Muscle Function in Health and Diseases

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Flashcards covering muscle function, motor control, contraction types, fatigue, fiber types, adaptation, and various muscle diseases and lesions, based on the provided lecture notes.

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28 Terms

1
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Differentiate between the three primary categories of movement generated by the motor system, providing an example for each.

The three categories are reflexive, rhythmic, and voluntary.

  • Reflexive: Involuntary, rapid, stereotyped responses to a stimulus, primarily mediated by spinal cord or brainstem circuits (e.g., knee-jerk reflex, withdrawal reflex).
  • Rhythmic: Stereotyped, repetitive movements with a central pattern generator (CPG) in the spinal cord or brainstem, initiated and modulated by higher centers (e.g., walking, breathing, chewing).
  • Voluntary: Goal-oriented, learned, and cortically-driven movements (e.g., reaching for a cup, writing).
2
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How does the origin of reflexive movements in the spinal cord and brainstem contribute to their characteristic speed and involuntary nature?

Their subcortical origin in the spinal cord and brainstem allows for rapid, direct processing and efferent signaling, bypassing conscious cortical involvement. This neural architecture facilitates quick, protective, and essential unconscious responses.

3
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Elaborate on the role of Central Pattern Generators (CPGs) in the spinal cord and brainstem for rhythmic movements.

CPGs are neural circuits within the spinal cord and brainstem capable of producing rhythmic patterns of motor output (e.g., alternating flexion/extension during locomotion) without rhythmic sensory or supraspinal input. They provide the fundamental oscillatory drive for movements like walking or breathing, which are then modulated by higher brain centers.

4
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Beyond the general motor cortex, specify key cortical areas and descending pathways primarily responsible for the initiation and execution of complex voluntary movements.

Voluntary movements primarily originate in the primary motor cortex (M1), premotor cortex, and supplementary motor area (SMA). These areas drive movement through direct pathways like the corticospinal tract and corticobulbar tract, which transmit commands to lower motor neurons.

5
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Explain how the association cortex and basal ganglia contribute to the "Motor Idea" stage of the Motor Hierarchy.

In the "Motor Idea" stage, the association cortex (e.g., prefrontal and parietal cortex) integrates sensory information and motivational states to determine the goal and overall strategy of a movement. The basal ganglia then play a critical role in selecting and initiating appropriate motor programs while suppressing unwanted ones, refining the abstract motor idea.

6
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Detail the contributions of the motor cortex and cerebellum during the "Motor Plan" stage of the Motor Hierarchy.

During the "Motor Plan" stage, the motor cortex (premotor and supplementary motor areas) translates the abstract motor idea into a detailed sequence of muscle contractions. The cerebellum integrates sensory feedback with motor commands, predicting the sensory consequences of movement and making real-time adjustments to ensure smooth, coordinated, and accurate execution, comparing desired movement with actual movement.

7
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Describe the process of "Execution" in the Motor Hierarchy, emphasizing the roles of the brainstem and spinal cord.

The "Execution" stage involves transmitting precise motor commands from the brainstem descending pathways and spinal cord to the muscles via lower motor neurons (LMNs). LMNs are the 'final common path' that directly innervate muscle fibers, translating neural signals into muscle contraction, with brainstem pathways controlling posture and gross movements, and spinal cord circuits mediating fine motor control.

8
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Define a motor unit and explain its fundamental physiological significance in muscle contraction.

A motor unit consists of a single alpha motor neuron and all the extrafusal muscle fibers it innervates. This arrangement is crucial because all muscle fibers within a single motor unit contract synchronously when the alpha motor neuron fires, serving as the indivisible functional unit of force generation.

9
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Explain the adaptive advantage of a low innervation ratio (3-6 muscle fibers per motor unit) for fine movements.

A low innervation ratio means each motor unit controls very few muscle fibers. This allows for precise, graded control of muscle force because activating a single motor unit produces a very small, discrete increase in tension, crucial for delicate tasks like eye movements or finger dexterity.

10
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Explain the functional benefit of a high innervation ratio (200-300 muscle fibers per motor unit) for gross movements.

A high innervation ratio means each motor unit controls many muscle fibers. This allows for the generation of substantial force with the activation of fewer motor neurons, making it energy-efficient for powerful, less precise movements like those in the quadriceps or gastrocnemius muscles.

11
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Justify why the Lower Motor Neuron (LMN) is termed the 'final common path' for muscle contraction.

The LMN is considered the 'final common path' because all motor commands, whether originating from reflex arcs, central pattern generators, or higher cortical centers, must ultimately converge upon and be transmitted by the alpha motor neurons (LMNs) to initiate muscle fiber contraction. No other neuron directly stimulates muscle fibers.

12
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Describe the 'size principle' of motor unit recruitment and its physiological basis in generating increasing amounts of muscle tension.

The 'size principle' states that during graded muscle contraction, motor units are recruited in an orderly fashion from smallest to largest. Small motor neurons, which innervate fewer, smaller muscle fibers, have higher input resistance and thus a smaller depolarization threshold. They are activated first by a given synaptic input, generating small, precise forces. As more force is required, larger motor neurons (with lower resistance) are recruited, activating more and larger muscle fibers to produce greater tension.

13
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Define isotonic contraction and distinguish it from isometric contraction based on force, load, and muscle length changes.

Isotonic contraction occurs when the force generated by the muscle exceeds the opposing load, resulting in muscle shortening (concentric) or lengthening (eccentric) while maintaining a relatively constant tension throughout the range of motion. In contrast, isometric contraction involves muscle tension increasing without a change in muscle length, as the force generated is less than or equal to the load.

14
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Describe the mechanical characteristics of an isometric muscle contraction, including its relationship between muscle force, external load, and muscle length.

An isometric contraction is characterized by the muscle generating force without a change in its overall length. This occurs when the external load equals or exceeds the maximal force the muscle can produce, preventing movement but causing a significant increase in internal muscle tension.

15
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Define concentric isotonic contraction and provide a common example, explaining the relationship between muscle force and load.

Concentric isotonic contraction occurs when the muscle shortens as it generates force, such that the muscle's contractile force is greater than the external load it is overcoming. A common example is the upward phase of a bicep curl or lifting a weight against gravity.

16
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Define eccentric isotonic contraction, detailing its unique mechanical characteristics and providing an illustrative example.

Eccentric isotonic contraction occurs when the muscle lengthens under tension because the external load exceeds the muscle's contractile force, causing it to resist the lengthening action. An example is slowly lowering a heavy object to the ground or the downward phase of a squat. These contractions are particularly effective at generating high forces and are associated with a higher risk of muscle damage.

17
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Mechanistically explain why eccentric (lengthening) muscle contractions are more prone to causing muscle injury and Delayed Onset Muscle Soreness (DOMS) compared to concentric contractions.

Eccentric contractions are more damaging because the muscle actively resists lengthening while force is being produced, putting significant strain on sarcomeres and cellular structures. This can lead to micro-tears in muscle fibers, disruption of the Z-disks, and inflammation, which are primary contributors to muscle injury and DOMS.

18
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Provide a comprehensive definition of muscle fatigue and briefly distinguish between central and peripheral fatigue.

Muscle fatigue is defined as the exercise-induced reduction in the ability of muscle to produce force or power. It can be categorized into:

  • Central fatigue: Involves the central nervous system, where decreased motor drive from the brain leads to reduced muscle activation.
  • Peripheral fatigue: Occurs at the neuromuscular junction or directly within the muscle fibers due to factors like accumulation of metabolic byproducts, ion imbalances (K^+), and depletion of energy substrates (ATP, glycogen).
19
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Detail at least three distinct physiological mechanisms contributing to muscular fatigue at the cellular or biochemical level.

Common physiological causes of muscular fatigue include:

  1. Metabolite Accumulation: Accumulation of inorganic phosphate (P_i) from ATP hydrolysis, H^+ from lactic acid (leading to decreased pH), and ADP can directly impair contractile protein function, calcium release/reuptake, and enzyme activity.
  2. Ion Imbalances: Alterations in intracellular (K^+) and (Na^+) concentrations can disrupt muscle fiber excitability and propagation of action potentials.
  3. Glycogen Depletion: Exhaustion of muscle glycogen stores, especially during prolonged exercise, limits the availability of substrate for ATP production.
  4. Neuromuscular Junction Fatigue: Reduced acetylcholine release or receptor sensitivity can impair transmission.
20
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Identify the muscle fiber type known as red muscle fibers or Type I, and list its key metabolic and contractile characteristics.

Slow-oxidative fibers (Type I) are characterized by:

  • Metabolism: High capacity for oxidative phosphorylation (aerobic metabolism), abundant mitochondria, high myoglobin content (red color), extensive capillary supply.
  • Contraction: Slow contractile speed, high fatigue resistance, low ATPase activity. Best suited for prolonged, low-intensity activity.
21
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Identify the muscle fiber type known as white muscle fibers or Type IIb, and list its key metabolic and contractile characteristics.

Fast-glycolytic fibers (Type IIb, or often Type IIx in humans) are characterized by:

  • Metabolism: High capacity for glycolysis (anaerobic metabolism), few mitochondria, low myoglobin content (white color), sparse capillary supply.
  • Contraction: Fast contractile speed, low fatigue resistance, high ATPase activity. Best suited for short-duration, high-intensity power activities.
22
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Elaborate on why oxidative phosphorylation is the primary ATP synthesis pathway for slow-oxidative (Type I) muscle fibers and its functional consequence.

Oxidative phosphorylation is dominant in Type I fibers due to their rich supply of mitochondria, extensive capillary networks, and high myoglobin content for oxygen delivery. This aerobic pathway allows for sustained ATP production, making these fibers highly resistant to fatigue and ideal for endurance activities.

23
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Elaborate on why glycolysis is the primary ATP synthesis pathway for fast-glycolytic (Type IIb) muscle fibers and its functional consequence.

Glycolysis is the primary ATP synthesis pathway for Type IIb fibers because they possess a high concentration of glycolytic enzymes and can rapidly produce ATP without oxygen. This enables quick, powerful contractions but leads to rapid fatigue due to lactate accumulation and depletion of glycogen stores.

24
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Describe the comprehensive physiological adaptations observed in slow-oxidative (Type I) muscle fibers in response to chronic endurance aerobic exercise.

Regular endurance aerobic exercise induces significant adaptations in Type I fibers:

  • Increased mitochondrial density and size, enhancing oxidative phosphorylation capacity.
  • Proliferation of capillaries, improving oxygen and nutrient delivery.
  • Elevated myoglobin content, boosting oxygen storage within muscle.
  • Enhanced activity of oxidative enzymes.
    These changes collectively augment aerobic ATP production, leading to substantially increased resistance to fatigue and improved endurance capacity.
25
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Describe the multifaceted physiological adaptations characteristic of fast-glycolytic (Type IIb) muscle fibers in response to short-duration, high-intensity resistance training.

Short-duration, high-intensity exercise primarily drives adaptations in Type IIb fibers, leading to:

  • Increased synthesis of glycolytic enzymes, bolstering anaerobic ATP production.
  • Muscle fiber hypertrophy (increase in diameter) due to increased synthesis of contractile proteins (actin and myosin).
  • An elevated number of myofibrils and cross-bridges.
    These adaptations collectively result in greater maximal force production and increased power output, although fatigue resistance does not significantly improve.
26
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Define Muscular Dystrophy, highlighting its underlying genetic nature and the progressive physiological consequence.

Muscular Dystrophy (MD) is a group of genetic, inherited disorders characterized by progressive weakness and degeneration of skeletal muscles. It typically stems from mutations in genes (e.g., dystrophin gene in Duchenne MD) responsible for producing proteins essential for maintaining the integrity and function of muscle fibers, leading to their gradual breakdown and replacement by fibrous and fatty tissue, resulting in loss of force-generating capacity.

27
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Describe the pathophysiology of Myasthenia Gravis, focusing on the specific immunological attack and its resulting impact on neuromuscular transmission.

Myasthenia Gravis is an autoimmune disorder where the immune system mistakenly produces antibodies that attack and destroy or block the abundant acetylcholine (ACh) receptors on the postsynaptic membrane of the motor end plate at the neuromuscular junction. This reduction in functional ACh receptors impairs the ability of ACh released from the motor neuron to fully depolarize the muscle fiber and initiate action potentials, leading to profound and fluctuating muscle weakness.

28
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Explain the characteristic clinical manifestations of a Lower Motor Neuron Lesion (LMNL) on muscle tone, deep tendon reflexes, and muscle morphology, providing the physiological rationale for these changes.

An LMNL disrupts the 'final common path' from the central nervous system to the muscle. This results in:

  • Hypotonia or Atonia (Flaccidity): Due to the loss of excitatory input from the LMN to the muscle, the muscle loses its resting tension.
  • Hyporeflexia or Areflexia: The reflex arc is interrupted, as the LMN is an integral component, preventing the muscle from contracting in response to stretch.
  • Muscle Atrophy: Denervated muscles lose trophic support and undergo severe wasting.
  • Fasciculations/Fibrillations: Spontaneous contractions of muscle fibers or bundles may occur due to denervation sensitivity.