Homeostasis: A Framework for Strength Gains

By: Barbell Logic Team

Stress-recovery-adaptation is a predictable process of survivability. One that we have learned to hijack in order to direct physical change. While the overarching process is fairly predictable, we are still figuring out exactly why certain types of stress lead to specific physical changes—exactly what is it about the forces encountered in barbell training that cause us to get stronger? And if we know that, can we better steward the process of recovery to improve our training outcomes? I have found it helpful to consider these questions from the beginning of the process, the disruption of the status quo that we covet with every training session. This change from and return to homeostasis may not provide any hard and fast answers right now, but it helps to understand the process of training and the best practices we’ve developed that go with it.

Homeostasis: A Framework for Strength Gains

Photo by Alora Griffiths on Unsplash

Sometimes in the course of developing best practices, intuition precedes understanding. The history and development of strength training are like this. As far back as 500 BC, there are stories of humans using the concept of progressive overload to get stronger. This makes sense. The idea that if you lift gradually heavier weights, you will get gradually stronger is reasonable. No “Eureka!” moment here; from the beginning of human history, we’ve grown, developed, and become stronger simply by interacting with our environment. As obvious an observation as this seems, we don’t really know why it happens.

So, we’ve reversed engineered some explanations. The concept of Stress-Recovery-Adaptation is one way to explain the changes we observe through training. It starts out with the simple principle that living organisms and living tissue want to stay that way. When they encounter stress that threatens to disrupt the status quo, they react, changing and adapting, rising to the level of the stress-event or, sometimes, falling to a level conserved activity and energy usage. When the stress is a physical activity for the purpose of training, it is followed by a period of decreased capacity while the body reroutes resources to support the adaptation.

Stress-recovery-adaptation is a predictable process of survivability. One that we have learned to hijack in order to direct physical change. In our calculated manipulations of this process, we are still figuring out exactly why certain types of stress lead to specific physical changes—exactly what is it about the forces encountered in barbell training that cause us to get stronger? And if we know that, can we better steward the recovery process and improve our training outcomes? It is helpful to consider these questions from the beginning of the process, the disruption of the status quo that we covet with every training session. This change from and return to homeostasis—the body’s dynamic state of equilibrium—may not provide any hard and fast answers right now, but it helps to understand the process of training and the best practices we’ve developed that go with it.   

Force Production and Trainability

We’ve discussed homeostasis as the constant regulation of the body’s systems that keep us alive and kicking. Core temperature, blood glucose levels, blood PH, fluid and energy balance, and the amount of oxygen in our blood are some of the dynamically regulated conditions of our bodies. When something in our environment disrupts these conditions, your body has built-in reactions for short- and long-term changes that either bring the system back into balance or that adapt the system to a changed environment, changing the body’s set point for that set of regulatory controls. As an example, we discussed the changes that occur when you move from sea-level to altitude, resulting in a change in your blood oxygen level. You can live at altitude because of this changed set point; you have a “new normal” so to speak.

This impressive resistance to disequilibrium has become a powerful tool that we use to manipulate our physiology in beneficial ways. If we are going to do so, however, it is helpful to know how our bodies tend to respond to intentionally induced change and how we can facilitate and maximize the benefits of that process. Endurance athletes will change their altitude for training purposes; we change our gravity.

At the most basic level, increases in strength come from loading. Strength is the ability to produce force, and we measure strength by our ability to produce force against an external resistance (the barbell). This is an important (somewhat catchall) definition of strength. Your ability to produce force involves neural-motor components, such as the rate and efficiency with which you recruit motor units; it includes mechanical, contractile components, including muscle size contractile capacity; and it includes coordination between the neural-motor and the mechanical properties muscles, meaning your natural and learned coordination affects your ability to produce force. Of these, we are most concerned with the mechanical component of force production, with your muscles’ contractile ability to produce force and overcome gravity.  

The trainability of an adaptation depends on our ability to cause an overload, the specificity with which we can direct that overload toward the desired adaptation, and the reversibility of that adaptation. Neural-motor components of strength change rapidly and to a small degree with targeted training, tapering off quickly. The same goes for your skill and coordination to produce force in specific ways. There is a narrow range of improvements in both these areas.

Muscle size and ability to produce force, however, are eminently trainable. We’ve seen people gain strength and maintain muscle mass beyond their eighth decade of life. You can start lifting right now and continue to induce muscular overload and adaptive responses with training for just about as long as you are able to get up from your bed every day. So, while the components of force production are more involved than just the contractile potential of your muscle cells, that’s where we are going to focus on changes for this a discussion of stress, recovery, and exhaustion through the lens of homeostasis.

What Stress is Causing Changes in Force Production

Homeostatic regulation involves a process that has a simple, overarching framework but that is exceedingly complicated and not completely understood at the cellular level: Receptors sense stimuli, receiving information about changes to your environment and transmitting that information to a control (or integration) center. The control center receives and processes the information, comparing it to the set point and signaling effector cells. These effector cells—muscles and glands—either oppose or enhance the stimulus. This can happen very quickly, as may have happened as a child when you decided to test your mom’s theory that the stove is, indeed, hot—pain led to an involuntary muscular response to jerk your hand back from the stimulus before you could think to cry out. Or this process can be more gradual, such as that which happens when we train, inducing a stimulus that leads to a greater ability to produce force.

An example of homeostatic regulation. In a negative feedback loop, a stimulus—a deviation from a set point—is resisted through a physiological process that returns the body to homeostasis. (a) A negative feedback loop has four basic parts. (b) Body temperature is regulated by negative feedback.
OpenStax [CC BY 4.0 (https://creativecommons.org/licenses/by/4.0)]

The observation that lifting heavy weights makes you stronger is a correct one; mechanical stress contributes to muscle protein synthesis. There are some different possible mechanisms that can cause this result, however. Because the mechanical stress of high-intensity lifting also causes muscle damage, it has been thought that exercise-induced damage to the sarcomeres (the smallest contractile component of muscle cells) is the driving force behind muscle growth and increased contractile properties. Mechanical stress strains the muscle fibers, signals the release of protein-damaging calcium proteases, and initiates an inflammatory response. The short-term result is muscle damage and a decrease in your ability to produce force followed by increased protein synthesis and a recovered state of improved ability to produce force. This, however, is a little bit problematic. If exercise-induced muscle damage were the only thing driving of strength increases, then we should observe that athletes who engage in the most muscle-damaging exercises are also the strongest. We would expect things like downhill running or eccentric-focused training to promote the greatest muscle hypertrophy. Instead, the exercise stimulus itself seems to affect the changes in muscle growth, and at least some hypertrophy can be shown with minimal muscle damage. It is possible, then, that muscle damage is a side effect and mechanical loading is the crucial part of resistance training for increased protein synthesis.

But it must be conducted at sufficient intensities. In the homeostatic framework, stress must be sufficient to disrupt the system’s happy state of equilibrium in order to signal change and cause muscle growth. Protein synthesis is directed by the mTOR signaling pathway. “The mTOR pathway regulates homeostasis by directly influencing protein synthesis, transcription, autophagy, metabolism, and organelle biogenesis and maintenance.” (The Neurology of mTOR) In the regulation of protein synthesis, mTOR signaling responds to mechanical loading. So, at least part of what makes us stronger is that when we train, the loading and mechanical strain of training signals an increase in muscle protein synthesis. (Mitsunori Miyazaki and Karyn A. Esser, “Cellular mechanisms regulating protein synthesis and skeletal muscle hypertrophy in animals,” (April 2009).) This is not the ONLY signal that causes increased protein synthesis. “We believe that this mechanical pathway likely acts synergistically with changes in amino acid uptake and growth factor availability to contribute to the prolonged activation of mTOR signaling following high resistance contractions/mechanical overload.” (Id.) Perhaps the only conclusion we can make is that it is necessary to lift sufficiently heavy weights in order to get stronger. Which receptors send what signals to the mTOR control center, leading to muscle growth is…complicated. The observations we can make at the cellular level may be involved in signaling or may just be symptoms of training stress unrelated to actual improvements in strength—more likely they are a little bit of both.

Our goal here is to set up a framework for discussing training stress, recovery, and exhaustion as the disruption and regulation or failure of our bodies’ homeostatic regulation. The stress that causes change is readily observable without us fully understanding the cellular mechanisms involved. The next step is to consider what happens after we lift weights, between bouts of training that actually makes us stronger. In this interim period that we call “recovery,” what happens on the inside to help us grow muscle and become better at producing force? And, perhaps more importantly, what can we do to aid recovery, facilitating the regulatory homeostatic processes? Should we be taking a closer look at the industry that has shot up around recovery, from cryo- and compression therapy to specially formulated drinks and supplements? What are the practices that actually help us move or maintain our set point for strength?

Next up, homeostasis and recovery….