Wave summation: Recall that a muscle twitch can last up to ms and that an action potential lasts only ms. Also, with the muscle twitch, there is not refractory period so it can be re-stimulated at any time. If you were to stimulate a single motor unit with progressively higher frequencies of action potentials you would observe a gradual increase in the force generated by that muscle.
This phenomenon is called wave summation. Eventually the frequency of action potentials would be so high that there would be no time for the muscle to relax between the successive stimuli and it would remain totally contracted, a condition called tetanus. Essentially, with the high frequency of action potentials there isn't time to remove calcium from the cytosol. Maximal force, then, is generated with maximum recruitment and an action potential frequency sufficient to result in tetanus.
Initial Sarcomere Length: It has been demonstrated experimentally that the starting length of the sarcomere influences the amount of force the muscle can generate. This observation has to do with the overlap of the thick and thin filaments. If the starting sarcomere length is very short, the thick filaments will already be pushing up against the Z-disc and there is no possibility for further sarcomere shortening, and the muscle will be unable to generate as much force.
On the other hand, if the muscle is stretched to the point where myosin heads can no longer contact the actin, then again, less force will be generated. Maximum force is generated when the muscle is stretched to the point that allows every myosin head to contact the actin and the sarcomere has the maximum distance to shorten.
In other words, the thick filaments are at the very ends of the thin filaments. These data were generated experimentally using frog muscles that were dissected out and stretched between two rods. Intact muscles in our bodies are not normally stretched very far beyond their optimal length due to the arrangement of muscle attachments and joints. However, you can do a little experiment that will help you see how force is lost when a muscle is in a very short or a very stretched position. This experiment will use the muscles that help you pinch the pad of your thumb to the pads of your fingers.
These muscles are near maximal stretch when you extend your arm and also extend your wrist. As your wrist is cocked back into maximal extension, try to pinch your thumb to your fingers.
See how weak it feels? Now, gradually flex your wrist back to a straight or neutral position. You should feel your pinch get stronger. Now, flex your elbow and your wrist. With your wrist in maximal flexion, the muscles you use to pinch with are near their most shortened position. Try pinching again. It should feel weak. But, again, as you extend your wrist back to neutral you should feel your pinch get stronger.
The ultimate source of energy for muscle contraction is ATP. Recall that each cycle of a myosin head requires an ATP molecule. Multiply that by all of the myosin heads in a muscle and the number of cycles each head completes each twitch and you can start to see how much ATP is needed for muscle function.
It is estimated that we burn approximately our entire body weight in ATP each day so it becomes apparent that we need to constantly replenish this important energy source. For muscle contraction, there are four ways that our muscles get the ATP required for contraction.
When we think of skeletal muscles getting tired, we often use the word fatigue, however, the physiological causes of fatigue vary considerably.
At the simplest level, fatigue is used to describe a condition in which the muscle is no longer able to contract optimally. To make discussion easier, we will divide fatigue into two broad categories: Central fatigue and peripheral fatigue.
Central fatigue describes the uncomfortable feelings that come from being tired, it is often called "psychological fatigue. Psychological fatigue precedes peripheral fatigue and occurs well before the muscle fiber can no longer contract. One of the outcomes of training is to learn how to overcome psychological fatigue.
As we train we learn that those feelings are not so bad and that we can continue to perform even when it feels uncomfortable. For this reason, elite athletes hire trainers that push them and force them to move past the psychological fatigue. Peripheral fatigue can occur anywhere between the neuromuscular junction and the contractile elements of the muscle.
It can be divided into two subcategories, low frequency marathon running and high frequency circuit training fatigue. High frequency fatigue results from impaired membrane excitability as a result of imbalances of ions. Muscles can recover quickly, usually within 30 minutes or less, following high frequency fatigue. It is much more difficult to recover from low frequency fatigue, taking from 24 hours to 72 hours. Please note that factors that are not on the list are ATP and lactic acid, both of which do not contribute to fatigue.
The reality is we still don't know exactly what causes fatigue and much research is currently devoted to this topic. Classically, skeletal muscle fibers can be categorized according to their speed of contraction and their resistance to fatigue. These classifications are in the process of being revised, but the basic types include:. Fast-twitch type II fibers develop tension two to three times faster than slow-twitch type I fibers.
How fast a fiber can contract is related to how long it takes for completion of the cross-bridge cycle. An example of this is the biceps brachii muscle contracting when a hand weight is brought upward with increasing muscle tension.
As the biceps brachii contract, the angle of the elbow joint decreases as the forearm is brought toward the body. Here, the biceps brachii contracts as sarcomeres in its muscle fibers are shortening and cross-bridges form; the myosin heads pull the actin. An eccentric contraction occurs as the muscle tension diminishes and the muscle lengthens. In this case, the hand weight is lowered in a slow and controlled manner as the amount of cross-bridges being activated by nervous system stimulation decreases.
In this case, as tension is released from the biceps brachii, the angle of the elbow joint increases. Eccentric contractions are also used for movement and balance of the body.
An isometric contraction occurs as the muscle produces tension without changing the angle of a skeletal joint. Isometric contractions involve sarcomere shortening and increasing muscle tension, but do not move a load, as the force produced cannot overcome the resistance provided by the load.
For example, if one attempts to lift a hand weight that is too heavy, there will be sarcomere activation and shortening to a point, and ever-increasing muscle tension, but no change in the angle of the elbow joint.
In everyday living, isometric contractions are active in maintaining posture and maintaining bone and joint stability. However, holding your head in an upright position occurs not because the muscles cannot move the head, but because the goal is to remain stationary and not produce movement. Most actions of the body are the result of a combination of isotonic and isometric contractions working together to produce a wide range of outcomes Figure All of these muscle activities are under the exquisite control of the nervous system.
Neural control regulates concentric, eccentric and isometric contractions, muscle fiber recruitment, and muscle tone. A crucial aspect of nervous system control of skeletal muscles is the role of motor units. As you have learned, every skeletal muscle fiber must be innervated by the axon terminal of a motor neuron in order to contract.
Each muscle fiber is innervated by only one motor neuron. The actual group of muscle fibers in a muscle innervated by a single motor neuron is called a motor unit.
The size of a motor unit is variable depending on the nature of the muscle. A small motor unit is an arrangement where a single motor neuron supplies a small number of muscle fibers in a muscle. Small motor units permit very fine motor control of the muscle. The best example in humans is the small motor units of the extraocular eye muscles that move the eyeballs.
There are thousands of muscle fibers in each muscle, but every six or so fibers are supplied by a single motor neuron, as the axons branch to form synaptic connections at their individual NMJs. This allows for exquisite control of eye movements so that both eyes can quickly focus on the same object.
Small motor units are also involved in the many fine movements of the fingers and thumb of the hand for grasping, texting, etc. A large motor unit is an arrangement where a single motor neuron supplies a large number of muscle fibers in a muscle. The best example is the large motor units of the thigh muscles or back muscles, where a single motor neuron will supply thousands of muscle fibers in a muscle, as its axon splits into thousands of branches. There is a wide range of motor units within many skeletal muscles, which gives the nervous system a wide range of control over the muscle.
The small motor units in the muscle will have smaller, lower-threshold motor neurons that are more excitable, firing first to their skeletal muscle fibers, which also tend to be the smallest. Activation of these smaller motor units, results in a relatively small degree of contractile strength tension generated in the muscle. However, thick and thin filaments—the components of sarcomeres—do not shorten. Instead, they slide by one another, causing the sarcomere to shorten while the filaments remain the same length.
The sliding filament theory of muscle contraction was developed to fit the differences observed in the named bands on the sarcomere at different degrees of muscle contraction and relaxation. The mechanism of contraction is the binding of myosin to actin, forming cross-bridges that generate filament movement Figure 6. Figure 6. When a a sarcomere b contracts, the Z lines move closer together and the I band gets smaller. The A band stays the same width and, at full contraction, the thin filaments overlap.
When a sarcomere shortens, some regions shorten whereas others stay the same length. A sarcomere is defined as the distance between two consecutive Z discs or Z lines; when a muscle contracts, the distance between the Z discs is reduced. The H zone—the central region of the A zone—contains only thick filaments and is shortened during contraction.
The I band contains only thin filaments and also shortens. The A band does not shorten—it remains the same length—but A bands of different sarcomeres move closer together during contraction, eventually disappearing. Thin filaments are pulled by the thick filaments toward the center of the sarcomere until the Z discs approach the thick filaments. The zone of overlap, in which thin filaments and thick filaments occupy the same area, increases as the thin filaments move inward.
The motion of muscle shortening occurs as myosin heads bind to actin and pull the actin inwards. This action requires energy, which is provided by ATP.
Myosin binds to actin at a binding site on the globular actin protein. ATP binding causes myosin to release actin, allowing actin and myosin to detach from each other. The enzyme at the binding site on myosin is called ATPase.
The myosin head is then in a position for further movement, possessing potential energy, but ADP and Pi are still attached. If actin binding sites are covered and unavailable, the myosin will remain in the high energy configuration with ATP hydrolyzed but still attached. If the actin binding sites are uncovered, a cross-bridge will form; that is, the myosin head spans the distance between the actin and myosin molecules.
Pi is then released, allowing myosin to expend the stored energy as a conformational change. The myosin head moves toward the M line, pulling the actin along with it. As the actin is pulled, the filaments move approximately 10 nm toward the M line. This movement is called the power stroke, as it is the step at which force is produced.
As the actin is pulled toward the M line, the sarcomere shortens and the muscle contracts. This energy is expended as the myosin head moves through the power stroke; at the end of the power stroke, the myosin head is in a low-energy position.
After the power stroke, ADP is released; however, the cross-bridge formed is still in place, and actin and myosin are bound together. ATP can then attach to myosin, which allows the cross-bridge cycle to start again and further muscle contraction can occur Figure 6.
With each contraction cycle, actin moves relative to myosin. Which of the following statements about muscle contraction is true? The power stroke occurs when ADP and phosphate dissociate from the myosin head. The power stroke occurs when ADP and phosphate dissociate from the actin active site.
View this video animation of the cross-bridge muscle contraction. When a muscle is in a resting state, actin and myosin are separated. To keep actin from binding to the active site on myosin, regulatory proteins block the molecular binding sites. Tropomyosin blocks myosin binding sites on actin molecules, preventing cross-bridge formation and preventing contraction in a muscle without nervous input. Troponin binds to tropomyosin and helps to position it on the actin molecule; it also binds calcium ions.
To enable a muscle contraction, tropomyosin must change conformation, uncovering the myosin-binding site on an actin molecule and allowing cross-bridge formation.
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