Skeletal Muscle: Properties, Fiber Types and Applied Aspects

Introduction

• Skeletal muscle demonstrates specialized properties such as summation, tetanus, and length–tension relationships that optimize force generation. It utilizes adenosine triphosphate and creatine phosphate for energy, shows oxygen debt after activity, and regulates force through motor unit recruitment.

Properties Of Skeletal Muscle

Important Properties

• Skeletal muscle exhibits specialized functional properties beyond basic excitability and contractility.
• These include summation, staircase phenomenon, tetanization, post-tetanic potentiation, length–tension relationship, and load–velocity relationship.
• These properties enable graded force production and efficient adaptation to varying functional demands.

Summation of Contraction

• Summation refers to the increase in isometric tension with repeated stimulation of a muscle fiber.
• The action potential is short, lasting about 1 to 4 milliseconds, while contraction lasts longer.
• The refractory period ends before contraction begins, allowing repeated stimulation during contraction.
• Successive stimuli generate multiple action potentials in the same muscle fiber.
• Contractile elements do not obey an all-or-none response and can produce graded contractions.
• When a second stimulus occurs before the first contraction ends, the responses combine. This produces a greater contractile force than a single twitch.
• Increased intracellular calcium ions from repeated stimuli enhance cross-bridge formation. This results in higher tension development.
• As the interval between stimuli decreases, the degree of summation increases. This mechanism allows muscles to produce stronger and sustained contractions during activity.

Staircase Phenomenon

• The staircase phenomenon is a gradual increase in contraction strength during repeated stimulation at sub-tetanic frequency.
• Each successive twitch shows higher tension until a steady maximal level is reached. This occurs when a new stimulus is applied before complete relaxation of the previous contraction.
• The second and subsequent contractions therefore produce greater force than the initial twitch.
• Residual calcium ions remain in the sarcoplasm because reuptake into the sarcoplasmic reticulum is incomplete.
• Additional calcium released with each stimulus increases intracellular calcium concentration. This enhances cross-bridge formation and increases contractile force.
• Repeated contractions also generate heat, which reduces sarcoplasmic viscosity.
• Improved enzyme activity further augments contraction efficiency.
• The amplitude of contractions rises stepwise, producing a pattern resembling a staircase.
• After a few stimuli, the force plateaus as calcium levels and contractile response reach a maximum. This phenomenon is also observed in cardiac muscle and contributes to improved performance during repeated activity.

Tetanization

• Tetanization is a sustained muscle contraction produced by very high-frequency stimulation without relaxation.
• Continuous activation of contractile elements results in a smooth and prolonged contraction.
• In complete tetanus, no relaxation occurs between successive contractions.
• In incomplete tetanus, brief partial relaxation is seen between contractions.
• As stimulus frequency increases, individual twitches fuse and produce progressively higher tension.
• Maximum tension is reached at tetanizing frequency, beyond which further increase in frequency does not increase force.
• The critical frequency is the minimum frequency required to produce summation.
• Tetanization is a sustained muscle contraction produced by very high-frequency stimulation without relaxation.
• Continuous activation of contractile elements results in a smooth and prolonged contraction.
• In complete tetanus, no relaxation occurs between successive contractions.
• In incomplete tetanus, brief partial relaxation is seen between contractions.
• As stimulus frequency increases, individual twitches fuse and produce progressively higher tension.
• Maximum tension is reached at tetanizing frequency, beyond which further increase in frequency does not increase force. ·  The critical frequency is the minimum frequency required to produce summation.
• For example, a twitch lasting 10 milliseconds corresponds to a critical frequency of about 100 stimuli per second.
• Fast muscle fibers require higher critical frequency, whereas slow fibers require lower values.
• Tetanic tension is usually about three to four times greater than a single twitch.
• During a single twitch, calcium release is brief and declines rapidly due to reuptake. Therefore, not all cross-bridges are activated simultaneously.
• In tetanus, repeated stimuli maintain a high calcium ion concentration in the cytoplasm. This ensures continuous exposure of myosin-binding sites on actin. As a result, maximal cross-bridge interaction occurs, producing greater force.
• Sustained tetanic contraction is physiologically important for maintaining posture and powerful movements.

Post-Tetanic Potentiation

• Post-tetanic potentiation is an increased contractile response following a tetanic contraction.
• A single stimulus applied after tetanus produces a stronger twitch than normal.
• Residual calcium ions remain in the sarcoplasm after tetanus due to delayed reuptake.
• Additional calcium released with the next stimulus raises cytosolic calcium levels further. ·  This enhances cross-bridge formation and increases the force of contraction.

Length-Tension Relationship

• Isometric tension depends on the initial length of the muscle before contraction.
• In experimental settings, muscle length is varied by altering the distance between fixed ends.
• Stretching a muscle generates passive tension, produced by elastic elements such as titin.
• Passive tension is not due to active contraction of myofilaments.
• When the stretched muscle is stimulated, it produces total tension.
• Active tension is calculated as total tension minus passive tension.
• Active tension represents force generated by cross-bridge interaction.
• As muscle length increases within physiological limits, active tension also increases. This occurs because optimal overlap between actin and myosin enhances cross-bridge formation.
• The length at which maximum active tension is produced is called the optimal length.
• Beyond this length, excessive stretching reduces filament overlap and decreases force.
• The resting length of skeletal muscle is slightly stretched in the body.
• This is evident as the muscle shortens when detached from its attachment.
• Resting length closely corresponds to optimal length, ensuring maximal force during normal activity. Thus, the length–tension relationship is essential for efficient muscle performance and force generation.

Length-Tension Relationship in a Sarcomere:

• The length–tension relationship is explained by the sliding filament mechanism of contraction.
• Tension depends on the number of cross-bridges formed between actin and myosin.
• At resting length, optimal overlap exists between thick and thin filaments. This allows maximal cross-bridge formation and produces maximum active tension.
• When the sarcomere is stretched beyond this length, filament overlap decreases.
• Reduced overlap leads to fewer cross-bridges and a proportional decline in tension.
• If there is no overlap, active tension becomes zero.
• When the sarcomere shortens below resting length, excessive overlap occurs.
• Thin filaments may overlap each other and interfere with cross-bridge formation. This reduces effective tension generation.
• At very short lengths, binding sites may lie in nonfunctional regions, further decreasing force.
• The optimal sarcomere length is about 2.0 to 2.2 micrometers, where maximum tension is generated.

Load-Velocity Relationship

• The velocity of muscle shortening during isotonic contraction is inversely related to the applied load.
• With no load, the muscle shortens at its maximum velocity.
• As the load increases, the velocity of shortening progressively decreases.
• When the load equals the maximum isometric tension, shortening velocity becomes zero.
• If the load exceeds this value, the muscle undergoes lengthening contraction.
• This principle explains daily activities, where light objects are lifted faster than heavy ones.
• The velocity of contraction depends on the rate of cross-bridge cycling, which is influenced by adenosine triphosphatase activity.
• With light loads, resistance to filament sliding is minimal, allowing rapid movement and fewer cross-bridges at a time. This results in faster contraction but lower tension.
• With heavier loads, cross-bridge movement slows, allowing more interactions between actin and myosin. This produces greater tension but reduces contraction speed.
• When correlated with the length–tension relationship, maximal shortening velocity occurs at resting muscle length.
• If the muscle is stretched before contraction, it is termed preloaded.
• If the load is applied after contraction begins, it is called afterloaded.
• These relationships are essential for understanding muscle performance and mechanical efficiency.

Energy Sources in Skeletal Muscle

Adenosine Tri-phosphate

• Adenosine triphosphate is the immediate energy source for muscle contraction.
• Hydrolysis of adenosine triphosphate releases about 7.3 kilocalories per mole, forming adenosine diphosphate and inorganic phosphate. It provides energy for cross-bridge cycling, enabling movement of myosin heads.
• Binding of adenosine triphosphate to myosin causes detachment from actin, allowing repeated cycles. It supplies energy to the calcium pump that transports calcium into the sarcoplasmic reticulum, initiating relaxation. It also fuels the sodium–potassium pump to maintain membrane excitability.
• The stored adenosine triphosphate in muscle is limited and supports contraction only for a fraction of a second. Therefore, continuous regeneration of adenosine triphosphate is essential.
• Regeneration occurs through three main pathways:

1. Transfer of phosphate from creatine phosphate to adenosine diphosphate.
2. Oxidative phosphorylation in mitochondria.
3. Metabolic breakdown of glucose to carbon dioxide and water.

• These mechanisms ensure a constant supply of energy during muscle activity.

Creatine Phosphate

• Creatine phosphate is a high-energy compound that rapidly regenerates adenosine triphosphate in muscle. ·  It transfers a phosphate group to adenosine diphosphate through the enzyme creatine kinase.
• This reaction is fast and does not require oxygen. It is activated when adenosine triphosphate levels fall and adenosine diphosphate levels rise.
• The concentration of creatine phosphate in resting muscle is about five times higher than adenosine triphosphate. However, its reserve is limited and supports contraction only for a few seconds.
• During recovery, creatine phosphate stores are replenished using energy derived from newly synthesized adenosine triphosphate.
• When creatine phosphate and adenosine triphosphate levels decline, other energy systems become active.
• At rest and during mild activity, muscles mainly use fatty acids for energy.
• During moderate to intense exercise, glucose and glycogen become the primary substrates.
• In the presence of oxygen, aerobic metabolism produces carbon dioxide, water, and about 36 to 38 molecules of adenosine triphosphate per glucose molecule.
• In oxygen deficiency, anaerobic metabolism produces lactic acid and only 2 molecules of adenosine triphosphate.

Oxygen Debt

• During intense exercise, oxygen supply becomes insufficient for complete aerobic metabolism.
• Muscles rely partly on anaerobic glycolysis, producing less energy and generating lactate.
• In prolonged moderate activity, most energy is derived from aerobic pathways.
• In short, high-intensity activity, a larger proportion comes from anaerobic metabolism.
• After exercise, additional oxygen is required to restore normal physiological state. This extra oxygen requirement is termed oxygen debt.
• Oxygen is needed to convert accumulated lactate back to pyruvate. It helps in regeneration of adenosine triphosphate and creatine phosphate stores. It also replenishes oxygen bound to myoglobin in muscle fibers. Therefore, respiratory rate remains elevated even after exercise stops.
• The magnitude of oxygen debt depends on the intensity and duration of activity.
• Efficient recovery mechanisms reduce oxygen debt in trained individuals.

Muscle Fatigue

• Muscle fatigue is the progressive decline in force during repeated stimulation despite continued activity. It is characterized by reduced contraction amplitude, decreased shortening velocity, and prolonged relaxation.
• Fatigue may occur early or late and may progress rapidly or slowly.
• The pattern depends on the type of muscle fibers and the nature of activity.
• Key factors influencing fatigue include:

1. Fiber composition of the muscle.
2. Intensity and duration of exercise.
3. Availability of oxygen and glucose.
4. Accumulation of metabolites such as lactate, hydrogen ions, and potassium.
5. Level of prior physical training.

• Central nervous system influence plays a major role in fatigue development.
• Psychological factors such as motivation and encouragement can delay fatigue.
• These effects may involve activation of endogenous opioid pathways that reduce perception of exertion.
• Muscles that fatigue rapidly tend to recover quickly.
• Muscles that fatigue slowly usually require a longer recovery period.
• Understanding fatigue mechanisms is important for optimizing performance and rehabilitation.

Rigor Mortis

• Rigor mortis is postmortem muscle stiffness due to failure of cross-bridge detachment.
• Lack of adenosine triphosphate prevents separation of actin and myosin.
• After death, cytoplasmic calcium ions remain elevated.
• Calcium is not pumped into the sarcoplasmic reticulum due to absence of energy.
• Membrane integrity is lost, allowing calcium entry from extracellular fluid.
• Calcium also leaks from the sarcoplasmic reticulum into the cytoplasm.
• Increased calcium exposes myosin-binding sites on actin.
• Cross-bridges form but cannot detach, producing sustained contraction. This results in progressive muscle stiffness.
• Rigor mortis begins about 3 to 4 hours after death. It becomes fully established within approximately 12 hours.
• The stiffness gradually disappears after 48 to 60 hours due to protein breakdown. The process is clinically useful for estimating the time since death.

Heat Production in Muscles

• During contraction, most energy is released as heat, while a smaller portion performs mechanical work.
• Mechanical efficiency is the percentage of energy converted into work.
• In isometric contraction, no external work is done, so efficiency is zero percent.
• In isotonic contraction, efficiency is about 20 to 25 percent and may reach up to 50 percent.
• Heat production can be measured using sensitive temperature-detecting instruments.

Types of Heat

• Resting heat is produced due to basal metabolic activity in a relaxed muscle.
• Initial heat is generated during contraction and exceeds resting heat.

1. Activation heat is produced after stimulation but before contraction begins.
2. Shortening heat occurs during muscle shortening and increases with the extent of shortening.

• Relaxation heat is released when the muscle returns to its original length after contraction.
• Recovery heat is generated during metabolic processes that restore muscle to its resting state. It persists for a longer duration and is approximately equal to initial heat.
• Heat production reflects energy utilization and is essential for understanding muscle efficiency and metabolism.

Fiber Types in Skeletal Muscle

• Skeletal muscle fibers are classified based on contraction speed and metabolic properties.
• Two main types are recognized: Type I fibers (slow, oxidative) and Type II fibers (fast, glycolytic or oxidative-glycolytic).

Table 28.1: Differences between type I and II muscle fibers.

Feature	Type I Fibers (Slow Oxidative)	Type II Fibers (Fast Glycolytic)
Contraction speed	Slow	Fast
Fatigue resistance	High	Low
Metabolism	Oxidative phosphorylation	Glycolysis
Mitochondria & myoglobin	Abundant	Limited
Glycogen content	Low	High
Motor unit size	Small	Large
Capillary supply	Dense	Sparse

Type I Muscle Fibers

• Type I fibers are slow-contracting fibers rich in myoglobin and capillaries, giving a red appearance.
• They contain abundant mitochondria and primarily generate adenosine triphosphate by oxidative phosphorylation.
• These fibers have low myosin adenosine triphosphatase activity, resulting in slower cross-bridge cycling.
• Consequently, contraction velocity is low, but endurance is high.
• Type I fibers are highly resistant to fatigue and can sustain prolonged activity.
• They are important for maintaining posture and are commonly found in back and proximal limb muscles.

Type II Muscle Fibers

• Type II fibers contract rapidly and appear pale due to lower myoglobin content.
• They have high myosin adenosine triphosphatase activity, leading to faster contraction.
• These fibers rely more on glycolytic metabolism for energy production.
• They fatigue more quickly but generate powerful and rapid movements.
• Type II fibers are prominent in muscles responsible for precise and quick actions, such as those of the hand and eye.

Motor Units

Definition

• A motor unit consists of a single motor neuron, its axonal branches, and all the muscle fibers it innervates.
• Activation of one motor neuron causes simultaneous contraction of all fibers in that unit.

Size of a Motor Unit

• Motor neuron cell bodies are located in the anterior horn of the spinal cord.
• A single neuron may innervate a variable number of muscle fibers.
• Small motor units supply few fibers and produce fine, precise movements.
• In intrinsic hand muscles, one neuron may innervate fewer than ten fibers, generating small tension.
• Large motor units supply many fibers and produce greater force.
• In back muscles, one neuron may control hundreds to thousands of fibers, resulting in strong contractions.

Recruitment of Motor Units

• At rest, very few motor units are active.
• Increased force is achieved by activating additional motor units, a process called recruitment.
• Recruitment allows graded control of muscle tension depending on functional demand.
• In muscles performing fine movements, recruitment occurs gradually.
• Each additional unit contributes a small increase in tension, allowing precise regulation.
• In muscles responsible for posture and powerful actions, recruitment adds large increments of force. This enables effective resistance against gravity and maintenance of body position. Thus, motor unit organization determines both precision and strength of muscle activity.

Size Principle

• The size principle states that motor units are recruited in an orderly manner based on neuron size.
• Each motor unit contains muscle fibers of the same metabolic type.
• Small motor neurons innervate slow, oxidative fibers with high fatigue resistance.
• Large motor neurons supply fast, glycolytic fibers that generate greater force but fatigue quickly.
• During low-intensity activity, small motor units are activated first.
• As demand increases, larger motor units are progressively recruited.
• This sequence ensures efficient energy use and smooth increase in force.
• Oxidative fibers dominate during sustained, moderate activity.
• Glycolytic fibers are recruited during high-intensity contractions requiring rapid force.
• Most muscles contain a mixture of both fiber types for versatile function.

Whole-Muscle Contraction

• Whole muscles consist of many fibers organized into multiple motor units.
• Voluntary movement is controlled by the central nervous system, which adjusts muscle force precisely.
• Smooth and graded contraction is achieved by:

• Increasing the number of active motor units (recruitment).
• Increasing the frequency of motor neuron discharge.

• Motor units fire asynchronously, allowing sustained contraction and delaying fatigue.

• Total muscle tension depends on:

1. The number of active motor units.
2. The number of fibers within each motor unit.
3. The type of muscle fibers, including their size, length, and fatigue resistance.

Muscle Strength

• Muscle strength is defined as the maximum load a muscle can lift.
• For comparison, strength is expressed as load per cross-sectional area.
• Average skeletal muscle strength is about 3 to 4 kilograms per square centimeter.
• This value is relatively consistent across mammalian species.
• Muscle strength varies with sex, age, genetics, and training status.
• Males generally exhibit higher strength due to the anabolic effects of testosterone.
• Regular training increases muscle size and functional capacity.
• Structural adaptations improve force generation and endurance. Thus, coordinated neural control and muscle properties determine overall performance.

Applied Aspects

Muscular Dystrophy

• Muscular dystrophy refers to a group of genetic disorders causing progressive degeneration of skeletal muscle.
• These conditions result from defects in proteins of the dystrophin–glycoprotein complex, which stabilizes muscle fibers.

Duchenne Muscular Dystrophy

• Duchenne muscular dystrophy is the most common and severe form, inherited as an X-linked recessive disorder. It primarily affects male children and presents with progressive muscle weakness by around 4 years of age.
• There is apparent muscle enlargement, especially in calf and pelvic muscles, due to fatty and fibrous tissue replacement.
• Children often use their hands to rise from the floor, indicating proximal muscle weakness.
• Cardiac involvement, including enlargement of the heart, is common.
• Most affected individuals lose the ability to walk by early adolescence.
• Life expectancy is reduced, often up to the third decade.
• The condition is caused by absence of dystrophin due to gene mutations on the X chromosome.

Baker’s Muscular Dystrophy

• Becker muscular dystrophy is a milder and less common variant.
• Dystrophin is present but reduced or structurally abnormal.
• Symptoms appear later and progress more slowly, allowing survival into adulthood.
• Experimental therapies aim to enhance production of dystrophin-related proteins.
• Proteins such as utrophin may partially compensate for dystrophin deficiency.
• Some forms also involve defects in proteins like laminin, affecting muscle stability and integrity.

Myopathies

• ·  Myopathies are muscle disorders caused by structural or metabolic abnormalities.
• ·  Mutations in desmin affect skeletal and cardiac muscle integrity.

Metabolic Myopathies

• These result from defects in enzymes involved in carbohydrate, protein, or fat metabolism.
• Accumulation of toxic metabolites leads to muscle damage and weakness.

Inflammatory Myopathy

• Poliomyelitis causes weakness due to destruction of anterior horn motor neurons. It leads to muscle paralysis and may result in respiratory failure.

Myotonia

• Myotonia is characterized by delayed muscle relaxation after voluntary contraction. It results from mutations affecting sodium or chloride ion channels.
• These channel defects lead to prolonged muscle excitability and stiffness.

Focal Dystonias

• Focal dystonia involves involuntary, repetitive, or sustained muscle contractions in a localized region.
• These contractions produce abnormal movements, postures, and may cause significant pain.

• Common forms include:

1. Cervical dystonia, affecting neck and shoulder muscles.
2. Blepharospasm, involving eyelid muscles.
3. Writer’s cramp, affecting hand muscles.
4. Spasmodic dysphonia, involving vocal cord muscles.

• These disorders may impair normal motor function and daily activities.
• Local injection of botulinum toxin reduces abnormal muscle activity and improves symptoms.

Muscle Sprain

• A muscle sprain occurs due to overstretching or excessive force during activity.
• Injury commonly involves the myotendinous junction or muscle fibers.
• Structural damage may affect contractile elements, especially near Z lines.
• Symptoms include pain, swelling, weakness, and tenderness.
• Management includes rest, ice application, immobilization, and analgesic medication.
• Severe cases may require surgical repair.

Muscle Cramp

• A muscle cramp is a painful, involuntary sustained contraction of muscle. It results from high-frequency nerve impulses causing tetanic contraction.
• Common causes include electrolyte imbalance, dehydration, and excessive exercise.
• Correction of fluid and electrolyte status helps relieve symptoms.