Length force relationship muscle contraction headache

Length tension relationship – Strength & Conditioning Research

It turns out that this banding pattern and the relationship between muscle length & active tension in skeletal muscle were the principal features. Clearly, such extreme elongation would take the muscle beyond the plateau in its length/tension relationship and, thus, preclude it from producing any more. Looking for online definition of muscle contraction in the Medical Dictionary? muscle Concentric—The muscle shortens in length as it overcomes resistance. See also excitation-contraction coupling, force-velocity relationship, myofibrils. . muscle conditioning; muscle contraction; muscle contraction headache · muscle.

The sequence of events that results in the depolarization of the muscle fiber at the neuromuscular junction begins when an action potential is initiated in the cell body of a motor neuron, which is then propagated by saltatory conduction along its axon toward the neuromuscular junction. Acetylcholine diffuses across the synapse and binds to and activates nicotinic acetylcholine receptors on the neuromuscular junction.

The membrane potential then becomes hyperpolarized when potassium exits and is then adjusted back to the resting membrane potential. This rapid fluctuation is called the end-plate potential[18] The voltage-gated ion channels of the sarcolemma next to the end plate open in response to the end plate potential.

Length-tension relationship

These voltage-gated channels are sodium and potassium specific and only allow one through. This wave of ion movements creates the action potential that spreads from the motor end plate in all directions.

The remaining acetylcholine in the synaptic cleft is either degraded by active acetylcholine esterase or reabsorbed by the synaptic knob and none is left to replace the degraded acetylcholine.

Excitation-contraction coupling Excitation—contraction coupling is the process by which a muscular action potential in the muscle fiber causes the myofibrils to contract. DHPRs are located on the sarcolemma which includes the surface sarcolemma and the transverse tubuleswhile the RyRs reside across the SR membrane.

The close apposition of a transverse tubule and two SR regions containing RyRs is described as a triad and is predominantly where excitation—contraction coupling takes place. Excitation—contraction coupling occurs when depolarization of skeletal muscle cell results in a muscle action potential, which spreads across the cell surface and into the muscle fiber's network of T-tubulesthereby depolarizing the inner portion of the muscle fiber.

Depolarization of the inner portions activates dihydropyridine receptors in the terminal cisternae, which are in close proximity to ryanodine receptors in the adjacent sarcoplasmic reticulum.

The activated dihydropyridine receptors physically interact with ryanodine receptors to activate them via foot processes involving conformational changes that allosterically activates the ryanodine receptors. Note that the sarcoplasmic reticulum has a large calcium buffering capacity partially due to a calcium-binding protein called calsequestrin. The near synchronous activation of thousands of calcium sparks by the action potential causes a cell-wide increase in calcium giving rise to the upstroke of the calcium transient.

Sliding filament theory Sliding filament theory: A sarcomere in relaxed above and contracted below positions The sliding filament theory describes a process used by muscles to contract. It is a cycle of repetitive events that cause a thin filament to slide over a thick filament and generate tension in the muscle.

However the actions of elastic proteins such as titin are hypothesised to maintain uniform tension across the sarcomere and pull the thick filament into a central position.

Length-tension relationship :: Sliding filament theory

A crossbridge is a myosin projection, consisting of two myosin heads, that extends from the thick filaments. The binding of ATP to a myosin head detaches myosin from actinthereby allowing myosin to bind to another actin molecule.

Once attached, the ATP is hydrolyzed by myosin, which uses the released energy to move into the "cocked position" whereby it binds weakly to a part of the actin binding site. The remainder of the actin binding site is blocked by tropomyosin. Unblocking the rest of the actin binding sites allows the two myosin heads to close and myosin to bind strongly to actin. The power stroke moves the actin filament inwards, thereby shortening the sarcomere.

Myosin then releases ADP but still remains tightly bound to actin. At the end of the power stroke, ADP is released from the myosin head, leaving myosin attached to actin in a rigor state until another ATP binds to myosin. A lack of ATP would result in the rigor state characteristic of rigor mortis. Once another ATP binds to myosin, the myosin head will again detach from actin and another crossbridges cycle occurs. The myosin ceases binding to the thin filament, and the muscle relaxes.

Thus, the tropomyosin-troponin complex again covers the binding sites on the actin filaments and contraction ceases. Gradation of skeletal muscle contractions Twitch Summation and tetanus Three types of skeletal muscle contractions The strength of skeletal muscle contractions can be broadly separated into twitch, summation, and tetanus.

A twitch is a single contraction and relaxation cycle produced by an action potential within the muscle fiber itself. Summation can be achieved in two ways: In frequency summation, the force exerted by the skeletal muscle is controlled by varying the frequency at which action potentials are sent to muscle fibers. Action potentials do not arrive at muscles synchronously, and, during a contraction, some fraction of the fibers in the muscle will be firing at any given time.

In multiple fiber summation, if the central nervous system sends a weak signal to contract a muscle, the smaller motor units, being more excitable than the larger ones, are stimulated first. As the strength of the signal increases, more motor units are excited in addition to larger ones, with the largest motor units having as much as 50 times the contractile strength as the smaller ones. As more and larger motor units are activated, the force of muscle contraction becomes progressively stronger.

A concept known as the size principle, allows for a gradation of muscle force during weak contraction to occur in small steps, which then become progressively larger when greater amounts of force are required.

Finally, if the frequency of muscle action potentials increases such that the muscle contraction reaches its peak force and plateaus at this level, then the contraction is a tetanus. Length-tension relationship Muscle length versus isometric force Length-tension relationship relates the strength of an isometric contraction to the length of the muscle at which the contraction occurs.

Muscles operate with greatest active tension when close to an ideal length often their resting length. When stretched or shortened beyond this whether due to the action of the muscle itself or by an outside forcethe maximum active tension generated decreases.

Due to the presence of elastic proteins within a muscle cell such as titin and extracellular matrix, as the muscle is stretched beyond a given length, there is an entirely passive tension, which opposes lengthening. Combined together, there is a strong resistance to lengthening an active muscle far beyond the peak of active tension. Force-velocity relationships Force—velocity relationship: Since power is equal to force times velocity, the muscle generates no power at either isometric force due to zero velocity or maximal velocity due to zero force.

The optimal shortening velocity for power generation is approximately one-third of maximum shortening velocity. Force—velocity relationship relates the speed at which a muscle changes its length usually regulated by external forces, such as load or other muscles to the amount of force that it generates.

Force declines in a hyperbolic fashion relative to the isometric force as the shortening velocity increases, eventually reaching zero at some maximum velocity. The reverse holds true for when the muscle is stretched — force increases above isometric maximum, until finally reaching an absolute maximum.

This intrinsic property of active muscle tissue plays a role in the active damping of joints which are actuated by simultaneously-active opposing muscles.

ForceVelocity

In such cases, the force-velocity profile enhances the force produced by the lengthening muscle at the expense of the shortening muscle. This favoring of whichever muscle returns the joint to equilibrium effectively increases the damping of the joint. Moreover, the strength of the damping increases with muscle force. The motor system can thus actively control joint damping via the simultaneous contraction co-contraction of opposing muscle groups.

Smooth muscles can be divided into two subgroups: Single-unit smooth muscle cells can be found in the gut and blood vessels. Because these cells are linked together by gap junctions, they are able to contract as a syncytium. Single-unit smooth muscle cells contract myogenically, which can be modulated by the autonomic nervous system. Unlike single-unit smooth muscle cells, multi-unit smooth muscle cells are found in the muscle of the eye and in the base of hair follicles.

Multi-unit smooth muscle cells contract by being separately stimulated by nerves of the autonomic nervous system. As such, they allow for fine control and gradual responses, much like motor unit recruitment in skeletal muscle. Mechanisms of smooth muscle contraction Smooth muscle contractions Sliding filaments in contracted and uncontracted states The contractile activity of smooth muscle cells is influenced by multiple inputs such as spontaneous electrical activity, neural and hormonal inputs, local changes in chemical composition, and stretch.

Some types of smooth muscle cells are able to generate their own action potentials spontaneously, which usually occur following a pacemaker potential or a slow wave potential.

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The calcium-calmodulin-myosin light-chain kinase complex phosphorylates myosin on the 20 kilodalton kDa myosin light chains on amino acid residue-serine 19, initiating contraction and activating the myosin ATPase. Unlike skeletal muscle cells, smooth muscle cells lack troponin, even though they contain the thin filament protein tropomyosin and other notable proteins — caldesmon and calponin.

Termination of crossbridge cycling and leaving the muscle in latch-state occurs when myosin light chain phosphatase removes the phosphate groups from the myosin heads. Phosphorylation of the 20 kDa myosin light chains correlates well with the shortening velocity of smooth muscle. During this period, there is a rapid burst of energy utilization as measured by oxygen consumption.

Within a few minutes of initiation, the calcium level markedly decreases, the 20 kDa myosin light chains' phosphorylation decreases, and energy utilization decreases; however, force in tonic smooth muscle is maintained. During contraction of muscle, rapidly cycling crossbridges form between activated actin and phosphorylated myosin, generating force.

It is hypothesized that the maintenance of force results from dephosphorylated "latch-bridges" that slowly cycle and maintain force.

Neuromodulation Although smooth muscle contractions are myogenic, the rate and strength of their contractions can be modulated by the autonomic nervous system. Postganglionic nerve fibers of parasympathetic nervous system release the neurotransmitter acetylcholine, which binds to muscarinic acetylcholine receptors mAChRs on smooth muscle cells.

These receptors are metabotropicor G-protein coupled receptors that initiate a second messenger cascade. It does so by maintaining a muscle tone, i. The myofilaments are also elastic.

They maintain enough overlap for muscular contraction. In cardiac muscles The length-tension relationship is also observed in cardiac muscles. However, what differs in cardiac muscles compared to skeletal muscles is that tension increases sharply with stretching the muscle at rest slightly. This contrasts with the gradual build up of tension by stretching the resting skeletal muscle see Graph 4.

Length-tension relationship observed in cardiac muscles. The optimum length is denoted as Lmax which is about 2. Like skeletal muscles, the maximum number of cross-bridges form and tension is at its maximum here. Beyond this, tension decreases sharply.

In normal physiology, Lmax is obtained as heart ventricles become filled up by blood, stretching the myocytes. The muscles then converts the isometric tension to isotonic contraction which enables the blood to be pumped out when they finally contract. The heart has an intrinsic control over the stroke volume of the heart and can alter the force of blood ejection. Force-velocity relationship Cardiac muscle has to pump blood out from the heart to be distributed to the rest of the body.

It has 2 important properties that enable it to function as such: It carries a preload, composed of its initial sarcomere length and end-diastolic volume.

This occurs before ejecting blood during systole. This is consistent with Starling's law which states that: Force-velocity relationship in cardiac muscles.

At rest, the greater the degree of initial muscle stretch, the greater the preload. This increases the tension that will be developed by the cardiac muscle and the velocity of muscular contraction at a given afterload will increase. Upon stimulation of cardiac muscle, it develops isometric tension without shortening.

Once enough tension has accumulated, the muscle can now overcome the afterload and eject the blood it was carrying. Tension however is maintained at this stage. Tension is greater in muscle stretched more initially as the preload at a given velocity for muscular shortening.