Week 3 Flashcards
(45 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
2
Q
Anatomical Divisions of the Nervous System?
A
- Central Nervous System (CNS):
Composed of the brain and spinal cord
Responsible for integration and processing of information
- 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)
3
Q
Structure of a Neuron?
A
Axon: Carries action potentials away from the cell body.
Schwann cells: Form the myelin sheath, insulating the axon and speeding up signal transmission.
Synapse: Junction between the axon of one neuron and the dendrite of another.
Signal speed increases with larger axon diameter and thicker myelin sheath
4
Q
Functional organisation of the nervous system?
A
- Input → Sensory Nervous System
- Detects stimuli and transmits information to the CNS.
- Somatic Sensory:
Consciously perceived input (e.g. eyes, ears, skin). - Visceral Sensory:
Not consciously perceived; from internal organs (e.g. heart, blood vessels).
- Output → Motor Nervous System
- Initiates and transmits information from the CNS to effectors.
- Somatic Motor:
Voluntary control of skeletal muscle. - Autonomic Motor:
Involuntary control of cardiac muscle, smooth muscle, and glands
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.
6
Q
Neuronal Electrical Activity and Action Potentials
A
Resting Membrane Potential (RMP):
- The inside of the neuron is negatively charged at rest (typically –40 to –75 mV).
Determined by:
- Selective membrane permeability
- Ion concentration gradients (Na⁺, K⁺, Cl⁻)
Sodium–Potassium Pump (Na⁺/K⁺ ATPase):
- Actively moves 3 Na⁺ out and 2 K⁺ in, helping maintain the negative RMP.
Action Potential (AP) – The Nerve Impulse:
- Triggered when a stimulus is strong enough to depolarise the membrane.
Depolarisation:
- Na⁺ channels open
- Na⁺ rushes into the cell
- Inside becomes more positive
Repolarisation:
- K⁺ exits the cell rapidly
- Na⁺ channels close
- Negative charge is restored
All-or-None Law:
- Once initiated, the action potential will fire completely travelling the entire length of the neuron without diminishing.
7
Q
Neurotransmitters & Synaptic Transmission?
A
Neurotransmitters are chemical messengers released from the presynaptic neuron.
They bind to receptors on the postsynaptic neuron, leading to depolarization of the membrane.
This depolarization may initiate an action potential in the postsynaptic neuron, allowing the signal to continue.
8
Q
Types of Synaptic Potentials?
A
- 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.
9
Q
Sensory Information and Reflexes?
A
Proprioceptors (“Sixth Sense”): Provide sensory feedback about body position in space and movement based on specialised receptors.
Joint Proprioceptors:
- Free nerve endings: Detect touch & pressure
- Golgi-type receptors: Sense joint movement (in ligaments)
Muscle Proprioceptors (Mechanoreceptors):
- Muscle spindles: Detect changes in muscle length
- Golgi Tendon Organs (GTOs):
— Monitor muscle force
— Prevent excessive tension
— stimulation results in reflex relaxation of muscle
— Strength gain can reduce GTO inhibition, allowing more force
Muscle Chemoreceptors (Metaboreceptors):
- Detect chemical changes (e.g., ↑ H⁺, CO₂, K⁺)
- Send feedback to CNS to regulate cardiovascular and pulmonary responses
10
Q
Key Structures of the Brain? Roles?
A
- Cerebrum (Cerebral Cortex)
- Controls voluntary movement.
- Stores learned experiences.
- Processes sensory input.
- Cerebellum
- Coordinates movement and balance.
- Brainstem (Midbrain, Pons, Medulla)
- Regulates cardiorespiratory function, posture, and muscle tone.
11
Q
Sports-Related Traumatic Brain Injury (TBI)?
A
Concussions (Mild TBI):
Symptoms span physical, cognitive, emotional, and sleep domains:
- Physical: headache, nausea, vomiting, vision problems
- Cognitive: Memory loss, confusion, slowed thinking
- Emotional: Irritability, sadness, anxiety
- Sleep-related: Insomnia, drowsiness, changes in sleep patterns
Risk:
- Repeated concussions increase the risk of long-term degenerative conditions (e.g., chronic traumatic encephalopathy).
12
Q
Spinal Cord Structure and Function? Tuning?
A
Structure:
- The spinal cord is approximately 45 cm long, protected by the vertebral column, and connects to the brainstem.
- Contains motor neurons, sensory neurons, and interneurons for signal integration.
Function:
- It acts as a major communication pathway, transmitting information to and from the brain.
- Responsible for relaying sensory input (from skin, joints, muscles) and motor output to muscles.
Spinal tuning refers to how the spinal cord’s neural circuits refine voluntary movements, adjusting commands from the brain before executing them
13
Q
Control of Voluntary Movement?
A
Involves cooperation between multiple brain regions and subcortical structures.
Motor cortex receives input from:
- Basal nuclei – involved in movement planning.
- Cerebellum – responsible for movement coordination.
- Thalamus – integrates sensory information.
Spinal tuning (spinal cord mechanisms):
- Refines motor signals before reaching muscles.
Proprioceptive feedback (from sensors in muscles/joints):
- Enables ongoing modification and fine-tuning of movements
14
Q
Exercise and Brain Health?How?
A
Regular exercise enhances cognitive function and provides protection against:
- Alzheimer’s disease
- Stroke
- Age-related cognitive decline
Mechanisms:
- Promotes neurogenesis (new neurons)
- Enhances memory and learning
- Improves brain blood flow and vascular function
- Reduces depression-related mechanisms
- Lowers inflammation, hypertension, and insulin resistance
15
Q
Muscles in the body? Main functions of skeletal muscle?
A
The human body contains 600+ skeletal muscles.
They make up approximately 40–50% of total body mass.
Functions:
- Locomotion & Breathing - Produces force for movement and ventilation.
- Postural Support – Maintains body position and stability.
- Heat Production – Generates heat to help regulate body temperature.
- Endocrine Function – Secretes hormones and signaling molecules (e.g. myokines).
16
Q
Muscle Actions?
A
- Flexors → Decrease joint angle.
- Extensors → Increase joint angle.
- Attachment: Origin (fixed) & Insertion (moves).
17
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.
18
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.
19
Q
Satellite Cells & Muscle Growth?
A
Function:
- Satellite cells support muscle repair and growth by donating nuclei to muscle fibers.
- This increases the number of myonuclei in mature muscle cells.
Myonuclear Domain:
- Each nucleus controls a specific volume of sarcoplasm (cytoplasm in muscle cells).
- A nucleus can only manage a limited area → more myonuclei = more area supported.
Impact:
- Hypertrophy: More myonuclei → increased capacity for protein synthesis → muscle growth.
- Atrophy: Loss of myonuclei → reduced protein synthesis → decreased muscle function.
20
Q
Neuromuscular Junction (NMJ)? Components?
Trainability?
A
Neurouscular junction - Space 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 causes end plate potential → Muscle depolarization → Contraction.
Trainability of NMJ:
- Larger NMJ
- More synaptic vesicles (containing ACh)
- More ACh receptors → Enhanced performance.
These adaptations lead to faster and more efficient neuromuscular transmission, contributing to enhanced muscular performance.
21
Q
Sliding Filament Model & Contraction Cycle? Source? Fact/Determinant?
A
Muscle shortens as actin filaments slide over myosin.
- Contraction Steps:
Cross-bridge formation: Myosin binds to actin. - Power stroke: Myosin pulls actin, driven by ATP hydrolysis.
- Cross-bridge detachment: New ATP binds, myosin releases actin.
- Reactivation: ATP is hydrolyzed, resetting myosin head.
ATP sources:
- Phosphocreatine (PCr)
- Glycolysis
- Oxidative phosphorylation
Each cycle shortens muscle by ~1% of resting length; some muscles can shorten up to 60%.
ATPase activity determines the speed of ATP hydrolysis and rate of contraction.
22
Q
Excitation-Contraction Coupling (E-C Coupling) Process ?
A
- Action potential arrives at the motor neuron terminal.
- Ca²⁺ enters axon terminal → Triggers ACh release.
- ACh binds to receptors on motor end plate → Opens ion channels.
- Na⁺ influx causes local depolarization → Muscle action potential is initiated.
- Action potential travels along the sarcolemma and down T-tubules.
- Ca²⁺ released from the sarcoplasmic reticulum (SR).
- Ca²⁺ binds to troponin → Tropomyosin shifts → Myosin binding sites exposed.
- Cross-bridge cycling begins → Muscle contracts (requires ATP & Ca²⁺).
- When stimulation stops, Ca²⁺ is pumped back into SR → Muscle relaxes.
23
Q
Exercise and muscle fatigue?
A
Muscle Fatigue = a decline in muscle power output.
Reasons:
- Decrease in muscle force production at the
cross-bridge/peripheral level - Changes in CNS – central fatigue
Causes of fatigue are multifactorial therefore the exact cause of muscle fatigue depends on the exercise
intensity that produce fatigue.
24
Q
Muscle Actions & Contraction Types?
A
- Dynamic (Isotonic)
- Concentric: Muscle shortens (lifting a weight).
- Eccentric: Muscle lengthens (lowering a weight).
- Static (Isometric)
- No length change (planks, wall sits).
- Isokinetic: Muscle contracts at a constant speed (requires specialized equipment like a dynamometer).
25
Muscle fibre type characteristics ? and which each fibre type is?
Type I (Slow-Twitch):
- Mitochondria Density: High
- Fatigue Resistance: High
- Primary Energy System: Aerobic
- ATPase Activity: Low
- Contraction Speed: Slow
- Efficiency: High
- Specific Tension: Moderate
Type IIa (Fast Oxidative-Glycolytic):
- Mitochondria Density: Moderate
- Fatigue Resistance: Moderate
- Primary Energy System: Mixed (aerobic + anaerobic)
- ATPase Activity: High
- Contraction Speed: Fast
- Efficiency: Moderate
- Specific Tension: High
Type IIx (Fast Glycolytic):
- Mitochondria Density: Low
- Fatigue Resistance: Low
- Primary Energy System: Anaerobic
- ATPase Activity: Highest
- Contraction Speed: Fastest
- Efficiency: Low
- Specific Tension: High
26
Fiber Type Distribution/Composition? Influences?Trends?
Most muscles contain a mix of fibre types:
- Type I (slow-twitch)
- Type IIa and IIx (fast-twitch subtypes)
Each fibre type has distinct functional properties (e.g. contraction speed, fatigue resistance).
Average composition in arm and leg muscles:
- Roughly 45–55% Type I fibres.
Distribution varies widely between individuals, influenced by:
- Genetics
- Hormones
- Training and activity habits
General Trends by Group:
- Endurance Athletes: ~70–80% Type I fibres
- Sprinters/Power Athletes: ~70–75% Type II fibres
- Non-athletes: Approximately 50% Type I, 50% Type II
Despite variations between people, fibre type distribution tends to be consistent across different muscles within the same person.
27
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)
28
Force-Velocity & Force-Power Relationships?
Force-Velocity Relationship
- As force increases, velocity of contraction decreases.
- Fast-twitch fibres produce greater velocity at any given force compared to slow-twitch fibres.
- Maximum shortening velocity occurs when force is minimal.
- Applies to both slow and fast fibres, but fast fibres are consistently faster.
Force-Power Relationship
- Peak power output is greater in muscles with a higher percentage of fast-twitch fibres.
- Power increases with velocity up to ~200–300°/sec.
- Beyond this speed, power decreases due to reduced force output at high velocities
29
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.
30
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%
31
Muscle Power? effects of ageing?
Muscle Power = Force × Velocity
Older adults show:
- Lower muscle power
- Slower rate of force development
- Increased risk of falls
Age-related decline in muscle power is significant.
- Women tend to lose velocity faster than men.
Key Study: Van Roie et al. (2018) – Highlighted the importance of muscle power in aging and mobility.
32
Causes of Age-Related Functional Declines?
1. Muscle Mass Loss (Sarcopenia & Atrophy)
- Begins after age 40: ~8% loss per decade (0.5–1% per year).
- After age 70: ~15% per decade (Janssen et al., 2000).
- By age 70–80, most people retain only 60–80% of the muscle mass they had at 30.
- Greater loss in lower limbs than upper limbs.
2. Decline in Muscle Quality
- Increased fat accumulation in and around muscles:
--- Intermuscular fat (IMF)
--- Subcutaneous fat (SF)
- Fat infiltration reduces force production.
- Power et al. (2014): Older adults have more fat, less muscle in thigh region.
- More fat = lower muscle quality.
3. Neuromuscular Alterations:
Motor Unit (MU) Changes:
- Fewer motor units with age.
- Denervated fibres lead to:
--- Atrophy
--- Fibre loss
- Reinnervation by Type I motor units (slower, less forceful).
- Compensatory larger MUs reduce fine motor control.
Denervation & Reinnervation Outcomes:
Type II fibres:
- Atrophy if not reinnervated.
- Reinnervated by Type I units = more fatigue-resistant but weaker.
Results in:
- Slower, less powerful contractions.
- Increased fall risk due to reduced force and speed.
Key Studies: (not as important)
- Campbell et al. (1973):
- Fewer MUs = less force.
- Wilkinson et al. (2018): Reinnervation by Type I MUs reduces efficiency.
33
Muscle Fibre Changes?
Muscle Fibre Changes (Age-Related):
- Type II fibres shrink more than Type I fibres with ageing.
- Total number of muscle fibres decreases, but the proportion of Type I fibres remains relatively stable.
(Lexell et al., 1988)
Key Findings:
- Loss of muscle mass does not fully explain loss of strength.
- Strength loss is significantly greater than muscle mass loss.
(Delmonico et al., 2009)
34
Fatigue Resistance in Old Age?
Older adults are less fatigable than younger adults in specific tasks.
Reasons include:
- A greater proportion of Type I-like fibres (slow-twitch, endurance-oriented).
- Altered neuromuscular activation patterns, promoting sustained force production.
35
Effect of Lifelong Exercise on Muscle Ageing?
Lifelong exercise preserves muscle function but doesn’t fully prevent ageing effects.
Master athletes show:
- Higher muscle power.
- Better preservation of Type I fibres.
- Greater force output—comparable to people 30 years younger.
Key Study: Piasecki et al. (2016).
- Motor unit enlargement still occurs, and muscle deterioration continues—though less severely
36
Roles of the brain stem?
Midbrain (Mesencephalon): Connects the pons and cerebral hemispheres
Controls:
- Responses to sight
- Eye movement
- Pupil dilation
- Body movement
- Hearing
Medulla Oblongata: Controls autonomic functions (e.g. heart rate, breathing)
- Relays signals between brain and spinal cord
- Coordinates body movements
Pons: Regulates sleep and autonomic functions
- Relays sensory info between cerebrum and cerebellum
37
What are the key brain structures and steps involved in planning and executing voluntary movement?
Initial drive to move: Subcortical and cortical areas
Movement “rough draft”: Association cortex
Refined movement design: Basal nuclei and cerebellum
Relay station: Thalamus
Final executor of motor plan: Motor cortex
Execution of movement: Motor units
38
Four categories of exercise intensity?
Moderate: lactate threshold, 76-85% max HR, <60-75% Vo2max, Hard perception
Very heavy: >lactate threshold, 86-100% max HR, <76-100% Vo2max, Very Hard perception
Severe : >lactate threshold, 100% max HR, >100% Vo2max, All out exercise/max effort perception
39
Mechanisms of muscle fatigue at different intensities?
Heavy Intensity Fatigue (1–10 min):
Peripheral mechanisms during heavy to severe exercise.
Causes:
- ↓ Ca²⁺ release from sarcoplasmic reticulum.
- Metabolite buildup inhibiting myofilament sensitivity to Ca²⁺ (Pi, H⁺, free radicals).
Effects:
- Pi and free radicals alter cross-bridge heads, reducing actin binding.
- H⁺ competes with Ca²⁺ on troponin, impairing contraction.
Moderate Intensity Fatigue (>60 min)
Causes:
- Increased free radicals (unstable molecules that can damage cells by reacting with important cell components.).
- Muscle glycogen depletion.
Effects:
- Pi and H⁺ do not contribute significantly here.
- Free radicals reduce cross-bridge binding.
- Glycogen depletion lowers TCA cycle intermediates → reduces ATP production via oxidative phosphorylation.
40
Exercise-associated muscle cramps (EAMS)?
Definition: Involuntary, spasmodic muscle contractions during exercise.
Common with: Prolonged, high-intensity exercise.
Myth: Not mainly caused by dehydration or electrolyte imbalance.
Cause: Likely due to hyperactive motor neurons in the spinal cord.
- Altered muscle spindle and Golgi tendon organ function.
- Increased excitatory input and reduced inhibition.
Relief: Passive stretching works best.
Other notes: Electrolyte imbalance might contribute only in extreme heat/prolonged conditions.
Interesting: Activating ion channels in mouth/throat may inhibit spinal motor neuron overactivity and relieve cramps.
41
Functional Differences Among Human Skeletal Muscle Fiber Types?
Human skeletal muscle fibers vary in key functional properties that influence performance:
Contractile Properties:
- Maximal force production, often expressed as specific force.
- Speed of contraction (Vmax), regulated by myosin ATPase activity.
- Maximal power output, calculated as force × shortening velocity.
- Fast, high-force fibers generate the greatest power.
Fatigue Resistance:
- Ability to sustain contractions over time varies among fiber types.
Muscle Fiber Efficiency:
- Some fibers use less ATP to produce the same amount of force, making them more energy efficient.
Muscle contraction speed is determined by the rate of cross-bridge cycling, which is governed by the type of myosin ATPase isoform present. During muscle shortening, changes occur primarily in the I band, while the A band length remains constant.
42
Methods for Identifying Muscle Fiber Types?
Muscle fibers are classified based on their contractile and metabolic properties using several techniques:
Muscle Biopsy:
- A small sample of muscle (<50 mg) is taken for analysis.
- Samples may not fully represent the entire muscle or body.
- Fiber distribution varies by depth—surface muscle tends to have more Type II fibers, deeper muscle more Type I fibers.
Oxidative Capacity Assessment:
- Measured by the number of capillaries, mitochondria, and myoglobin content.
Myosin ATPase Staining:
- Uses specific chemical stains that highlight differences in myosin ATPase activity between fiber types.
Immunohistochemical Staining:
- Employs antibodies that selectively bind to unique myosin proteins.
- Fibers appear in different colors, allowing easy differentiation.
Gel Electrophoresis:
- Separates and identifies distinct myosin isoforms specific to each fiber type.
43
Speed of muscle contraction and relaxation
Muscle Twitch: A single muscle contraction triggered by one stimulus.
Latent Period: A brief delay after stimulation, corresponding to muscle fiber depolarization.
Contraction Phase: Calcium is released from the sarcoplasmic reticulum (SR), allowing cross-bridge formation and tension development.
Relaxation Phase: Calcium is pumped back into the SR, causing cross-bridge detachment and muscle relaxation.
Fast Fibers:
- Shorten more quickly due to faster calcium release from the SR.
- Exhibit higher myosin ATPase activity, enabling rapid contraction and relaxation.
44
Force regulation in muscles?
Motor Unit Recruitment:
- More motor units activated → greater force.
- Fast motor units produce more force than slow ones.
Muscle Length:
- There is an optimal muscle length (“ideal length”) for maximum force generation due to maximal cross-bridge formation.
Motor Neuron Firing Rate:
- Force increases with higher frequency of stimulation:
--- Single twitch → Summation → Tetanus (sustained contraction).
Contractile History:
- Force output varies depending on muscle condition:
--- Rested muscle generates more force than fatigued muscle.
--- Warm-up exercises cause postactivation potentiation, temporarily enhancing force.
45
The Motor Unit
One α-motoneuron innervates multiple muscle fibers, forming a motor unit.
A single nerve impulse activates all fibers in that unit simultaneously.
Fibers in a motor unit are scattered throughout the muscle.
Motor unit size varies: small units for fine control, large units for high force.
All fibers in a motor unit share the same fiber type.
