Muscle Physiology

Chapter 8

There are three kinds of muscle tissue: skeletal, cardiac, and smooth.

• These three kinds of muscle tissue compose about 50 percent of a human’s body weight.

• Skeletal muscle tissue is striated and subject to voluntary control.

• The skeletal muscles make up the muscular system.

• The skeletal muscles are innervated by the somatic nervous system.

A muscle fiber is a skeletal muscle cell. It is large, elongated, and cylinder-shaped. The fibers extend the entire length of a skeletal muscle.

• A muscle fiber contains contractile elements called myofibrils. A myofibril contains thick filaments called myosin and thin filaments (e.g., actin).

• Actin and myosin are arranged in units called sarcomeres. A sarcomere is found between two Z lines. The sarcomere is the functional unit of the muscle. Its regions are:

– A band - myosin (thick) filaments stacked along with parts of the actin (thin) filaments

– H zone - middle of the A band where actin does not reach

– M line - extends vertically down the center of the A band

– I band - has part of actin that do not project into A band

The thick filaments of myosin have cross bridges. The cross bridges can attach to actin binding sites. The cross bridges also have myosin ATPase activity.

• Actin is the main, thin structural protein in the sarcomere. Each actin molecule has a binding site that can attach with a myosin cross bridge.

• Actin and mysoin are contractile proteins.

Tropomyosin and troponin are thin proteins. They are regulatory proteins.• Tropomyosin covers the actin binding sites,

preventing their union with myosin cross bridges.• Troponin has three binding sites: one binds to

tropomyosin, one to actin, and one to Ca ions. – When calcium combines with troponin, tropomyosin

slips away from its blocking position between actin and myosin.

– With this change actin and myosin can interact and muscle contraction can occur.

Skeletal muscle contraction is a molecular phenomenon. • The myosin cross bridges can bind to the actin, pulling these thin

filaments toward the center of the sarcomere. This is the sliding filament mechanism.

– The width of the A band remains unchanged.– The H zone is shortened horizontally.– The I band decreases in width as the actin overlaps more with the myosin.– Neither the thick nor thin filaments change in length. They change their

position with one another.– The actin slides closer together between the thick filaments.

By the power stroke the myosin cross bridges pull the thin actin filaments inward. The cross bridges bind to the actin and bend inward.• A single power stroke pulls the actin inward only a

small percentage of the total shortening distance. Complete shortening occurs by repeated cycles of the power stroke.

• This interaction can occur when troponin and tropomyosin are pulled out of the way by the release of calcium.

• The link between myosin and actin is broken at the end of one cross bridge cycle. A cross bridge returns to its original position and can return to the next actin molecule position, pulling the actin filament further.

By excitation-coupling a series of events link muscle excitation to muscle contraction.• Calcium is the link for this process.

– A somatic efferent sends action potentials to muscle fibers.– This neuron releases acetylcholine at the neuromuscular junction.– This produces an action potential over the entire muscle cell membrane.– This action potential passes along the membrane of the T tubule in the

central part of the muscle fiber.– This action potential meets the membranes of the adjacent sarcoplasmic

reticulum (SR) deep inside the muscle cell.– A permeability change is produced in the membranes of the SR, releasing

calcium from the SR.

The release of calcium ions from the SR into the cytosol allows it to bind with troponin.• By this event, tropomyosin is pulled off the binding

sites of actin, allowing the myosin cross bridges to bind to actin and slide this protein.– Myosin cross bridges had been previously energized by

splitting ATP into ADP plus P. The cross bridges have binding sites for this change. This energy places the myosin cross bridges into a cocked position.

– The contact between myosin and actin “pulls the trigger”, allowing myosin to pull the actin toward the center of the sarcomere (power stroke). This shortens the sarcomere.

– P is released from the cross bridges during the power stroke. ADP is released with power stroke completion.

The addition of a new ATP to myosin cross bridges detaches them from actin. The bridges return to their original conformation.

• The cross bridges return to their original shape for a repeat of the power stroke cycle.

• By the continued, repetition of the cycle, the “rowing” of the myosin cross bridges slide the actin toward the center of the sarcomere for muscle contraction.

• However, for this repetition, calcium ions must be available.

Relaxation of a skeletal muscle depends on the reuptake of calcium ions, from the cytosol into the SR.

• With the absence of calcium, troponin and tropomyosin can resume their blocking role.

• However, calcium can be released again from the SR into the cytosol if a somatic efferent neuron signals the muscle cell with another action potential.

A whole muscle is a group of muscle fibers.

• A muscle is covered by a sheath of connective tissue. It divides the muscle internally into bundles. Each individual muscle fiber is enveloped by a layer of connective tissue.

• A tendon attaches a muscle to a bone.• A single action potential is a muscle fiber produces a

twitch. • Gradations of whole muscle tension depend on the

number of muscle fibers contracting and the tension developed by each contracting fiber.

A motor unit is one motor neuron and the muscle fibers it innervates.

• Whole muscle tension depends on the size of the muscle, the extend of motor unit recruitment, and the size of each motor unit.

• The number of muscle fibers varies among different motor units.– Muscles performing refined, delicate movements have few

muscle fibers per motor unit. – Muscles performing coarse, controlled movements have a

large number of fibers per motor unit.– The asynchronous recruitment of motor units delays or

prevents muscle fatigue.

The tension developed by a muscle depends on the frequency of stimulation.

• Repetitive stimulation of a muscle increases its tension by twitch summation.

• Contractile responses (twitches) can add together by two actions potentials signaling a muscle fiber closely together in time.

• If a muscle fiber is stimulated very rapidly, it cannot relax between stimuli. The twitches merge into a smooth, sustained, maximal contraction called tetanus.

• Twitch summation results from sustained elevation of calcium in the cytosol.

The tension of a tetanic contraction also depends on the length of the fiber at the onset of contraction.

– The optimal length is the resting muscle length. It offers the maximal opportunity for cross-bridge interaction.

– At lengths other than the optimal length, not all cross bridges are able to interact for muscle shortening.

• Whole muscle tension also depends on he extent of fatigue and the thickness of the fiber.

• Muscle tension is transmitted to bone as the contractile component tightens the series-elastic component.

– The origin is the fixed end of attachment of a muscle to a bone. The insertion is the movable end of attachment. If

– If muscle tension overcomes a load, it pulls the insertion toward the origin.

The two primary types of contraction are isotonic and isometric.

• By isometric contraction the muscle tension developed is less than its opposing load. The muscle cannot shorten and lift the object with that load.

• By isotonic contraction the muscle tension developed is greater than its opposing load. The muscle usually shortens and lifts an object. The muscle maintains a constant tension throughout the period of shortening.

• The velocity of muscle shortening is inversely proportional to the magnitude of the load.

Skeletal muscles can perform work.

• Work is calculated by multiplying the magnitude of the load times the distance the load is moved (Force times distance).– Much of the energy applied is converted

into heat.– About 25 percent is realized work. – About 75 percent is converted to heat.

Bones, muscles, and joints interact to form lever systems. • A lever is a rigid structure capable of moving around a pivot.

• The pivot is the fulcrum.

• The power arm is the part of the lever between the fulcrum and the point where an upward force is applied.

• The load arm is the part of the lever between the fulcrum and the downward force from the load.

• Often the velocity and distance of muscle shortening is increased to increase the speed and range of motion of the body part moved by muscle contraction. The muscle must exert more force than the opposing load for this increased speed and range.

ATP is generated three ways for the muscle contraction. • Creatine phosphate plus ADP is converted enzymatically to creatine plus

ATP. This is the first source of ATP for the first minute or less of exercise.• Oxidative phosphorylation generates large amounts of ATP in the

mitochondria if oxygen is available for the muscle cell. This supports aerobic exercise. Some types of muscle fibers have myoglobin which can transfer oxygen into muscle cells.

• Glycolysis makes a small amount of ATP in the absence of oxygen. A net of 2ATPs is formed per glucose molecule. This process uses large quantities of stored glycogen and produces lactic acid. The accumulation of this acid produces muscle soreness.

• Glycolysis supports anaerobic exercise. One glucose molecule is converted into two molecules of pyruvic acid.

• It the absence of oxygen for the muscle cell, pyruvic acid does not enter oxidative phosphorylation. It is converted to pyruvic acid.

These are two types of fatigue.

• Muscle fatigue occurs when an exercising muscle can no longer respond to the same degree of stimulation with the same degree of contractile activity.– Factors for this include an increase in inorganic phosphate,

accumulation of lactic acid, and the depletion of energy reserves. Increased oxygen consumption is needed to recover from exercise (paying off an oxygen debt).

• Central fatigue occurs when the CNS can no longer activate motor neurons supplying working muscles.– It is often psychological and is related to biochemical changes

at the synapses in the brain.

The three types of skeletal muscle fibers are:

– slow oxidative (type I) fibers– fast-oxidative (type IIa) fibers– fast-glycolytic (type IIb) fibers

• Most humans have a mixture of all three types of fibers.

• They are classified by the pathway used for ATP synthesis (oxidative vs. glycolytic) and the rapidity by which they split ATP and contract (fast vs. slow).

• Oxidative fibers are red with a high concentration of myoglobin.

Muscle fibers can adapt to the different demands placed on them.• Regular endurance exercise (e.g., long-distance jogging) promotes

improved oxidative capacity in oxidative fibers.

• The fibers use oxygen more efficiently.

• High-intensity resistance training promotes hypertrophy of fast glycolytic fibers. The fibers increase diameter. Testosterone promotes protein synthesis for this increase.

• The extent of training determines the interconversion of the two types of fast-twitch fibers. Whether a fiber is fast- twitch or slow-twitch depends on its nerve supply.

• Fast-twitch and slow-twitch fibers are interconvertible. For example weight training can convert fast -oxidative fibers to fast-glycolytic fibers.

• Skeletal muscles atrophy when not used. There is disuse atrophy and denervation atrophy.

• Skeletal muscles have a capacity for limited repair.

Multiple neural inputs influence motor unit output. There are three inputs of control for motor neuron output.

• (1) spinal reflex pathways that arise from afferent neurons

• (2) corticospinal (pyramidal) motor system that arise from the primary motor cortex; It is involved mainly with the intricate movements of the hands.

• (3) pathways of the multineuronal (extrapyramidal) motor system that originate from the brain stem; It is involved mainly with postural adjustments and involuntary movements of the trunk and limbs.

Muscle receptors provide afferent information needed to control skeletal muscle activity.

– This input can communicate changes in muscle length (monitored by muscle spindles) and muscle tension (monitored by Golgi tendon organs). Golgi tendon organs are located in the tendons of muscles.

• A stretch reflex is triggered when a whole muscle is passively stretched.– Muscle spindles are stretched. This triggers the reflex

contraction of that muscle. This response resists passive changes in muscle length.

– The classic example of the stretch reflex is the patellar-tendon or knee jerk reflex.

Smooth muscle composes the internal, contractile organs except the heart. The heart is composed of cardiac muscle.

• Smooth muscle cells are small and unstriated.– These cells have actin and myosin. Their

arrangement is not organized compared to skeletal muscle cells. Therefore, smooth muscle cells are not striated.

– Smooth muscle cells contract when calcium ions enter the cells from the ECF. Calcium is also released from intracellular stores.

– This release activates a series of biochemical reactions leading to myosin cross bridge movement.

– Myosin cross bridges are phosphorylated and bind to actin.

Multiunit smooth muscle is neurogenic.

• It has properties partway between skeletal muscle and single-unit smooth muscle.

• Smooth muscle is supplied by the involuntary autonomic nervous system.

• Multi-unit smooth muscle is found in the walls of large vessels, the large airways of the lungs. the ciliary muscle, the iris of the eye, and the base of hair follicles.

• Single-unit smooth muscle cells form functional syncytia.• A syncyticium is a group of interconnected cells. When an action

potential develops in one cell, it quickly spreads to other cells. • Therefore, the cells in a syncyticium contract as a single,

coordinated unit.

Single-unit smooth muscle is myogenic.

• It is self-excitable. It does not require nervous stimulation for contraction. It can develop pacemaker potentials or slow-wave potentials.

• Automatic shifts in ion concentrations in the ECF and ICF cause spontaneous depolarizations to threshold potential.

• By myogenic activity the smooth muscle develops nerve-independent contractile activity. It is initiated by the muscle itself.

Single-unit smooth muscle can produce gradations of contraction.• It differs from the mechanism for producing the gradations of

skeletal muscle contraction.• It depends on the level of calcium ions in the cytosol. • Many single-unit smooth muscle cells have enough calcium in

the cytosol to maintain tone (low level of tension). This occurs in the absence of action potentials.

• Signaling by the ANS and hormones alter the strength of self-induced, smooth muscle contractions.

• Other factors, such as local metabolites and certain drugs, alter the contraction of smooth muscle.

• All of these influences alter the level of calcium ions in the cells’ cytosol.

Smooth muscle can develop tension when it is stretched significantly. It inherently relaxes when stretched.

• Its contraction is slow and energy-efficient.– Single-unit smooth muscle can exist at a

many lengths without a change in tension. It is well-suited for forming the walls of distensible, hollow organs.

Cardiac muscle has properties of skeletal and smooth muscle. • It is found in the walls of the heart.

• It is highly organized and striated. These are similarities to skeletal muscle tissue.

• It can generate action potentials which spread throughout the walls of the heart. This is similar to single-unit smooth muscle.