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134 Cards in this Set

  • Front
  • Back

Peripheral Nervous System (PNS)

Cranial nerve & spinal nerves


Communication line between the CNS & body

Sensory (afferent) nerves

Somatic & visceral nerves


Conducts impulses from receptors to CNS

Motor (efferent) nerves

Motor nerves


Conducts action potentials from CNS to effectors (muscles & glands)

Sympathetic Division

Mobilises body systems for activity (i.e. flight or fight)

Autonamic nervous system (ANS)

Visceral motor (involuntary)


Conducts action potentials from CNS to cardiac muscles, smooth muscle & glands

Somatic Nervous System

Somatic motor (voluntarily)


Conducts action potential from the CNS to skeletal muscle

Parasympathetic Division

Conserves energy


Promotes digestion (rest & repair)

How does ANS function?

Sympathetic - noradreline (NA) acting on adrenoceptors


Parasympathetic - acetylcholine (Ach) acting on muscarinic Ach receptors

Ganglia neurotransmitter

Ach for both symp. & parasymp. ganglia acting on nicotinic Ach receptors

Localisation of Ganglia

Symp: close to spinal cord


Parasymp: close or within target organs

The neurotransmitter at all autonamic ganglia & parasymp. neuroeffector junctions is

Acetylcholine

The neurotransmitter at all symp. neuroeffector junctions is

Norepinephrine

Synthesis of noradrenaline & adrenaline

Tyrosine ---> DOPA ---> Dopamine ---> Noradrenaline (synthesis stops here for symp. nerve endings) ---> Adrenaline

Where is Tyrosine derived from?

From dietary proteins

Where is DOPA derived from?

In cytoplasm of nerve ending

Where is Dopamine derived from?

Accumulated in storage granules

Enzyme responsible for converting Tyrosine into DOPA

Tyrosine Hydroxylase

Enzyme responsible for converting DOPA into Dopamine

Dopa Decarboxylase

Enzyme responsible for converting Dopamine into Noradrenaline

Dopamine B-Hydroxylase

Enzyme responsible for converting Noradrenaline into Adrenaline

Phenylethandomine N-Methyl Transferase

Where is Adrenaline derived from?

Adrenal medulla only

Function of Sympathetic Division

Maintain the normal functioning of double innervated autonomic effectors by opposing the effects of parasym. impulses (e.g. slowing heart & weakening heart beat)

Function of Sympathetic Impulses

Maintain the heartbeat's normal rate & strength.

Only sympathetic fibres

innervate the smooth muscle in blood vessel walls

Inactivation of Catecholamines

1) Uptake


2) Enzymatic Inactivation


3) Diffusion

Uptake 1

Into nerve ending (neuronal uptake)


specific for noradrenaline


rapid & efficient major route


90% of released noradrenaline

Uptake 2

Into other cells & tissues (extra-neuronal uptake)


less specific - Adrenaline removed, faster than noradrenaline


important at synapse when uptake 1 impaired

MAO (Monoamine oxidase)

In nerve ending - associated with mitochondria


In extracellular fluid

COMT (Catechal-o-methyl transferase)

In extracellular fluid

Under which conditions do parasympathetic systems predominate?

Non-stressful & the in-between times of "rest & repair)

Function of Parasympathetic System

Slows heartbeat


Promotes digestion


Gland secretion

Autonomic Effectors (Glands)

Sweat


Lacrimal


Digestive


Liver


Adrenal Medulla

a-Adrenoreceptors

a1 (postsynaptic at sympathetic neuroeffector synapses)


a2 (presynaptic at sympathetic neuroeffector synapses)

B-Adrenoreceptors

B1 (heart, intestinal smooth muscle)


B2 (broncheal, vascular & uterine smooth muscle)

When is acetylcholine nicotinic/muscarinic?

Nicotinic (in sympathetic & parasympathetic ganglia)

Muscarinic (parasympathetic neuroeffector synapses)

What are Sympathomimetics?

Drugs that mimic the actions of norepinephrine & epinephrine

B2 Adrenoreceptor Agonist

agonists cause bronchial dilation & are used in treatment of asthma

B1 Adrenoreceptor Agonist

Agonists are sometimes used to stimulate the force of heart contraction

a1 Adrenoreceptor Agonist

Agonists are used to dilute the pupil

a2 Adrenoreceptor Agonist

agonists are centrally acting hypotensive drugs

a-Adrenoreceptor Antagonist

a1- Adrenoreceptor blockers reduce arteriolar & venous tone

B-Adrenoreceptor Antagonist

B1- Adrenoreceptor blockers reduce rate & force of contraction of heart rate with less effect on blood vessels & bronchioles

Sympathetic Innervation

Thoracolumbar

Parasympathetic Innervation

Craniosacral

Cardiovascular System

Provides rapid transport of nutrients to the tissues in the body & allow rapid removal of waste products

Cardiovascular System Function

Transport & secret hormones (e.g. atrial natriuretic peptide)


Host defence, transport immune cells & antigens & other mediators (e.g.antibody)


Temperature regulation

3 Components of CVS

The Heart


Blood


Blood vessels or vascular system

Precardium

Heart is located within a fluid filled membrane sac

Epicardium

Inner lining of the pericardium is continuous with the covering of the heart itself

Myocardium

Walls of the heart are composed of cardiac muscle cells

Endocardium

Inner surface of walls that is in contact with blood

Myocardium is supplied with blood by:

Coronary Arteries


Coronary Blood Flow

What are cardiac muscle walls joined together by & why?

Gap junctions to allow for the spread of excitation from one cell to another

Conducting System

Myocardium contains specialised cells that constitute the Conducting System & are essential for heart excitation

2 Phases of Cardiac Cycle

Contractile Phase (systole)


Relaxation (filling) phase (diastole)

What does the alternation between contraction & relaxation produce?

The differences in pressure which push the blood into the heart chambers & the circulation

Events leading to Cardiac Contraction

1)Depolarisation of plasma membrane


2)Opening of voltage-sensitive Ca2+ channels


3)Flow of Ca2+ into cell (Ca2+ release from sarcoplasmic reticulum)


4)Rise in cytosolic Ca2+ concentration


5)CONTRACTION



Sino - atrial node

Pacemaker

After electrical excitation

Contraction

Atrioventricular Node

Tactical Pause

Ventricular conducting fibers

Freeways

Ventricular Myocardium

Surface Roads

Intrinsic Conduction System

Originates at the sinoatral (SA) node

Define Action Potential

A transient depolarization of the cell membrane


Initiated when membrane is depolarized


Occur spontaneously (in nodal cells)


Transmission from adjacent myocytes through gap junctions

The electrical potential across a plasma membrane is determined by 2 main factors:

Distribution of ions across the membrane


Selectively permeability of cell membrane

The Resting Membrane Potential

K+ (potassium) ions are the major determinants of resting membrane potentials


The resting membrane is only slightly permeable to Na+ (sodium)

Refractory Periods

Absolute refractory period (ARP)


- ~250ms in myocytes




Relative refractory period (RRP)

(CHRONOTROPIC CONTROL) Sympathetic Fibres - Noradrenaline

B1 Receptors increasing the permeability of nodal cell plasma membrane to Na+ & Ca2+

(CHRONOTROPIC CONTROL)Parasympathetic - Acetylcholine

M2 Receptors, increasing the permeability to K+ & decreasing the Na+ & Ca2+ permeability

What is Pacemaker Rate affected by?

Temperature. This is why heart rate increases when a person has a fever

What does the slope of phase 4 depolarisation in SA nodal cells determine?

Heart Rate

Heart rate at rest

50 to 70 > 200 at max. exercise

Stroke Volume (SV)

Volume of blood pumped per contraction


Is only 50% end-diastolic volume at rest

End-Diastolic Volume (EDV)

Volume of blood in ventrical after contraction

End-Systolic Volume (ESV)

Volume of blood in ventricle after contraction

How to calculate Stroke Volume (SV)

End-Diastolic Volume (EDV) - End-Systolic Volume (ESV)

What increases Stroke Volume (SV)?

Expelling end-diastolic volume


-e.g. catecholamines increasing force of contraction



Regulation of Arterial Blood Pressure

Baroreceptor reflex


Chemoreceptor reflex


Cardiopulmonary reflexes (CO/resp rate)

Hormonal Control (long term)

Vasopressin


Angiotensin II


Aldosterone


Atrial natrineretic peptide (ANP)

How is Arterial Blood Pressure calculated?

Cardiac Output (CO) x total peripheral resistance (TPR)

Factors influencing Blood Pressure

Stroke Volume, Heart Rate, Blood Viscosity, Arteriolar Diameter, Cardiac Output, Peripheral Resistance, Arterial Blood Pressure

Arteriolar Radius

Symp. nerves, Noradrenaline, a1, CONSTRICT




Symp. cholinergic, Nerves (skeletal muscle), Acetylcholine, Muscarinic (M3), DILATE




Plasma Membrane, B2, DILATE




Local Controls: PO2,PCO2,K+, Adenosine, DILATE

How to calculate flow of lungs

Change in Pressure/ Resistance



Pressure of a gas in a mixture is called

Partial Pressure (P)

Ventilation

Exchange of air between atmosphere & alveoli by bulk flow (e.g transfer of CO2 & O2 through pulmonary & system circulation)

Gas exchange of O2 & CO2 between alveolar air & blood in lung capillaries by

Diffusion

5L of arterial blood contains:

15ml physically dissolved O2


remainder (985ml O2) bound to haemoglobin


4 x subunits = 4 x globin - haeme (Fe2+ binds O2)

Metabolically active tissue

Lower PO2


Higher PCO2 (thus H+)


Increased temperature


Greater O2 unloading



Oxygen Transport by Haemoglobin

Oxygen unloads from Haemoglobin to Tissue


CO2 moves from tissue to blood


CO2 moves from blood to alveoli

What does Carbonic Anhydrase (CA) in erythrocytes catalyse?

CO2 + H2O ---> HCO3 + H+

In breath (Inspiration)

Diaphragm contracts


External intercostal muscles pull ribs up & out

Out Breath (Expiration)

Diaphragm relaxes & abdominal organs press upwards


Lung elasticity recoils inwards

Maximum Inspiration

Sternum moves up & out


Diaphragm contracts more

Maximum Expiration

Internal intercostal muscles pull ribs down & out


Abdominal muscles compress organs & force diaphragm higher

Chemical Inputs that stimulate ventilation

Arterial PO2


Production of non-CO2 acids


Arterial PCO2

Skeletal Muscle Control: Motor Nerves

Muscle action potential


Ca2+ rise


Contraction

Contractile filaments

Myosin (Thick)


Actin (Thin)

Acetylcholine released by nerves binds

Nicotinic Ach-receptors


Acetylcholine binding opens ion channels

Afferent cholinergic innervation from...

Brainstem/spinal cord

Neuromuscular Junction

No inhibitory nerves


Na+ influx --> end-plate potential



What does the Action Potential propagate?

Across the plasma membrane into T-tubules

Voltage-sensor activates...

Ryanodine Receptor on Sarcoplasmic Retiulum

Function of Ca2+ at Neuromuscular Function

Ca2+ release into cytosol


Ca2+ enters voltage-gated channels


Ca2+ released from terminal cistemae


Ca2+ binding --> myosin able to bind troponin

Why does Myosin head - group bind actin?

To drive contraction

What does ATP hydrolysis energise/drive?

Energises Myosin


Drives:


1)Cross-bridge cycling


2)Restoration of plasma-membrane ion gradients (Na+/K+ - ATPase)


3) Removal of Ca2+ from cytosol back into sarcosplasmic reticulium (Ca2+ - ATPase)

Cycle of ATP binding, hydrolysis, ADP/Pi release drives...

Ratchets myosin toward Z-line

Ca2+ removal from Troponin

Restores tropomyosin blocking action

Ca2+ binding to Troponin

Removes blocking action of tropomyosin

Resupply of ATP within the Skeletal Muscle

Phosphorylation of ADP by Creatine Phosphate


Mitochondrial Oxidative Phosphorylation


Oxygen (aerobic)


Glycolisis supplied by blood & catabolism of muscle glycogen

Whole muscle tension

Sum of recruitment of motor units

Exercise decreases muscle

ATP


O2


Phospho-creative

Thermoregulation

Increased peripheral blood flow & sweating


Increased ATP production


Increase size of muscle fibres

Low-Intensity: Aerobic

Increased mitochondria


Increased capillaries

Endurance training

Fast-glycolytic fbres become fast-oxidative-glycolytic fibres (IIb --> IIa)

High-Intensity "strength - training"

Increased diameter of fast-twitch fibres (Hypertrophy)

Increased expression of glycolytic enzymes


Greater synchronisation of motor unit recruitment

Effect of exercise on Cardiovascular & Respiratory Systems

Supplying O2 from lungs to skeletal muscle via increased blood flow


Control body temp. by thermoregulation


Increasing peripheral blood flow & sweating

Extremely fast change in rate of breathing

Not due to gradual chemical changes

Maximal O2 Consumption

VO2 Max = arterial O2 content - venous O2 content) x CO (cardiac output)


(limiting factor = cardiac OUTPUT)

Increased mitochondria

Does not affect VO2 max, BUT does increase endurance

Endogenous Anabolic Steroids

Testosterone, Nandrolone, DHEA

Exogenous Anabolic Steroids

Metandienone, Stanozold

Hormones & Hormone Modulator (Anabolic Steroids)

Choriomic gonadotrophin


--> increased testosterone production




Aromatose Inhibitors


--> decreased testosterone breakdown

Desired effects of Anabolic Steroids

Increased muscle development


Increased competitiveness & aggression

Growth hormone produced in children

Somatotrophin (GH)


(release stimulated by GHRH (GH-releasing factor))

Desired effects of somatotropin

Increased lean body mass


Decreased fat


Increased recovery/repair

Red Blood Cell Production

Manually: blood doping


Hormonally: erythropoietin (epoitin/EPO) - recombinant expressed glycoprotein; hypoxia-mimicking agents (argon/xenon; cobalt) but altitude training is legal

B-adrenergic receptor agonists

B1-receptors on heart


B2 receptors on vascular/bronchial smooth muscle

Bronchodilation

Increased oxygen uptake

B2-specific agonists

Salbutamol (limited concentration allowed)


Terbutaline


Clenbutarol

B1/2-specific agonists

Epinephrine (local administration allowed)

B2-adrenergic Receptor Antagonists

Propanolol


Reduce tremor in precision sports (shooting, archery)

Stimulus (CNS)

Ephedrine, Amphetamine, Cocaine


Locomotor stimulation


Increased stamina & excitement


a-adenosine anatagonist


Inhibits phosphodiesterase


--> inc cAMP --> mimics B-stimulation

CNS + Peripheral Stimulant

Cardiac & Smooth Muscle Action

Other Gene Doping

Mouse Experiments (genetic mutations produced that alter muscle mass, power & endurance)


Naturally occurring genetic mutations/ polymorphisms can affect physical performance