T7: Run For Your Life Flashcards
Bones function
Allow movement
Levers
Rigid, lightweight, long
Ligament function
Connect bones
Elastic
Tendon function
Connect muscle and bone
Inelastic
Cartilage function
End of bones/joints
Smooth, reduce friction
Spongy, cushion impact
Synovial fluid
Muscle function
Antagonistic pairs
Flexor closes joint
Extensor opens joint
Name two types of muscle fibre
Type I - slow twitch
Type II - fast twitch
Type I / slow twitch muscle fibre
Stamina
Aerobic
Lots of blood vessels
Lots of NRG
More mitochondria
More myoglobin
Type II / fast twitchy
Rapid
Anaerobic
Fewer blood vessels
Little NRG
Less mitochondria
Less myoglobin
Describe the muscle cell structure
Myofibrils
Sarcolemma (muscle coating)
Nuclei
Mitochondria
Sarcoplasmic reticulum
Describe a Sarcomere repeating unit
Thick filament (myosin)
Thin filament (actin)
Many make up a myofibril
M line connects thick filaments
A line connects Sarcomere units
H zone between thin filaments
Sliding filament theory stages
Nerve impulses, neurone —> muscle fibre
Sarcoplasmic reticulum release Ca2+
Binds to troponin
Tropomyosin moves
Reveals myosin binding sites on thick filaments
Thin filament actin bind to myosin-ADP-Pi
Pi released, myosin-ADP changes shape, pulls on actin
ADP released, myosin remains bound to actin
ATP binds to myosin, releases actin
ATP hydrolysed
Myosin-ADP-Pi returns to original position
Repeat process until impulse/Ca2+ stops
Name 4 stages of aerobic respiration
Glycolysis
Link reaction
Kerb cycle
Electron transport chain/oxidative phosphorylation
Glycolysis
Cytoplasm
Input (glucose 6C, 2NAD, 2ATP, 2ADP)
Output (2 pyruvate 3C, 2 reduced NAD, 4 ATP)
Link reaction
Mitochondria
Input (pyruvate 3C, Co-A, NAD)
Output (acetyl CoA, reduced NAD, CO2)
Cycle happens twice
Krebs cycle
Mitochondria matrix
Input (Acetyl CoA, 3 NAD, 1FAD, 1 ADP)
Output (CoA, 2CO2, 3 reduced NAD, 1 reduced FAD, 1 ATP)
Electron transport chain/oxidative phosphorylation
Mitochondria inner membrane
Input (reduced NAD, reduced FAD, O2, ADP+Pi)
Output (H2O, NAD, FAD, ATP)
Reduced NAD is oxidised/loses e-s
H+ —> outer membrane
H+ impermeable inner membrane, proton gradient
H+ back in via ATP synthase, Chemiosmosis, releases ADP+Pi! make ATP
Electron transport chain, reduces O2/gains e-s, makes H2O
Compare reduced NAD and FAD
NAD better for ATP synthesis as it makes 3 molecules whereas FAD only makes 2
Anaeorbic respiration
Limited/no oxygen
NAD can’t give e- to electron transport chain/O2
ETC/Kreb cycle/Link reaction stop
Pyruvate + reduced NAD —> lactate + 2 NAD (reversible reaction)
No ATP itself (glycolysis incomplete)
Pyruvate —> link reaction/glucose/lipids
Lactic acid
Toxic
High conc, low pH
Metabolise lactate, not wasted
Neutralise oxygen debt (NAD amount needed to remove lactate)
Ventilation in exercise vs rest
Rest: passive exhale
Exercise: active exhale
Inhalation mechanism
Diaphragm contracts/flattens
External intercostal muscles contract
Ribs move up and out
Increase thorax volume
Lower pressure
Air moves in
Exhalation mechanism
Diaphragm relaxes/moves up
Intercostal muscles relax
Rib cage moves down and in
Decrease thorax volume
Higher pressure
Air moves out
Cardiac output
Cardiac output (dm3/min) = stroke volume (dm3/ml) x heart rate (bpm)
Stroke volume
Rest = 60-70
Exercise = 90-110
Heart rate
Rest = 60-80
Exercise = up to 200
Oxygen consumption
Dm3/min
Dm3/min/Kg
Breathing rate
Rest = 12-20bpm
Exercise = 40-50bpm
Tidal volume
Rest = 0.5dm3
Exercise = 2.5dm3
Respiratory minute ventilation
Minute ventilation rate = tidal vol x breathing rate
Rest = 6-10dm3/min
Exercise = 100-125 dm3/min
Spirometer trace
Y = spirometer volume (dm3)
X = time (s-1)
Vertical distance between peak and trough = tidal volume
Vertical distance between two peaks/troughs =vol O2 absorbed
Cardiac muscle structure
Myogenic: contracts without nerve impulse
Striated
Same as general muscle fibre
Multi uncleated
Intercalated disc
Cardiac muscle coordination process
Impulse —> sinoatrial node (SAN)
Atrial wall contraction (systole)
Impulse —> atrioventricular node (AVN)
Heart wall layer is non conducting
Impulses —> purkyne fibres —> apex —> ventricle wall
Blood squeezed into arteries (systole)
ECG
Electrocardiogran
P wave = atria contract
QRS complex = ventricles contract
T wave = vent rules relax
Heart rate receptors
Chemoreceptors (CO2 conc/pH)
Thermoreceptors (blood temp/respiration rate)
Mechanoreceptors (artery wall stretch)
CNS
Cardiovascular control centre in medulla oblongata
2 nerves connected to SAN
Sympathetic nerve sends impulse (increase heart rate/noradrenaline neurotransmitter)
Parasympathetic vegus nerve sends impulse (decrease heart rate/acetylcholine neurotransmitter)
Adrenaline effect on heart rate
Increases
Increase contraction strength
Fight/flight
Homeostasis
Maintaining internal body conditions in a dynamic equilibrium
Name 4 homeostatic systems
Water potential of blood
Core body temperature
Blood glucose concentration
Blood pH
Describe the homeostatic process that occurs when your core body temperature DECREASES
Low temp environment/activity
Thermoreceptors detect
Impulse to heat GAIN centre in hypothalamus
Decrease sweat vasoconstriction and shivering
Less heat loss via evaporation and radiation
Describe the homeostatic process that occurs when your core body temperature INCREASES
High temp exercise/environment
Thermoreceptors detect
Impulse to heat LOSS centre of hypothalamus
Increase sweat production and vasodilation
More heat loss via evaporation and radiation
Negative feedback loop
Homeostatic mechanism for dynamic equilibrium
Change detected by sensory receptors
Hormones/impulses released
Effector response returns to normal
Positive feedback loop
Change detected by sensory receptors
Hormones/impulses released
Effector response increases change
Too little training effects
Input > output
Excess stored as fat
Obesity/high bp/CVD/diabetes
Increased risk of poor mental health
Too much training effects
Correlation to immune system supression
Natural killer cells reduced
Inflammatory response reduces circulated phagocytes
Joint damage
Cartilage/ligaments
Name and describe 3 drugs used in sport
Anabolic steroid
- Increase muscle mass/recovery/training intensity
EPO
- More red blood cell production
Beta blockers
- Control heart rate
Describe 2 arguments about drug use in sport
Fair as everyone is doing it, bodily autonomy
Fair if everyone competes clean, drug misuse risk
Keyhole surgery
Less invasive
Faster recovery
East infection risk
Don’t always need anaesthetic
Prosthetics
Limbs/joints
Normal mobility
Sport participation
Hormones definition
Chemical messengers desired by endocrine glands into the blood plasma and responded to by target cells
Name 3 types of hormone
Proteins
Tyrosine derivatives
Steroids
Steroid hormones
Lipid based
Can cross phopholipid bilayer
Bind to receptor proteins in cytoplasm
Hormone + receptor complex act as transcription factors
Transcription initiation complex
