Muscle fatigue
- It is the reduction in muscle ability to generate force.
- It usually follows high intensity or prolonged low/ moderate intensity exercise.
It also occurs easily when there is an interruption of the muscle blood flow.
- It can be explained by:
■ Depletion of energy stores in the muscle (glycogen, ATP, creatine phosphate).
■ Depletion of acetylcholine at the neurons supplying the muscle.
■ Accumulation of metabolites
- It is the reduction in muscle ability to generate force.
- It usually follows high intensity or prolonged low/ moderate intensity exercise.
It also occurs easily when there is an interruption of the muscle blood flow.
- It can be explained by:
■ Depletion of energy stores in the muscle (glycogen, ATP, creatine phosphate).
■ Depletion of acetylcholine at the neurons supplying the muscle.
■ Accumulation of metabolites
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TYPES OF CONTRACTION:
1/ Isometric ("same measure" or length):
Contraction without an appreciable decrease in the length of the whole muscle.
In isometric contraction there is Increasing tone.
Isometric = No change in length + Increased tension
2/ Isotonic ("same tension").
Contraction against a constant load with a decrease in muscle length, (e.g. when lifting a light object).
Isotonic= No change in tension + Decreased length
Note: because work is the product of force times distance, isotonic contractions do work, whereas isometric contractions do not.
1/ Isometric ("same measure" or length):
Contraction without an appreciable decrease in the length of the whole muscle.
In isometric contraction there is Increasing tone.
Isometric = No change in length + Increased tension
2/ Isotonic ("same tension").
Contraction against a constant load with a decrease in muscle length, (e.g. when lifting a light object).
Isotonic= No change in tension + Decreased length
Note: because work is the product of force times distance, isotonic contractions do work, whereas isometric contractions do not.
The oxygen debt mechanism :
Is extra amount of oxygen consumed after exercise.
1/ It takes oxygen from myoglobin.
2/ It metabolizes glucose anaerobically to lactic acid to synthesize ATP.
3/ It uses phosphorylcreatine to synthesize.
⭕️ After exercise extra amount of oxygen (oxygen debt) is provided by hyperventilation.
Oxygen debt it is used to:
1/ Repay oxygen taken from myoglobin
2/ Catabolize lactic acid to carbon dioxide and water
3/ Replenish phosphorylcreatine.
N.B: Oxygen debt does not occur in the cardiac muscle
Is extra amount of oxygen consumed after exercise.
1/ It takes oxygen from myoglobin.
2/ It metabolizes glucose anaerobically to lactic acid to synthesize ATP.
3/ It uses phosphorylcreatine to synthesize.
⭕️ After exercise extra amount of oxygen (oxygen debt) is provided by hyperventilation.
Oxygen debt it is used to:
1/ Repay oxygen taken from myoglobin
2/ Catabolize lactic acid to carbon dioxide and water
3/ Replenish phosphorylcreatine.
N.B: Oxygen debt does not occur in the cardiac muscle
Physiology
Photo
Post = noradrenaline except:
Sweet glads
arterioles of skeletal muscles
Pilo_erector muscles
Sweet glads
arterioles of skeletal muscles
Pilo_erector muscles
Hydrolysed by :
1/Monoamine oxidase MAO
2/Catechol_O_methyl_transferase COMT
Metabolites of catecholamines → vanillylmandelic acid VMA (urine )+ Metaepinephrine + Metanephrine
High excretion of VMA indicates hyper production of catecholamines due to
1/Monoamine oxidase MAO
2/Catechol_O_methyl_transferase COMT
Metabolites of catecholamines → vanillylmandelic acid VMA (urine )+ Metaepinephrine + Metanephrine
High excretion of VMA indicates hyper production of catecholamines due to
pheochromocytoma (tumor in adrenal medulla)
Other neurotransmitter:
Substance P: released by some GIT postganglionic parasympathetic neurons.
Nitric oxide (NO); released by some GlT postganglionic parasympathetice.
Dopamine: Released by some interneurons in sympathetic ganglial.
GnRH: Released by some preganglionic neurons.
Co-transmitters:
VIP (vasoactive intestinal peptide) : May be released with acetylcholine.
ATP, Neuropeptide Y: May be released with noradrenaline.
Substance P: released by some GIT postganglionic parasympathetic neurons.
Nitric oxide (NO); released by some GlT postganglionic parasympathetice.
Dopamine: Released by some interneurons in sympathetic ganglial.
GnRH: Released by some preganglionic neurons.
Co-transmitters:
VIP (vasoactive intestinal peptide) : May be released with acetylcholine.
ATP, Neuropeptide Y: May be released with noradrenaline.
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Acetylcholine receptors:
1- Nicotinic receptors (N1 & N2)
- Described as nicotinic because they can be stimulated by small amount enicotine (the chemical substance found in tobacco).
- They act as ion channels (their stimulation results in Na+ influx & K+ efflux)
- They are found at the following sites: Motor end plate (N1),
sympathetic ganglial (N2), parasympathetic ganglia (N2), Adrenal medulla (N2) &
the brain (N2),
2- Muscarinic receptors :(M1-M5)
Described as muscarinic because they can be stimulated by small amount muscarine (a toxin that is derived from a poisonous mushroom).
There are many subtypes of muscarinic receptors (M1-M5).
* Their stimulation:
results in either activation of phospholipace C to increase inositol triphosphate (IP3) & intracellular calcium (M1, M3 & M5), or inhibition of adenylate cyclase decreased cAMP (M2 & M4).
- They are found in the organs (not ganglia).
These include:
_All organs supplied by postganglionic parasympathetic neurons.
_The organs supplied by cholinergic postganglionic sympathetic neurons(sweat glands, arterioles of skeletal muscles & piloerector muscles).
_The brain (has both nicotinic & muscarinic receptors).
-Their stimulation causes parasympathetic effects.
1- Nicotinic receptors (N1 & N2)
- Described as nicotinic because they can be stimulated by small amount enicotine (the chemical substance found in tobacco).
- They act as ion channels (their stimulation results in Na+ influx & K+ efflux)
- They are found at the following sites: Motor end plate (N1),
sympathetic ganglial (N2), parasympathetic ganglia (N2), Adrenal medulla (N2) &
the brain (N2),
2- Muscarinic receptors :(M1-M5)
Described as muscarinic because they can be stimulated by small amount muscarine (a toxin that is derived from a poisonous mushroom).
There are many subtypes of muscarinic receptors (M1-M5).
* Their stimulation:
results in either activation of phospholipace C to increase inositol triphosphate (IP3) & intracellular calcium (M1, M3 & M5), or inhibition of adenylate cyclase decreased cAMP (M2 & M4).
- They are found in the organs (not ganglia).
These include:
_All organs supplied by postganglionic parasympathetic neurons.
_The organs supplied by cholinergic postganglionic sympathetic neurons(sweat glands, arterioles of skeletal muscles & piloerector muscles).
_The brain (has both nicotinic & muscarinic receptors).
-Their stimulation causes parasympathetic effects.
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Noradrenaline receptors:
1/ Alpha receptors (a)
Have many subtypes (a1& a2).
Alpha 1 receptors (a1 Rs):
a1 Rs are found in smooth muscle of many organs (e..g., blood vessels.
urethral sphincter & dilator pupillae muscle).
They induce induce smooth muscle contraction resulting in many effects
(e.g., vasoconstriction, reduced urine flow and dilation of the eye pupil).a1 Rs act through activation of phospholipase C (PLC), which increases intracellular inositol triphosphate (IP3), calcium & diacylglycerol (DAG).
Alpha 2 receptors (a2 Rs ):
_a2 Rs are found in the presynaptic membranes of sympathetic neurons.
_The released norepinephrine acts on them to inhibit its own release (Negative Feedback). This results in reduction of the sympathetic effects.
_Sites of a2 Rs include the pancreas and GIT sphincters. Their stimulation results in reduced insulin secretion and contraction of GIT sphincters.
- Other sites of a2 Rs include the GIT wall (causing relaxation) and the CNS (causing analgesia & sedation).
_a2 Rs act through inhibition of adenylate cyclase to decrease cAMP.
Beta receptors (B):
Beta 1 receptors (B1 Rs):
- B1 Rs are dominant in the heart, renin secreting cells & adipose tissue:
_Their stimulation in the heart increases the heart rate (+ve chronotropeffect), contractility (+ve inotropic effect) & conduction velocity +ve dromotropic effect). Other effects include renin secretion & lipolysis.
Beta 2 receptors (ẞ2 Rs):
B2 Rs cause relaxation of smooth muscle. They are dominant in many organs (e.g., lung bronchioles, GIT wall, urinary bladder wall & uterus). Their stimulation results in bronchodilation reduced GIT motility, relaxation of the urinary bladder wall & relaxation of the uterus.
Beta 3 receptors (B3 Rs):
B3 Rs are also dominant in the adipose tissue. They cause lipolysis.
1/ Alpha receptors (a)
Have many subtypes (a1& a2).
Alpha 1 receptors (a1 Rs):
a1 Rs are found in smooth muscle of many organs (e..g., blood vessels.
urethral sphincter & dilator pupillae muscle).
They induce induce smooth muscle contraction resulting in many effects
(e.g., vasoconstriction, reduced urine flow and dilation of the eye pupil).a1 Rs act through activation of phospholipase C (PLC), which increases intracellular inositol triphosphate (IP3), calcium & diacylglycerol (DAG).
Alpha 2 receptors (a2 Rs ):
_a2 Rs are found in the presynaptic membranes of sympathetic neurons.
_The released norepinephrine acts on them to inhibit its own release (Negative Feedback). This results in reduction of the sympathetic effects.
_Sites of a2 Rs include the pancreas and GIT sphincters. Their stimulation results in reduced insulin secretion and contraction of GIT sphincters.
- Other sites of a2 Rs include the GIT wall (causing relaxation) and the CNS (causing analgesia & sedation).
_a2 Rs act through inhibition of adenylate cyclase to decrease cAMP.
Beta receptors (B):
Beta 1 receptors (B1 Rs):
- B1 Rs are dominant in the heart, renin secreting cells & adipose tissue:
_Their stimulation in the heart increases the heart rate (+ve chronotropeffect), contractility (+ve inotropic effect) & conduction velocity +ve dromotropic effect). Other effects include renin secretion & lipolysis.
Beta 2 receptors (ẞ2 Rs):
B2 Rs cause relaxation of smooth muscle. They are dominant in many organs (e.g., lung bronchioles, GIT wall, urinary bladder wall & uterus). Their stimulation results in bronchodilation reduced GIT motility, relaxation of the urinary bladder wall & relaxation of the uterus.
Beta 3 receptors (B3 Rs):
B3 Rs are also dominant in the adipose tissue. They cause lipolysis.
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N.B:
Certain organs are not supplied by the parasympathetic (although they supplied by the sympathetic); and therefore, they are do not have muscarinic receptors. These include ventricles of the heart, radial muscle of the iris & some blood vessels (of the skin, abdominal viscera and the kidney).
Certain organs are not supplied by the parasympathetic (although they supplied by the sympathetic); and therefore, they are do not have muscarinic receptors. These include ventricles of the heart, radial muscle of the iris & some blood vessels (of the skin, abdominal viscera and the kidney).
⭕️ Epinephrine acts better on beta-receptors whereas, norepinephrine acts better on alpha-recpeptors.
Blockers of Acetylcholine:
1/Competitive nicotinic blockers:
_Curare.
_Hexamethonium.
2/Depolarizing nicotinic blocker:
Large amount of nicotine
3/Competitive muscarinic blockers:
_Atropine.
_Scopolamine.
4/Depolarizing muscarinic blocker:
_large amount muscarine
1/Competitive nicotinic blockers:
_Curare.
_Hexamethonium.
2/Depolarizing nicotinic blocker:
Large amount of nicotine
3/Competitive muscarinic blockers:
_Atropine.
_Scopolamine.
4/Depolarizing muscarinic blocker:
_large amount muscarine
Blockers of Noradrenaline:
1/ Alpha-blockers:
phentolamine, prazosin→ alpha 1
yohimbine → Alpha 2
Effect vasodilation (to treat hypertension) and relaxation of sphincters (to facilitate micturition in prostatic hypertrophy patients).
2/ Beta-blockers:
_B1 & B2 Rs (e.g., propranolol)
_ẞ1 Rs (e.g., atenolol)
_ẞ2 Rs (e.g., butoxamine)
Effect: decreased heart rate & decreased contractility (to treat
diseases like hypertension & myocardial infarction).
1/ Alpha-blockers:
phentolamine, prazosin→ alpha 1
yohimbine → Alpha 2
Effect vasodilation (to treat hypertension) and relaxation of sphincters (to facilitate micturition in prostatic hypertrophy patients).
2/ Beta-blockers:
_B1 & B2 Rs (e.g., propranolol)
_ẞ1 Rs (e.g., atenolol)
_ẞ2 Rs (e.g., butoxamine)
Effect: decreased heart rate & decreased contractility (to treat
diseases like hypertension & myocardial infarction).
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The Frank Starling Law :
states" within certain limits, the energy of contraction is directly proportional to the initial length of the muscle fibres"
states" within certain limits, the energy of contraction is directly proportional to the initial length of the muscle fibres"