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YEAR 1 > Muscles/Exercise/Booze & Fags Physiology > Flashcards

Muscles/Exercise/Booze & Fags Physiology Flashcards

1
Q

What are characteristics of skeletal muscles?

A

Excitable
Contractile
Extensible
Elasticity

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2
Q

What are major functions of skeletal muscle?

A

Locomotion - movement
Stabilise - posture
Stabilise joints
Produce/generate heat

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3
Q

What is the structure of striated skeletal muscle?

A

Muscle attached to bone
Surrounded by connective tissue

Epimysium - connective tissue covering muscle belly of fasicles

Perimysium - connective tissue covering fasicles

Endomysium - connective tissue covering muscle fibres

Sarcolemma - phospholipid bilayer plasma membrane in muscle fiber

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4
Q

What is the unit of contraction in a myofibril?

A 
Sarcomere - z line to z line
M line - made of myosin, stabilises thick filament 
A band - dark band 
I band - light band 
H zone - distance between thin filaments 
Thick filament - myosin 
Thin filament - actin 
Z line
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5
Q

What are the steps of excitation-coupling neuromuscular transmission pre-synapse?

A
  1. Stimulus arrives and reaches threshold for AP
  2. Sodium voltage gates open and sodium enters the cell
  3. Calcium channels open from depolarisation at +30mV
  4. Vesicles move to membrane in the presence of calcium
  5. Vesicles fuses with membrane and release ACh into cleft via exocytosis
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6
Q

What are the steps of excitation-coupling neuromuscular transmission post-synapse?

A
  1. ACh diffuses across cleft to nicotinic receptor - ligand gated ion channel. Sodium in and potassium out
  2. Influx of sodium - more sodium voltage gates open - more sodium comes in = becoming electropositive
  3. Sodium channels inactivate from influx of sodium - membrane at +30mV
  4. Positive flow from sodium influx stimulates activation of dihydropyridine receptor on T tubule(invagination of sarcolemma)
  5. DHP receptor on T tubule binds to Ryanodine receptor on SR to open
  6. Entry in SR allows calcium to flow out into cell
  7. Calcium binds to troponin C - Sliding Filament Theory
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7
Q

What are the 3 processes used to terminate muscle contraction?

A
  1. SERCA (Ca-ATPase) pump - active transport across the sarcoplasmic reticulum
  2. Na/Ca exchanger leadings to facilitates diffusion across the sarcolemma membrane into extracellular space.
  3. Ca-ATPase active transport across the sarcolemma membrane into the extracellular space.
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8
Q

What is the sliding filament theory for muscle contraction?

A
  1. Calcium binds to Troponin C
  2. Tropomyosin moves out of the way = free active site for myosin
  3. Myosin hydrolyses ATP to ADP + P to put myosin heads in cocked position
  4. Myosin heads form a cross bridge with actin filament
  5. Release of energy = power stroke - sliding of thin filament over thick filament
  6. Release of ADP + P
  7. New ATP joins, cross bridge broken, actin goes back to original position.

steps repeated until calcium no longer present in the sarcoplasm.

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9
Q

What shortens in the structure during muscle contraction

A

H band and I band shorten

A band stays the same

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10
Q

What does the force of a muscle contraction depend on?

A

Size of muscle fibres

Numbers of muscle fibres

Frequency of stimulation

Length of the sarcomere

Velocity of muscle shortening

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11
Q

What is the difference between isotonic and isometric contraction?

A

Isotonic - muscle length changes, tension stays the same.

Isometric - produces tension without change in length

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12
Q

What are Type I - Slow, Oxidative Twitch Muscle Fibres?

A 
Small fibre diameters 
Large amounts of mitochondria 
Slow contractions
Low power 
Aerobic metabolism - make ATP
High levels of myoglobin - RED
Fatigue resistance - endurance, marathons
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13
Q

What are Type IIa - Fast, Oxidative Twitch Muscle Fibres?

A 
Large diameter fiber
Aerobic and anaerobic respiration 
Fast contractility 
Moderatelty fatigue resistant - walking + sprinting
Myoglobin - RED/PINK
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14
Q

What is a muscle twitch and what are the different types?

A

Rapid contraction of muscle from one neural stimulus

Single muscle twitch
Temporal summation - Multiple stimulus from one AP
Complete tetanus - Sustained contraction, excessive stimulus

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15
Q

What are respiratory changes that occur during exercise?

A

Increased oxygen demand from respiratory system during exercise leads to…
- Increased ventilate rate
- Increased tidal volume
(more rapid and deeper breaths)

VO2 max - when steady state oxygen consumption does not increase with work intensity. When reach max = reached aerobic threshold and convert to anaerobic metabolism which lowers blood pH

Alveolar diffusion - oxygen and CO2 diffusion capacity increases with exercise. Related to increase in perfusion rather than increased ventilation

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16
Q

What are controls of respiration?

A
  • CNS
  • Psychological influences
  • CO2 levels
  • H+ levels
  • O2 levels
  • Core body temperature
  • Peripheral joint receptors - increased chemoreceptors
  • Pulmonary stretch receptors
17
Q

What are benefits of regular exercise?

A

Reduced blood pressure

Increased circulating HDL and reduced triglycerides

Changes in arterial wall homeostasis reusing atherosclerotic disease

Improved aortic value function and reduction in calcification

Increased ventricular chamber wall thickness

Overall reduced risk of cardiovascular disease

Reducing insulin resistance
- Training increases protein turnover, increased lipid oxidation = resulting in decreased fat mass, decreased plasma lipid levels = decrease in insulin resistance

Moderate clinical effect in a decline in depression

High intensity weight bearing improves bone density

Can improve muscle mass and strength in patients with RA who suffer from cachexia

Resistance training can increase tendon stiffness, strengthen connective tissue

Mobility exercise to increase range of motion

18
Q

What is cardiac output and how much does it change in exercise?

A

CO = heart rate x stroke volume(volume of blood pumped out with each contraction)

Cardiac output increases 4-5 times resting output

19
Q

What is Starlings Law?

A

The more full the heart is - the harder it will contract = increase stroke volume

(contracting skeletal muscle improves venous return - increased pressure and volume on the heart = starlings law = increase stroke volume)

Force of contraction related to how stretched the cardiac muscle is

20
Q

What are early cardiovascular responses to exercise?

A

Vasoconstriction of inactive muscles, splanchnic, renal and cutaneous circulation = makes more blood available for diversion to contracting muscles

Vasodilation of active muscles

Increased stroke volume, cardiac output from sympathetic output causes tachycardia and increased contractility

21
Q

What are delayed cardiovascular responses to exercise?

A

Delayed vasodilation from the release of histamine, kalikreins, epinephrine - triggered by contracting skeletal muscle

Exercise pressor reflex
- Stretch receptors sense muscle contraction, receptor signals travel through fibres to spinal cord and medullary cardiovascular control centre = sustains sympathetic outflow to heart

Aterial baroreflexes
- Central command resets arterial baroreflex threshold (higher mean arterial pressure needed to slow HR)

Histamine release
- Potent vasodilator- cells near arterioles release histamine when sympathetic tone wanes (less norepinephrine). Relaxed arterioles = muscle capillary pressure rises = extravasation into muscle tissue(fluid leak)

Epinephrine release
- Preganglionic sympathetic fibres to adrenal medulla = epinephrine release → acts on cardiac beta-1 adrenoreceptors = enhance neural effects on heart/ increased cardiac output

Core body temp regulation
- Increased metabolism = core body temp rises → temperature-sensitive cells in hypothalamus = 1. signals medulla to inhibit sympathetic vasoconstrictor outflow to skin. 2. Activates sympathetic cholinergic fibres to sweat glands = more sweat + co-release neurotransmitters = dilate cutaneous vessels

22
Q

What are the effects of nicotine on the body at a physiological level?

A
  • Increased heart rate
  • Cardiac contractility
  • Increased blood pressure
  • Decreased skin temperature
  • Increased platelet aggregation
  • Increased oxygen demand
  • Mobilisation of blood sugar
  • Reduction of GI motility
  • Sweating
  • Plaque formation
  • Osteoporosis
  • Infertility or erectile dysfunction
23
Q

What are the effects of nicotine on the body at a cellular level?

A
  • Increased synthesis and release of hormones
  • Activation of tyrosine hydroxylase enzyme
  • Activation of several transcription factors
  • Induction of heat shock proteins
  • Induction of oxidative stress
  • Effects on apoptosis
  • Induction of chromosome aberrations
  • Induction of sister chromatid exchange
24
Q

What affect does nicotine have on the sympathetic and parasympatic nervous system?

A

Nicotine increases sympathetic activity

Nicotine reduces parasympathetic effects

25
Q

What are acute effects of alcohol on the CNS?

A
  • Slurred speech
  • Increased self confidence
  • Euphoria + Mood changes
  • Intellectual and motor performance impaired
26
Q

What are chronic effects of alcohol on the CNS?

A
  • Irreversible neurological effects – dementia, peripheral neuropathy
  • Wernicke’s encephalopathy - thiamine deficiency
  • Cerebral atrophy, cerebellar degeneration, optic neuropathy
27
Q

What are the effects of alcohol on the body?

A

Cardiovascular system

- Acute - vasodilation – feeling warm but increasing heat loss
- Chronic - Cardiomyopathy, coronary heart disease, increases HDL and inhibits platelet aggregation, hypertension

Endocrine system
- Diuresis – inhibiting release of ADH from pituitary

GI tract

- Acute - Increased salivary and gastric secretion
- Chronic Bleeding from gastritis, gastric ulcers, oesophageal varices

Liver

- Fat accumulation – hepatitis – hepatic necrosis – fibrosis, cirrhosis
- Effects lipid metabolism, platelet function, atherosclerosis

Fetal development

- Fetal alcohol syndrome
- Alcohol-related neurodevelopmental disorder
- Consumption during the first trimester has the most damaging effects

Carcinogenesis
- Increased risk of cancers of the oral cavity, eosophagus, liver and breast

Malnutrition
- Alcoholism often associated with malnutrition and deficiencies - particularly B vitamins

28
Q

What are the 4 products of ethanol metabolism?

A
  1. Alcohol oxidation - causes fat accumulation in the liver
  2. Acetaldehyde toxicity - acute effects of alcohol
  3. ROS generation - lipid per oxidation of cell membranes
  4. Endotoxin release - stimulates TNF and cytokine release
29
Q

What effect does alcohol have on the nervous system?

A

Ethanol can enhance GABAa mediated inhibition – allosteric modulator – inhibition of neural firing

Ethanol inhibits activity of glutamate receptors- reduction of neural activity – disruption in memory loss, consciousness and alertness

Inhibit opening of calcium gated channels at axon terminals = reducing NT release

Increased serotonin and glycine receptor function

Alcohol stimulates dopamine transmission in the mesolimbic dopamine pathway

30
Q

What is the pathway of nicotine in the brain?

A

Nicotine and Alcohol release endorphins which activate mu opioid receptors in the ventral tegmental area - VTA

Activation of receptors inhibits release of inhibitory GABA

Release of dopamine in the Nucleus Accumbens

31
Q

How does de-sensitization occur in alcohol and smoking addiction?

A

Continued high release of dopamine(overstimulation) – body thinks too much dopamine so reduces dopamine receptors on post-synaptic (homeostasis) – means you need more dopamine to get the same response

De-sensitization – continued dopamine over-stimulation leads to…

  • A reduction in dopamine receptors
  • A reduced sensitivity to dopamine
  • A reduced dopamine production

YEAR 1 (17 decks)

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