Blood flow regulation is one of the most interesting aspects of human physiology. When we perform high intensity exercise we utilize oxygen at a greater rate than it can be supplied to the skeletal muscle, and as a result there is a net deoxygenation of the skeletal muscle. In response to this hypoxia in the skeletal muscle we experience ‘metabolic vasodilation’ which is a process by which we increase blood flow. This process is relatively simple during single joint or small muscle mass exercise, like a bicep curl for example. However, it becomes increasingly complex when we progress to regional exercise using multiple muscle groups in close proximity to one another or full body exercise. The reason for this is that we have a finite ability to metabolically vasodilate tissue before we outstrip our cardiac output and cannot maintain our arterial blood pressure. As a result our body has built in protective mechanisms to ensure that we never vasodilate so much that it threatens our arterial blood pressure, which would lead to a loss of consciousness. One mechanism by which this occurs is an increase in sympathetic nervous system activity, termed sympathetic vasoconstriction. This sympathetic regulation of peripheral resistance guards against the extreme vasodilator capacity of skeletal muscle invoked by exercise and protects us from extreme hypotension or low blood pressure.
This is never more apparent that when doing full body, all out, exercise like Crossfit or Cross Country-Skiing. During these full body endurance sports the demand for oxygen by skeletal muscle can be increased by multiple orders of magnitude and as a result skeletal muscle blood flow is very high. This creates some problems during full body exercise where there are two potentially competing physiological needs. First, skeletal muscle blood flow needs to be matched to meet the metabolic costs of muscle contraction. Second, blood pressure needs to be regulated to ensure there is adequate perfusion pressure to all organs. The idea that these two important needs ‘compete’ arises when we consider the total mass and vasodilator capacity of skeletal muscle compared to the maximal pumping capacity of the heart. With enough skeletal muscle vasodilation there exists a risk that cardiac output is outstripped and blood pressure regulation will be threatened.
So, in addition to considering the heart as a pump, the blood vessels as an oxygen delivery system, and the muscle as an end user of oxygen we also need to consider the overall need of the human body to maintain arterial blood pressure in order to ensure the brain and vital organs get enough blood flow. One way that arterial blood pressure is regulated is that the sympathetic nervous system restrains blood flow to the contracting skeletal muscles. This was first explained by Loring B. Rowell in his ‘sleeping giant hypothesis’ which reflected the idea that the vast ability of skeletal muscle to vasodilate can outstrip the ability of the heart to generate adequate cardiac output and arterial blood pressure. If the ‘sleeping giant’ awakens and blood flow to the skeletal muscle is not restricted, then autonomic failure will ensue and blood pressure will fall so low that an individual will quickly lose consciousness.
In addition to blood flow to the working muscles being restrained, there is also a diversion of blood flow away from less active skeletal muscle and other tissues so that the vast majority of cardiac output (after the brain and vital organs are perfused) is directed to active skeletal muscle. This adaptation is most impressive in elite endurance athletes. In these individuals vasodilating factors in the skeletal muscle outcompete sympathetic vasoconstriction in the arterioles closest to the contracting muscle (which is termed (functional sympatholysis) while allowing for continued vasoconstriction upstream. This interplay allows for high degrees of oxygen extraction while maintaining high flow rates and simultaneously ‘protecting’ cardiac output. In this way, elite athletes straddle the line between supplying the muscle with sufficient oxygen while keeping cardiac output as high as possible without threatening the ability to maintain consciousness.
If an aeronautical engineer were to analyze a bumblebee they would quickly conclude that it could never fly. Yet, it does. Similarly, if a hydrodynamic analysis were done on the human circulatory system it would lead to the conclusion that human beings cannot stand upright, Yet, they do. We partly owe this ability to our ‘second heart’. While the heart acts as the ‘master pump’ in our bodies, it’s just one part of an integrated system and it could not function without a secondary pump, called the ‘muscle pump’. The muscle pump acts as a secondary heart on the venous (return) side of circulation. Without this second heart an exercising human could not force enough blood back to the right ventricle of the heart to maintain an adequate level of cardiac output to keep them upright, and conscious, let alone exercising.
If you’ve ever stood up for an extended period of time, without the slightest movement, you’re familiar with the sensation of teetering on the bring of unconsciousness. Thankfully, even the most modest muscle contractions of the leg muscles are enough to act as an effective pump driving blood back to the heart and preventing you from blacking out. The reason for this is that these muscles contract rapidly to restore ventricular filling pressures and stroke volume. However, cardiovascular control is extremely complex, and there are instances where we can’t rely on the ‘second heart’ to help control cardiac output. For example, when exercising in high heat conditions. Exercising in high temperatures forces humans to cope with two of the most powerful regulatory demands they can face: the competition between the skin and muscle for large fractions of cardiac output and blood flow.
The cutaneous (skin’s) circulation is second only to the skeletal muscle in its capacity to receive large amounts of blood flow and can therefore seriously compete with skeletal muscle for cardiac output during exercise. Simply put, we can’t increase blood flow to a great extent in one highly compliant region without decreasing it somewhere else. This means that at some level of physical output, in high heat conditions, cardiac output just can’t rise enough to supply both the skin and muscle with necessary blood flow. This competition between the skin and muscle for blood flow provides a perfect example of how peripheral circulation determines the performance of the heart and lines up with the mid 20th century physiologist, August Krogh’s, beliefs that the distribution of cardiac output determines the volume of blood available to the heart at any moment. When we shunt more blood to the skin's surface (to dissipate heat) it means that a lower fraction of blood volume is passing through the ‘second heart’ (muscle pump), and as a result less blood is being driven back to the heart between contractions.
The price we pay for pumping more blood through the skin (or any ‘non-pumping circuit’) during exercise is a fall in ventricular filling pressure, cardiac preload, stroke volume, and consequently cardiac output. We cannot sacrifice cutaneous blood flow for the sake of maintaining ventricular filling pressure and cardiac output, otherwise disabling hyperthermia (heat stroke) would quickly ensue. This is one of the reasons why our performance is lowered when we exercise in very high temperatures, and it is also a cause of 'cardiac drift’. Cardiac drift is a consequence of progressive increases in the fraction of cardiac output directed to vasodilated skin as body temperature rises. This causes decreases in thoracic blood volume, and consequently stroke volume with an upward ‘drift’ in heart rate at a fixed work bout.
Muscle Oxygenation Responses to Regional Versus Systemic Exercise
Have you ever wondered that the physiologic differences are between regional and systemic muscular work? For example, if you wanted to do an interval session have you wondered if there is a meaningful difference between using a watt bike where only your legs are involved versus an airdyne bike that incorporates both lower and upper limb activity? If so, you’ve pondered questions about cardiovascular control mechanisms. Starting with a simple example, when intense upper body movement is added to intense lower body movement blood flow to the legs at a given work rate will reduce by up to 10%. So, for example, if I was pedaling on an airdyne bike with my legs only, then started using both my arms and legs, blood flow to my lower body would be reduced. A similar effect also occurs in the upper body, as would be the case if I was powering the airdyne bike with my arms only and then started using my legs. nThese reductions in blood flow to the extremity muscles are a product of peripheral vasoconstriction, which is caused by the arterial baroreflex whose key functions include supporting and maintaining blood pressure.This mechanism is also seen when an athlete is limited by the maximal pumping capacity of their heart during high intensity exercise and cannot increase cardiac output to cope with an increased work demand. In these cases cardiac output is not sufficient to maintain blood pressure and the arterial baroreflex increases peripheral resistance by augmenting SNS activity and restricting blood flow to working skeletal muscles. This is an effective strategy because very small changes in the radius of a blood vessel have huge impacts on resistance.This is common in Crossfit athletes who are strong, have great local muscular endurance, but weak cardiac output. These athletes often end up in a scenario where the demand for blood flow is higher than the cardiac system is capable of supplying. In these cases blood flow to low priority areas is selectively reduced, which eventually impacts the working muscle. When this occurs we can look for signs of vasoconstriction or occlusion to see if the cardiac system is implicated as well as other red flags. This can be seen on a step test where the working muscles progressively vasoconstrict as intensity increases.
Oxygen Transport in Deep Versus Superficial Muscles
In addition to understanding the differences between exercise that involved regional vs local muscle work, we also need to appreciate the differences in oxygen kinetics between deep and superficial muscles of the same regional muscle groups. In the picture above I have NIRS data from a collegiate rower performing a 2,000m row in 6:22 at a fixed stroke rate of 32-36 SPM. This trend shows his muscle oxygenation trends from his vastus lateralis and rectus femoris muscles. You'll notice that the desaturation curves are quite different between these two heads of the quadricep, which may seem perplexing at first glance.
In order to understand why this is the case we need to appreciate the fact that NIRS allows us to sample muscle oxygenation in both deep and superficial muscles. Deeper muscles tend to have greater capillarity and blood flow than superficial muscles, and they also tend to be more oxidative. As a result, deeper muscles present with slower rates of oxygen desaturation than superficial muscles at a given power output, and they also have higher nadirs. Additionally, deep and superficial muscles have different oxygen transport strategies. Deep muscles rely more of perfusive transport and superficial muscles rely more on diffusive transport. This is an often underappreciated aspect of oxygen transport and metabolic control, and can account for much of these differences between the vastus lateralis (superficial muscle) and rectus femoris (deep muscle) trends above.
In addition to different active muscles having different oxygen kinetic profiles, we also need to consider how changes in coordination and recruitment impact muscle oxygenation trends as fatigue set in. For example, a rower may start with more of a knee flexion dominant pattern and as the knee flexors fatigue they may rely more on hip extension to power their stroke. This would result in less oxygen extraction in the VL as fatigue onsets and more oxygen extraction in the rectus femoris. As a result, monitoring oxygen saturation in just one working muscle can potentially misrepresent the status of overall systemic energy reserves.
So, going back to the rower’s muscle oxygenation trends, we see that deoxygenation occurs in both the vastus lateralis and rectus femoris muscles as soon as the activity starts. Within the first ~600 meters muscle oxygen saturation in both the vastus lateralis and rectus femoris reach a relative low point and this low muscle oxygen saturation level is maintained up to ~1300 meters, indicating that the rower is working at a maximum steady state between ~600 meters to ~1300 meters. However, once he hits the 1300 meter mark we see that muscle oxygen saturation in the vastus lateralis begins to climb and while muscle oxygen saturation in the rectus femoris begins to drop down further. This indicates a change in coordination and recruitment which is an unconscious strategy employed to keep him powering through his event while his 'primary' working muscles begin to fatigue. By observing this we can better understand the energetic constraints of his event and how he copes with those demands, which will allow for greater precision in his training, even preparation, and pacing on subsequent events.
Mixed Modal Sporting Applications
One of the things I find so interesting about mixed work capacity sports, like Crossfit, is the discrepancy between local and systemic energy reserves that tend to occur. Most 'work capacity' sports involve regional muscle groups working in concert with one another (think running, for example), or large groups of muscles across the body working in harmony (like during rowing). Crossfit certainly has movements that fall into these broad categories, but what complicates things are the liberal sprinkling of small muscle mass exercises scattered across events. For example, stringing together combinations rowing, box jumps, and strict handstand pushups which are systemic, regional, and local movements respectively. Since so many muscle groups are used in a Crossfit metcon, and we're often limited by one small muscle group [like during a handstand pushup], monitoring muscle oxygen saturation in any one area can potentially misrepresent the status of overall systemic energy reserves. As a result, I'll typically advocate for using two to three NIRS sensors during a metcon. This often entails one sensor on the largest ‘primary’ working muscles, another sensor on a ‘secondary’ working muscle, and the third on an intercostal muscle to assess the work of breathing or on a non-involved, or minimally involved, muscle. What this allows us to do is parse out whether someone is systemically limited, or locally limited. If someone is systemically limited then we need to improve the athlete's maximum integrated capacity for the respiratory, cardiovascular, and muscular system to uptake, transport, and utilize oxygen respectively [which in that case we'd want to improve their VO2max]. On the other hand, if they are 'locally limited' we may need to prioritize strength of a certain muscle group (or muscle groups), coordination, local mitochondrial density, or localized blood flow. Understanding which of these factors is limiting an athlete is critical, and it's a lot more complex than saying they need to improve their 'engine' to get better at metcons. In the picture above we have muscle oxygen saturation trends from an elite Crossfit athlete’s right vastus lateralis and right deltoid, as well as their respiratory muscle blood flow trends taken from the left intercostal between the 7th and 8th ribs. Note that the vastus lateralis and deltoid oxygen saturation trends follow the same pattern, but only with different magnitudes of oxygen utilization. Additionally, there is a near inverse relationship between vastus lateralis and deltoid muscle oxygen saturation and respiratory muscle blood flow. This means that as oxygen is consumed in the extremity muscles there is a proportional increase in the work of breathing. Collectively, we can use this to discern that a systemic limitation is present, which can help us guide their training and pacing in metcons in a more strategic manner.
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