is that muscle tissue is well supplied by blood and has the potential to heal quite rapidly, even when trauma is severe. A rule of thumb taught in academic education is that it takes about 1 week to heal a muscle tear of 1 cm (33).
Tendons, ligaments and other connective tissue are perfused to a lesser extent by the cardiovascular system. The most common injuries are a tear of the wrist flexors, the Achilles tendon, the tendons of the rotator cuff or the dreaded anterior cruciate ligament injuries (ACL). All these injuries take a substantial longer time to heal than muscle tissue. In a review by Yang et al (5), it took about 9-12 months for recovery with residual impairments following the injury. Surgical treatment of rotator cuff tears is quite depressing: 20-95% of chronic tears fail to heal (13). That means you start out as quite the mess, get an operation disabling you for about a year and you end up being the same mess afterwards. Life is good. In another meta-analysis (14), the overall re-tear rate was 25.9% in the single-row group and 14.2% in the double-row group. After an ACL surgery, only 8 of the 11 patients examined 6–12 months postoperatively had regeneration of the semitendinosus tendon with normal anatomical topographies to the level of the tibia plateau (6). In conclusion, connective tissue takes longer to heal than muscle tissue.
Lastly, the nervous system takes even longer to regenerate. The CNS can’t regenerate to full function spontaneously because its environment is too hostile for axon growth to occur (16). The presence of inhibitory molecules in the brain and spinal cord limits axon regeneration and growth in the adult CNS. This is why spinal cord lesions are still permanent and why the brain has to adapt the homunculus functionally after a regional infarct. This means that adjacent cells have to take over the function of the cells that die. The classic is the story of Phineas Gage. An iron rod pierced completely through Phineas’ left frontal brain lobe which consequently changed his behavior and personality. Later in his life, he returned to being more functional and socially adapted because of his brain making the functional adaptation. Hooray for the brain! In the past, it was commonly accepted that the brain only had the potential to develop structurally before birth. Nowadays, there is emerging evidence that it has a limited capacity for regeneration with availability of stem cells in the brain (18). It is, however, insufficient to restore the full function and structure of an injured brain.
The peripheral nervous system (PNS) begins where the nerves leave the spinal cord and ends at the innervated tissue (or the other way around). It is more stimulatory to growth and contrary to the CNS, has the potential to regenerate. Damage can range from a mild praxis of the nerve, to demyelination and destruction of the axon, to complete disruption of the nerve. Neuropraxia is the mildest type of nerve injury where the coating around the nerve sheet (the myelin) is damaged. This demyelination makes the transmission of signals harder. The coating increases the conductivity of a nervous system signal. Axonotmesis is when there is a disruption of the axon without destroying the surrounding connective tissue framework. Neurotmesis is when there is a complete disruption of continuity. A picture speaks a thousand words:
From Martins et al(32): This picture shows a normal nerve fiber and the different grades of nerve injury.
The severity of the trauma predicts the time it takes to fully recover. With neural damage, the distal axon degenerates after which a growth cone develops at the proximal bud. A translation from Martian language: “The part that’s further away from the CNS dies and the part that’s still connected begins to grow.” From Menorca (15) et al: “The rate of regeneration may vary depending on location along the neuron in which proximal segments, closer to the CNS, may see an increase of 2-3mm/day while more distal segments, further away from the CNS, may progress at a rate of 1-2mm/day.” Afterwards, this growth cone needs to become myelinated and the axon needs to enlarge to progress towards functional re-innervation. Big words to say it’ll probably take a while… Muscle tissue can recover for as long as a year when denervated. By two years, chances to recuperate melt as ice in the sun. At that point, chances are very slim that muscle architecture is still intact and endplate integrity is maintained. The structure that receives the axon of the nerve on a muscle is simply too far gone at this stage. Recovery of sensory function in patients with various cutaneous nerve injuries after foot and ankle surgery requires at least 6 months (9). Regaining full sensory function after surgical trauma can take 2-3 years to fully recuperate (15).
This whole and somewhat hefty section gives you an idea about the time it takes to structurally alter the tissue at hand. In order, muscle tissue is structurally more adaptive than connective tissue than neural tissue. Hypertrophy will be more rapid than laying down lines of connective tissue along the lines of force. In a strength trainee, the current most plausible theory is that hypertrophy is dependent on specific tension, muscular damage and metabolic stress (20). In a recent MASS issue, Eric Helms showed that muscular damage doesn’t seem to be related to muscle growth since growth only seems to occur after the damage is healed (21).
Metabolic stress also seems to be less meaningful than originally thought of. In KAATSU, muscle growth seems to happen in the muscles that aren’t being occluded. Occlusion of a limb just makes the muscles which aren’t occluded work harder (22). This was apparent in a study by Kashiwanoha et al (22): arm occluded bench press training resulted in 16% pec growth vs 8% growth of the triceps. Specific tension thus seems to be the main driver for hypertrophy in the drug-free athlete. It was Menno, the Bayesian Bodybuilder himself, who introduced me to this concept. A stronger nervous system gives you the potential to gain more muscle mass by producing more tension. More muscle mass gives you more potential to produce this specific tension.
The maximal neural potential
The maximal possible adaptation can be more or less calculated by taking a look at world class performances in the different lifts. It’d be possible to derive a formula for each different lift by using a database of elite lifting performances. This would be quite the task. Luckily for us, it would be also quite unnecessary, since Greg Nuckols already made such a calculator on his website (17). Kudo’s to the most pettable person in the whole industry. It can give you an idea what part of your strength is attributed to neural efficiency with it topping off at about 85-115% of the calculated value. It’s simply the maximal amount of gains you can make fully disregarding hypertrophy from the untrained to the elite state.
The whole article gives an idea about the total contribution of the rapid plasticity of the nervous system and the resilience of its structural adaptations. Mingled with hypertrophy, people can become exceptionally strong in a movement pattern without training it specifically. If your nervous system is already strong and you don’t achieve hypertrophy, you’re not going to get meaningfully stronger or faster. We all heard the stories about an advanced sprinter picking up strength training for a whole year and progressing to lifting borderline insane weights without ever making progress on the track.
What part is attributed to the central or the peripheral nervous system remains in the dark. Central adaptations will have a total body effect. Peripheral adaptations will only have an effect on the innervated body part or tissue. If the CNS would adapt positively to a squat and your bench would increase immediately, that would be a central effect. If it only had a peripheral effect, your bench wouldn’t increase because of the limited upper body training effect of the squat. Of course, there are certain processes, like myelination, that do occur centrally. Axons get “isolated” more and more which increases the conductivity of the signal. But given the smaller potential of the central nervous system to produce new cells, it seems plausible that the main structural adaptations happen outside of it. It could be that the key for Broz’ Olympic lifters to a stellar bench is training the peripheral nervous system of the upper body by Olympic Jerking away. Perhaps there is a more permanent central neural effect from the heavy squats. Either way, doing heavy taxing compound movements with an explosive effort and repeating this for a long time is just a lot of time spent giving the right stimulus to the nervous system to structurally adapt to being strong and explosive. Broz was onto something…
This picture has absolutely nothing to do with the article. But if you made it so far in this article, you deserve it.
Take home messages
- In the past, only short term adaptations to strength training were attributed to adaptations of the nervous system. Long term structural adaptations, like myelination of the central axons or new cell growth to a certain degree, are probably also made in the nervous system. However, they are slower than the structural adaptations of muscle or connective tissue. This makes them more permanent.
- The speed of adaptation is correlated to the speed of decay. The longer it takes to bring about change, the more permanent the change will be with the nervous system leading the way.
- For the moment, we’re still too ignorant to know for certain what’s really attributable to the central or to the peripheral nervous system. It seems logical that the central nervous system is able to alter its structure to a lesser degree than the peripheral.
- You can get an idea of the potential magnitude of these adaptations by using the calculator at Nuckols’ site. Simply calculating your max possible squat/bench/deadlift at a certain lean body mass gives you an idea of your room for improvement. Since the calculator is based upon a population, your lifts will plateau somewhere between 85-115% of the calculated value.
- Recknor, J.B. and S.K. Mallapragada, Nerve Regeneration: Tissue Engineering Strategies, in The Biomedical Engineering Handbook: Tissue Engineering and Artificial Organs, J.D. Bronzino, Editor. 2006, Taylor & Francis: New York
About the author
Jasper De Coninck is a Belgian physio and strength coach with a main focus on the athletic population. He has a MS in sports and rehab and prides himself in constant education. His main specialties are mobility, movement based therapy, structural balance and weakness correction.