Skeletal Muscle Structure, Function, and Fatigue

Comprehensive review flashcards covering skeletal muscle physiology, connective tissue organization, cross-bridge cycling, motor unit recruitment, force regulation, fiber typing, sites and mechanisms of fatigue, DOMS, and muscle cramps.

How many skeletal muscles are in the human body, and what percentage of total body weight do they account for?

The body contains over $400$ skeletal muscles, which account for $40\text{--}50\%$ of total body weight.

What are the primary functions and characteristics of skeletal muscle?

Functions include force production (for locomotion, breathing, and postural support) and heat production during cold stress. Key characteristics are irritability, contractility, extensibility, and elasticity.

What are the distinguishing characteristics of Type I muscle fibers?

Type I fibers are red, tonic, slow-twitch, and slow-oxidative; they are rich in myoglobin ($\text{Mb}$), have high mitochondrial content and fatigue resistance, low ATPase activity and $V_{\max}$, high efficiency, and are adapted for long, continuous, low-intensity contractions.

What are the distinguishing characteristics of Type IIx muscle fibers?

Type IIx fibers are white, phasic, fast-twitch, and fast-glycolytic; they have high phosphocreatine ($\text{CP}$) content, low mitochondrial density and fatigue resistance, the highest ATPase activity and $V_{\max}$, low efficiency, and are adapted for short, high-intensity work.

How do Type IIa muscle fibers compare to Type I and Type IIx fibers in terms of characteristics?

Type IIa fibers are intermediate (fast-oxidative glycolytic); they feature high/moderate mitochondria and fatigue resistance, use a combination energy system, have high ATPase activity and $V_{\max}$, moderate efficiency, and high specific tension.

How does muscle fiber type distribution typically differ between nonathletes, power athletes, and endurance athletes?

Nonathletes have approximately $50\%$ slow and $50\%$ fast fibers; power athletes (e.g., sprinters) have a high percentage of fast fibers; endurance athletes (e.g., distance runners) have a high percentage of slow fibers.

What is an isometric muscle contraction, and what are typical examples?

An isometric contraction occurs when the muscle exerts force without changing its length (e.g., pulling against an immovable object or actions of postural muscles).

What is the difference between concentric and eccentric isotonic muscle actions?

In concentric action, muscle length decreases (shortens) during force production; in eccentric action, muscle length increases while producing force.

What are the three connective tissue layers surrounding skeletal muscle, and what do they enclose?

Epimysium surrounds the entire muscle; Perimysium surrounds bundles of muscle fibers called fascicles; Endomysium surrounds individual muscle fibers.

What are satellite cells and what is their functional importance?

Satellite cells are muscle stem cells that play a key role in muscle growth and repair by increasing the number of nuclei. This expands the myonuclear domain (cytoplasm supported by each nucleus) to allow greater protein synthesis during adaptations to strength training.

What does the Principle of the Sliding Filament state?

Sarcomere length shortens during contraction, but the individual lengths of actin (thin) and myosin (thick) filaments do not change.

What is a motor unit and a motor end plate?

A motor unit consists of a motor neuron and all the muscle fibers it innervates. A motor end plate is the pocket formed around the motor neuron terminal by the sarcolemma.

What are the sequential steps of muscle excitation at the neuromuscular junction?

1. An action potential in the motor neuron causes the release of acetylcholine ($\text{ACh}$) into the synaptic cleft; 2. $\text{ACh}$ binds to receptors on the motor end plate, causing depolarization that travels down transverse tubules ($\text{T-tubules}$) to stimulate $\text{Ca}^{2+}$ release from the sarcoplasmic reticulum ($\text{SR}$).

What role does $\text{Ca}^{2+}$ play in the transition from a weak to a strong cross-bridge binding state?

$\text{Ca}^{2+}$ binds to troponin, triggering a conformational shift in tropomyosin that uncovers the active binding sites on actin, allowing myosin cross-bridges to form a strong binding state.

What causes the mechanical cross-bridge movement (power stroke) and the detachment of myosin from actin?

The release of inorganic phosphate ($\text{P}_i$) from myosin causes the cross-bridge movement (power stroke). Subsequent binding of ATP to myosin breaks the cross-bridge, returning it to a weak binding state.

How does skeletal muscle blood supply adapt during exercise?

Oxygen uptake increases by up to $70\times$, capillary beds undergo rapid dilation, up to $4000\,\text{capillaries}$ can deliver blood to each $\text{mm}^2$ of muscle, and exercise training increases overall capillary density.

According to the force-velocity relationship, at what force is the maximum velocity of shortening attained?

The maximum velocity of shortening ($V_{\max}$) is greatest at the lowest force, a principle that holds true for both slow- and fast-twitch fibers.

At what movement velocity is peak power generated in skeletal muscle?

Peak power increases with velocity up to a movement speed of $200\text{--}300^\circ\cdot\text{sec}^{-1}$; beyond this velocity, power declines because force decreases sharply with further increases in speed.

What are the three phases of a muscle twitch and their approximate durations?

The latent period lasts $\sim 5\,\text{ms}$, the contraction phase (during which tension is developed) lasts $40\,\text{ms}$, and the relaxation phase lasts $50\,\text{ms}$.

What is the Size Principle of motor unit recruitment and what is the recruitment sequence?

The size principle states that the smallest motor units are recruited first because they produce larger excitatory postsynaptic potentials ($\text{EPSPs}$) and reach threshold sooner. The recruitment order is Type S (slow) $\rightarrow$ Type FR (fast, fatigue-resistant) $\rightarrow$ Type FF (fast, fatiguable).

At what percentages of $\dot{V}\text{O}_{2\max}$ are Type I, Type IIa, and Type IIx muscle fibers recruited?

Type I fibers are recruited up to $40\%\,\dot{V}\text{O}_{2\max}$, Type IIa fibers are recruited between $40\text{--}75\%\,\dot{V}\text{O}_{2\max}$, and Type IIx fibers are recruited at exercise intensities exceeding $75\%\,\dot{V}\text{O}_{2\max}$.

What three factors regulate force generation in skeletal muscle?

1. Types and number of motor units recruited (more and faster motor units produce greater force); 2. Initial muscle length ('ideal' resting length maximizes cross-bridge formation); 3. Nature/frequency of neural stimulation (simple twitch, summation, or tetanus).

How is muscle fatigue defined?

Muscle fatigue is the inability to maintain power output or force generation during repeated muscle contractions, characterized by a decrease in force production and shortening velocity.

What primary metabolic changes cause fatigue during short-term, high-intensity exercise ($\sim 60\,\text{seconds}$)?

The accumulation of lactate, $\text{H}^+$, $\text{ADP}$, $\text{P}_i$, and free radicals, which diminishes the number of cross-bridges bound to actin and increases intracellular $\text{Ca}^{2+}$ levels.

How does free radical production during exercise contribute to peripheral muscle fatigue?

Free radicals damage contractile proteins (myosin and troponin), limiting cross-bridges in the strong binding state, and depress $\text{Na}^+/\text{K}^+$ pump activity, disrupting $\text{K}^+$ homeostasis.

What physiological factors limit aerobic performance lasting $3\text{--}20\,\text{minutes}$ versus $1\text{--}4\,\text{hours}$?

Performances lasting $3\text{--}20\,\text{minutes}$ are primarily limited by $\dot{V}\text{O}_{2\max}$ (cardiac output, $\text{CaO}_2$, capillary/mitochondrial density, and Type I fiber percentage). Performances lasting $1\text{--}4\,\text{hours}$ are limited by glycogen depletion, dehydration, heat load, bioenergetics, and steady-state $\dot{V}\text{O}_2$ / running economy.

What sequence of events causes Delayed Onset Muscle Soreness (DOMS)?

1. Structural and membrane damage to muscle fibers; 2. $\text{Ca}^{2+}$ leaks from the $\text{SR}$ and accumulates in mitochondria, inhibiting ATP production; 3. Protease activation causes cellular protein degradation; 4. Inflammatory response elevates prostaglandins and histamines; 5. Edema and histamines stimulate local pain receptors (peaking at $\sim 48\,\text{hours}$).

Why is the accumulation of lactic acid considered a myth as the cause of DOMS?

Lactate levels return to baseline within $15\text{--}50\,\text{minutes}$ post-exercise, soreness is greatest following eccentric contractions rather than high-glycolytic concentric bouts, and patients with McArdle's disease (lacking glycogen phosphorylase, unable to form lactate) still develop DOMS.

What three theories explain the 'Repeated Bout Effect'?

1. Neural theory (altered motor unit recruitment across larger muscle areas); 2. Connective Tissue theory (increased intramuscular connective tissue protecting fibers); 3. Cellular theory (synthesis of protective stress proteins within muscle fibers).

What is sarcopenia and how does muscle mass decline with aging?

Sarcopenia is age-related loss of muscle mass. Approximately $10\%$ of muscle mass is lost between ages $25\text{--}50\,\text{years}$, and an additional $40\%$ is lost between ages $50\text{--}80\,\text{years}$, along with a loss of fast-twitch fibers and a relative gain in slow-twitch fibers.

What are the two proposed theories explaining exercise-related skeletal muscle cramps?

1. Dehydration and electrolyte depletion theory (sweat loss of water and $\text{Na}^+$ causes spontaneous contractions); 2. Altered neuromuscular control theory (muscle fatigue causes increased muscle spindle activity and impaired Golgi tendon organ inhibitory drive, increasing motor neuron firing).

What four methods are used to determine skeletal muscle fiber types?

1. Muscle biopsy; 2. Myosin ATPase staining (Type I stains darkest, IIa lightest, IIx intermediate); 3. Immunohistochemical staining (selective antibodies binding specific myosin proteins); 4. Gel electrophoresis (separating specific myosin heavy chain isoforms).