2009. augusztus 26., szerda

Napi olvasmány: a szívizom adaptációja az edzéshez

Az alábbi olvasmányból megtudhatjuk, hogy a sportoló és az átlagember szive között a legnagyobb különbség a stroke volumen. A nagyobb stroke-volumen (vér kipumpálása a balkamrából szivverésenként) eredményezi az alacsony nyugalmi pulzust. A nagyobb stroke-volumen szorozva sok összehúzódással pedig nagyobb szívteljesítményhez vezet, ezáltal növekszik a vo2max.

Myocardial Adaptations to Training

© 1996 Stephen Seiler

The heart, in cellular composition, structure, and mechanics, is an absolute marvel of "biological engineering". Even among human couch potatoes, it is an astoundingly well-equipped endurance muscle. It has an incredibly dense network of capillaries (over 2000 capillaries per cubic millimeter!) designed to provide reliable delivery of oxygen to the working muscle with a minimum diffusion distance to intracellular mitochondria. The individual heart cells (called myocytes) are densely packed with mitochondria; they take up about 20-25% of the human heart cell volume. In contrast, mitochondria make up less than 5% of the untrained skeletal muscle cell volume. The specific biochemistry of the muscle cells is designed to minimize lactate production even at very high workloads (H isoform of lactate dehydrogenase for you scientists). The heart can metabolise fat, lactate, and blood glucose with equal effectiveness.

So, how can endurance training improve a muscle that is already superbly designed and equipped to perform constant work? The answer is fairly simple. IT GETS BIGGER! (OK, it's slightly more complicated than that). Endurance trained hearts do not beat faster at maximum. They do not beat more powerfully, gram for gram. They also do not change significantly in terms of mitochondrial or capillary density. The distinction between the athlete's heart and the sendentary heart is the larger stroke volume of the trained heart. This improvement is critical to improved endurance performance. Why? The heart is first and foremost a pump. It pumps oxygenated blood to the body to support the production of cellular energy. During exercise, working muscles increase their cellular energy requirements up to 100X. Generating more energy (ATP) requires more oxygen delivery to the mitochondria.

The quantity of work that can be performed by the muscles over an extended period of time is critically dependent on the volume of blood that can be delivered by the heart. A body supplied more oxygen by a bigger pump has the potential to sustain work at a greater maximal intensity. Maximal Cardiac Output = Maximal Heart Rate X Stroke Volume. Stroke volume is the volume of blood ejected from the left ventricle each beat. Endurance training impacts myocardial function 1) at rest, 2) during sub-maximal exercise, and 3) during maximal exercise.

Resting Hemodynamics and Exercise

At rest the stroke volume and resting heart rate of the average person can be remembered easily as approximately 70 ml/beat and 70 beats/minute. This gives us 70X70 or roughly 5 liters/minute resting cardiac output (5,000ml/min). The resting cardiac output is determined by the oxygen demand at rest, and also by the need for high blood flow to the kidneys for filtration purposes. It doesn't change appreciably with endurance training. However, the manner in which the heart delivers this resting demand does change. After 6 months of endurance training, the resting heart rate may decrease to 55 bpm. At the same time, resting stroke volume increases to about 90 ml (HR x SV stays the ~same before and after training). So a reduced resting heart rate is a hallmark of endurance training. Resting heart rate (RHR) can be much lower. In champion endurance athletes, RHR is often in the 30s and low 40s. Since resting oxygen demand still hasn't changed, this should tip you off that these athletes have extremely high resting stroke volumes! Thus, the resting heart of the athlete is more efficient. It performs the same work with fewer beats and less myocardial energy demand. However, since some medical symptoms are also marked by a reduced resting heart rate, your physician may initially raise his/her eyebrow to your low frequency lub-dub during checkups.

Having said all that, I feel I need to muddy the water a bit. First, while a lower resting heart rate is a typical feature of the endurance-trained heart; there is substantial variability in the resting heart rate and its response to training. Recent studies (i.e. the Heritage Study for those interested) have demonstrated a substantial genetic variability in the responsiveness to training. So, some people will respond more dramatically to the same training stimulus than others. Second, another typical feature of the highly endurance trained heart is arrhythmias. It is not unusual for well-rained athletes to show some conduction abnormalities. Often, these are present at rest, but disappear as soon as exercise starts. So, while a low heart rate in and of itself is no reason to worry, doctors do understandably take notice if that steady lub-dub sound shows repeated hiccups. Some heart hiccups are more serious than others, so humor them.

Myocardial Responses to Sub-maximal Exercise Before and After Training

When we begin to exercise at any given intensity, more oxygen must be delivered to the working muscle. Cardiac output increases in proportion to the increased energy demand. If we measure the responses of an individual to running at 8 min mile pace before and after 3 months of regular exercise, here is what we will see. First, the metabolic cost of working at this intensity will be unchanged (assuming no major improvement in running efficiency). Therefore cardiac output will be the same. However, just as during rest, the heart will deliver more blood each beat. Therefore heart rate at this and any sub-maximal exercise intensity will be reduced. Using the analogy of a car engine, we have replaced a small motor with a larger one that achieves the same horsepower at lower rpms. Of course, this change is a major reason why Polar Electro in Finland sells so many fancy “computer downloadable” heart watches around the world. The reduction in heart rate at sub-maximal workloads is a quantifiable, easy to measure indicator that we are adapting to training, and they have convinced us that we need to keep track of that!

Hemodynamic Response to Maximal Exercise

There is for all of us an exercise intensity that will elicit our maximum cardiac output. Once this limit is achieved, further increases in work intensity will result in no further increase in heart rate. By definition, this is then the maximum heart rate. The maximum heart rate in humans varies from individual to individual and decreases with age. Therefore the only way to know precisely what a specific person's maximal heart rate is would be to do a maximal exercise test. Without such precise knowledge, we often use the formula "220 minus age" to approximate maximal heart rate. This formula will generally give results within plus or minus 10 bpm of reality. True maximal heart rate may not be achieved in some forms of exercise that do not employ a large enough muscle mass, or if the person is unfamiliar with the mode of exercise employed. For example, one person may have a true maximum heart rate of 195 achieved during uphill running, but only 191 during a cycling test, and 187 during swimming. These latter heart rates are termed peak heart rates and should be used as a basis for determining training intensity for a specific exercise mode.

The important thing to remember is: Maximal heart rate does not increase after training. It stays the same (or might even decrease just slightly). However, maximal stroke volume increases. Therefore maximal cardiac output increases in response to exercise. This is the primary reason for the increase in VO2 max!

So, in response to endurance exercise the heart adapts by increasing stroke volume at rest, during sub-maximal exercise, and during maximal exercise. There is some debate regarding whether stroke volume increases BECAUSE heart rate is decreased (increasing diastolic filling time), or because of an increase in ventricular volume due to eccentric hypertrophy of the heart muscle. Both factors probably contribute based on the available data. Both changes also rapidly revert towards normal with the cessation of training. One other important change that takes place is an increased blood volume. Increased blood volume helps to take advantage of the increased filling capacity of the heart and facilitates increased stroke volume. This adaptation occurs fairly rapidly with training, but is also the first adaption lost if we stop training for several days!

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