Performance Physiology 101: Identifying & Training Respiratory Limitations

Evan Peikon
13 min readJan 28, 2021

When I think about hydrogen ion (H+) accumulation the first that comes to mind is the unpleasant burning sensation in a muscle during high intensity work bouts. But, is H+ accumulation all bad? The answer is no. Pain and fatigue don’t exist to stop us from hitting PR’s — they serve an important protective function. Similarly, H+ also has a protective role.

“At first sight [fatigue] might appear an imperfection of our body, is on the contrary one of its most marvelous perfections. The fatigue increases more rapidly than the amount of work done saves us from the injury which lesser sensibility would involve for the organism” — Angelo Mosso

One of the functions of H+ is to help us avoid dangerously low levels of ATP, which would lead to muscle rigor (this is the reason why rigor mortis occurs). When ATP levels get too low H+ stops calcium ions (Ca2+) from binding with Mg2-, which inhibits the splitting of ATP molecules, consequently helping us prevent ATP from reaching dangerously low levels. When H+ levels get too high, we have a downward shift in pH which causes us to slow down or stop our efforts. Again, this is a protective.

Knowing this it allows us to ask another question — if we can maintain H+ homeostasis can we keep pushing for longer? And, if so how can we accomplish that? One way this can happen is through the lactate shuttle. People often make the mistake of thinking that the lactate shuttles primary function is to get rid of lactate, for it’s own sake, by shuttling it to other areas of the body. This assumes that lactate is a fatigue byproduct or poisonous metabolite that we want to get rid of. However, lactate is a fuel source for oxidation and one of the primary roles of the lactate shuttle is to transport H+ from the muscle cells to the blood stream.

Typically when we’re in a state where H+ is in excess there is also a lot of CO2 build up. If an athlete is able to shuttle the excess H+ out of the working muscles, now there ability to continue performing will come down to breathing off the excess CO2 at a fast enough clip. This is something that can be trained whether that’s using the

to improve expiratory muscle strength, improving breathing coordination, or improving the fatigue resistance of the diaphragm and other accessory breathing muscles.

Athelte who develop these qualities can often push for extended periods of time while presentign with low muscle oxygen saturation levels and a right shift in the oxygen dissociation curve. They are able to accomplish this by shuttlign H+ out of the working muscles at a fast rate and breathing with a sufficient volume and frequecy to clear CO2 quickly enough. However, once these atheltes respiritory msules start to fatigue they often run into issues.

This raises two questions…..
1) How do we know when someone has a respiratory limitation, whether that’s an inspiratory muscle weakness, expiratory muscle weakness, lack of fatigue resistance in the diaphram, poor breathing coordination, or even a structural issue?

2) What do we do about it?

The rest of the article will be dedicated to answering both of these questions.

Before delving into respiratory limitations i’ll start with a broad overview of the three primary energetic limiters which include pulmonary (respiratory) limitations, cardiovascular (delivery) limitations, and muscular (utilization) limitations. Its important to acknowledge that these limitations function as the rate limiting factors for VO2max, as discussed in the paper “Weak Beliefs, Strongly Held: Challenging Conventional Paradigms of Maximal Exercise Performance.”

Broadly speaking, we can separate these three limiters into two categories, supply limitations and utilization limitations.

Figure I. In the picture above we see NIRS trends from two athletes performing a wingate test. Athlete 1 (left) is limited by their rate of oxygen utilization while Athlete 2 (right) is limited by their oxygen supply, as indicated by muscle oxygen saturation (SmO2) reaching 0% during the work bout. Respectively, these represent the two broad categories of limitations.

When assessing for utilization limitations i’m looking at the ability of the muscle to consume oxygen compared to the ability of the body to delivery oxygen.

Figure II. Athlete 1 (top) presents with a utilization limitation while Athlete 2 (bottom) presents with a supply limitation, as indicated by the muscle oxygen saturation response (green line) as they transition from a sustainable to an unsustainable intensity.

I’m most interested in what happens when an athlete transitions from a sustainable intensity to an unsustainable intensity that they can only support for a very brief of time. If their oxygen utilization limit performance we will see high muscle oxygen saturation levels even at high intensities. This is the primary indication of a utilization limitation, though an extraction limitation can also be present, which is when an athletes ventilatory exchange can have an impact on the athletes ability to extract oxygen. this occurs when an athlete breaths in a shallow, rapid, manner that can induce hypocapnia (low CO2 in the blood). Low CO2 reduced the acidity of blood which increases hemoglobins affinity for oxygen, thus reducing it’s ability to unload oxygen into the muscles.

Supply limitations on the other hand can be broken into delivery and respiritory limitations.

Figure III. Athlete 1 (Top) Presents with a respiratory limitation while Athlete 2 (bottom) Presents with a Delivery Limitation

A delivery limitation means that cardiac output is not sufficient to meet the demand for all of the organs and muscles. The body places a very high priority on preserving blood flow for the brain and heart. When the body is in a scenario where the demand for blood flow is higher than the cardiac system is capable of supplying it selectively reduces blood flow to low priority areas which eventually impacts the working muscle. When O2 is low we also look for signs of vasoconstriction or occlusion to see if the cardiac system is implicated. If the body is vasoconstriction the working muscle to ration blood flow SmO2 (muscle oxygen saturation) will be lower during rest periods, which is generally a progressive condition rather than a sudden one. A respiratory limitation is similar to a delivery limitation in that it is an oxygen supply limitation. Both typically lead to overall lower SmO2 levels at moderate to high intensities, but they come with different THb trends. While there are many types of respiratory limitations, i’m primarily going to talk about that which occurs to to insufficient ventilatory exchange. This generally manifests with a decrease in SmO2, less reload during rest periods, but increased THb due to vasodilation from Co2 build up, which is indicative of a hypercapnic state.

Next we’ll cover the broad strokes of how to identify respiritory limitations.

Figure IV. The green line represents SmO2 (muscle oxygen saturation), light red is THb (total hemoglobin), and dark red is heart rate.

Respiratory limited athletes typically present with very good cardiac output, good mitochondrial and capillary density, but a ‘weak’ respiratory system.This can be due to a lack of strength in the inspiratory or expiratory muscles, or a lack of fatigue resistance in the diaphragm

During high intensity exercise the diaphragm has a very large energy requirement and that muscle will need to contract with a lot of force and with a high frequency. If it starts to fatigue there will be a few dowstream effects. For starters, we’ll see progressive decreases in SmO2 from work bout to work bout, less oxygen will be reloaded into the muscle during rest periods, and there will be increasing THb due to vasodilation from CO2 build up, as seen in figure IV. We will also see some athletes present with hypoxemia, which is a drop in peripheral oxygen saturation. This is measured with a pulse oximeter.

We may also see a low LBM to FVC6 ratio. FVC6 is forced vital capaicity, which is a proxy for functional lunge volume. Additionally, in respiratory limited athletes we will different spirometry trends associated with inspiratory versus expiritory limitations. An inspiritory limited athelte will have a low FVC6, low FEV1, but the ratio between the two will be ~76–80%. An expiratory limited athlete will have a low FVC6 and low FEV1 as well, but the ratio between the two will be <76%.

Often times respiratory limited athletes also have trouble gaining muscle mass which can be attributed to their excellent cardiac output. In a previous article titled, “NIRS, Muscle Oxygenation, and Hypertrophy: What Is The Lowest Intensity You Can Use While Still Eliciting A Growth Response” I discuss the idea of individualized intensity cut offs for hypertrophy training. Respiratory limited athletes are often the individuals who do not experience venous or arterial occlusion until higher percentages of their 1RM, and as a result they may have trouble desaturating local muscles, it can be difficult to get a meaningful stimulus for hypertrophy.

They also often have lower neural drive, great tissue quality, and they adapt very well to both oxygenating and deoxygenating training, which is something I discuss at length in The Science & Practice of Performance Enhancement with NIRS. Before discussing practical interventions for training respiratory limitations, it’s important to understand why they are so prevalent in elite endurance athletes in the first place.

As you know, exercise has a profound ability to alter our bodies over time. For example, many of the ‘systems’ that contribute to oxygen transport undergo substantial adaptations to intense training. For every increase in VO2max, we are likely to see an increase in hemoglobin mass, improved circulation, increased left ventricular volume, or increased muscle mitochondrial and capillary density [and subsequently improved oxygen utilization].

Given how adaptable all of these systems appear to be, we would expect the airways, respiratory muscles, pulmonary vasculature, and lungs to adapt as well. After all, the bulk of exercise science literature asserts that the ‘limiting factor’ for maximum oxygen transport and utilization centers around the cardiovascular response to exercise. Additionally, it’s traditionally been said that the respiratory system is overbuilt for the demands posed by maximal exercise.

However, more recent research has revealed several circumstances in which one or more parts of the respiratory system are shown to be imperfect, anatomically underbuilt, and incur high biological costs during maximal effort exercise. Even trained endurance athletes, with very high VO2max values, may not have enhanced diffusion capabilities or lung volumes than the average sedentary adult. This absence of training effects on lung structure is shocking given the cardiovascular and muscular system’s capacity to adapt to exercise. In addition to not showing significant signs of adaptation to exercise, several respiratory system components can be negatively impacted via intense exercise training. For example, elite endurance athletes have a high prevalence of airway narrowing during or immediately following high-intensity exercise. Additionally, high-intensity training in elite endurance athletes can cause disruptions and remodeling of the airways, often accompanied by hypersensitive airways. This is because the high ventilatory demands of exercise require flow rates in excess of ten times resting levels which can injure the airways.

In Crossfit athletes, i’ve often observed arterial desaturation as low as 5–12% below resting values during maximal effort exercise. In these athletes, arterial desaturation almost always occurs at intensities above the lactate balance point and reaches the lowest value at maximal intensity. Additionally, using Moxy, we can see that oxygen transport to the respiratory muscles does not meet the metabolic requirements of ventilation. As a result, there is significant deoxygenation of the trunk’s accessory respiratory muscles during maximal effort exercise. In the picture above [at the beginning of this subsection] we have a coastal muscle SmO2 trend and an SpO2 trend for an advanced Crossfit athlete performing a step test. Note the change in both SmO2 and SpO2 as both reach a nadir at the highest workout intensities. This is indicative of both a pulmonary diffusion limitation, as well as a lack of fatigue resistance of the inspiratory and expiratory musculature.

It’s also worth noting that this phenomenon may be more exaggerated in female elite endurance athletes versus male elite endurance athlete, though it is also quite common in the later population. High resolution computed tomography has shown that airway cross-sectional areas are comparable between the sexes throughout the maturation process, but postpubescent females show a 20–30% reduction in the diameter of the trachea and main stem bronchi. A smaller lung size in adult females accounts for much of these differences in airway size, but even when a limited number of comparisons were made at equivalent lung volumes the adult female had narrowed trachea and bronchi compared to males of an equal body mass. Resting diffusion capacity and lung volumes are also lower in women versus men, even when adjusted for age, height, and hemoglobin concentration. Additionally, complete expiratory flow limitations, during maximum exercise, are observed in trained females at maximum VE much lower than in men. According to Demsey et al., 2020, “we can interpret these data to mean that adult women of all ages and over a wide range of fitness levels have hormonally determined trachea, bronchi, and lung sizes that are underbuilt for the flow rates demanded by heavy intensity exercise. Because the consequences of airway dysanapsis are likely to exist in the majority of women and be manifested even in moderately heavy exercise, we would predict that adult women across the fitness range would experience a greater suscepti- bility to respiratory limitations to exercise than do men.”

Now that we’ve covered some of the basic trends and compensation patterns associated with respiratory limitations, we’ll quickly cover some practical training interventions. I typically break these interventions into 5 primary categories: (1) Foundations, (2) General Adaptations for EST, (3) Tier 1 & Tier 2 Training Interventions, (4) Training Tools, and (5) ‘Other’ interventions.

When I think about the foundations for improving a respiritory limited athletes performance, the first thing that comes to mind is structure. The reason why A&P are paired together is because structure dictates function. The 4 main structural points I think about in this case are the position of the pelvis, the thoracic spine, the ribcage, and the infrasternal angle. Addressing these are relatively straight forward, but some things to consider are the fact that there is a ‘chicken and egg’ interplay between respiratory muscle strength limitations and structural limitations. For example, an athelte who is stuck in thoracic extension may be in that position because they have an expiritory muscle strenght limitation. This is a case where function impacts structure. On the other hand, we can have a scenario where structure dictates function as is the case when kyphotic athletes present with inspiratory muscle weakness. Once structure is in place, then I start to think about how these structures move. This is where we need to start thinking about breathing mechanics and the ability to breath with sufficient depth and frequency in sport specific positions.

The next set of foudnatiosn deal with with function. These include the strength of inspiratory and expiratory muscles including the diaphragm, external obliques, and abdominal muscles, diaphragm muscle endurance, as well as breathing coordination. The Spirotiger is one of my ‘go to’s for developing these qualities, but there are plenty of ways these can be accomplished on the cheap.

In terms of general training adaptations for energy system training we’re looking for improvements in cardiac-respiritory coordination, an improved maximum steady stat, increased functional lung volume, and improve respiratory muscle endurance. I won’t get into all the minutia here, but to give you a practical protocol one way to develop these qualities is through ‘hard start’ interval training.

One of the things we need to consider is that the amount of work accumulated at a high % of athlete’s peak oxygen consumption is one of the most essential training variables for improving resp limited athletes performance. However, the amount of volume that an athlete’s muscles, bones, and joints can tolerate week after week is finite, which puts a limit on how much work they can conceivably do at a high % of peak O2 consumption.

This is especially true in Crossfit, or mixed sport, athletes who can only dedicate so much time to their EST development given all of the other sport-specific qualities that need to be trained. As a result, it’s crucial to find ways to elicit specific adaptations with as little volume as necessary.

One way to add this degree of precision is by manipulating intra-interval pacing structures to stress different ‘systems’ more than others. For example, let’s say we had a respiratory limited athlete, and we wanted to train at a high % of their VO2peak. We could either have them do a traditional interval training session where they complete a series of fixed pace intervals or use a ‘hard start’ interval method. The latter entails starting at a very fast pace and descending in speed across the interval.

Numerous studies have shown that hard start intervals induce higher mean VO2 and lower RPE’s than traditional interval structures despite similar average speeds, indicating that hard start intervals are a good strategy for interval sessions aiming to accumulate more time at a high % of VO2peak with less wear and tear.Practically, this could be doing something like….

If you’re interested in learning more about the concepts discussed in this article feel free to reach out at “”. I offer consulting, and additional services for coaches, sports teams and organizations, which you can learn more about here. Additionally, if you’re interested in learning how to identify and train limitations on your own, i’ve partnered with Moxy Monitor to produce an NSCA CEU approved courses called the Science & Practice of Performance Enhancement with NIRS, which you can find here. This course is packed with information and practical takeaways for athletes and coaches, whether or not they use a NIRS device.



Evan Peikon

Evan Peikon is an integrative physiologists with an interest in enhancing human performance. IG: @Evan_Peikon. Website: