Cardiovascular Control During Full-Body Exercise
The Tug of War Between Metabolic Vasodilation and Sympathetic Vasoconstriction & It’s Implications
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 (Figure I).
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 [ie, 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 [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 ensure 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 allows 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 where to analyze a bumblebee they would quickly occlude 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 it’s capacity to receive large amount 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 skins 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 disabiling 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 ‘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 a upward ‘drift’ in heart rate at a fixed work bout.
For Moxy Monitor users, you’ll first notice the signs of cardiac drift and blood flow redistribution to the cutaneous circulation in the non-working muscles. This will look like progressive decreases in total hemoglobin (THb), and as you continue to push for an extended duration you’ll eventually see decreases in THb to the working muscles as well, which will result in major performance losses. These can be mitigated to an extent by cooling the skin’s temperature (or drinking slushied ice), but it also opens the door for improving thermoregulation in athletes, especially those who compete in endurance sports in extreme conditions.
That said, it’s very difficult to improve that which we cannot quantify. Up to this point it’s been difficult to get accurate measures of skeletal muscle blood flow, and thermal distribution throughout the body. This is no longer the case as non-invasive measurement of skeletal muscle oxygen kinetics (Moxy Monitor), core temperature (CoreTemp), and skin temperature (Thermo Human) become cheaper and easier practically implement.
The CORE development team recently posted a ‘heat ramp test’, which is intended to compare changes in physiological responses over time.
The protocol begins with a gradual warm-up, or ‘thermal accumulation phase‘. They recommend starting at 50% of your functional threshold power (FTP) or critical power (CP) and gradually increasing your output over a 20:00 period. The recommended ramp structure is as follows: 5:00 at 50, 60, 70, 80% FTP. This ramping period ensures the core temperature rises slowly from baseline upto 38 °C (100.4ºF).
Once the core body temperature reaches 38 °C (100.4ºF) you are instructed to reocrd your heart rate and power output. Now the test has officially begun and you are instructed to hold your heart rate steady by allowing your power output to decline over time, which will counteract the ‘cardiac drift’ (heart rate rising at a fixed power output) discussed earlier in this article. During this phase your heart rate will remain stable while your power output decreases and your core temperature increases. Once your power output declines by >20% from the first check point you should record your core temperature again and stop the work bout.
This test is interesting from a descriptive and a prescritive standpoint. It tells us both how well an athlete is able to maintain their output while counteracting cardiac drift, and it also allows one to calculate ‘heat training zones’ if desired. However, what’s more interesting is where we can overlay this data with that taken from other technologies like NIRS and infrared thermography.
What does NIRS measure?
“NIRS measurements reflect the balance of O2 delivery to working muscles and muscle O2 consumption in capillary beds” -Ufland et al. 2012“Combining NIRS with simple physiological interventions, such as venous or arterial occlusions,allows quantitative measurements to be made from skeletal muscle. This provides a tool for assessing two major determinants of the capacity of muscles to exercise: O2 delivery and O2 utilization. The non-invasive nature of NIRS makes it an appealing technique for use in adynamic environment and for activities of daily living.” -Jones et al. 2016
What is Infrared Thermography ?
A thermogram is a representation of heat radiating from the body. Skin temperature regulation is impacted by blood flow, muscle recruitment pattern, inflammation, and injury. As a result, IT allows one to detect these thermal asymmetries, which represent regions of interest (ROI’s). ROI’s show potential injury risk from workload mismanagement, biomechanics, tissue pathologies, or other sources of thermal asymmetry.
By implementing infrared thermography into the ‘heat ramp’ test above we can measure the thermal gradient from core to skin, which would allow you to measure thermal flux (the balance of heat generation in the body and heat dissipation via active and passive thermoregulation). Because increase in cutaneous blood flow are a primary mechanism for offloading heat, this can help us understand how increased thermal loads impact an individuals cardiovascular control.
Additionally, we can use a NIRS device (like a Moxy Muscle Oxygenation Monitor) how increases in cutaneous flow impact both the non-working and working muscles. For example, when blood is redistributed from the skeletal muscle to the skin we will first see a decrease in total hemoglobin to the non-working muscle, which allows a large fraction of cardiac output to be maintained to the working muscles while still increased flow to the skin. As temperature increases, and additonal blood needs to be partioned to the cutaneous circulation, we will see decreases in flow to the skeletal muscle, which will result in a drop in performance.
Over time, as heat tolerance increases, we will want to see an athelte:
(1) Extend the time it takes for power output to drop by >20% at a fixed heart rate as temperature climbs from 38 °C (100.4ºF) upward.
(2) Improve the ability to counteract cardiac drift at a fixed power out when core temperature is elevated.
(3) Increase thermal flux. As the muscles generate heart we want to see an improved ability to offload heat, which will likely result in improvements in (1) and (2).
(4) Maintain blood flow (without compromise) to the active muscles for a longer duration after core temperature exceeds 38 °C (100.4ºF).
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