Heart rate training (Part II) exercise and metabolism.
The primary objectives of this series are to briefly discuss the scientific rationale supporting the use of heart rate (HR) as a practical measure of exercise performance and present some ideas (coming up in Part III) about how one may incorporate HR training methods into their exercise routine.
In Part I, we explored heart function by looking at the determinants of cardiac output. These were stroke volume (SV) and heart rate. In the absence of changes in contractility, both end systolic and end diastolic volume decrease with increased heart rate. The results of research studies depend heavily on the experimental method. While there is debate over this issue, HR and SV seem to decrease proportionately due to reduced ventricular filling time. Most studies indicate that stroke volume probably remains relatively unchanged as HR increases. Heart rate is also influenced by the sympathetic and parasympathetic nervous system which also can have a major effect on contractility. These changes are impossible to measure in routine training so HR remains the practical measure of exercise intensity.
Intuitively we know that there are certain responses of our bodies to exercise. These include elevations in respiratory rate, heart rate, body temperature, and muscle fatigue. All of these are sensible to us in one way or another as we have all experienced during exercise. Technically speaking, one's heart rate may increase more than 300 percent above its resting level. Cardiac contractility, measured as the rate of pressure generation in the heart, dP/dt, also increases substantially. Most importantly, our consumption of oxygen dramatically increases. Sports physiologists measure this as V02. In the laboratory we find that heart rate correlates very well with oxygen consumption through very high levels of exertion. So what drives oxygen consumption?
If we have any hope of connecting heart rate with exercise and training, the link must be through metabolism of fuel to create chemical energy After all, it is the production of chemical energy in the form of ATP adenosine triphosphate, that propels us in sport and enables skeletal and heart muscle contractions.
Let's start with primary energy sources of which there are two, carbohydrates and fats. Some of you will say that protein can be used as well and you are correct, but it's total contribution to energy generation is quite small. Therefore, for this discussion, we'll just ignore it. In the following description, I will not worry about the intermediary steps in the metabolic pathways or the nitty-gritty chemical reaction details of the electron transport mechanism. It will be sufficient to look superficially at two metabolic pathways paying particular attention to a couple of important steps, the energy produced, and ultimately the metabolic cost and athletic performance implications of energy production.
[FIGURE 1 OMITTED]
When we consume carbohydrates, our bodies store them as sugars, mainly in the form of glucose, a six carbon sugar, attached end to end to form glycogen, a polymer of glucose. In 1918, Otto Meyerhof and Jakub Parnas showed that glucose was utilized as a fuel and lactic acid produced as an end-product during muscle cell contractions. Gustav Embden described the detailed steps of the biochemical pathway that bears their names (The Embden-Meyerhoff-Parnas Pathway). This is also called the Glycolytic Pathway and the metabolism of glucose is referred to as glycolysis. In the cytosol of the cell, the 10-step glycolytic pathway eats up glucose and initially consumes energy through the conversion of glucose to fructose, another six carbon sugar. Fructose, as many of you know, has received some bad press because it is associated with malabsorption in the GI tract. However, in this metabolic case, fructose is simply produced during glycolysis and then split into two three carbon sugars. En-route to fructose, two ATP molecules are consumed. The bottom half of the pathway produces four ATP high-energy molecules for every fructose. A net of two ATP molecules are produced for every glucose molecule metabolized. When sufficient oxygen is present, the end point of glycolysis is the production of pyruvate which soon enters the Tri Carboxylic Add Cycle (TCA). However, when extremely high levels of exertion are demanded by an athlete and there is insufficient oxygen available, pyruvate cannot enter the TCA cycle and glycolysis is fermented to lactic acid. Ouch! To add insult to injury, we can only sustain this extreme level of exertion for up to 90 seconds before "hitting the wall." We often refer to this level of exertion as being in the "red zone."
[FIGURE 2 OMITTED]
The endurance engine for all athletes is the TCA cycle, also known as the Kreb's Cycle or the Citric Add Cycle. This energy producing powerhouse requires a plentiful supply of oxygen and fat to fuel its elaborate biochemical oxidation and reduction reactions that take place in the mitochondria of cells. Pyruvate, triglycerides, and phospholipids are converted to citric acid where they enter the cycle. Without going into the gory details of intermediary metabolism, it is sufficient to say that the TCA cycle produces 34 ATP molecules or 17 times that of glycolysis. This is why fat burning during extended exercise is so vitally important. It also explains why endurance training must be designed to prepare the body to depend upon this cycle for energy production instead of glycolysis
Athletes may glibly refer to oxygen debt when discussing physical effort where lactic acid is produced in high concentrations in our muscles. When we exercise or compete at high intensity we can easily or sometimes inadvertently enter the "red zone." Intuitively, we understand the jargon because we feel the bum, exhaustion, muscle fatigue, and difficult recovery if we remain in the red zone too long. A dear understanding of this concept is sometimes hard to find. Oxygen is the cash currency of intermediary metabolism. When an athlete is burning fat and has adequate oxygen supply from respiration, pyruvate formation connects glycolysis to the TCA cycle. But when oxygen demand outstrips the supply, V02 max, and the muscle machinery needs more ATP, it has to borrow from somewhere else to replace the missing oxygen. As we saw above, when this happens, the end product of glycolysis becomes lactic add, which then accumulates in the muscles. Oxygen can be used later to burn off the lactic add and the amount of oxygen cash required to metabolize the lactic add is the oxygen debt. If the oxygen debt is small, such as during a short acceleration or climbing a small hill, it is possible to reduce the lactic add level as one continues to exercise at a more oxygen efficient level. If the effort is exhaustive, it may functionally end one's workout or the days competition.
Linking oxygen metabolism to heart rate and the red zone
We have now completed the linkages between exercise intensity, oxygen consumption, cardiac output, and heart rate. In addition we have reviewed the connection between oxygen consumption with the type of fuel we burn during exercise, either carbohydrate or fat. And we have also seen that aerobic metabolism uses fuel from carbohydrate and fat sources producing carbon dioxide and water, while anaerobic metabolism uses carbohydrates and produces lactic add. The exercise intensity at which the body begins to produce lactic add is the anaerobic threshold (AT).
Figure 3 shows us the empirical relationship between heart rate effort (x-axis) and the mix of fuel we use. The absolute heart rate will vary from person to person, but in general we can consider the intersection of the X and Y coordinates at about 70 percent of the subject's maximum heart rate. At these low efforts, a significant part of energy generation comes from fat and a much smaller component from carbohydrate. The amount of carbohydrate metabolized increases along with heart rate, until the fat burning engine can no longer keep up. As we enter the red zone, HR typically above 90 percent, muscles must get most of their ATP energy from glucose metabolism. Consequently, lactic acid is created, and oxygen debt builds up.
[FIGURE 3 OMITTED]
In the next issue, we will discuss ways in which we can use heart rate training to teach our bodies to burn fat and extend the red zone onset to higher and higher heart rate levels.
By Douglas F. Munch, PhD
Dr. Douglas Munch is a medical consultant and longtime competitive athlete in track and swimming He received his doctorate in medicine and biomedical engineering from the Johns Hopkins University School of Medicine in Baltimore, Maryland.
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|Title Annotation:||TALKING ABOUT TRAINING|
|Author:||Munch, Douglas F.|
|Date:||Sep 22, 2012|
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