Many coaches are of the belief that if heart rate is maintained between 120 and 150 beats per minute, any activity or combination of exercises will elicit structural and functional cardiovascular adaptations and promote recovery. Unfortunately, this simple story is both incomplete and inaccurate, and leads to many coaches and athletes accumulating far more stress than they recognize, resulting in insufficient recovery, decreased performance, autonomic dysregulation, undesirable adaptations to training, a decrease in respiratory and movement variability, and pain/injury.
Including “low intensity” cardiac output work in a training program has become a common practice of many performance coaches and medical practioners, with the goal of increasing cardiac efficiency and local tissue aerobic capacity via angiogenesis and mitochondrial biogenesis, as well as facilitating active recovery in between high intensity training sessions by increasing blood flow and oxygen delivery throughout the body. It is said that as long as heart rate is maintained between 120 and 150 BPM, stroke volume is optimized, the preload of the left ventricle required for (potential) eccentric hypertrophy is maximized, the working tissue is performing in an aerobic, oxidative environment, and the intensity of the training is low enough to enhance recovery.
The picture above was taken during what I believed to be a low intensity, active recovery run. I was running at about 11 minutes/mile, which is very slow considering the fact that I’ve run a half marathon at 8:40/mile, have a PR mile of 6:19, and my heart rate never got above 155 BPM at any point. In fact, it was much lower during the majority of the run.
Yet, the Moxy data displayed on the watch tells a very different story. The muscle oxygen saturation (SMO2) in my right quad was between 13 and 23% for about 58 minutes of my 60-minute run…
This means that for almost the entirety of my “low intensity, active recovery” run, my quad was operating in a low oxygen environment where O2 utilization exceeded O2 supply by a substantial margin.
These tissues were in “survival mode” for most of the run, where O2 had all but bottomed out. In this scenario, glycolysis is upregulated and relied upon in order to meet the demands of the activity.
The low O2 environment and upregulation of glycolysis will draw water into the cell, altering cell structure, ion gradients, membrane potential, and the ordering of water in the cell. This will move the cell out of the ready state and demand significant recovery before structure and function can be restored.
The “ready state” of the cell is a concept introduced to me by Aaron Davis of Train Adapt Evolve. The ready state of the cell is characterized by:
- The internal protein structure of the cell is in an unfolded state
- High concentrations of PCr in the cell
- Low levels of structured water in the cell
- Potassium in the cell
- Sodium out of the cell
- Calcium out of the cell
- An internal environment within the mitochondria that allows for optimal Electron Transport Chain function and oxidative metabolism
If the cell is not in this state, oxidative metabolism is compromised, which leads to increased reliance on glycolysis to replenish PCr, the direct donor of a phosphate to ADP to make ATP.
Glycolysis, though always active, is much less efficient, has a far lower capacity, and a much greater cost, than oxidative metabolism. This leads to the early onset of fatigue and to the employment of compensatory movement strategies in order to continue to produce a certain output.
The key to understanding the ready state is to understand that the management of energy underlies every reaction in our bodies. Not only do actions that cells must carry require energy, but the very structure of the cell that allows the maintenance of optimization of function, response, and adaptation demands energy.
In order to understand how energy plays a critical role in the maintenance of order in the cell, it’s vital to understand that the cell is not the spacious, gelatinous blob that we are shown in textbooks in school. The interior of the cell is actually incredibly crowded with proteins that are vital to cell function including transferring substances throughout the cell, translating forces to the cell’s nucleus to induce gene transcription and translation, allowing the cell to move and change shape, etc.
ATP is not only the energy currency of the cell, but a critical molecule in maintaining the separation of the crowded, protein-dense cellular interior. The structure of the interior of the cell is vital to the maintenance of the ion gradients and internal/external environment indicative of the ready state detailed above. Energy, structure, and function are highly interrelated and dependent on one another.
Despite my low heart rate and perceived exertion (I’m not sure I could run any slower and still actually be running), this kind of work is immensely taxing and highly fatiguing. It comes as no surprise that I’ve noticed the day after these long runs my lower body feels thrashed, my quads feel incredibly toned up and “tight”, and I tend to experience more of the locking, catching, and pain symptoms in my right knee that I’ve had periodically since running the half marathon in Philadelphia last November.
If you, your athletes, or your patients have this response to “low intensity” training, you are layering on a great deal more stress than you are accounting for that demands resources and recovery.
If this kind of reaction occurs on your low intensity training days, you are likely compromising the quality of your high intensity days and accumulating more stress than you body can recover from. This may be one of the key factors in why concurrent training programs fail. People point the finger of blame at the antagonizing physiological cascades associated with resistance training and endurance training, but the reality just may be a dosage issue that they don’t even realize exists and not a physiological mismatch.
In addition to the fact that you may not be facilitating recovery if your low intensity work is not actually low intensity, you not be eliciting the cardiovascular adaptations that you believe are taking place in response to cardiac output work.
Past a certain point in development, it takes a tremendous amount of very specific stimuli to get structural changes to the heart such as eccentric left ventricular hypertrophy. This requires a substantial preload of the left ventricle, allowing the walls of the heart to eccentrically lengthen to a significant degree before concentrically contracting to eject the blood.
Over time, repeated exposure to this type of work could theoretically increase the diameter of the left ventricle, leading to an increased capacity to fill and eject larger volumes of blood with each beat, therefore improving efficiency and reducing heart rate for a given intensity.
If you are strong, muscular, highly trained individual with a bias toward force production, you may occlude venous outflow or arterial inflow during contraction. While muscular contraction should temporarily compress blood vessels, the compression should be released during the relaxation phase of the contractile cycle, allowing deoxygenated blood to leave the tissue and return to the heart while fresh, oxygenated blood reaches the muscle. If, however, the muscle contracts extremely forcefully, or remains in a concentrically oriented state while it should be lengthening, the compression may not be released, and the muscular contraction may block venous outflow or arterial inflow.
If an athlete has this reaction during work intended to elicit structural and functional adaptations to the heart, you will not only not get eccentric hypertrophy of the left ventricle, you will likely get concentric adaptations to the heart as the heart pumps harder to try to overcome the blockage.
This response can be seen by monitoring THB trends with the Moxy, which gives us a measurement of the concentration of hemoglobin and myoglobin under the probe. If THB increases during the work bout, and then decreases during rest, this is indicative of a venous occlusion. In this situation, venous outflow is restricted during the work, like a garden hose being kinked, and then during the rest period, once muscular contraction has ceased, the kink is released, and blood is once again able to leave the tissue and return to the heart.
If THB flat lines during work, this is indicative of an arterial occlusion, which means that oxygenated blood is not able to get to the working muscle due to the compressive force of the contractile tissue.
Both of these scenarios will result in premature fatigue in the local tissue and potentially disadvantageous adaptations to the heart.
The moral of the story is, just because heart rate is under 150 BPM, does not automatically mean that you are getting cardiovascular adaptations associated with improved efficiency such as eccentric left ventricular hypertrophy, increased stroke volume, and decreased resting heart rate OR facilitating recovery.
Many people, including those who use heart rate to track intensity, are working at too high an intensity to get the benefits that they believe their getting from their low intensity aerobic work. They are living in the middle, performing low intensity work that is intense enough to demand significant recovery resources, but not intense enough to result in adaptations associated with true high intensity work. At the same time, the fatigue accumulated from this work detracts from the ability to execute quality high intensity work during sessions that are intended to be high intensity, leading to alterations in motor control and coordination, decreased outputs, and impaired adaptations.
In some cases, planned low intensity training sessions are actually the most intense stimuli the individual is exposed to in their entire program!
Consider this: when I perform a heavy set of squats, I will likely desaturate the muscle as completely as I’m able to, but I will then rest 3-5 minutes before performing another set. My exposure to a local environment of low O2 is brief, and then I allow myself to recover completely before performing another set of squats. Across the course of a workout, I might be exposed to 8-12 sets of exercises that full desaturate my quads.
However, when I went for a run, I spent 58 minutes of the 60-minute session in a low O2 environment, where O2 had all but bottomed out. The stress of this training session likely exceeded anything else I was doing in my training program at the time EVEN THOUGH MY HEART RATE AND PERCEIVED EFFORT WAS VERY LOW.
While some people may argue that this response is only occurring in one muscle, in one small area of the muscle belly under the probe, and that we can’t know what is happening throughout the rest of the body just from one Moxy alone, the reality is that even if this type of ischemic response is occurring in one small area of the body (it’s likely not, given what we know about an individual’s contractile bias and the integrated nature of the biotensegrity human system) it is feeding back to the brain through bidirectional feedback loops and being registered as a substantial threat to the integrity of the system. So even if the response itself is only being measured in one local tissue area, it will elicit a response from the entire system to deal with the threat. Existing in a low oxygen environment for such an extended duration is extremely threatening to the entire system.
The accumulation of intense sessions like this layered on top of high intensity training sessions in the weight room as well as high intensity, interval-based conditioning work on other days of the week leads to poor recovery, decreased movement variability, autonomic dysregulation, increased perception of threat, pain experiences, and eventually, injury. This is EXACTLY what has happened to me over the year two years since I began training for and participating in endurance races.
The best coaches recognize that effective training is polarized. A stimulus should either be high enough intensity to significantly disrupt homeostasis and move the needle towards increasing performance, or it should help to enhance recovery and maintain health. Training that exists in the middle is left out of the program because it doesn’t accomplish either goal, and carries with it the negative secondary consequences associated with both ends of the spectrum with none of the benefits.
This is a perfect demonstration of why any attempt to make blanket, black and white statements about the human organism will inevitably be incorrect. Though all humans share some commonalities and have to work within common constraints, the reality is that we are all structurally and functionally unique to some degree, and we will have unique physiological and neuromuscular responses to the same stimuli.
We need to appreciate that responses and adaptations to training stressors are much more unique to each individual than we generally appreciate. Give an elite marathon runner 60 minutes of low intensity running, and they’ll likely feel recovered, refreshed, and rejuvenated.
Give a former collegiate offensive lineman with a lengthy history of high intensity, high volume strength training, considerable lower body hypertrophy, and a wide ISA with a strong concentric, compressive bias 60 minutes of low intensity running, and what you get are sore, fatigued quads, joint pain, and decreased performance for days after.
This does not just apply to running. High resistance spin biking, riding an assault bike, continuous sled pushing and sled dragging, and high-incline treadmill walking are all examples of popular aerobic modalities that are automatically assumed to be low intensity, but elicit unfavorable responses such as those described above in some individuals, especially in those with a history of heavy strength training, those carrying a significant amount of muscle mass, and/or those with significant limitations in movement variability.
1) “Aerobic work” is not inherently low intensity. Just because you are maintaining a heart rate of 150 BPM or less and the activity does not feel that strenuous does not mean that it is truly low intensity, facilitating recovery, and leading to the intended adaptations to the heart. There are many people out there whose low intensity aerobic work is actually medium or high intensity, and in some cases, it is the highest intensity stimulus they may be getting throughout their entire training week.
2) Everyone’s physiology, coordinative strategies, and bias towards high pressure/low pressure strategies are unique. Individual responses to the same stressor will therefore, be unique. We cannot make blanket statements about a particular exercise or particular exercise prescription. What might be a low intensity aerobic stimulus for one individual may actually be incredibly stressful for another.
3) Performing frequent work in a low oxygen, ischemic environment for long periods of time and/or occluding arterial inflow and venous outflow of working tissue is incredibly stressful, rife with secondary consequences, and unsustainable.
So What Can We Do To Improve This?
Since I originally posted the Moxy data from this run on my Instagram story, I’ve received a number of questions, but the two most common have been:
“So what did you do to stop this from happening?”
“If someone has this reaction, how do you go about improving it?”
I will be perfectly honest and say that I don’t have an exact answer for these questions yet. I’m still in the process of considering the variables that are likely responsible for this reaction, and trying to determine how I can modify training to reduce these reactions and prescribe exercise that more appropriately fits the intent of the session.
However, I do have a number of ideas based on principles on physiology, energetics, and mechanics that I am currently testing to reduce the influence of these reactions and improve my performance with an eye toward competing in another adventure race next year as well as regain some elements of health that I have compromised to increase performance.
1) Alter Axial Skeleton Position/Restore Respiratory Variability
The position of the axial skeleton, consisting of the cranium, spine, rib cage, and sacrum, as well as the ilia of the pelvis, sets the foundation for the movement options available to the appendicular skeleton as well as the orientation and length/tension relationships of the tissues that attach to these structures.
In many cases, lack of respiratory variability (the ability to exhale and inhale fully with corresponding movement of the entire skeleton) leads to compensatory strategies in order to maintain the ability to inhale and/or exhale to satisfy the need to breathe while meeting the demands of the stressors of daily life and exercise/sport performance.
During respiration, the entire skeleton needs to be able to move to accommodate the oscillation of gases and fluids throughout the body. If the entire skeleton is unable to express the motion necessary to complete a normal inhalation and exhalation, we will still find a way to breathe, and this will come in the form of compensatory strategies that move us toward either an exhalation or inhalation strategy.
(For a visual of the movement of the entire skeleton, check out the video attached below)
A common compensatory strategy that we will employ as we continue to deal with internal forces, gravity, and the need to breathe, is to compress the posterior pelvis and posterior thorax, driving the spine forward into extension and the pelvic girdle as a whole into anterior orientation. This is a compensatory exhalation strategy.
An anteriorly oriented pelvis is a position of acetabulum on femur flexion, which means that the hip flexors will pick up concentric orientation. One of these hip flexors in the rectus femoris muscle, the two-joint quadriceps muscle that attaches to the anterior inferior iliac spine, the superior acetabulum, the tibial tuberosity, and the patella.
Additionally, posterior compression of the thorax driving the spine into extension will further bias the diaphragm toward concentric orientation. When the diaphragm contracts in a descended position it actually pulls the spine further down and forward into extension via its crural attachments to the lumbar vertebrae. The diaphragm and the psoas are actually in essence, one muscle, sharing fascial connections that are so integrated that they cannot be dissected apart.
Therefore, posterior compression of the spine has a cascading effect that impacts the polyarticular chains of muscles that attach to the spine and run down the front of the hip to the knee joint.
With the appreciation that muscles are a man-made construct, only truly separated and isolated based on arbitrary distinctions that we have made by dissecting apart what is truly a continuous, integrated system, the position of hip flexion will drive tension and concentric orientation in all of the tissues that share attachments with the diaphragm, psoas, iliacus, rectus femoris, the rest of the quadriceps muscles, tensor fascia latae, etc.
The result is that the muscles on the front of the hip and thigh will be biased toward concentric orientation, and therefore, a compressive, high-pressure strategy.
Chronic concentric orientation means that these muscles are maintained for long periods of time in a state that is identified as shorter than some imaginary mid length. This means that the muscle is constantly slightly (or more than slightly in some cases) contracted. The physiological consequences of maintaining a muscle in a constant state of low-level contraction is a chronically low oxygen environment, restricted blood flow to the tissue, and high-energy utilization.
Therefore, if the goal is to increase resting SMO2, decrease oxygen utilization during low intensity activities, improve oxygen supply/deliver, and eliminate occlusion reactions, and we are monitoring the quadriceps, we should probably attempt to reduce the concentric orientation of these tissues.
This is accomplished by bringing the pelvis back from anterior orientation, reducing the posterior compression of the thorax and pelvis, and restoring respiratory variability so that the individual doesn’t need to utilize compensatory strategies to continue to breathe.
Breathing is the brain’s number one priority, and it will sacrifice anything in order to continue to breath and meet the respiratory demands of whatever activities we engage in in life. Lack of respiratory variability will lead us to continually utilize certain positions and compensatory strategies to continue to maintain the ability to inhale and exhale against a skeleton that is incapable of moving through the full range of both phases of the respiratory cycle.
Additionally, a bias towards exhalation/compression/force production may predispose the individual to an occlusion reaction, as they’re naturally more likely to create high levels of tension with each contraction and will be more likely to struggle with gaining eccentric orientation to allow inflow and outflow between contractions.
How to assess this, what activities to select, and how to coach them is beyond the scope of this article, but keep an eye out for more information on this on this blog going forward, and be sure to check out Bill Hartman, The Intensive, and all of the information he has been putting out on social media recently for more information.
2) Choose A Less Intense Activity
It may seem exceedingly obvious, but if you’re performing an activity at the lowest intensity you possibly can and are still desaturating to such a substantial degree that you’re spending the majority of your time in a low O2 environment or you have an occlusion reaction that restricts the flow of blood, you need to choose a lower-intensity activity if your intent is to train cardiac output or facilitate recovery.
For me, this has included using a spin bike set at a low resistance, low intensity assault bike rides, dusting off the elliptical (yeup I said it), and treadmill walking on an extremely low incline.
The elliptical has been particularly useful, as it is a low-impact option that allows me to integrate the arms into the equation to further reduces my propensity to create high forces with every contraction of my quads.
As overly-intellectualized strength and conditioning professionals, I believe that we look down on machines like the elliptical because they conjure in our heads the imagery of commercial gym goers reading, texting, and talking on the phone as they mindlessly cruise on them, gaining virtually nothing from the activity. But we need to remember that the elliptical is simply an object. It is a tool and utilized in the appropriate context, with the right perspective and intent, I think it can be a valuable tool for an individual looking to train at an intensity that is characteristic of true cardiac output work.
I’ll typically perform 45-90 minutes of work on a low resistance and low incline setting on the elliptical while monitoring SMO2 with Moxy.
Monitoring Moxy during these activities has demonstrated that I am able to maintain steady SMO2 (true cardiac output work) when I want to, and even over deliver SMO2 in some cases (more on this later).
Not shockingly, since making the switch to some of these lower intensity options, I feel minimal fatigue in my legs immediately after the activity, and sometimes even feel refreshed and rejuvenated, I have an easier time creating expansion in areas of my thorax that are often so compressed that I can’t even create a shift in volume there with manual assistance, my high intensity lifts are far more productive because I feel recovered, the pain, swelling, and frequency of my knees “flare ups” has decreased, and even the quality of my sleep has improved.
3) Use General Circuits
One of the problems with continuous cyclical work with individuals who tend to be utilization dominant and display occlusion reactions is that if they are unable to contract and relax effectively due to their concentric orientation and high-pressure, contractile strategy, the working tissue is never able to eccentrically orient. They are constantly in a cycle of “more contracted” and “slightly less contracted,” but the tissue is ALWAYS creating tension and high pressure.
So if we want to reduce the influence of this constant state of concentric orientation, we can force the issue by creating a general circuit of activity that features activities that tend to alternate lower body and upper body biases. This is also a great time to include triplanar exercises that bias expansion/compression in areas where the individual cannot shift fluids and volumes and address certain ranges of the propulsive cycle that the individual needs to recapture elements of variability.
While cyclical activities certainly have unique benefits in terms of the demand placed on the cardiac system and therefore, the adaptations to the training, if the goal is to facilitate recovery or train true cardiac output that allows me to maximize left ventricular preload, a low intensity circuit may be the best option.
Ideally, we would construct a circuit that allowed the individual to move continuously from one exercise to another, while monitoring SMO2 in the relevant tissue to ensure that we are not occluding or desaturating fully, and if we do desaturate O2 to a significant degree, we fully recover it prior to the next exercise that taxes that tissue. This is why alternating lower/upper activities or ensuring that the chosen exercise doesn’t predispose the individual to significant O2 utilization in a working tissue or an occlusion reaction is critical.
Additionally, circuits that include shorter work bouts per exercise exposure will bias more cardiac development, while circuits that feature lengthier work intervals per exercise will facilitate more local tissue oxidative development. In this case, we want to bias central development, and therefore, would want short exposures to each exercise with frequent switches in order to ensure we aren’t continuously desaturating or occluding to a significant degree.
I like to use activities within these circuits that bias inhalation/expansion as I am a wide infrasternal angled individual with a strong concentric strategy who is also very compressed A – P at the thorax and the pelvis. This allows me to perform activities that will help to restore movement and respiratory variability while facilitating recovery and creating adaptations to the heart.
The following is one example of a circuit of this type that I performed last week.
Work continuously but rest as needed to maintain heart rate within appropriate range (somewhere between 110-140 BPM) for this type of work if you do not have access to NIRS technology while choosing activities that may elevated your heart rate but don’t cause significant local tissue fatigue.
4) Break Up The Training Into Intervals
One of the primary benefits of interval work is that you can break up training that would be too intense to perform continuously into manageable segments with recovery in between that allows you to accumulate more total volume at particular intensity.
In this specific scenario, we could use “tempo” intervals to train at a similar “low intensity pace,” but cut the activity when SMO2 bottoms out or reaches a critical threshold. Then, you would recover until SMO2 is fully restored and perform another bout. In this way, you could accumulate more quality volume in an aerobic, oxygenated environment, and then cut the session when you are unable to recover effectively between bouts. This would ensure that you maximize the quality of the work being done and minimize the time spent in an ischemic environment.
The other option is to simply do more general, low intensity activity for active recovery/cardiac output work, and save specific work like running or cycling at race pace or desired training intensities for high intensity sessions. In this scenario you would use intervals to accumulate quality, highly-coordinated, specific work at the desired pace in an oxygenated environment that minimizes the time spent in “survival mode” and allows for sufficient recovery between work intervals. In this way, increasing the number of bouts and the frequency of this kind of work can optimize volume without requiring substantial periods of recovery in between sessions.
5) Perform “Over Delivery” Work To Increase Resting SMO2
Over delivery work is characterized by supply of O2 exceeding utilization.
When this occurs, after an initial desaturation, we should see SMO2 actually increase steadily throughout the session. The desaturation at the onset of exercise is the time delay that it takes for the cardiac and respiratory systems to react to the increased activity.
After this initial period, SMO2 will actually steadily climb throughout the session. This indicates that more oxygen is being supplied to the tissue than is needed to meet the demands of the work.
This idea is taken directly from Aaron Davis, and is a fantastic strategy to use as a warm up or active recovery day activity.
In a warm up scenario, a few key goals are to:
- Increase tissue temperature
- Increase blood flow
- Increase oxygen supply to working tissue
By increasing tissue temperature, CO2 production and decreasing tissue pH, we decrease hemoglobin’s affinity for oxygen, which will lead to more oxygen being dropped off at the site of work. This is advantageous as we prepare for more strenuous activity, as oxygen is essentially our fuel source and is analogous to gasoline in a car engine. The more we are able to deliver to the working muscles, the more substrate we have available to run oxidative metabolism in the electron transport chain of the mitochondria, which has the largest ATP yield of any of the primary energy pathways.
Additionally, we want to increase blood flow, allowing more oxygen to be supplied to the working tissue and products of energy metabolism to be removed.
Finally, we want to increase heart rate as an indication of sympathetic arousal and the heart responding to the increased activity. This response by the heart is a critical element in the body’s allostatic response to the increased activity demand in order to supply blood and oxygen to the peripheral contractile tissue.
All of these things are accomplished with true over delivery work, making it a fantastic options following movement prep and before beginning more intense elements of the training session. Some examples are low-resistance spin bike riding, elliptical, or a quality dynamic warm up.
Another option is to use short bursts of max effort sprints, as long as the individual doesn’t have an occlusion reaction. Max effort sprints of 10-15 seconds with full recovery typically lead to an over-delivery of oxygen during the recovery period, increasing SMO2 and effectively filling the gas tank.
As a training session in its own right, over delivery work should be performed for 45-90 minutes at a time depending on the individual’s goals and physiological reaction to the training.
This is true regeneration work, as SMO2 should be higher at the end of the session than at the beginning. In addition to the acute recovery effects of over delivery work, this type of work will lead to structural adaptations to the heart via left ventricular preload, mitochondrial biogenesis, capillarization, and increased blood flow.
The goal of frequent over delivery work is to facilitate recovery while also eliciting systemic, structural adaptations that allow the individual to have higher levels of resting SMO2.
Typically, utilization-dominant individuals such as those who will tend to desaturate SMO2 rapidly during even low intensity work or those that exhibit an occlusion reaction will also have low resting SMO2.
Low resting SMO2 means that the individual is only operating with a portion of their gas tank filled even at rest. Imagine someone gave you a car. This car had a gas-guzzling engine, and could, for whatever reason, only be filled to half a tank. Would you want that car? (Analogy stolen directly from Aaron Davis)
The concept is the same here. If at rest only 50% of my hemoglobin and myoglobin are saturated with oxygen that means I have a much smaller percentage of my gas tank available to desaturate at the onset of work. I’m much more likely in this case to operate at a very low SMO2 during any sort of exertion, especially higher intensity exercise.
Additionally, this low resting SMO2 is indicative of increased demand for oxygen utilization in the tissue, and a lack of the supply infrastructure in place to deliver enough oxygen to support the local demand.
Over delivery work can be performed frequently because it is very low intensity. Ideally, you’d monitor SMO2 throughout to determine the most appropriate exercise modality for the individual and then cut the session when over delivery ceases.
Without NIRS technology, choosing a low intensity activity with minimal resistance is the best option. We frequently use a spin bike with relatively low RPMS and low resistance, low resistance elliptical, low incline treadmill walking, a rower, etc.
Most people would be amazed at just how low intensity this work needs to be to elicit the desired outcome. I will typically perform a spin bike session with almost no resistance whatsoever between 70-85 RPMs. Even still, I have to monitor SMO2 closely, because I utilize oxygen so quickly and easily.
6) Perform True Cardiac Output Work
“True” cardiac output work would be exercise performed at an intensity that allows for balanced, steady SMO2 throughout the activity, this would be indicative of an intensity and an activity where oxygen supply adequately meets oxygen utilization.
Heart rate during such an activity would likely be higher than that of an over delivery session, and therefore, stroke volume would be more maximal as the intensity is low enough to allow for a full preload of the left ventricle, but high enough that heart rate would increase to a level where stroke volume would be maximized.
As such, this type of work is critical to eliciting structural and functional adaptions to the myocardium.
However, the key difference between what coaches typically prescribe and this type of work is once again, that the intensity is often much lower than what most people appreciate. Heart rate should be between 110-140 BPM, and it is critical that the individual does not have an occlusion reaction to the particular activity and that they do not desaturate quickly or significantly. This is why heart rate may give us some correlative information, but can’t give us the whole picture, and without knowing what is happening at the local tissue environment, cardiac output training can quickly become more intense than intended or evoke an occlusion reaction in some individuals, in which case adaptations to the heart may not happen at all, or worse, may actually be exactly the opposite of what was intended.
Cardiac output work can be performed with low intensity, cyclical exercise modalities like spin bike riding, treadmill or incline treadmill walking, elliptical, assault bike riding, or even circuits when prescribed properly. Cardiac output work should last between 30-90 minutes or longer if you have lofty endurance sport goals in order to actually elicit an adaptation to the heart.
7) Decrease Hypertrophy
I can hear an angry mob of hypertrophy-junkies approaching my door with torches and pitchforks as I type these words but…if someone truly wants to prioritize endurance performance and wants to reduce these reactions associated with negative secondary consequences in order to perform a certain activity they enjoy doing like running or biking, reducing hypertrophy may be a necessary part of the process, especially for individuals who already possess large muscle mass, have a predisposition to easily gaining size, or have a lengthy history of heavy strength training and hypertrophy work.
The mechanisms of hypertrophy are controversial, but include increases in the size of individual muscle fibers, sarcoplasmic hypertrophy, and potentially muscle hyperplasia.
If we dig a bit deeper, increases in the thickness of individual muscle fibers are actually caused by the addition of myosin proteins, which cause the myosin filaments to become thicker, thereby demanding that the cell expand in size to create enough space to maintain the arrangement and function of the contractile elements of the muscle tissue.
In terms of sarcoplasmic hypertrophy, while it is traditionally thought that the primary mechanism of sarcoplasmic hypertrophy is increases in glycogen stores, it turns out that this is not exactly the case. Instead, the primary driver is an increase in sarcoplasmic protein content.
Muscle hyperplasia is the most controversial of all the proposed mechanisms of muscle hypertrophy, and consists of an increase in the number of muscle fibers.
What is the common element present in all three of these mechanisms that underlie muscle hypertrophy?
In the eloquent words of Bill Hartman, “When we hypertrophy a muscle, we’re actually jamming more stuff into the muscle, that takes up space, that stuff brings fluid with it, and now I have a compartment that is bigger than it used to be, that allows me to squeeze harder.”
Regardless of the exact type of hypertrophy, we are stuffing more proteins and/or molecules of glycogen into the compartment of the muscle. Those proteins all bring with them fluid, constituted mostly by structured water (H203), which takes up additional space. The result is a larger tissue biased toward greater force production and higher pressure that squeezes harder with each contraction. This increased bias toward compression/force production may potentially predispose the tissue to an occlusion reaction, as every time it squeezes, it is more likely to strongly kink the “garden hose” of the blood vessels and not allow a full relaxation to restore both inflow and outflow between contractions.
Additionally, because there are a greater number of thicker contractile proteins, there is a greater demand for energy utilization in order to fuel the contraction/relaxation cycle of the muscle.
With the greater demand for ATP to meet the energetic needs of the larger contractile tissue comes the need for greater oxygen supply. The problem with this is that greater muscular hypertrophy actually reduces capillary density in the tissue. This makes it more difficult to supply the larger muscle with the increased oxygen it needs while removing the CO2 it produces during work because there is a smaller number of capillaries per muscle fiber.
Now you’ve basically got yourself a big, gas-guzzling engine. There’s a reason that elite endurance athletes aren’t extremely muscular. At a certain point, too much muscle becomes energetically inefficient. It’s expensive, it’s difficult to supply, and it demands substantial remodeling from the cardiac, respiratory, and delivery system to meet the oxygen demands and remove the products of increased energy metabolism.
With this in mind, it may be prudent for an individual whose priority is endurance performance or who wants to perform a certain type of activity (i.e. running), to decrease their muscular hypertrophy and potentially reduce the frequency/volume/intensity of resistance training that may lead to increased hypertrophy.
8) Improve Coordination
Inter and intramuscular coordination is a highly individualized and adaptive component to this equation that isn’t often considered because until now we really haven’t had a good way to measure it, though coaches have appreciated it’s importance since the days of Supertraining. Coaches often this site this classic text for articulating that more elite athletes don’t necessarily contract faster than their lesser qualified counterparts, but instead are able to relax muscles much faster.
Specifically referring to occlusion reactions, in which arterial inflow or venous outflow is restricted to the working tissue, what we are seeing is mismatches between the individual’s ability coordinate the cycle of contraction/relaxation and the intensity of the exercise.
During low force/high velocity contractions, we should see a compression of the blood vessels, which temporarily restricts flow followed by a relaxation of the contractile tissue that not only allows blood to flow through the vessels once again, but also helps to increase the velocity of the flow as a result of the previous contraction to help pump blood through the vessel. To understand this, picture kinking a garden hose and then unkinking the hose, the fluid flow through the hose would stop briefly and then accelerate rapidly leading to a temporary higher velocity of flow after the blockage was released. This would be indicated by a decreasing THB line during work.
A compression reaction is probably ideal for a marathon runner or a team sport athlete that has to run in open spaces like a wide receiver in football, but probably not ideal for a high level powerlifter whose entire sport is based on the ability to exert maximal force against huge loads.
During moderate force/moderate velocity contractions, we should see a venous occlusion, which would temporarily stop blood flow from leaving the working tissue, leading to increased pooling of blood and byproducts of energy metabolism in the tissue, and forcing the heart to have to work harder to break through the blockage. In this case, we’d see THB increase during work and decrease during rest, indicating that blood volume is increasing due to the blockage and then dropping when the blockage is released during the rest period.
This may be a necessary reaction from a linebacker or running back in football, who has to exert high forces for very brief periods to take on a block or a tackler which requires a strong, but often not maximal contraction, but would be problematic for a Crossfitter who has to lift submaximal loads many times across the course of a metcon.
Finally, during high force/low velocity contractions, we should see an arterial occlusion, where blood flow to the working tissue is temporarily blocked, leading to an inability to supply fresh oxygen to the tissue and the heart once again needing to increased its work rate to try to compensate. In this case, we’d see THB flat line, as blood can’t get into or out of the working tissue, leading to stagnation of the blood trapped there.
This is an appropriate reaction if we’re talking about a powerlifter performing a competition single or even an offensive lineman in football, as both need to create extremely high amounts of tension in high force situations, but would be wildly inappropriate for a marathoner or field or court sport athlete like a wide receiver or defensive back if they were to do it all the time.
Our structural biases and training/athletic history tend to predispose use to these type of reactions, and if we lack to ability to coordinate the optimal contractile strategy in the appropriate scenario, performance will often suffer and in some cases, both acute and long-term recovery and health are impacted.
For example, an individual with a wide infrasternal angle has a structural bias toward exhalation/compression and higher force production, with a compensatory inhalation/expansion strategy of the lower rib cage superimposed on the axial skeleton presentation.
Due to the larger surface area of the diaphragm in these individuals, they will already be predisposed to a high-force production, concentric strategy.
Take this individual, and now put them into sports like football and have them play offensive line, Olympic weightlifting, and powerlifting, and they will likely excel, but they will also likely develop further compensatory inhalation and exhalation strategies to meet the physical demands of their chosen endeavor. This will further deepen their bias towards compression, concentric orientation, and high force outputs, as they are already predisposed to that type of strategy, and then we layered on activities and sports that further require those type of outputs.
Now, take this individual and apply their competitive drive to a sport or activity that involves a significant endurance component once their competitive sport career is over. In some cases, these types of individuals gravitate towards competitive outlets like Crossfit that allow them to combine their love of hard training and lifting heavy loads with the dopaminergic sensation of striving to compete in a workout against themselves and the community. In other cases, these individuals transition to something like running 5ks and half marathons, competing in triathlons, adventure races, or obstacle course races.
The problem is, these individuals were born and trained their entire athletic careers to produce high forces and against heavy loads and high resistance. Now, they’re satisfying their need for competition by transitioning to activities that demand the exact opposite of what they’re structurally and neuromuscularly wired for. The result is that they continue to create venous and arterial occlusions while performing activities that demand long durations and have a substantial endurance component to them, leading to undesirable adaptations, secondary consequences, reduced performance, chronic pain, and eventually, tissue damage/injury.
This is exactly what happened to me. Activities like a bodyweight squat, sprint on an assault bike, sprint on a spin bike with no resistance, etc. ALL elicit a venous occlusion reaction. Even in exercises that require very low force contractions, my structure and coordinative strategy still yields a high force contraction that does not relax enough in between contractions to allow blood to leave the tissue and return to the heart. This is a good thing if I wanted to compete in powerlifting or put my helmet back on to go play offensive line, but not a good thing with my current goals and at this stage of my life. I am literally incapable of compressing and relaxing in anything that requires even some force output, and as soon as I try to increase force/velocity, I contract hard and sustain the contraction across the work bout. The result is that I can’t clear products of energy metabolism from the muscle effectively during intense work bouts, local tissues fatigue faster, and my heart has to work significantly harder.
To put this into the context of athletes still playing field and court sports, there are many athletes who are either too strong or too weak for the demands of their sport or position, leading to occlusion reactions.
If an athlete is “too strong” and produces high force contractions during inappropriate tasks or is “too weak” and can’t create enough tension to meet the force demands of a given activity, we may see occlusion reactions.
To use an example, we have a linebacker with a wide infrasternal angle who began lifting weights with his father when he was 11. He believed lifting weights was the key to his early success, and continued to train as heavy as possible to get as strong as possible in high school and college. He pushed his maximal strength in the weight room to the point where he could back squat 600 lbs.
The problem is, now his tissues and his nervous system have adapted to high loads, compression, and high force production, to the point where when he sprints, jumps, and cuts, he occludes. He fatigues quickly, and in the third and fourth quarter when his team needs him the most, he doesn’t have the explosiveness he does in the first half.
How do we alter an individual’s contractile strategy and improve coordination so that an athlete can compress and relax, reducing occlusion reactions and thereby improving local tissue capacity while setting the individual up for more favorable chronic adaptations associated with training?
In an individual biased towards high forces a compressive strategy, and concentric orientation, we need to increase expansive capabilities while retraining the ability to contract and relax quickly at low loads, high velocities, and in elastic/reactive activities.
This means reducing the volume/frequency/and intensity of heavy, slow, bilateral exercises like back squats, deadlifts, and bench presses, while using lower load, higher velocity exercises that will help the individual learn to compress and relax without needing to create more excessive muscular tension. Additionally, exercises and activities that bias eccentric orientation, expansion, and inhalation with the goal of restoring respiratory variability and reducing the influence of the compressive strategy.
In terms of exercise selection to improve specific coordination:
- Running/sprinting drills that emphasize relaxation, rhythm, fluidity, rapid turnover of the limbs, and short ground contact times.
- High velocity/low load lifts using timed sets of velocity based training to emphasize contraction/relaxation.
- Oscillatory exercises a la Triphasic Training
- High velocity/low resistance sprints on spin bike at a rate and duration that does not elicit an occlusion response.
Conclusion & Disclaimer
I want to make a few things very clear:
- I am NOT saying you should not train hard. Do not take this article as a free pass to never work hard.
- I am NOT saying that high intensity conditioning doesn’t have a place in a training program.
- I am NOT saying that low-intensity, cyclic aerobic work like running or cycling does not have value.
- I am NOT saying that muscle hypertrophy is bad or that you should throw away resistance training.
My hope is that if you’ve made it this far into this article, you already recognize all of those things. However, it’s become quite clear to me that even highly educated physical preparation coaches and therapists love to live at the ends of the spectrum, which is why I felt the need to articulate the above points.
There is security and clarity in simple answers, but the reality is that we live in a world where we work with the complex, emergent outputs of complex, adaptable, biological systems. There is no black and white. There is only gray. Everything we deal with exists on a continuum and can move in either direction.
What I am saying is this:
Responses to training are highly individualized.
One individual’s physiological reaction may be completely different than another’s to the same stimulus. By making black and white statements like “low intensity aerobic work between 120 and 150 BPM improves recovery and cardiac output” we fail to realize the range of responses and adaptations that could occur based on a myriad of individual characteristics, environment, and task-related variables at play here. What may be active recovery work for one individual could bury another individual for days. What may elicit increased cardiac efficiency, structural adaptations to the myocardium, and improved recovery capabilities for one individual may lead to compressive, concentric adaptations to the entire system (heart included).
Keep your highs high and your lows low.
There is a select subset of the population that includes coaches and PTs who are ex-athletes who are still meatheads. We hear the narrative that most people never actually train hard and we watch society as a whole do absolutely nothing productive in the gym. We talk about the need to simplify our exercise selection, stop getting bogged down in minutia, stop being afraid of hard work, and just get after it. We try to lead by example and show people that they’re capable of working so much harder and doing so much more than they realize.
I am one of those people. The problem is, I’ve taken it too far, and I fear there are many others like me. This had lead to a situation where every single day is high intensity. Instead of polarizing my training, getting after it when it’s time to work hard, but backing off and performing true low intensity work on other days, every day has become a different version of “how hard can I push myself to maximize the adaptation I’m getting from this.”
The result of this is that ALL of my training sessions became medium intensity. I’d show up to my high days and work hard, but I was so fatigued and so mentally drained that there was no way I was maximizing my outputs on those days. Conversely, on my low intensity days, I’d guilt myself into thinking, “I should be working harder than this, I should be doing more,” and the session would turn into something it was never intended to be. Over time, I compromised my ability to recover, I compromised the quality of my high intensity work, and eventually, I compromised my movement capabilities and my health.
Most normal people whose thoughts and priorities don’t center on training need to do simple things and learn to work really hard. But if you are part of the population who would take the time to read this lengthy article, whose livelihood and passions center early entirely around training and human performance, I implore you to reflect on whether you are actually keeping your high intensity work high and low intensity work low. If you’re not, you are not eliciting the adaptations that you desire, and you are likely setting yourself up for failure in the long run.
Heart rate only gives you a part of the picture and is not a reliable indicator of the systemic stress of a particular activity.
Heart rate may remain in a range that we have defined as low intensity, active recovery, aerobic exercise while local tissues continue to perform work in a low oxygen, reduced blood flow environment. This type of local tissue environment will not only lead to unfavorable structural adaptations to the heart, but will be profoundly stressful to the entire organism, especially when it is maintained for long periods of time. If this type of activity is performed on a low intensity day, it will add significantly more stress than the individual is accounting for in the training program, demand more resources and time for recovery, and potentially set the person up for diminished performance, pain experiences, and injury.
References & Recommendations For Further Study
Aaron Davis & Train Adapt Evolve (Now Evolve Health & Performance)
Cells, Gels, and The Engines of Life by Gerald Pollack
The Fourth Phase Of Water by Gerald Pollack
The Glycogen Shunt In Exercising Muscle: A Role For Glycogen In Muscle Energetics & Fatigue
Role Of The Phosphocreatine System On Energetic Homeostasis In Skeletal & Cardiac Muscles
Bill Hartman On The Secondary Consequences Of Hypertrophy & Concentric Orientation
Aaron Davis “Programming Conditioning For Field & Court Sports Using Muscle Oxygen Sensors”
“Omegawave & Moxy As Complimentary Training Technologies”
What Is Muscle Hypertrophy: 5-Minute Physiology With Dr. Andy Galpin
To Learn More About Or Purchase A Moxy Monitor