UNDERSTANDING How the body adapts

Building from a previous article found here, this present article aims to take a deeper look at the physiological adaptations that occur particularly in the cardiovascular system in relation to oxygen transport.

As we perform exercise and/or encounter different environmental stresses (ex., heat, cold, altitude, humidity levels), our body works to maintain homeostasis. Homeostasis is a state of equilibrium that is maintained by our body, and it is influenced by many factors some of which include temperature, acidity/pH, ion and glucose concentrations. When our body undergoes any kind of stress, our physiology – how our body works – is challenged to return to homeostasis. Let’s say our stress is due to increases in metabolic load (increased demand for energy, with or without the use of oxygen, to allow our muscles to contract or organs to function) from a training stimulus of exercise. Our bodies respond to this increased metabolic stress by stimulating our nervous system to help us regulate our blood pressure, releasing hormones to facilitate our cardiovascular response, improve our respiration and ability for oxygen to be transported from the lungs all the way to the cells. We do this to find a way back to homeostasis in our bodies, it is a stress/stimulus and then time for the body to regain function and regulation of our systems. This sounds tricky, right? I agree.

A question we often have is, what is our limit? How much can our bodies handle? (related to training volume, intensity, and load; life stresses included) We want to understand more about how our body responds to training. As we introduced above, during training we have an increased metabolic demand for our system. We want to go faster, farther, be stronger – so we have an increased demand for oxygen to supply energy to do that. Our training stimulus can be a variety of different avenues, think – intensity/reduced recovery/duration/altitude/heat/etc. Each of us is different, and we respond differently to the variations in training such as time needed to develop a response to a stimulus, ability to handle training load/recovery, etc. There are many factors in addition to training that impact our physiology, including relationships, school/career, responsibilities, family, finances, illness, emergencies, etc. 

First of all, this information of lack of oxygen is detected in our vessels by chemoreceptors (located in the aortic sinus by our aortic arch on the ascending aorta – just after blood is pumped by our heart, AND by our carotid sinus on our neck) and passed to our medulla oblongata and pons in the brain to allow our nervous system to react either in our heart (increase heart rate or stroke volume) or lungs (increase respiration, ventilation) to help us get more oxygen.

The most logical place to begin getting more oxygen is by increasing our breathing – we bring more oxygen into our lungs by increasing our inhalation – ventilation. There might be some issues with this, but that is for another day. For now, knowing that our body can change the rate of ventilation (breathing frequency) and the depth of our respirations (shallow versus deep breathing) is helpful for improving our oxygen availability. 

As mentioned above, our heart also assists in helping us improve our oxygen delivery. The heart is a crucial pump in our body, providing the rest of our body with oxygenated blood. If we increase our heart rate (HR), we can improve the amount of blood being delivered as the rate-speed increases. Additionally, we can increase the volume of blood being ejected with each beat (stroke volume, SV). Heart rate multiplied by stroke volume is equal to cardiac output (CO, a.k.a., systemic blood flow). This is to say that by altering heart rate and/or stroke volume, we can change the blood flow to the rest of our system. It is incredibly important, are you following me? Oxygen is being transported via the lungs, into the bloodstream, into the heart, pumped out of the heart into our arteries and vascular system, delivered via the bloodstream to our capillaries to make an exchange (unload oxygen to the tissues, and pick up carbon dioxide - deoxygenated blood - to return to the heart and exhale via the lungs). By increasing cardiac output, we deliver more blood (flow) and thus oxygen to our tissues. 

Going deeper in the heart now, heart rate is influenced by the sodium ion – if our body can make sodium more available with the release of norepinephrine – then our heart rate will increase. Sodium is required for our cardiac myocytes (heart muscle cells) to begin depolarization (excitation for contraction). Heart rate is one of our bodies main responses not only to provide more oxygen, but also for regulation of our blood pressure. Remember HR x SV = CO, so stroke volume is another way our body improves oxygen delivery. Contractility (inotropy) is a factor that increases myocardial oxygen consumption (i.e., heart muscle oxygen uptake), and contractility has a direct relationship with SV to eject more blood with each beat (stroke). With increased contractility, we have increased SV, which increases CO, and blood pressure to help our tissues receive more oxygen. Heart muscle contraction is improved by increasing the amount/availability of the calcium ion, as with more calcium our excitation-contraction coupling allows the muscle to contract (this action of contraction has the same mechanism in skeletal muscles and cardiac muscles). Specifically, the release of calcium from T-tubules to the sarcoplasmic reticulum stimulates the ryanodine receptor – Type 2 to release more calcium. Calcium binds with a protein called troponin which changes the shape of tropomyosin and moves it out of the way so that two filaments can interact together (myosin and actin), and with the help of ATP hydrolyzation (ADP + Pi) this creates a cross-bridge (position for muscle contraction) where Pi is released from the myosin filament and contraction happens by sliding these filaments and releasing a kind of coiled energy in the power stroke of contraction. Energy in the form of ATP is needed for this process of contraction and relaxation, but without calcium, there can be no contraction – no cross-bridge between these filaments. So now we know sodium and calcium are important ions for our heart to improve oxygen delivery. The heart is one of our vital organs and keeping healthy and fit will allow us to deliver more oxygen to our muscles and quicker. 

It is not only our lungs and heart that make adaptations to help us improve oxygen transport – but also our vessels. When we do not have enough oxygen available to our tissues, our systemic vessels vasodilate (expand) to allow more blood flow and more oxygen to pass through to the capillaries for circulating oxygen to our tissues. Vasodilation is relaxation of the smooth muscle cells in the tunica media layer of our resistance vessels (arterioles – smaller arteries). This happens as no norepinephrine is released, which prevents its binding of alpha 1 adrenergic receptors – allowing relaxation and thus vasodilation. This increases the vessel’s radius and decreases resistance in the vessel, allowing a decrease in blood pressure and thus more blood flow through the vessel providing more oxygen along the cascade of oxygen transport. Through this article, we have found our way so far along this cascade from lungs to the heart to the vessels.

This leads us into the uptake by the tissues. Our capillaries (smallest vessels) allow an exchange between oxygen and carbon dioxide through a process called microcirculation – where these gases move along the pressure gradient between hydrostatic pressure and osmotic pressure. This is where we can begin to imagine how our tissues consume oxygen. A parameter of interest is then the arterial and venous oxygen difference, however, this requires a more invasive collection of both arterial and venous blood. 

Now, the cool thing is that we just figured out how to understand what goes into a measurement of oxygen consumption (oxygen uptake). Have you heard of VO2max? That is the maximal volume of oxygen our body can consume/uptake in a minute. It is represented through the Fick equation, VO₂ = CO (cardiac output) X A-V O₂ difference (difference in oxygen uptake by the tissues, arterial and venous). The greater amount of oxygen extraction from the tissues – the greater the A-V O₂ difference. Oxygen extraction depends on workload, muscle fibers, muscle metabolism related to the glycogen stores, and cellular use of oxygen for energy related to mitochondrial respiration. We will dive into efficiency of oxygen utilization another time.

When we don’t have enough oxygen due to increased intensity of our exercise (speed, workload, duration, etc.) or decreased recovery time – the metabolic demand increases our body’s need for oxygen. From there we discussed that our body increases CO via HR and SV, also the vasodilation of our vessels to support delivery of oxygen, and indeed this is related to how our body utilizes that oxygen (oxygen extraction). Our oxygen consumption (VO₂) by relationship is then a parameter we use to understand how our body adapts to training. 

Measuring VO2 from submaximal or VO2max from maximal exercise testing allows us to contextualize the adaptations our body has made in training and over time (from different points in the seasons, year to year, or related to training interventions).

In the previous article on adaptation, we learned that the initial 1-4 weeks of training/intervention is about the body working to delivery more oxygen to the tissues through the cardiovascular system and creating more capillaries for improved oxygen availability. I hope from this current article, you have gotten a deeper understanding of how our cardiovascular system adapts to training.