The Right Stuff, Part 2

The Cutting-Edge Runner: How to Use the Latest Science and Technology to Run Longer, Stronger, and Faster
by Matt Fitzgerald

(Page 2 of 5)

Like the bones, the muscles and tendons are especially vulnerable to injury during the early stages of a new running program as tissue remodeling struggles to keep up with the tissue damage that stimulates it. And these same impact forces also contribute to muscle fatigue. Conventional wisdom holds that "hitting the wall" in a marathon or long training run is caused by depletion of stored energy–specifically glycogen. A more important cause of declining performance in long runs is impairment of the muscles' capacity for elastic recoil due to the effects of repetitive impact forces. The damage that accumulates in the muscle fibers reduces their stretching capacity and ability to contract. Then, to top it off, nerves send information about this damage to the brain, which responds by essentially shutting the muscles down to protect them from further damage. The net effect is that the physical cost of maintaining your desired speed increases dramatically. Your legs become increasingly sore, which reduces your desire to continue running at the current pace.

The same muscle and tendon adaptations that allow runners to run farther and more often without getting injured also increase resistance to this type of neuromuscular fatigue. The best way to train for impact tolerance is to begin with a small volume of running and increase it gradually, reducing volume every third or fourth week to give your legs a chance to recover, or "catch up."

CHARACTERISTIC #2: A BIG, STRONG HEART

As I explained above, one of the major factors that affects running performance is your aerobic capacity, or VO₂max. This is your maximum capacity to consume oxygen (relative to your body mass) while running. Why is this so important? Because your muscle fibers need oxygen to release the energy that allows them to contract repeatedly at the moderate work intensities associated with distance running.

There are two components of aerobic capacity: the delivery of oxygen to the muscles, and how oxygen is metabolized within the muscles. Because oxygen is transported in the blood, there is a close relationship between your maximum rate of blood circulation and your VO₂max. A strong heart is the cornerstone of good circulation–better runners tend to have larger, more powerful, and more efficient hearts than do lesser runners. Training increases the size, power, and efficiency of the heart muscle.

Oxygen consumption begins, of course, with the lungs, which draw oxygen from the air you breathe. (Interestingly, the lungs themselves do not adapt to training.) Much of the oxygen drawn into the lungs is trapped by capillaries and absorbed through them into the bloodstream. Hemoglobin proteins attached to red blood cells transport oxygen molecules to every cell throughout the body, where oxygen is used to break down fats, carbohydrates, and to a much lesser extent, amino acids (the building blocks of proteins) to release energy. The heart's role in this process is to keep the blood (and the oxygen within it) flowing throughout the body. When you're running, your body needs more oxygen to keep it moving, so the rate and force of the heart's muscle contractions must increase so that bloodflow and oxygen delivery to the working muscles can also increase. When you sustain very high running speeds long enough, your heart will reach its maximum pumping capacity, which, again, is determined by its size, strength, and efficiency. It's perhaps also determined by a protective mechanism that is regulated by the brain and may just prevent us from exercising to death (as inadequate oxygen flow to the heart itself would cause a heart attack).

The major adaptation of the heart to training is an increase in its size; in fact, it becomes more powerful and more efficient primarily by growing. The heart's maximum pumping capacity is a function of the amount of blood it pumps per contraction (stroke volume) and its maximum rate of contraction. Training does not increase maximum heart rate, but it does increase stroke volume. As the size of the heart increases, its blood storage capacity increases, allowing the heart to pump more blood per contraction. The maximum stroke volume of an average sedentary adult is 70 to 80 milliliters per contraction, while in elite endurance athletes, it can be as high as 160 to 170 milliliters per contraction. This adaptation allows the heart to perform any given amount of work at a lower heart rate. Consequently, trained runners can achieve a faster running speed before reaching their maximum heart rate (which remains unchanged) and maximum rate of bloodflow (which is now greater). A larger heart can also contract with greater force than a smaller one, which further reduces the rate of contraction needed to sustain any given work rate.

Science Says Through training, runners can double the stroke volume (the volume of blood pumped per contraction) of their hearts.

Heart growth happens relatively slowly and is believed to continue for years in runners who train consistently. However, there is a related training adaptation that happens much more quickly. Within days of the onset of training, blood plasma volume begins to increase (plasma is the fluid component of the blood). This change allows for greater blood pressure in the pumping chamber (left ventricle) of the heart, resulting in greater stroke volume. Ultimately, training can increase blood plasma volume by nearly 10 percent. There is also evidence that the blood vessels of trained runners have a greater dilating capacity, which allows for higher rates of bloodflow as well.

All types of training provide circulatory benefits. However, research shows that high-intensity intervals performed at or near 100 percent VO₂max are the most effective way to increase cardiovascular adaptations, and to increase VO₂max itself. Runners can achieve substantial gains in the pumping capacity of their hearts with as little as 8 weeks of training, especially if it features vVO₂max intervals. But structural changes in the heart cannot happen fast enough to account for such rapid improvement. So what's behind these fitness gains? It appears that neurological factors account for much of this early improvement. The brain actively limits the work rate of the muscles in order to protect the heart from oxygen deprivation. When you make it through your first bouts of hard training unharmed, the brain learns to relax a bit and allows the heart to work harder, so that the skeletal muscles can work harder too.

That's the first half of the VO₂max equation. The other half is the capacity of the muscles to draw oxygen from the blood and use it to break down fuel molecules and release energy. The muscles of faster distance runners have a very large capacity to use the oxygen that is delivered to them, and training can greatly increase this capacity.

As mentioned above, oxygen is transported to the muscles by hemoglobin molecules in the blood and passes into individual muscle cells through tiny blood vessels called capillaries. Myoglobin proteins located inside the muscle cell bind to oxygen molecules and store them until they are needed. Mitochondria, also located within the muscle cell, serve as the site of aerobic metabolism. In the mitochondria, oxygen and special enzymes break down carbohydrates (individual glucose molecules and long chains of glucose molecules called glycogen), fats (triglycerides), and some amino acids to produce molecules of adenosine triphosphate (ATP), which is the fundamental energy currency of the muscles. It is the splitting of ATP that ultimately fuels every muscle fiber contraction. Fats and carbohydrates are broken down not to provide energy directly but to replenish ATP, which the muscle cell stores in very small amounts (enough to fuel a few seconds of high-intensity work). The breakdown of one glucose molecule, for example, which requires two long series of reactions, yields 38 ATP molecules. This process takes only a fraction of a second.

Training increases the density of capillaries in the muscles, their myoglobin concentration, the number of mitochondria within the muscle cells, and the concentration of mitochondrial enzymes. In addition, it increases the number of glucose and fatty acid transporters in the muscle cell membranes, which in turn increases the efficiency with which the muscle cells can draw carbohydrate and fat fuel from the blood. These adaptations, which happen to the greatest degree in slow-twitch muscle fibers (one of two general classes of muscle fibers, which I'll describe below), add up to significant increases in oxygen consumption capacity. This allows the muscles to produce work aerobically at high rates.

Muscle cells are also able to break down glucose outside the mitochondria and without the help of oxygen, through a process known as anaerobic glycolysis. This process produces ATP less efficiently–only two or three ATP molecules per glucose molecule–yet much faster than aerobic metabolism. Therefore, as the intensity of work increases, the muscle cells depend more and more on anaerobic metabolism. For example, at a comfortable jog, more than 99 percent of your muscle energy is produced aerobically. During a 90-second sprint, aerobic and anaerobic pathways contribute energy about equally. And during a 10-second sprint, about 95 percent of your muscle energy comes from anaerobic metabolism.

The larger your aerobic capacity is, the less you have to rely on anaerobic metabolism at higher running speeds. Or, put another way, the larger your aerobic capacity is, the faster you can run before you begin to rely heavily on anaerobically produced energy. This is beneficial because the fast-twitch muscle fibers that specialize in anaerobic energy production fatigue much faster than the slow-twitch fibers that specialize in aerobic energy production. While runners with a lot of fast-twitch muscle fibers can often produce more total energy for running, and therefore sprint faster, runners with a lot of well-developed slow-twitch muscle fibers can maintain a relatively high running speed for a much longer duration.

How should you train to maximize the aerobic energy capacity of the muscles? Research tells us that the overall volume of training has the greatest influence on these adaptations. Since moderate aerobic-intensity running is conducive to high training volume, this type of running is probably most beneficial as a foundation for aerobic development. However, highly trained runners need to mix in some high-intensity running in order to stimulate further adaptations. Workouts performed at or near anaerobic threshold pace (explained below) seem to offer the greatest "bang for the buck" in terms of stimulating adaptations that increase this threshold.

CHARACTERISTIC #3: MAGNETIC MUSCLES

Until recently, scientists believed that fatigue during high-intensity exercise was related to lactic acid buildup. The theory went like this: In anaerobic glycolysis, described in the previous section, one of the intermediates of glucose metabolism, pyruvate, is produced faster than it can be used by the mitochondria to make ATP. Unused pyruvate quickly breaks apart into lactic acid and hydrogen ions, which accumulate in the muscle cells and "leak" into the bloodstream. The buildup of lactic acid and hydrogen ions in the muscle cells causes them to become more acidic and interferes with further energy production. It also stimulates nerve endings, causing the "lactic acid burn" sensation familiar to every competitive runner. The end result (said the theory) is plummeting performance–it becomes harder and harder, and eventually impossible, to sustain the desired running pace.

The latest research suggests that lactic acid buildup (known as acidosis) is a relatively weak contributor to muscle fatigue at high intensities. It now seems that a much stronger cause is a type of neuromotor fatigue, specifically, depolarization of the muscle cells resulting from a shift in calcium-potassium balance.

Here's the new theory: Muscle contractions are stimulated by electrical currents that flow throughout the body via minerals including sodium and potassium. Each muscle cell contraction involves a lightning-fast exchange in which potassium molecules inside the muscle cell and sodium molecules outside the muscle cell switch places. These exchanges are most efficient when there is a high degree of polarization (a difference in the strength of the electrical charge) between the spaces inside and outside the cells. At the beginning of high-intensity exercise, the inside of the muscle cell has a much stronger positive charge than the area outside the muscle cell. This difference in charge strength makes it easy for sodium and potassium to cross the cell membrane. During sustained high-intensity activity, potassium is released from the muscle cells faster than it can be taken up outside the muscle cells. The resulting buildup of potassium outside the muscle cells causes a progressive lessening of the difference in charge strength between the intracellular and intercellular spaces, hence weaker and less efficient muscle contractions (i.e., fatigue).

Picture the nerve signals that cause muscle contractions as little marbles rolling down a sand hill. Each grain of sand is a potassium molecule. The top of the hill is the inside of the muscle cell, and the bottom of the hill is the outside of the muscle cell. Each time a marble (nerve signal) rolls down the hill, a small avalanche of sand (potassium molecules) follows it. Consequently, as marble after marble rolls down the hill, the hill becomes less and less steep as sand shifts from the top to the bottom. So the marbles roll down slower and slower until eventually they don't roll at all. That's neuromotor fatigue.

Training leads to several adaptations that enhance a runner's resistance to muscle cell depolarization. One of them is an increase in slow-twitch muscle fiber characteristics. Fast-twitch muscle fibers are more susceptible to depolarization. Training also increases potassium storage within muscle cells and the density and efficiency of the so-called calcium-potassium pumps that are responsible for those lightning-fast calcium-potassium exchanges.

An interesting wrinkle is that muscle cell depolarization almost always occurs at the same time as muscular acidosis (lactic acid buildup) even though the mechanisms are distinct. This is what led scientists to believe for so long that acidosis was a major cause of fatigue. One of the strongest predictors of distance running performance is the ability to keep blood lactate levels low at higher running speeds (a phenomenon referred to as a high lactate threshold, or a high anaerobic threshold). One study found that a high anaerobic threshold speed explained 87 percent of the variability in 3,000-meter running performance in a group of high-level runners. However, it is now understood that this is mostly a coincidence. It's not the low lactic acid levels themselves but the corresponding low levels of intercellular potassium buildup that matter. Nevertheless, since it's not possible to measure potassium buildup in humans during exercise, and since lactic acid buildup and potassium buildup correspond so closely, blood lactate measurements will probably continue to be used to assess aerobic strength and performance potential.

© 2005 by Matt Fitzgerald

About the Author

Matt Fitzgerald, runner, triathlete, and coach, is a former editor and current contributor for Triathlete magazine. He writes articles for such national publications as Men's Health, Men's Fitness, Outside, Fitness Runner, and the Runner's World Web site, and serves as managing editor of the sports nutrition Web site, Pioneering Muscles.