Calisthenics Instructor Certification Chapter 7: Physiology of Muscles

 

Chapter 7: Physiology of Muscles

Structure of Skeletal Muscles

Skeletal muscles make up approximately 40% of body weight in men and 32% in women. The remaining ~10% of muscle mass is composed of smooth muscles and the cardiac muscle.

Through contraction, muscles generate tension, produce movement, and perform mechanical work.

Types of Muscle Tissue

Muscle tissue is categorized in two ways:

  1. By appearance:
    • Skeletal muscle and cardiac muscle are striated (show visible banding under a microscope).
    • Smooth muscle is non-striated.
  2. By control mechanism:
    • Skeletal muscles are voluntary, meaning they are controlled consciously.
    • Cardiac and smooth muscles are involuntary, functioning independently of conscious control.

Skeletal Muscle Fibers

Skeletal muscles are made up of bundles of elongated, cylindrical cells called muscle fibers, each surrounded by connective tissue.

  • Formation: During embryonic development, muscle fibers form by the fusion of smaller cells called myoblasts.
  • Structure: Each muscle fiber contains multiple nuclei and numerous mitochondria, which supply the large amounts of energy required for contraction.

Inside each fiber are myofibrils—specialized contractile structures that account for about 80% of the cell’s volume.

Myofibrils and Sarcomeres

Myofibrils are composed of alternating thick and thin filaments arranged in repeating units called sarcomeres.

  • Striations:
    • Thick and thin filaments overlap to form alternating dark A-bands and light I-bands, creating the striated appearance of skeletal muscle.
  • Sarcomere:
    • The section between two Z-lines.
    • It is the functional unit of skeletal muscle contraction.

Filaments

  • Thick Filaments: Composed primarily of myosin proteins. Each myosin molecule has a globular head that forms cross-bridges with actin during contraction.
  • Thin Filaments: Composed mainly of actin. Actin contains binding sites that interact with myosin heads.

Regulatory Proteins

Two key proteins regulate contraction:

  • Tropomyosin: Blocks actin’s binding sites at rest.
  • Troponin: Controls the position of tropomyosin.
    Together, they act as regulatory proteins, covering or exposing actin’s binding sites depending on the presence of calcium ions.

Titin

  • Titin is a giant, elastic protein (≈30,000 amino acids long).
  • It runs from the M-line to the Z-lines within the sarcomere.
  • Functions:
    • Anchors thick filaments.
    • Provides structural stability.
    • Acts as a spring, contributing to muscle elasticity (parallel elastic component).
    • Plays a role in signal transmission inside the muscle fiber.

Muscle Structure Hierarchy

  • Muscle (organ) → composed of multiple muscle fibers (cells)
  • Muscle fiber → contains numerous myofibrils
  • Myofibrils → made up of repeating sarcomeres
  • Sarcomeres → contain thick (myosin) and thin (actin) filaments
  • Filaments → built from proteins (myosin, actin, troponin, tropomyosin, titin)

 

Molecular Basis of Skeletal Muscle Contraction

The contraction of a skeletal muscle fiber is initiated when it is stimulated by a motor neuron. This triggers a series of events that culminate in the sliding of thin filaments (actin) over thick filaments (myosin) within the sarcomere, shortening the muscle fiber.

Cross-Bridge Cycling

Each myosin cross-bridge contains two functional regions:

  1. Actin-binding site – where the myosin head attaches to actin filaments.
  2. ATPase site – where adenosine triphosphate (ATP) binds and is hydrolyzed.

The hydrolysis of ATP provides the energy required for contraction.

  • ATP is split into ADP + Pi (inorganic phosphate) by the myosin head before binding to actin.
  • This reaction places the myosin head into a “high-energy” state.
  • When binding sites on actin are exposed, the myosin head attaches and undergoes a power stroke, pulling the thin filament toward the center of the sarcomere.
  • A new ATP molecule must then bind to detach the myosin head and reset the cycle.

This repeated cycle of attachment, power stroke, detachment, and re-cocking is the essence of the sliding filament mechanism.

Sliding Filament Mechanism

  • Thin filaments slide inward toward the center of the sarcomere (A-band).
  • Z-lines are pulled closer together, shortening the sarcomere.
  • Since all sarcomeres shorten simultaneously, the entire muscle fiber shortens, producing contraction.

Importantly, the filaments themselves do not shorten—it is their relative movement (sliding) that causes contraction.

Role of Calcium (Ca²⁺)

Muscle contraction is tightly regulated by calcium ions.

  • When an action potential travels along the sarcolemma, it enters the fiber via T-tubules.
  • This triggers the sarcoplasmic reticulum (SR) to release Ca²⁺ from its terminal cisternae (lateral sacs).
  • Ca²⁺ binds to troponin, causing a conformational change that shifts tropomyosin, exposing the binding sites on actin.
  • Cross-bridge cycling then proceeds.

When stimulation ceases:

  • Ca²⁺ is actively pumped back into the SR.
  • Troponin and tropomyosin return to their resting positions.
  • Actin-myosin interaction is blocked, and the muscle relaxes.

Excitation–Contraction Coupling

The term excitation–contraction coupling refers to the sequence of events that links:

  1. Excitation: the action potential in the muscle fiber.
  2. Contraction: the cross-bridge activity that produces shortening.

Calcium acts as the key link between the two processes.

Timing of Contraction

The phases of a single twitch contraction include:

  • Latent Period: The brief delay (~a few milliseconds) between the action potential and the start of contraction, representing the time required for excitation–contraction coupling.
  • Contraction Time: The period (15–50 ms) during which tension develops as cross-bridge cycling occurs.
  • Relaxation Time: The period (15–50 ms) during which Ca²⁺ is re-sequestered into the SR, leading to muscle relaxation.

Different muscle fiber types (fast-twitch vs slow-twitch) display different contraction and relaxation times.

 

Skeletal Muscle Mechanics

Sarcomere Tension

Sarcomeres are the contractile units of skeletal muscle. When their length decreases through the repeated cross-bridge cycle of actin and myosin, tension (force) develops inside the muscle fiber. This tension is transmitted to the skeleton through tendons—tough, collagen-based connective tissue that connects muscle to bone.

  • Origin: attachment on the less movable part of the skeleton.
  • Insertion: attachment on the more movable part.
    When sarcomeres shorten, the force passes through the tendon to move the bone at the insertion point. The external load is the opposing force, such as gravity or an object’s weight.

Types of Muscle Contraction

Muscle contraction does not always mean the muscle shortens—it simply means tension is produced. The main contraction types are:

  1. Isotonic contractions (constant tension)
    • Concentric: muscle shortens while producing force (e.g., lifting a weight).
    • Eccentric: muscle lengthens while producing force (e.g., lowering a weight).
    • In eccentric contractions, muscles often act as “brakes,” resisting gravity or external forces.
  2. Isometric contractions (constant length)
    • Muscle develops tension without changing length.
    • Example: holding a heavy book still, or contracting the biceps while the triceps balance the force.
  3. Isokinetic contractions (constant speed)
    • Occur only with specialized equipment.
    • Muscle contracts at a constant speed through the entire range of motion while resistance adapts to match force.

Work and Force

  • Force is the tension produced by the muscle.
  • Work is the product of force × distance moved.
  • Only 20–25% of the energy used by contracting muscle is converted into work; the rest is lost as heat.
  • Because muscles act as levers, they can amplify speed and movement distance at the expense of force.

Motor Units and Force Control

  • A motor unit is a motor neuron plus all the muscle fibers it innervates.
  • All fibers in a motor unit contract together when the neuron fires (“all or nothing”).
  • Muscles vary in motor unit size: some control only a few fibers (for fine movements), others hundreds (for strength).
  • Force regulation happens by:
    1. Recruitment: activating more motor units.
    2. Rate coding: increasing firing frequency of active motor units.

To prevent fatigue during prolonged activity, the nervous system alternates motor unit activation—called asynchronous recruitment. In maximal contractions, all units fire together, so fatigue cannot be avoided.

Twitch, Summation, and Tetanus

  • A single action potential in a muscle fiber causes a brief contraction known as a twitch.
  • When a fiber receives repeated stimulation before it fully relaxes, contractions add up—this is summation.
  • If stimulation is rapid enough that the muscle has no time to relax, a smooth, sustained contraction occurs. This is called tetanus and represents the muscle’s maximum force output.

Length–Tension Relationship

The ability of a muscle to produce force depends on its initial length before contraction.

  • At the optimal length, overlap between actin and myosin filaments is ideal, allowing maximum cross-bridge formation and maximal tension.
  • If the muscle is too short or too stretched, fewer cross-bridges form, and force decreases.

 

Muscle Metabolism and Fiber Types

ATP as the Energy Currency

Muscle contraction and relaxation require a constant supply of ATP. ATP is the only direct source of energy that powers cross-bridge cycling, calcium transport, and ion pumps in the muscle cell. Because muscles store very little ATP, they must continuously regenerate it during activity.

Pathways of ATP Production

Skeletal muscles use three main energy systems to maintain ATP supply:

  1. Creatine Phosphate System (Phosphagen System)
    • Provides immediate ATP at the onset of exercise.
    • A high-energy phosphate group from creatine phosphate is transferred to ADP, rapidly forming ATP.
    • Fuels short, explosive efforts (e.g., sprint starts, heavy lifts).
  2. Oxidative Phosphorylation (Aerobic Metabolism)
    • Uses oxygen to break down nutrients (mainly carbohydrates and fats).
    • Produces large amounts of ATP efficiently, but more slowly.
    • Dominates during endurance activities (running, cycling, swimming).
  3. Glycolysis (Anaerobic Metabolism)
    • Breaks down glycogen and glucose without oxygen.
    • Produces ATP quickly, but in limited amounts, and generates lactate.
    • Becomes crucial during high-intensity exercise when oxygen delivery is limited.

ATP in Muscle Contraction

ATP is required at four key steps of excitation–contraction and relaxation:

  1. Power stroke of the myosin cross-bridge.
  2. Detachment of myosin from actin.
  3. Active reuptake of calcium (Ca²⁺) into the sarcoplasmic reticulum during relaxation.
  4. Operation of the sodium-potassium pump after each action potential.

Muscle Fiber Types

Skeletal muscle fibers differ in contraction speed and energy system preference:

  1. Slow Oxidative Fibers (Type I)
    • Contract slowly, resist fatigue.
    • Rely mainly on oxidative phosphorylation.
    • Suited for endurance activities (e.g., marathon running, posture muscles).
  2. Fast Oxidative Fibers (Type IIa)
    • Contract faster than Type I, but still have good endurance.
    • Use both oxidative phosphorylation and glycolysis.
    • Adapted for sports requiring both power and stamina (e.g., middle-distance running).
  3. Fast Glycolytic Fibers (Type IIb/IIx)
    • Contract very quickly, fatigue rapidly.
    • Depend primarily on glycolysis.
    • Suited for short, explosive movements (e.g., sprinting, weightlifting).

👉 For fitness professionals: Understanding muscle metabolism and fiber types helps design training programs. Strength and power training emphasize fast glycolytic fibers and the phosphagen system, while endurance training develops oxidative fibers and aerobic capacity.

 

Creatine Phosphate (Phosphocreatine)

Creatine phosphate (PCr) is the first energy reserve activated at the onset of muscle contraction. It acts as an immediate buffer for ATP, the body’s direct energy source.

When exercise begins, the high-energy phosphate group of creatine phosphate is transferred to ADP, rapidly regenerating ATP. This reaction is catalyzed by the enzyme creatine kinase and is reversible:

Creatine Phosphate + ADP ↔ Creatine + ATP

Role at Rest vs. Exercise

  • At rest: ATP levels are relatively high, so energy and phosphate groups are transferred from ATP to creatine, forming phosphocreatine stores.
  • During contraction: ATP is broken down rapidly by myosin ATPase. As ATP levels drop, phosphocreatine donates its phosphate group to ADP, quickly replenishing ATP.

Muscle cells contain about five times more phosphocreatine than ATP, making it the main short-term energy reservoir. This system can sustain high-energy demands for only about 10–30 seconds, and in some cases up to one minute, depending on intensity.

Performance Relevance

  • Explosive activities such as sprinting, jumping, or heavy lifting rely heavily on the phosphocreatine system.
  • Because it works through a single enzymatic step, ATP resynthesis from PCr is extremely fast, making it ideal for short bursts of maximum effort.
  • Once phosphocreatine stores are depleted, muscles must switch to glycolysis or oxidative phosphorylation for continued energy.

Nutrition and Supplementation

Creatine is obtained naturally from the diet (mainly meat and fish) and also produced by the liver and kidneys. Athletes sometimes take creatine supplements to increase muscle phosphocreatine stores.

  • Benefits: Slight improvements in performance for activities requiring short-term, high-intensity effort (e.g., sprints, weightlifting).
  • Limitations: No benefit for endurance activities, which rely on aerobic metabolism.
  • Caution: Long-term effects of supplementation are not fully known, so use should be considered carefully.

👉 For fitness professionals: The phosphocreatine system is critical for understanding explosive power training. It explains why short, intense efforts can be repeated after brief rest periods (as PCr levels replenish) and why endurance training does not rely on this system.

 

Oxidative Phosphorylation

Oxidative phosphorylation is the body’s most efficient but slowest system of ATP production. Unlike phosphocreatine or glycolysis, which provide rapid energy, oxidative phosphorylation supplies ATP at a lower rate but can sustain activity for long durations.

This process occurs in the mitochondria and requires a continuous supply of oxygen (O₂). Oxygen is essential for the electron transport chain, where the chemical energy released from the breakdown of nutrients is used to generate ATP through a process known as chemiosmosis, powered by the enzyme ATP synthase.

Key Fuel Sources

  • Glucose (from blood sugar and stored glycogen in muscle and liver)
  • Fatty acids (mobilized from body fat stores, especially during longer efforts)

Depending on exercise intensity and duration, muscles switch between glucose and fatty acids as the dominant energy source.

Efficiency and Capacity

  • Yield: About 32 ATP per molecule of glucose – far more than glycolysis or phosphocreatine.
  • Speed: Relatively slow because of the many enzymatic steps required.
  • Capacity: High – can support energy demands for hours, as long as oxygen and nutrients are available.

This makes oxidative phosphorylation the primary energy system during aerobic or endurance-type exercise, such as walking, jogging, swimming, or cycling.

Oxygen Delivery During Exercise

To sustain oxidative phosphorylation, muscles require continuous oxygen delivery. The body adapts during exercise in several ways:

  • Faster and deeper breathing increases oxygen levels in arterial blood.
  • The heart pumps more forcefully and rapidly, sending more oxygen-rich blood to working muscles.
  • Blood vessels dilate to direct more blood flow to active muscles.
  • Hemoglobin releases more oxygen, while myoglobin inside muscle fibers helps transfer and store small amounts of oxygen for immediate use.

Practical Implications for Fitness

  • Endurance athletes benefit most from this system. Training increases mitochondrial density, capillary networks, and oxygen utilization efficiency.
  • Carbohydrate loading (increasing glycogen stores before competition) can improve performance in endurance events like marathons.
  • Once glycogen stores are depleted, the body shifts more toward fat metabolism, which is slower but nearly limitless compared to carbohydrate reserves.

👉 For trainers and coaches: Oxidative phosphorylation is the backbone of aerobic conditioning. Understanding how oxygen and nutrients fuel this system helps in designing programs that improve endurance, recovery, and overall metabolic health.

 

Glycolysis

Glycolysis is the second major energy system for ATP production in skeletal muscle. It becomes increasingly important when oxygen delivery to the muscle is limited or when exercise intensity is too high for oxidative phosphorylation to meet the energy demand.

Why Muscles Rely on Glycolysis

  • Oxygen limitations: The heart and lungs can only supply oxygen up to a certain level. In addition, during near-maximal contractions, the blood vessels within the muscle are compressed, reducing oxygen delivery.
  • High energy demand: During intense activity, muscle energy consumption may increase up to 100 times compared to rest. In these conditions, oxidative phosphorylation is too slow to supply enough ATP, so muscles rely more heavily on glycolysis.

How Glycolysis Works

  • In glycolysis, one molecule of glucose is broken down into two molecules of pyruvate, producing a net gain of two ATP molecules.
  • The pyruvate may either:
    1. Enter the mitochondria for oxidative phosphorylation if oxygen is available.
    2. Be converted into lactic acid if oxygen is insufficient.

Advantages of Glycolysis

  1. Anaerobic capacity: It can produce ATP without oxygen (supports anaerobic exercise).
  2. Speed: It produces ATP much faster than oxidative phosphorylation, which is critical during short bursts of high-intensity activity.

Limitations

  • Glycolysis alone provides less ATP per molecule of glucose than oxidative phosphorylation.
  • The byproduct lactic acid can accumulate, lowering pH and contributing to muscle fatigue.

Role in Exercise

  • Glycolysis is the primary system supporting high-intensity, short-to-medium duration activities, such as sprinting, heavy lifting, or interval training.
  • Because of its anaerobic nature, it is often referred to as the anaerobic energy pathway.

👉 For trainers and coaches: Glycolysis explains why athletes can sustain explosive effort for a limited time and why recovery periods are essential for clearing lactate and restoring balance.

 

Lactic Acid Production and Fatigue

Glycolysis provides an anaerobic pathway for ATP production during high-intensity exercise, especially when oxygen delivery or oxidative phosphorylation cannot meet the energy demands of the muscles. However, relying on this pathway has two key consequences:

  1. Inefficient ATP yield – Glycolysis produces only 2 ATP per glucose molecule, compared to 32 ATP generated via oxidative phosphorylation. As a result, large amounts of glucose must be consumed, rapidly depleting the limited glycogen stores in skeletal muscle.
  2. Lactic acid accumulation – When pyruvate cannot enter oxidative pathways, it is converted to lactic acid (lactate). Accumulation of lactate contributes to the burning sensation felt during intense exercise and is linked to metabolic acidosis. However, the soreness and stiffness experienced the next day are more likely due to reversible structural damage (microtears) in the muscle fibers, not lactate.

Because of these limitations, anaerobic high-intensity exercise can only be sustained for short durations, unlike aerobic endurance exercise which can continue for long periods.

Types of Fatigue

Muscle activity cannot be maintained indefinitely at high levels. As tension decreases, fatigue develops. Two forms are recognized:

1. Muscle Fatigue

Occurs when a muscle can no longer respond with the same contractile force despite continued stimulation.

  • Protective role: Prevents muscles from reaching the point where ATP depletion could cause rigor (permanent contraction).
  • Main causes:
    • Increased inorganic phosphate (Pi) from ATP breakdown, which interferes with cross-bridge function and calcium release.
    • Glycogen depletion, especially during prolonged or exhaustive exercise.
  • Influence of fiber type: Some fibers are more resistant to fatigue than others, and fatigue develops faster during high-intensity activity.

2. Central Fatigue

Occurs when the central nervous system (CNS) reduces stimulation of motor neurons, even though the muscles are still capable of contracting.

  • Often psychological in origin, linked to discomfort, monotony, or general tiredness (e.g., lack of sleep).
  • Can involve neurotransmitter changes in the brain (e.g., increased serotonin levels).
  • Overcoming central fatigue requires strong motivation or external incentives (e.g., competition).

Recovery and Oxygen Debt

Recovery after intense exercise requires increased oxygen consumption. This is known as Excess Post-Exercise Oxygen Consumption (EPOC). During recovery:

  • Breathing remains deep and rapid to restore oxygen balance.
  • The oxygen deficit created during exercise is repaid, replenishing ATP and creatine phosphate, and clearing lactate from the blood.
  • This process helps restore muscle function and prepares the body for the next effort.

👉 Practical Insight for Trainers:
Understanding lactic acid and fatigue helps explain why rest intervals, proper nutrition, and structured recovery strategies are critical in training programs. Lactate is not just “waste” – it is also a fuel that can be reused by other tissues (like the heart and slow-twitch fibers).

 

Oxygen Debt (O₂ Deficit) and Recovery

During intense exercise, the muscles’ demand for oxygen can exceed the supply that the circulatory and respiratory systems can deliver. When this happens, energy production shifts toward anaerobic pathways (creatine phosphate breakdown and glycolysis), resulting in lactate accumulation. This state is called oxygen debt (O₂ deficit), and the work done during this period is termed anaerobic work.

After heavy muscular work, the body continues to breathe deeply and rapidly for several minutes. This increased oxygen intake serves to “repay” the oxygen debt, restoring the body to pre-exercise metabolic conditions.

What Happens During Recovery

  1. Phosphocreatine Restoration
    • ATP generated through oxidative phosphorylation during recovery is primarily used to resynthesize creatine phosphate, which typically takes just a few minutes.
  2. Lactate Removal
    • Lactate produced during anaerobic metabolism is converted back into pyruvate, which can either:
      • Enter oxidative phosphorylation to produce ATP, or
      • Be transported to the liver and converted into glucose (Cori cycle), replenishing glycogen stores in muscles and liver.
    • This process can take several hours.
  3. Glycogen Replenishment
    • If glycogen stores have been significantly depleted (e.g., after a marathon), full recovery may take up to a day or more and depends on adequate carbohydrate intake.
  4. EPOC (Excess Post-Exercise Oxygen Consumption)
    • The elevated oxygen consumption after exercise supports:
      • Restoring creatine phosphate and glycogen reserves.
      • Removing lactate.
      • Returning body temperature and hormone levels (e.g., adrenaline/epinephrine) to baseline.
    • EPOC is therefore more than just “repaying” oxygen; it reflects a general metabolic reset of the body after strenuous activity.

👉 Practical Note for Trainers:

  • Short, high-intensity exercise (like sprinting or weightlifting) creates a large O₂ debt that is repaid quickly (minutes).
  • Long, exhaustive exercise (like marathon running) requires longer recovery (hours to a full day), not just for oxygen balance but for nutrient and glycogen restoration.
  • Recovery nutrition (especially carbohydrate intake) is crucial to speed up glycogen replenishment.

Types of Skeletal Muscle Fibers

Skeletal muscle fibers are categorized into three main types, based on their ATP hydrolysis rate and their primary metabolic pathways for ATP resynthesis:

  1. Slow oxidative fibers (Type I)
  2. Fast oxidative fibers (Type IIa)
  3. Fast glycolytic fibers (Type IIx)

Comparison of Slow and Fast Fibers

  • ATPase activity:
    Fast fibers have higher myosin ATPase activity than slow fibers. This means they hydrolyze ATP faster, allowing quicker cross-bridge cycling and contraction.
  • Contraction speed:
    • Fast fibers reach peak tension in 15–40 ms.
    • Slow fibers reach peak tension in 50–100 ms.
  • Determinants of contraction speed:
    1. The load applied (force-velocity relationship).
    2. Myosin ATPase activity.

Comparison of Oxidative and Glycolytic Fibers

  • ATP synthesis capacity:
    • Oxidative fibers: High capacity for ATP synthesis through oxidative phosphorylation. They are more resistant to fatigue.
    • Glycolytic fibers: Rely mainly on glycolysis, producing ATP rapidly but less efficiently, leading to faster fatigue.
  • Mitochondria:
    • Oxidative fibers contain many mitochondria.
    • Glycolytic fibers have few mitochondria.
  • Myoglobin & color:
    • Oxidative fibers are rich in myoglobin, giving them a red color (also called red fibers).
    • Glycolytic fibers have low myoglobin, making them pale or white fibers.
  • Capillary supply:
    • Oxidative fibers have a dense capillary network, ensuring good oxygen delivery.
    • Glycolytic fibers have fewer capillaries, as they depend less on oxygen.
  • Fuel storage:
    • Oxidative fibers mainly use fatty acids and glucose with steady O₂ supply.
    • Glycolytic fibers store large amounts of glycogen, necessary for rapid ATP production during anaerobic activity.

 

Characteristics of Skeletal Muscle Fiber Types

Characteristic Slow Oxidative Fibers (Type I) Fast Oxidative Fibers (Type IIa) Fast Glycolytic Fibers (Type IIx)
Myosin ATPase activity Low High High
Contraction speed Slow Fast Fast
Fatigue resistance High Moderate Low
Oxidative phosphorylation capacity High High Low
Glycolytic enzyme content Low Moderate High
Mitochondria Many Many Few
Capillaries Many Many Few
Myoglobin content High High Low
Fiber color Red Red White
Glycogen content Low Moderate High

 

Muscle Fiber Types and Genetic Factors

In humans, most muscles contain a mixture of all three fiber types. The proportion of each type in a given muscle depends primarily on the muscle’s function. Muscles that must perform low-intensity, prolonged contractions without fatiguing easily (e.g., the postural muscles of the back and the leg muscles that support body weight) have a high percentage of slow oxidative fibers. By contrast, fast glycolytic fibers dominate in the muscles of the arms, which are often required to produce rapid and powerful movements, such as lifting heavy objects.

The percentage of fiber types not only varies between different muscles within an individual but also between individuals. Athletes genetically endowed with a higher proportion of fast glycolytic fibers often excel in sprinting and explosive sports, while those with more slow oxidative fibers are better suited for endurance events such as the marathon. Of course, success in any sport depends not only on genetics but also on multiple other factors, including the type and intensity of training.

Importantly, the mechanical and metabolic properties of muscle fibers can change significantly in response to the demands placed upon them. Muscle fibers adapt to the functional requirements imposed through different forms of training. Distinct exercise types induce different neural activation patterns in the engaged muscles. Over time, these patterns drive adaptive changes in the fibers, making them more efficient at meeting functional demands. These adaptations mainly affect:

  1. Their capacity for aerobic metabolism
  2. Their fiber diameter

 

Improvement of Oxidative Capacity

Regular aerobic endurance exercise, such as swimming or jogging, promotes metabolic adaptations in oxidative fibers, since these are the fibers primarily recruited during such activities. For example, the number of capillaries supplying blood to the fibers increases, as does the number of mitochondria within them. These changes allow muscles to utilize oxygen more efficiently, enabling them to sustain prolonged activity without fatigue. In this case, however, no change in muscle size is observed.

Muscle Hypertrophy

Muscle size can increase through regular, short-duration, high-intensity anaerobic resistance training (e.g., weightlifting). The increase in muscle size, or hypertrophy, is due mainly to the enlargement of fast glycolytic fibers, which are recruited during strong, high-force contractions. This enlargement is primarily caused by the increased synthesis of actin and myosin filaments, enhancing the fiber’s capacity for cross-bridge cycling and thus its contractile strength.
Mechanical stress from resistance training activates signaling proteins within the fibers, which in turn activate genes responsible for producing contractile proteins. Intense resistance training can double or even triple muscle volume. Hypertrophied muscles are better adapted for powerful, short-duration contractions, but their endurance does not improve.

The Role of Testosterone

Muscle fibers in men generally have a larger diameter, making their muscles bigger and stronger than those of women, even without resistance training. This difference is largely due to the hormone testosterone, a steroid hormone secreted predominantly in males. Testosterone promotes the synthesis of actin and myosin proteins.

Fiber-Type Transformation

All muscle fibers within a single motor unit are either slow or fast. However, the two subtypes of fast-twitch fibers (oxidative and glycolytic) can transform into one another depending on the type of training performed—that is, based on the functional demands repeatedly imposed by their motor neurons. In contrast, slow-twitch and fast-twitch fibers cannot convert into one another.

Limited Repair Capacity of Muscles

When a muscle is damaged, limited regeneration is possible, even though muscle cells themselves cannot divide mitotically to replace lost cells. Near the surface of muscles lies a small population of muscle stem cells known as satellite cells, which normally remain in a dormant state.
When a fiber is damaged, local signals activate these satellite cells, which divide and produce myoblasts (the same undifferentiated cells that form muscle fibers during embryonic development). These myoblasts fuse into large, multinucleated cells that immediately begin synthesizing the intracellular components of mature fibers, eventually differentiating into fully functional muscle fibers. However, in cases of severe injury, this repair mechanism is insufficient to replace all the lost fibers.

Rigor Mortis

Each cross-bridge cycle requires a new ATP molecule to bind to myosin in order to release it from actin. Although ATP is not hydrolyzed during this detachment step, its presence is essential. The importance of ATP becomes clear in the phenomenon of rigor mortis.
Rigor mortis is the generalized stiffening of skeletal muscles after death, beginning about 3–4 hours postmortem and completing within roughly 12 hours. After death, calcium concentration in the cytoplasm rises because cell membranes no longer maintain ionic gradients and calcium leaks from the sarcoplasmic reticulum. Elevated Ca²⁺ levels shift troponin and tropomyosin, exposing actin’s binding sites and allowing myosin cross-bridges (which were “primed” with ATP before death) to attach. Because ATP can no longer be produced, actin and myosin cannot detach, locking the filaments together and producing stiffness. Rigor mortis gradually dissipates over the following days as muscle proteins degrade.

 

Control of Motor Activity

The control of motor activity is carried out through three categories of neural signals transmitted to the motor neurons of different muscles:

  1. Signals from spinal reflex arcs, originating from afferent neurons.
  2. Signals from the corticospinal (pyramidal) motor system, which begins in the primary motor cortex and regulates precise, fine movements of the hands.
  3. Signals from the multineuronal (extrapyramidal) motor system, which extends from the brainstem and regulates posture through involuntary movements of large muscle groups in the trunk and limbs. The output of the brainstem is influenced by the cerebellum, basal ganglia, and cerebral cortex.

Effective regulation of motor commands requires continuous feedback, especially information about changes in muscle length (monitored by muscle spindles) and muscle tension (monitored by Golgi tendon organs).

Motor units define motor activity, ranging from postural contractions and stereotyped movements (e.g., walking) to highly skilled movements (e.g., gymnastics). Regardless of complexity, movement is determined by neural inputs to motor neurons, which then trigger muscle fiber contractions.

Neural Inputs to Motor Neurons

Three categories of neural inputs affect motor neurons and regulate excitation of the muscle fibers they innervate:

  1. Afferent signals from sensory neurons – transmitted via interneurons in the spinal cord, forming spinal reflex arcs.
  2. Signals from the primary motor cortex – pyramidal cells project directly to motor neurons (or local interneurons) in the spinal cord. These fibers form the corticospinal (pyramidal) motor system, responsible for voluntary control.
  3. Signals from the brainstem – part of the extrapyramidal (multineuronal) system, a network of interconnected brain regions. It involves the reticular formation, influenced by the motor cortex, cerebellum, and basal ganglia, as well as premotor and supplementary motor areas via the thalamus.

The primary motor cortex and brainstem are the only regions that directly influence motor neurons. Other brain regions regulate motor commands indirectly.

Reflexes and Motor Systems

  • Spinal reflexes are crucial for posture and protective movements (e.g., withdrawal reflex).
  • The corticospinal system governs fine, voluntary movements of the hands and fingers (e.g., texting on a phone).
  • The extrapyramidal system governs posture and large, involuntary movements of trunk and limb muscles.
  • Both systems interact and overlap—for example, voluntary thumb movements when texting also involve subconscious postural adjustments to hold the phone.

Excitatory vs. Inhibitory Inputs

Motor neurons receive both excitatory and inhibitory inputs. Smooth and coordinated movement depends on balancing these signals.

  • Loss of inhibitory input → spastic paralysis (increased muscle tone, exaggerated reflexes).
  • Loss of excitatory input → flaccid paralysis (limp muscles, loss of voluntary control, reflexes remain).
  • Damage to the motor cortex → paralysis on the opposite side of the body (hemiplegia).
  • Spinal cord injury → flaccid paralysis below the lesion, leading to quadriplegia (all four limbs) or paraplegia (lower limbs).
  • Destruction of motor neurons (cell bodies or axons) → flaccid paralysis and loss of reflexes.
  • Damage to the cerebellum or basal ganglia → clumsy, uncoordinated movements, but not paralysis.
  • Damage to premotor or supplementary motor areas → impaired planning and initiation of voluntary movements.

Sensory Feedback and Proprioception

Coordinated skeletal muscle activity depends on afferent input:

  • Simple reflexes (e.g., touching a hot surface → withdrawal).
  • Complex tasks (e.g., catching a ball), where the CNS integrates visual input and proprioceptive feedback to plan sequential movements.

Proprioceptive receptors provide continuous information about body position and movement:

  • Muscle spindles (length changes).
  • Golgi tendon organs (tension changes).
  • Additional inputs from joints, vestibular system, eyes, and skin.

Muscle Spindles

Muscle spindles are bundles of intrafusal fibers enclosed in a connective tissue capsule, aligned parallel to regular extrafusal fibers. Unlike extrafusal fibers (contractile along their length), intrafusal fibers have a non-contractile central region.

  • Innervated by both sensory afferents and gamma motor neurons.
  • Primary endings detect changes in length and rate of stretch.
  • Secondary endings detect static length only.
  • They play a central role in the stretch reflex.

Stretch Reflex

When a muscle is stretched, spindles are activated, increasing afferent firing. This excites alpha motor neurons, causing contraction of the same muscle—a negative feedback mechanism resisting further stretch.

  • Classic example: patellar (knee-jerk) reflex, where tapping the patellar tendon stretches the quadriceps, leading to sudden leg extension.
  • Clinical importance: reflex testing indicates proper functioning of spindles, afferents, motor neurons, synapses, and neuromuscular junctions.

Stretch reflexes stabilize posture. For example:

  • Quadriceps reflex keeps the knee extended during standing and walking.
  • Biceps reflex helps maintain grip when holding or filling a glass.

Coactivation of Alpha and Gamma Motor Neurons

During voluntary or reflex contractions, alpha motor neurons activate extrafusal fibers while gamma motor neurons adjust intrafusal fiber tension. This coactivation ensures spindle sensitivity to stretch is maintained even as the muscle shortens.

  • If load is heavier than expected, spindles signal alpha motor neurons to increase contraction.

Golgi Tendon Organs

Located in tendons, these receptors detect tension rather than length. Each organ consists of afferent fibers interwoven with collagen bundles.

  • When tension increases, collagen stretches, compressing the afferent endings, which fire in proportion to tension.
  • Information is relayed to the brain for unconscious movement regulation and conscious awareness of muscle force.
  • Unlike spindles, Golgi organs do not trigger reflexes directly—they act as sensors, preventing excessive tension through higher-level control.

 

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