Week 3 Flashcards

(36 cards)

1
Q

Functions of the Nervous System?

A

Controls the internal environment (in coordination with the endocrine system)

Regulates voluntary movement

Processes and responds to sensory input

Integrates spinal cord reflexes

Facilitates memory and learning

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2
Q

Anatomical Divisions of the Nervous System?

A
  1. Central Nervous System (CNS):
    Composed of the brain and spinal cord

Responsible for integration and processing of information

  1. Peripheral Nervous System (PNS):
    Consists of all neurons outside the CNS

Divided into:

Sensory (afferent) division: Carries signals to the CNS from receptors

Motor (efferent) division: Carries signals from the CNS to effectors (muscles and glands)

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3
Q

Structure of a Neuron?

A

Axon: Transmitsaction potentialsaway from the cell body.

Schwann cells: Insulate axon by forming themyelin sheath, which speeds up signal transmission.

Synapse: Connection between the axon of one neuron and the dendrite of another.

Also, Larger axon diameterandthicker myelin sheath=faster signal transmission

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4
Q

Functional organisation of the nervous system?

A

Input = Sensory nervous system ( detects stimuli and transmits information from the receptors to CNS)

Branches into:

  • Somatic sensory - sensory input consciously perceived from receptors eg eyes, ears, skin
  • Visceral sensory - not consciously perceived from receptors of blood vessels and internal organs eg heart

Output = Motor nervous system - initiates and transmits information from the CNS to effectors

Branches into:

  • Somatic motor - motor output that is consciously or voluntarily controlled, effects is skeletal muscle
  • Autonomic motor - not consciously or is involuntarily controlled, effects are cardiac, and smooth muscle and glands
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5
Q

Multiple Sclerosis (MS)?

A

Autoimmune disorderthat destroysmyelin sheaths, leading to:
- Muscle weakness
- Fatigue
- Loss of motor control
- Poor balance
- Depression
Exercise trainingcan improvefunctional capacityandquality of life.

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6
Q

Electrical Activity in Neurons?

A
  • Negative chargeinside the cell at rest (40 to -75 mV in neurons).
  • Maintained by:
    1. Selective permeabilityof the membrane.
    2. Ion concentration differences(Na+, K+, Cl-).

🔄Sodium-Potassium Pump

  • Activelymoves 3 Na+ out and 2 K+ intothe cell, maintainingnegative RMP.

Action Potential (AP) – The Nerve Impulse

  1. Depolarization:
    • Na+ channels open, Na+ rushesintothe cell.
    • Inside the neuron becomesmore positive.
  2. Repolarization:
    • K+ exitsthe cell quickly, restoringnegative charge.
    • Na+ channels close.
  3. All-or-None Law:
    • Once an action potential starts, ittravels the full length of the neuron.
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7
Q

Neurotransmitters & Synaptic Transmission?

A
  • Neurotransmitters: Chemical messengers released from thepresynaptic neuron.
  • Bind to receptors onpostsynaptic neuron, causingdepolarization.
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8
Q

Types of Synaptic Potentials?

A
  1. Excitatory Postsynaptic Potentials (EPSPs)
    • Promote depolarization, bringing the neuroncloser to threshold.
    • Summation mechanisms:
      • Temporal summation: Rapid, repeated EPSPs from a single neuron.
      • Spatial summation: Multiple neurons releasing EPSPs simultaneously.
  2. Inhibitory Postsynaptic Potentials (IPSPs)
    • Causehyperpolarization(more negative potential).
    • Inhibit depolarization, making neuronless likely to fire.
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9
Q

Sensory Information and Reflexes?

A

Proprioceptors – The “Sixth Sense”

  • Providesensory feedbackaboutbody position and movement.
  1. Joint Proprioceptors
  • Free nerve endings: Detect touch and pressure.
  • Golgi-type receptors: Found injoint ligaments, detect movement.
  1. Muscle Proprioceptors (Mechanoreceptors)
  • Muscle spindles: Detect changes inmuscle length.
  • Golgi Tendon Organs (GTOs): Monitormuscle force, preventing excessive force generation.

💡Training adaptation: Athletes canoverride GTO inhibition, leading toincreased strength.

  1. Muscle Chemoreceptors (Metaboreceptors)
  • Detect chemical changes:
    • H+ ions (pH changes), CO2, and K+.
  • Provide feedback toCNSfor cardiovascular and pulmonary regulation.
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10
Q

Key Structures of the Brain?

A
  1. Cerebrum (Cerebral Cortex)
    • Controls voluntary movement.
    • Storeslearned experiences.
    • Processessensory input.
  2. Cerebellum
    • Coordinatesmovement and balance.
  3. Brainstem (Midbrain, Pons, Medulla)
    • Regulatescardiorespiratory function, posture, and muscle tone.
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11
Q

Sports-Related Traumatic Brain Injury (TBI)?

A

Concussions (Mild TBI)

Symptoms can bephysical, cognitive, emotional, or sleep-related:
Physical - Headache, nausea, vomiting, vision issues
Cognitive - Memory loss, confusion, slow responses
Emotional - Irritability, sadness, nervousness
Sleep - Insomnia, excessive sleepiness

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12
Q

Spinal Cord and Voluntary Movement?

A
  • 45 cm long, encased and protected by bony vertebral
    column, and attaches to brainstem
  • Major conduit for two-way transmission of information from
    skin, joints, and muscles to brain
  • Major pathway forsensory and motor information.
  • Containsmotor, sensory, and interneurons.
  • Spinal tuning: Central networksrefine voluntary movement.
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13
Q

Control of Voluntary Movement?

A
  • Motor Cortex(Brain) receives input from:
  • Basal nuclei(movement planning).
  • Cerebellum(movement coordination).
  • Thalamus(sensory integration).
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14
Q

Exercise and Brain Health?

A

Regularexercise enhances cognitive functionand protects against:
Alzheimer’s Disease, Stroke, Cognitive decline with aging

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15
Q

Mechanisms of Exercise Benefits?

A
  • Stimulatesneurogenesis (new neurons).
  • Improvesblood flow and vascular function.
  • Reducesinflammation, hypertension, insulin resistance.
  • Enhancesmood and reduces depression risk.
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16
Q

Main functions of skeletal muscle?

A

Locomotion & breathing (force production).
Postural support (stability).
Heat production (thermoregulation).
Endocrine function (hormone secretion).

17
Q

Muscle Actions?

A
  • Flexors → Decrease joint angle.
  • Extensors → Increase joint angle.
  • Attachment: Origin (fixed) & Insertion (moves).
18
Q

Structure of Skeletal Muscle?

A

Connective Tissue Layers: Surrounding skeletal muscle
- Epimysium → Surrounds the entire muscle.
- Perimysium → Surrounds fascicles (muscle fiber bundles).
- Endomysium → Surrounds individual muscle fibers.
- Basement membrane → Below endomysium.
- Sarcolemma → Muscle cell membrane.

19
Q

Microstructures of muscle fibres?

A
  • Myofibrils & Contractile Proteins:
    • Actin (thin filament) & Myosin (thick filament).
    • Sarcomere structure: Z line, M line, H zone, A band, I band.
  • Tubular Systems:
    • Sarcoplasmic Reticulum (SR): Calcium storage.
    • Terminal Cisternae: Expanded SR regions.
    • Transverse Tubules (T-tubules): Carry electrical signals.
20
Q

Satellite Cells & Muscle Growth?

A
  • Satellite cells aid in muscle repair and hypertrophy.
  • Myonuclear domain: Sarcoplasm controlled by one nucleus.
  • Hypertrophy → More myonuclei → Greater protein synthesis.
  • Atrophy → Fewer myonuclei → Decreased muscle function.
21
Q

Neuromuscular Junction (NMJ)?

A
  • Junction between motor neuron & muscle fiber.
  • Key Components:
    • Motor end plate → Sarcolemma pocket around the neuron.
    • Neuromuscular cleft → Small gap for neurotransmitter exchange.
    • Acetylcholine (ACh):
      • Released from neuron → Binds to receptors → Muscle depolarization → Contraction.
  • Trainability of NMJ:
    • Larger NMJ, more synaptic vesicles (ACh), more ACh receptors → Enhanced performance.
22
Q

Sliding Filament Model & Contraction Cycle?

A
  • Muscle shortens as actin slides over myosin.
  • Steps:
    1. Cross-bridge formation (actin-myosin binding).
    2. Power stroke (filament movement via ATP hydrolysis).
    3. Cross-bridge detachment (new ATP binds).
    4. Reactivation of myosin head (ATP hydrolysis resets position).
  • ATP sources:
    • Phosphocreatine (PCr), glycolysis, oxidative phosphorylation.
23
Q

Excitation-Contraction Coupling (E-C Coupling)?

A
  • Process:
    1. Action potential travels down T-tubules.
    2. Calcium released from SR.
    3. Calcium binds to troponin → Tropomyosin moves.
    4. Myosin binding sites on actin exposed → Cross-bridge formation.
    5. Contraction continues with ATP & calcium.
    6. When neural activity stops, calcium is pumped back into SR → Muscle relaxes.
24
Q

Muscle Fatigue & Exercise-Associated Muscle Cramps (EAMC)? Solutions?

A
  • Muscle Fatigue Causes:
    • Heavy exercise (1-10 min):
      • ↓ Calcium release from SR.
      • Accumulation of Pi, H+, free radicals → Weakens actin-myosin interaction.
    • Moderate exercise (>60 min):
      • Glycogen depletion → Less ATP production.
      • Increased radical production damages muscle proteins.
  • EAMC Causes:
    • Not primarily electrolyte imbalance.
    • Likely due to hyperactive spinal motor neurons.
    • Altered muscle spindle & Golgi tendon organ activity.
  • Solutions:
    • Stretching.
    • Activating transient receptor potential channels (mouth/throat stimulation).
25
Muscle Actions & Contraction Types?
- Dynamic (Isotonic) - Concentric: Muscle shortens (lifting a weight). - Eccentric: Muscle lengthens (lowering a weight). - Static (Isometric) - No length change (planks, wall sits). - Isokinetic: Constant velocity contractions (dynamometer testing).
26
Muscle fibre type characteristics ? and which each fibre type is?
Mitochondria density Fatigue resistance Energy systems ATPase Activity Contraction speed Efficiency Specific tension Type I - High High Aerobic Low Slow High Moderate Type IIa - Moderate Moderate Mixed High Fast Moderate High Type IIx - Low Low Anaerobic Highest Fastest Low High
27
Fiber Type Distribution?
- Endurance Athletes: ~70-80% Type I fibers. - Sprinters: ~70-75% Type II fibers. - Non-athletes: ~50% Type I, 50% Type II.
28
Motor Units & Force Regulation?
- Motor Unit = Motor Neuron + All Innervated Muscle Fibers. - Henneman's Size Principle: - Small units (low force, fatigue-resistant) recruited first. - Large units (high force, fatigue-prone) recruited as needed. - Force Regulation Factors: 1. Number & type of motor units activated. 2. Muscle length (optimal sarcomere overlap). 3. Firing rate of motor neurons (twitch, summation, tetanus). 4. Contractile history (fatigue vs. potentiation from warm-up)
29
Force-Velocity & Force-Power Relationships?
- Force-Velocity: - Higher force → Lower velocity. - Fast-twitch fibers = Greater velocity at any given force. - Force-Power: - Peak power at 200-300°/sec. - Beyond this, force decreases at higher speeds.
30
Muscle Aging & Disease? Brief summary?
- Sarcopenia (Age-Related Muscle Loss): - 10% loss from 25-50 years. - 40% additional loss from 50-80 years. - Shift from fast to slow fibers. - Resistance training slows progression. - Cachexia (Disease-Related Muscle Loss): - Common in cancer & diabetes. - 50% of cancer patients experience severe muscle wasting. - Exercise & nutrition therapy help. - Muscular Dystrophy: - Genetic disorder causing progressive muscle fiber loss. - Duchenne MD most common in children.
31
Strength Loss with Age?
- Annual decline: - Men: ~3–4% per year. - Women: ~2.5–3% per year. *(Goodpaster et al., 2006)* - Lower body muscles experience greater strength losses. 40% compared to 33%
32
Muscle Power & Function?
- Power = Force × Velocity - Older adults exhibit: - Lower muscle power. - Slower rate of force development. - Higher risk of falls. Key Study: Van Roie et al. (2018) - Muscle power declines significantly with age. - Women tend to lose velocity faster than men.
33
Causes of Age-Related Functional Declines?
Muscle Mass Loss (Sarcopenia & Atrophy) - Muscle loss rate: - 40+ years: ~8% per decade (0.5–1% per year). - 70+ years: ~15% per decade. *(Janssen et al., 2000)* - By 70–80 years, most individuals have only 60–80% of the muscle mass they had at age 30. - Greater loss in lower limbs than upper limbs. Muscle Quality Decline - Increased fat accumulation in and around muscles: - Intermuscular fat (IMF). - Subcutaneous fat (SF). - Fat infiltration reduces muscle force production. Key Studies: - Older adults have more fat & less muscle in thigh muscles. *(Power et al., 2014)* - Increased fat content = Lower muscle quality. Neuromuscular Alterations Motor Unit (MU) Changes - Fewer motor units with age. - Muscle fibres become denervated, leading to: - Fibre atrophy. - Fibre loss. - Reinnervation by Type I motor units (slower contractions). - Larger motor units compensate but reduce fine motor control. Key Studies: - Campbell et al. (1973): Fewer motor units = Less force. - Wilkinson et al. (2018): Reinnervation by Type I units leads to less efficient muscle function. Denervation & Reinnervation - Type II fibres either: - Atrophy (due to lack of innervation). - Get reinnervated by Type I motor units. - Reinnervated fibres are less powerful but more fatigue-resistant. Effects: - More fatigue resistance. - Less force & slower movements → Higher fall risk.
34
Muscle Fibre Changes?
- Type II fibres shrink more than Type I fibres. - Total muscle fibre numbers decrease, but Type I proportion remains stable. *(Lexell et al., 1988)* Key Findings: - Muscle loss ≠ Strength loss. - Strength loss is much greater than muscle mass loss. *(Delmonico et al., 2009)*
35
Fatigue Resistance in Old Age?
- Older adults are less fatigable than young adults in certain tasks. - Due to: - More Type I-like fibres (slow-twitch, endurance). - Altered neuromuscular activation patterns.
36
Effect of Lifelong Exercise on Muscle Ageing?
Master Athletes & Lifelong Exercisers - Lifelong training preserves muscle function but does not prevent all ageing effects. - Master athletes maintain: - Higher muscle power. - Better Type I fibre preservation. - Greater force production (similar to people 30 years younger). Key Study: Piasecki et al. (2016) - Lifelong exercise does not prevent motor unit enlargement. - Muscle deterioration still occurs but is less severe.