Are You Getting Enough O2? — Oxygen's Role in Muscle Growth

The idea of infinite hypertrophy is somewhat of a pipe dream, chased after by the multi-billion dollar sports supplement industry and the athletes devoted to figuring out how to achieve it.  We know that the structural capabilities of our tendons, bones, and joints limit their abilities to support never ending muscle hypertrophy; however, many still search for ways to manipulate the intrinsic muscle factors that limit muscle growth.

The supplement industry will tell you that there are magic pills and powders that help you evade hypertrophy plateaus. I’m not here to say that those things can’t help you gain muscle, because they can. Sometimes though, they crash your wallet in trial and error process of figuring out which supplements work for you. While there are many things that limit muscle growth, I’m here to talk to you about just one. This “supplement“ is free, easily accessible, and critical to acquiring muscle mass.

The “supplement” I’m talking about is oxygen, and it is essentially everything when it comes to continual muscle growth. Now, for those of you thinking, “Jenn, we all need oxygen,” I agree. But, I’m here to talk to you about why oxygen is critical for hypertrophy (muscle fiber growth) and how you can maximize this free magical substance to help keep you muscles growing.

Before we get going, we’re going to backtrack. We are going to cover some basics about muscle contractions and hypertrophy, as well as, review fiber types and the role of oxygen in muscle growth. Then, once we’re all on the same page, we will go over simple ways to tackle this limitation in your quest for infinite hypertrophy.

Hypertrophic Growth and Energy

We could talk all day about what supplements work and why they work when it comes to skeletal muscle hypertrophy, but the truth is, none of that matters if we don’t understand hypertrophy in general. There are three types of growth going on in muscle in your lifespan: incremental growth, reparative growth, and hypertrophic growth. To make hypertrophic growth happen, we train and induce stressors that tell the muscle to increase in shape, functionality, density, and mass as a way to meet the demands that training imposes. Thus, as you increase the stimuli to the muscle, and increase the functional demands, muscle adapts by increasing contractile, structural, and enzymatic proteins.

Many people will tell you that hormones and nutritional support are what drive hypertrophic growth, but the truth is, it’s relatively independent from those factors. Actually, that’s one of the things that make hypertrophic growth different from incremental and reparative growth. So what does that mean? Well, it means that you can have hypertrophic growth in the absence of exogenous nutrient intake and hormones, as long as your body has the ability to reallocate existing energy supplies to the process. Sorry, fan of bulking, I’m basically telling you hypertrophy can happen without a massive amount of calories¹. You see, each time you lift weights, mechanical tension is applied to the membrane of cells within your muscles. This can activate the same anabolic pathways that hormones and nutrients do. Thus, mechanical tension alone can induce protein synthesis². Don’t misunderstand me, nutrients and hormones obviously help the growth process and increase its magnitude. But, it is the metabolic (O₂ supply) and mechanical (training induced overload) demands that really run the muscle growth show.

Oxygen’s Role in Making Your Muscles Move

When you lift weights and train, you do hundreds and thousands of repetitions in an attempt to induce sufficient damage to your muscles so that they can repair and come back bigger and better than ever. Let’s zoom into what’s happening during each repetition. First, your brain sends signals called action potentials to your muscles telling them to contract. As muscles contract, or shorten, contractile units within each myofibril shorten. These contractile units are called sarcomeres, and they run in a stacked pattern throughout muscle tissue³. Within each sarcomere, there are contractile proteins called myosin and actin that use ATP and calcium to promote sarcomere shortening. We actually call this the sliding filament theory. Thus, we need both calcium and adenosine triphosphate (ATP) to keep muscle contractions going.

During your training session, muscle glycogen and glucose are continuously broken down to make ATP. Fat, or more specifically fatty acids, can also be broken down to yield ATP, but this tends to take a lot longer. To get ATP made in large quantities, your muscles have these structures called mitochondria. Mitochondria are the powerhouses of cells.  We call mitochondria the powerhouses because they generate energy for the cell, in the form of ATP. Through the transportation of oxygen to working muscles via its diffusion from the capillaries, your mitochondria use O₂ to convert macronutrients (carbohydrates, fats, and/or proteins) into ATP.  We call that process aerobic metabolism.

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Since ATP drives the muscle contraction, you need O₂ to make ATP when you rely on aerobic metabolism. O₂ in the muscle can become limited if contraction intensities become to great or if the demand of O₂ exceeds its availability. Thus, ATP levels become depleted and your anaerobic energy supplies become depleted, fatigue sets in. Don’t get me wrong, your anaerobic metabolism is very important and working hard to generate ATP while you lift. However, in those long, high rep sets, you also heavily rely on your aerobic metabolism because your anaerobic system gets depleted first. Furthermore, it’s your aerobic system that promotes your recovery and generation of new anaerobic energy supplies for the next set. Thus, the ability for you to get oxygen into your muscle following the set is a huge mediator of the intensity you can apply to your next set.

Muscle Fiber Types and Hypertrophy

Hypertrophic growth means that you are increasing in the size of muscle fibers. Muscle fibers set out to accomplish the tasks that you ask of them during exercise, and as a result, fibers adapt. Fiber can be classified into different types: Type I, IIA, IIX, and IIB (sometimes you will see IIX and IIB written as IIX/B). These fibers types are classified by the myosin motor protein isoform they express (MHC I, IIA, IIX) or co-express (MHC I/IIA, MHC IIA/IIX, MHC I/IIA/IIX). Myosin, which we mentioned earlier, is one of those contractile proteins that drives the shortening of your muscles as they contract³.  Additionally, myosin isoforms dictate the speed and durations of contractions. Depending on the demand you impose on the body, it is possible to induce a fiber type shift so that your muscles can execute the movements you ask of them at a minimal metabolic cost⁴. Thus, you can imagine that there is an internal muscle feedback loop which links information about the contractile demand, the ATP needed to supply that demand, and the amount hypertrophic growth that occurs.

Your Type I fibers are known as the slow-twitch fibers. This means they have slow contraction rates. They also have a lot of mitochondria. Thus, your Type I fibers, can generate a lot of ATP using aerobic metabolism. Because Type I fibers can make a lot of ATP, they are more resistant to fatigue than Type II fibers. Thus, in the presence of sufficient oxygen and exogenous/endogenous macronutrient supply, these fibers can keep cranking out energy. With a lot of cardiovascular activity, you can shift the metabolic activity within the muscle by acquiring more oxidative enzymes. This can promote the predominance of Type I fibers. Because of this, you might hear people say, “don’t do too much cardio if you want to be a fast, explosive, lifter.” However, please note, fiber type shifting overnight and takes a large amount of training to induce. One run is not going to make you a Type I predominate athlete.

Your Type II (IIX and IIB) fibers are both your easily fatiguable, glycolytic, fast-twitch fibers. This makes sense considering that they have less mitochondria to pump our energy. Thus, to be explosive, they rely more heavily on your anaerobic metabolism (without O₂) to generate energy when working (not at baseline). Type IIX and IIA are not exactly the same though, as Type IIAs are your glycolytic-oxidative fast-twitch fibers. Thus, they have benefits of being glycolytic, powerful, and explosive, while still being somewhat fatigue resistant and oxidative. With the exception of one study, most of the research has shown that bodybuilders have predominantly MHC IIA fibers.

Additionally, they have very few, to no, MHC IIB/X fibers^5-7. Strength training has been show to promote a unilateral shift from IIX to IIA fibers^8-11 and explosive activities like sprinting are reported to elicit a bidirectional shift where MHC I and IIX both shift towards IIA¹². Thus, bodybuilders, or those in search of infinite hypertrophy actually have a greater proportion of IIA fibers, and not IIX or I/IIA/IIX fibers compared to normal individuals who exercise. If you’re wondering why, that is a good question. But think about it.  As you train, your muscles are working. In the heavy sets, you are predominately pounding your anaerobic metabolism to supply you with energy to move the weight and during rest periods, your aerobic metabolism is working hard to replenish your depleted energy stores. Additionally, those high rep failure sets really push blood and oxygen to the muscle, which helps promote the generation of a lot of energy when you have sufficient mitochondrial content. Thus, shifting to a IIA fiber, AKA adding more mitochondria while keeping the fast fiber phenotype, is really just your muscles adapting to the demands you’re imposing.

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Not to confuse you, but Type IIX has been known to be the largest type of fiber. These fibers break down ATP the fastest and have the least amount of mitochondria. I know, this seems to make almost makes no sense at first, because I’m essentially tell you the fibers which have the potential to be the biggest have the least ATP powerhouses? But think about where you find the people with the most Type IIX fibers. These are often the people who have become immobilized or inactive. Inactivity alone leads to the conversion of muscle fibers into IIX. That, of course, should be surprising to some, as many people will tell you it is the Type II fibers that make you explosive. However, elderly people who have more Type IIX fibers also have lower maximal oxygen consumption rates (vO_2max). These people are usually weaker and experience the opposite of hypertrophy, atrophy. Elderly people are often immobile and as they age, the oxidative capacity of their working muscles declines. We actually know that mitochondrial biogenesis (making new mitochondria) declines occurs with aging¹³ and concurrently elderly people experience a shift to more type IIX fibers. Thus, their fibers become more glycolytic, less oxidative, and make less ATP because they have less mitochondria. It all starts to make sense when you consider that glycolytic fibers have longer diffusion distances, and as a result, a larger fiber is required to supply adequate amounts of O₂.  With less O₂ being delivered, the muscle responds by reducing its metabolic demands and metabolic costs of normal function by converting to a IIX fiber¹⁴. At that same time, muscle that isn’t being used becomes lost. Thus, in the absence of directing blood flow to the muscle and remaining active, the muscle gets rid of its fibers that consume higher basal levels of O₂, and allows those with less O₂ demands to predominate^15,16. Keeping this train of thought in mind, it is almost as if we can make the observation that oxygen availability, and the oxidative capacity of a muscle, are critically important in the regulation of muscle growth.

Oxygen and Muscle Growth

As your muscles grow in response to training, existing capillaries that supply O² get pushed away, thus increasing the diffusion distance, or distance of a muscle that a capillary must oxygenate. Capillary neoformation occurs with muscle growth to attempt to increase the O₂ available to fuel that muscle, but not to the extent that your muscle is hypertrophying. This mismatch results in a decreased O₂ supply and capillary density in larger muscles^17,18, thus providing a checkpoint to unchecked muscle growth.

A state without oxygen is known as anaerobic, but this anaerobic environment also hypoxic, because by definition, a hypoxic state is one where there is not an adequate oxygen supply. When your muscle is faced with an anaerobic environment like resistance training, it adapts by upregulating the expression of genes that provide more blood and oxygen to the muscle. Specifically, the mitochondria have a protein within them that senses the training induced hypoxic environment. This then causes a series of events that results in an increase in genes and proteins, like erythropoietin (EPO)^19,20 and vascular endothelial growth factor (VEGF)²¹, which promote getting more O₂ into the muscle.

So perhaps you are thinking, why would muscles have a built in mechanism to sense low energy and why would they respond to that signal by increasing proteins that promote the increase in O₂ supply? Well, it’s because when you demand that your muscles give you hypertrophy, they respond by making sure you have the necessary things for hypertrophy to occur. And, O₂ just happens to be one of those necessary things.

Now, I’m sure there are some of you sitting there thinking, “Jenn, cardio builds oxidative capacity, and cardio kills muscle mass gains. “  I’m here to tell you though that you need O² for your muscles to continue to growth, and without a sufficient oxidative capacity, your muscles can’t keep growing. Don’t believe me? Well, mammalian target of rapamycin (mTOR), the thing most people think about when we think about activation of anabolic pathways on the molecular level, is actually involved in controlling oxygen consumption and genes that regulate mitochondrial biogenesis (the formation of new mitochondria)²². Thus mTOR’s ability to activate metabolic genes could be a way to view that the muscle is always looking for ways to increase its energy levels to support its anabolic growth. Additionally, without sufficient O₂, we activate proteins that increase myofibriliar degradation, thus limiting muscle fiber size. There are physiological mechanisms in place to make sure muscle can grow in an environment of sufficient O₂. When that environment is no longer supplied with sufficient oxygen though, muscle growth is halted. When this halt on growth is implement, it promotes sufficient oxygenation of the muscle, and thus more energy. Remember what I said earlier: muscle doesn’t need nutrients to hypertrophy if it has the means to do mobilize internal energy²². And, those cellular energy levels really rely on the presence of O₂, since it is aerobic, not anaerobic metabolism, which predominately supplies the basal day-to-day energy needs of skeletal muscle.

What to Do

By now, hopefully I’ve convinced you that your muscles need O₂ to keep growing. I won’t lie, though, there is data out there showing that cardio blunts hypertrophy^23,24. Some people hypothesize that cardio-induced catabolic pathways inhibiting anabolic ones²⁵, thus halting training gains. Others believe hypertrophy is halted by cardio because training volume becomes greater than your ability to recover. What side of the fence I sit on in regards to that debate is a topic for another time. However, please note that cardiovascular activity can help you on your quest for hypertrophic gains. To do this, we need to think about ways to increase the oxidative capacity of your muscles, without inhibiting your explosiveness or recovery. So, without further ado, here are my suggestions (which have no scientific support because there is limited research on this topic, to my knowledge).

1. Walking on the treadmill.  Walking will increase your aerobic capacity, because it is a form or aerobic cardiovascular exercise. At a low intensity, it should not be enough of a stressor to cause your muscles to become masses of Type Is. Also, at a low intensity it should help balance an overactive sympathetic response to resistance training, since it is a parasympathetic stimulus. Thus, with low intensity walking, you can prevent overtraining and enhance the oxidative capacity of your muscles. This is what we call a double win.
2. Assistance exercise with high rep band work. This type of concentric-only exercise, at a low intensity, will push blood flow and oxygen into the muscles. Pretty much, it’s giving your muscles the things they need to grow. Also, it shouldn't add more work to recover from, since concentric movements, unlike eccentric or triphasic movements, are not as hard to recover from. Actually, a lot of people use sled work (concentric only) to help improve their recovery.

3. Short rest intervals between sets. Short rest intervals, like on dynamic work or supersets, will increase your heart rate and thus increase stress to the circulatory and respiratory systems. Short rest intervals actually help train your cardiovascular fitness, believe it or not. Thus, when you use submaximal loads and keep the rest short between sets, you are doing cardio, to an extent. How great is that? Also, since it is not adding more training volume, it shouldn’t hinder your ability to recover from your training session.

Now, get out there and get jacked and oxygenated!

References

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