Week 3 Flashcards
Functions of the Nervous System?
Controlsinternal environment(in coordination with the endocrine system).
Regulatesvoluntary movement.
Processes and respondsto sensory input.
Integrates spinal cord reflexes.
Facilitatesmemory and learning.
Anatomical Divisions of the Nervous System?
Central Nervous System (CNS)
Brainandspinal cord.
Peripheral Nervous System (PNS)
Neuronsoutside the CNS.
Sensory (afferent) division: Transmits impulses from receptors to CNS.
Motor (efferent) division: Transmits impulses from CNS to effectors (muscles, glands)
Structure of a Neuron?
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
Functional organisation of the nervous system?
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
Multiple Sclerosis (MS)?
Autoimmune disorderthat destroysmyelin sheaths, leading to:
- Muscle weakness
- Fatigue
- Loss of motor control
- Poor balance
- Depression
Exercise trainingcan improvefunctional capacityandquality of life.
Electrical Activity in Neurons?
- Negative chargeinside the cell at rest (40 to -75 mV in neurons).
- Maintained by:
- Selective permeabilityof the membrane.
- 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
- Depolarization:
- Na+ channels open, Na+ rushesintothe cell.
- Inside the neuron becomesmore positive.
- Repolarization:
- K+ exitsthe cell quickly, restoringnegative charge.
- Na+ channels close.
- All-or-None Law:
- Once an action potential starts, ittravels the full length of the neuron.
Neurotransmitters & Synaptic Transmission?
- Neurotransmitters: Chemical messengers released from thepresynaptic neuron.
- Bind to receptors onpostsynaptic neuron, causingdepolarization.
Types of Synaptic Potentials?
- 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.
- Inhibitory Postsynaptic Potentials (IPSPs)
- Causehyperpolarization(more negative potential).
- Inhibit depolarization, making neuronless likely to fire.
Sensory Information and Reflexes?
Proprioceptors – The “Sixth Sense”
- Providesensory feedbackaboutbody position and movement.
- Joint Proprioceptors
- Free nerve endings: Detect touch and pressure.
- Golgi-type receptors: Found injoint ligaments, detect movement.
- 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.
- Muscle Chemoreceptors (Metaboreceptors)
- Detect chemical changes:
- H+ ions (pH changes), CO2, and K+.
- Provide feedback toCNSfor cardiovascular and pulmonary regulation.
Key Structures of the Brain?
- Cerebrum (Cerebral Cortex)
- Controls voluntary movement.
- Storeslearned experiences.
- Processessensory input.
- Cerebellum
- Coordinatesmovement and balance.
- Brainstem (Midbrain, Pons, Medulla)
- Regulatescardiorespiratory function, posture, and muscle tone.
Sports-Related Traumatic Brain Injury (TBI)?
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
Spinal Cord and Voluntary Movement?
- 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.
Control of Voluntary Movement?
- Motor Cortex(Brain) receives input from:
- Basal nuclei(movement planning).
- Cerebellum(movement coordination).
- Thalamus(sensory integration).
Exercise and Brain Health?
Regularexercise enhances cognitive functionand protects against:
Alzheimer’s Disease, Stroke, Cognitive decline with aging
Mechanisms of Exercise Benefits?
- Stimulatesneurogenesis (new neurons).
- Improvesblood flow and vascular function.
- Reducesinflammation, hypertension, insulin resistance.
- Enhancesmood and reduces depression risk.
Main functions of skeletal muscle?
Locomotion & breathing (force production).
Postural support (stability).
Heat production (thermoregulation).
Endocrine function (hormone secretion).
Muscle Actions?
- Flexors → Decrease joint angle.
- Extensors → Increase joint angle.
- Attachment: Origin (fixed) & Insertion (moves).
Structure of Skeletal Muscle?
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.
Microstructures of muscle fibres?
- 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.
Satellite Cells & Muscle Growth?
- 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.
Neuromuscular Junction (NMJ)?
- 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.
Sliding Filament Model & Contraction Cycle?
- Muscle shortens as actin slides over myosin.
- Steps:
- Cross-bridge formation (actin-myosin binding).
- Power stroke (filament movement via ATP hydrolysis).
- Cross-bridge detachment (new ATP binds).
- Reactivation of myosin head (ATP hydrolysis resets position).
- ATP sources:
- Phosphocreatine (PCr), glycolysis, oxidative phosphorylation.
Excitation-Contraction Coupling (E-C Coupling)?
- Process:
- Action potential travels down T-tubules.
- Calcium released from SR.
- Calcium binds to troponin → Tropomyosin moves.
- Myosin binding sites on actin exposed → Cross-bridge formation.
- Contraction continues with ATP & calcium.
- When neural activity stops, calcium is pumped back into SR → Muscle relaxes.
Muscle Fatigue & Exercise-Associated Muscle Cramps (EAMC)? Solutions?
- 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.
- Heavy exercise (1-10 min):
- 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).
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).
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
Fiber Type Distribution?
- Endurance Athletes: ~70-80% Type I fibers.
- Sprinters: ~70-75% Type II fibers.
- Non-athletes: ~50% Type I, 50% Type II.
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:
- Number & type of motor units activated.
- Muscle length (optimal sarcomere overlap).
- Firing rate of motor neurons (twitch, summation, tetanus).
- Contractile history (fatigue vs. potentiation from warm-up)
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.
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.
Strength Loss with Age?
- Annual decline:
- Men: ~3–4% per year.
- Women: ~2.5–3% per year.(Goodpaster et al., 2006)
- Lower body musclesexperience greater strength losses. 40% compared to 33%
Muscle Power & Function?
- Power = Force × Velocity
- Older adultsexhibit:
- Lowermuscle power.
- Slower rateof force development.
- Higher risk offalls.
Key Study: Van Roie et al. (2018)
- Muscle power declinessignificantlywith age.
- Womentend to lose velocityfasterthan men.
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)
- By70–80 years, most individuals haveonly 60–80%of the muscle mass they had at age 30.
- Greater loss in lower limbsthan upper limbs.
Muscle Quality Decline
- Increasedfat accumulationin and around muscles:
- Intermuscular fat (IMF).
- Subcutaneous fat (SF).
- Fat infiltrationreduces muscle force production.
Key Studies:
- Older adults havemore fat & less musclein thigh muscles.(Power et al., 2014)
- Increased fat content = Lower muscle quality.
Neuromuscular Alterations
Motor Unit (MU) Changes
- Fewer motor unitswith age.
- Muscle fibres become denervated, leading to:
- Fibre atrophy.
- Fibre loss.
- Reinnervation byType I motor units(slower contractions).
- Larger motor unitscompensate 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.
Muscle Fibre Changes?
- Type II fibresshrink more thanType Ifibres.
- Total muscle fibre numbers decrease, butType I proportion remains stable.(Lexell et al., 1988)
Key Findings:
- Muscle loss ≠ Strength loss.
- Strength loss is much greaterthan muscle mass loss.(Delmonico et al., 2009)
Fatigue Resistance in Old Age?
- Older adults are less fatigablethan young adults in certain tasks.
- Due to:
- MoreType I-like fibres(slow-twitch, endurance).
- Altered neuromuscular activationpatterns.
Effect of Lifelong Exercise on Muscle Ageing?
Master Athletes & Lifelong Exercisers
- Lifelong training preservesmuscle 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 exercisedoes not preventmotor unit enlargement.
- Muscledeterioration still occurs but is less severe.
