Muscle Physiology - Introduction to Muscle
Muscle contraction is the activation of tension-generating sites within muscle fibers. If the muscle length changes while muscle tension remains the same, then the In relation to the elbow, a concentric contraction of the biceps would cause .. "Redox biology of exercise: an integrative and comparative consideration of. The force -length relationship indicates that muscles generate the greatest force when at their resting (ideal) length, and the least amount of force when. All skeletal muscles have a resting length. When our muscles are stretched to the ideal length, it can maximize muscular contraction.
A neuromuscular junction is a chemical synapse formed by the contact between a motor neuron and a muscle fiber. 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  The voltage-gated ion channels of the sarcolemma next to the end plate open in response to the end plate potential.
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[ edit ] 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[ edit ] Main article: 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. 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[ edit ] 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.Whole muscle 3- Length/tension relationship
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.
Muscle contraction - Wikipedia
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. Hill's muscle model 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[ edit ] 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. 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 muscle Swellings called varicosities belonging to an autonomic neuron innervate the smooth muscle cells. 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[ edit ] 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. 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.
Introduction For more than three centuries, physiologists have known that a contracting muscle maintains a constant volume [ 1 ]. Contraction under constant volume dictates that muscle must grow wider as it shortens, thus expanding radially.
This, in turn, dictates that the distance lattice spacing between adjacent thick myosin and thin actin filaments must increase [ 23 ]. Historically, most attention paid to how the force of contraction changes with muscle length has ignored changes in lattice spacing, focusing instead on changes in filament overlap. Here, we demonstrate that changes in lattice spacing can play a little-recognized and critical role in determining the length—tension LT curve, a basic property of contracting muscle.
The LT curve of isometric muscle contraction provides key experimental support for the sliding-filament hypothesis [ 4 ]. The LT curve describes the maximum isometric force a muscle generates as sarcomere lengths vary.
The length–tension curve in muscle depends on lattice spacing
As muscle is stretched from extremely short to extremely long lengths, the force it generates increases over the ascending limb, peaks in the plateau region and decreases over the descending limb [ 5 ]. The rise and fall of force with sarcomere length is an indicator that the basic mechanism of force generation is myosin cross-bridge interaction with actin binding sites along the thin filament. Because the LT curve describes the behaviour of muscle across a wide range of lengths, the maintenance of a constant cell volume dictates that lattice spacing must change dramatically.
This makes the LT curve an ideal mechanism to demonstrate whether and how changes in lattice spacing alter the force muscle generates. Evidence that lattice spacing changes as sarcomere length changes comes from X-ray diffraction measurements and from the requirement that muscle remain at a constant volume if only approximately [ 23 ]. This isovolumetric assumption posits that the lattice volume of muscle is constant over the time scale of contractions, implying there is no bulk flow of fluids into or out of the myofibrils.
Aside from the difficulty in removing fluid from a tightly packed lattice, the sarcolemma surrounding each fibre enforces a constant cell volume at the subsecond time scale. Although the fibre maintains a constant volume over a contraction, this constraint is slightly relaxed over longer durations [ 6 ].
- Sarcomere length-tension relationship
- Muscle contraction
- Length tension relationship