Basic Skeletal Muscle Physiology
This is intended to be a bare-bones review of physiology of muscle function. There are numerous sources on the internet for those who are interested in a more in-depth exploration of skeletal muscle physiology. The concepts here have direct application to understanding how specific training improves (or decreases) endurance performance capacity.
Interior ComponentsEvery muscle cell contains a series of common components that are directly associated with contraction in some way, and influenced by training. I will briefly describe these. For now we will not worry about the rest (like the nucleus, ribosomes etc.).
The Motor UnitA motor unit is the name given to a single alpha motor neuron and all the muscle fibers it activates (neurophysiologists use the term innervates). With 250 million skeletal muscle fibers in the body (give or take a few million), and about 420,000 motor neurons, the average motor neuron branches out to stimulate about 600 muscle fibers. Interestingly, large muscles may have as many as 2000 fibers per motor unit, while the tiny eye muscles may have only 10 or so fibers per motor unit. The size of a motor unit varies considerably according to the muscle’s function. Muscles with high force demands but low fine control demands (like a quadriceps muscle) are organized into larger motor units. Muscles controlling high precision movements like those required in the fingers or the eyes are organized into smaller motor units. The motor neuron branches into many terminals, and each terminal innervates a specific muscle fiber. The motor unit is the brain’s smallest functional unit of force development control; if a motor unit comprising 600 muscle fibers in the left biceps is stimulated, than all 600 of those fibers will contract simultaneously and contribute to the total force produced by the biceps. The brain cannot stimulate individual fibers one at a time. Even for our sophisticated nervous system, that would require far too much wiring.
Regulation of Muscular ForceThe brain combines two control mechanisms to regulate the force a single muscle produces. The first is RECRUITMENT. The motor units that make up a muscle are not recruited in a random fashion. Motor units are recruited according to the Size Principle. Smaller motor units (fewer muscle fibers) have a small motor neuron and a low threshold for activation. These units are recruited first. As more force is demanded by an activity, progressively larger motor units are recruited. This has great functional significance. When requirements for force are low, but control demands are high (writing, playing the piano) the ability to recruit only a few muscle fibers gives the possibility of fine control. As more force is needed the impact of each new motor unit on total force production becomes greater. It is also important to know that the smaller motor units are generally slow units, while the larger motor units are composed of fast twitch fibers.
The second method of force regulation is called RATE CODING. Within a
given motor unit there is a range of firing frequencies. Slow units operate at a
lower frequency range than faster units. Within that range, the force generated
by a motor unit increases with increasing firing frequency. If an action
potential reaches a muscle fiber before it has completely relaxed from a
previous impulse, then force summation will occur. By this method, firing
frequency affects muscular force generated by each motor unit.
Firing PatternIf we try and relate firing pattern to exercise intensity, we see this pattern. At low exercise intensities, like walking or slow running, slow twitch fibers are selectively utilized because they have the lowest threshold for recruitment. If we suddenly increase the pace to a sprint, the larger fast units will be recruited. In general, as the intensity of exercise increases in any muscle, the contribution of the fast fibers will increase.
For the muscle, intensity translates to force per contraction and contraction frequency/minute. Motor unit recruitment is regulated by required force. In the un-fatigued muscle, a sufficient number of motor units will be recruited to supply the desired force. Initially desired force may be accomplished with little or no involvement of fast motor units. However, as slow units become fatigued and fail to produce force, fast units will be recruited as the brain attempts to maintain desired force production by recruiting more motor units. Consequently, the same force production in fatigued muscle will require a greater number of motor units. This additional recruitment brings in fast, fatiguable motor units. Consequently, fatigue will be accelerated toward the end of long or severe bouts due to the increased lactate produced by the late recruitment of fast units.
Specific athletic groups may differ in the control of the motor units. Top athletes in the explosive sports like Olympic weightlifting or the high jump appear to have the ability to recruit nearly all of their motor units in a simultaneous or synchronous fashion. In contrast, the firing pattern of endurance athletes becomes more asynchronous. During continuous contractions, some units are firing while others recover, providing a built in recovery period. Initial gains in strength associated with a weight training program are due to improved recruitment, not muscle hypertrophy.
IntroductionAdaptability is a fundamental characteristic of skeletal muscle (and the body in general). The nature of this adaptation can be summarized using the following principle: cells will adapt in a manner that tends to minimize any movement away from homeostasis, or resting conditions. In exercise physiology we refer to the acute changes that occur in a system, organ, or cell during exercise as responses. An example is the increase in heart rate that occurs when we jump up from our chair and start jogging. The long-term changes that occur as a result of repeated bouts of exercise are called adaptations. Cellular adaptations generally involve an increase or decrease in the rate of synthesis of a specific cellular protein. All muscle cells are in a constant state of synthesis and degradation. If synthesis rate exceeds degradation rate, an increase in the cellular component occurs. A change in protein synthesis requires a cellular signal. Biologists and physiologists continue to explore the communication process by which different forms of muscular work induce cellular changes. At the cellular level, there are some theories, but no complete understanding. However, we do know quite a bit about what adaptations do occur, even if all the details regarding how remain unclear just yet.
Contrast Between Maximal Strength and Maximal EnduranceIf we could build a skeletal muscle for the purpose of endurance, what would the recipe be? Since the heart is the supreme endurance muscle, let's cheat by taking a look at it first.
Characteristics of Fatigue Resistant Muscle Cells
Olympic Champions are OddballsIf you want to win an Olympic medal in the 100 meter dash, you had better be born with about 80% fast twitch fibers! Want to win the Olympic marathon? Put in an order for 80% slow twitch fibers in your quads. The fast twitch fibers benefit the absolute sprinter because they reach peak tension much faster than their slow twitch counterparts. Gram for gram, the two types are not different in the amount of force they produce, only their rate of force production. So, having a lot of fast twitch fibers only makes a positive difference when the time available for force production is very limited (milliseconds), like the 100ms or so the foot is in contact with the ground during a sprint or long jump. It makes no difference to the power-lifter who may use 3-4 seconds to execute a slow, smooth lift.. In cycling, the only event that they are decidedly advantageous for is the match sprint, analogous to the track 100 meter dash, but with more anticipatory tactics and theatrics.
For the pure endurance athlete, more slow twitch fibers that are advantageous. These fibers give up lightning contraction and relaxation velocity for fatigue resistance. Lots of mitochondria and more capillaries surrounding each fiber make them more adept at using oxygen to generate ATP without lactate accumulation and fuel repeated contractions, like the 240 or so in a 2000 meter rowing race, or the 15,000 plus in a marathon.
Does Fiber Type Change with Training?This has been one of the 10,000 dollar questions in exercise physiology. It has been documented that elite endurance athletes possess a higher percentage of slow twitch fibers in the muscles they use in their sport, compared to untrained individuals. Is this due to genetic endowment or years of rigorous training? The answer is difficult to get at directly because we don't have comparative muscle biopsies of great athletes before and after they started training and excelling in their sport. However, good basic investigation using experimental models has helped generate some answers. The critical knowledge to remember is that fiber type is controlled by the motor nerve that innervates a fiber. Unless you change the nerve, you won't change fiber types from fast to slow or vice versa. Just this type of experiment has been performed in animals (generally rats). So, remember, there is no compelling evidence to show that human skeletal muscle switches fiber types from "fast" to "slow" due to training..
Then Why Am I Training So Hard?Two reasons; first, skeletal muscles respond to chronic overload (training), by trying to minimize the cellular disturbance caused by the training. With intense endurance training, fast fiber types can develop more mitochondria and surrounding capillaries. So can the slow fibers. So training improves your existing fiber distribution's ability to cope with the exercise stress you create for it.
Second, even among a group of elite endurance athletes, fiber type alone is a poor predictor of performance. This is especially true in the intermediate duration events. There are many other factors that go in to determining success! In fact, there is also evidence to suggest that a mixed fiber composition is ideal for success in an event like the mile run, or if good performances are to be possible in a range of events.
Changes in Muscular StrengthIt is well documented that a person's maximal strength decreases with increasing age. Is this due to an unavoidable effect of aging or the typical decrease in physical activity that often accompanies getting older? The answer appears to be BOTH.
Fiber Type and AgingThere have been conflicting reports and myths developed regarding fiber type changes with aging. Cross-sectional studies of post-mortem bodies between age 15 and 83 have suggested that fiber type composition is unchanged throughout life. This is also supported by comparing muscle biopsy results of younger and older endurance athletes. In contrast, one longitudinal study of a group of runners examined in 1974 and again 1992, suggested that training could play a role in fiber distribution. Those athletes who continued training showed unchanged fiber composition. Those who stopped training appeared to have greater slow-twitch fiber percentage. This was primarily due to selective atrophy of the fast fibers. This is not difficult to explain since they are seldom recruited. There is also some evidence that the actual number of fast motor units decreases slightly with aging after age 50, about 10% per decade. The reasons or mechanisms for such a change are unclear. So, the net effect of aging for the endurance athlete is unchanged fiber composition or a slight relative increase in Slow fiber type due to selective Fast fiber loss. The Fast motor units do not become Slow motor Units.
Muscle Endurance Capacity and AgingThe good news for the endurance athlete is that there appears to be little change in skeletal muscle oxidative capacity with age, as long as training is maintained. The number of capillaries per unit area of muscle is the same in young and old endurance athletes. Oxidative enzyme levels are similar or slightly lower in older athletes. This small decrease is probably attributable to decreased training volume in the older athletes. Furthermore, it appears that the older individual who starts endurance training retains the potential to improve muscle endurance capacity.
SummaryIt appears that the Masters athlete who continues endurance training at high intensities and maintains a maintenance strength training program experiences few changes in skeletal muscle through age 50. After age 50, declines in the quantity, but not the quality of muscle occur. These declines are also diminished by continued training. In general the changes that occur diminish maximal strength and power more than endurance capacity. This helps to explain the tendency for older athletes to more toward longer events within their sports discipline.
Aging and Cardiovascular Function
IntroductionWorld records in endurance sports are not accomplished at age 55. Why? Because one of the unavoidable consequences of aging is a decline in the maximal capacity of the cardiovascular system to pump blood and deliver oxygen while removing metabolic waste products. The components of cardiovascular pump performance are 1) the maximal heart rate that can be achieved. 2) The size and contractility of the heart muscle 3) The compliance (stiffness) of the arterial tree. We will look briefly at what is known about aging effects on each of these variables.
Maximal Heart RateYoung children generally have a maximal heart rate approaching 220 beats per minute. This maximal rate falls throughout life. By age 60 maximal heart rate in a group of 100 men will average about 160 beats per minute. This fall in heart rate seems to be a linear process so that maximal heart rate can be estimated by the formula 220- AGE. This is an ESTIMATE, however. If we actually measure the maximal heart rates of those same 100 men during a maximal exercise test we would probably see a range of heart rates between 140 and 180. There is no strong evidence to suggest that training influences the decline in maximal heart rate. This reduction appears to be due to alterations in the cardiac electrical conduction system (SA node and Bundle of His), as well as down regulation of beta-1 receptors, which decreases the heart's sensitivity to catecholamine stimulation.
Maximal Stroke VolumeThe research picture regarding age effects om maximal stroke volume is far less clear. This is in part due to the technical challenges involved in making these measurements. Studies showing a decline, an increase, and no change can be found in the literature. It appears that if middle-aged and older adults continue to train intensely, stroke volume is well maintained. Heart size in older athletes has been shown to be similar to that of young athletes, and bigger than their sedentary, same-aged peers. Ultimately, maximal stroke volume appears to decrease due to a 1) decrease in training volume and 2) an increase in peripheral resistance.
The Peripheral ResistanceThe blood pumped out of the heart enters the systemic arterial system. In our youth, this system of arteries is quite flexible or compliant. This is important for the performance of the heart. Compliant vessel walls stretch when blood is pumped through them, lowering the resistance that the heart must overcome to eject it volume of blood each beat. As we age, these vessels lose their elasticity. Consequently, resting blood pressure and blood pressure during exercise slowly increase as we age. Continued training appears to reduce this aging effect, but does not eliminate it. Increased peripheral resistance results in a decrease in maximal blood flow to working muscles. However, at submaximal exercise intensities, the 10-15% decrease in blood flow is compensated for by increased oxygen extraction (a-v O2 difference). This compensation is probably possible due to the increased transit time of the blood through the capillary tree.
The Big PictureIn the sedentary population, cardiovascular performance declines progressively with age. However, much of this decline is due to 1)physical inactivity and 2) increased body weight (fat). Maximal oxygen consumption declines about 10% per decade after age 25. However, if body composition is maintained and physical activity levels are kept constant, the decline in VO2max due to aging is only about 5% per decade. Prior to age 50, this decline may even be less, perhaps 1-2% per decade in hard training masters athletes. Ultimately, cardiovascular capacity is reduced however, due to the unavoidable decline in maximal heart rate.