Topic 7: Process Details

Sliding Filament Theory:

1. Nerve impulses arrives at a neuromuscular junction.
2. Calcium ions are released from the sarcoplasmic reticulum.
3. Calcium ions difuse through the sarcoplasm.
4. This initiates the movement of the protein flaments.
5. Calcium attaches to the troponin molecule causing it to move.
6. The tropomyosin on the actin flament shifts its position
exposing the myosin inding sites on the actin flaments.
7. !yosin heads ind "ith myosin inding sites on the actin
flament forming cross#ridges.
8. $hen the myosin head inds to the actin %&' and 'i on the
myosin head are released.
9. The myosin changes shape causing the myosin head to nod
for"ard.
10. This movement results in the relative movement of the
flaments( the attached myosin moves over the myosin.
11. %n %T' molecule inds to the myosin head causing the myosin
head to detach.
12. %n %T'ase on the myosin head hydrolyses the %T' forming
%&' and 'i.
13. This hydrolysis causes a change in shape of the myosin head.
14. The myosin head returns to it)s upright position and the cycle
can start again.
*lycolysis
+. Stores of glycogen are converted into a hexose sugar( glucose.
,. *lucose is stale and unreactive so energy from %T' is needed
to start the reactions.
-. T"o phosphate groups are added to the glucose from , %T'
molecules( this increases the reactivity of the glucose.
.. The glucose is no" split into , molecules of -#caron
compounds.
/. 0ach intermediate -C sugar is oxidised producing pyruvate.
1. T"o hydrogen atoms are removed during the reaction and
ta2en up y the co#en3yme N%&.
4. Fate of hydrogen)s and N%& is seen in the 5res cycle and
0lectron transport chain.
6. *lucose is at a higher energy level than the pyruvate and so
on conversion some energy ecomes availale for the direct
creation of %T'.
7. 'hosphate from intermediate compounds is transferred to %&'
creating %T' "hich is called Sustrate 8evel 'hosphorylation
ecause the energy for the formation of %T' comes from the
sustrates.
8in2 9eaction
1. 'yruvate is : # decaroxylated :caron dioxide released as a
"aste product; < dehydrogenated : t"o hydrogen)s are
removed and ta2en up y the coen3yme N%&;.
2. , caron molecule comines "ith coen3yme % to form acetyl
coen3yme.
3. , hydrogen atoms released are involved in %T' formation.
5res Cycle
+. , caron acetyl Co% comines "ith a .#caron compound to
create a 1#caron compound.
,. T"o steps involve decaroxylation "ith the formation of
caron dioxide.
-. Four steps involve dehydrogenation( the removal of hydrogen
atoms to convert N%& to reduced N%& or F%& to reduced F%&.
.. =ne of the steps involves Sustrate 8evel 'hosphorylation
"ith direct synthesis of a single %T'.
/. This is a cycle 2no"n as the 5res Cycle.
0lectron Transport Chain
+. $hen a coen3yme accepts the hydrogen "ith its electron the
coen3yme is reduced ecoming reduced F%& or reduced N%&.
,. The reduced coen3ymes carries the hydrogen to the electron
transport chain on the mitochondrial inner memrane.
-. 0lectrons pass from one electron carrier to the next in a series
of redox reactions> the carrier is reduced "hen it receives the
electrons and "hen it passes them on.
.. 'roton :?@; move across the inner mitochondrial memrane
creating high ?@ concentration in the intermemrane space.
/. ?@ difuses ac2 into the mitochondrial matrix do"n the
electrochemical gradient via a stal2ed particle.
1. ?@ difusion allo"s %T'ase to catalyse %T' synthesis.
4. 0lectrons and ?@ ions recomine to form hydrogen atoms
"hich then comine "ith oxygen to create "ater.
6. Af the supply of oxygen stops the electron transport chain and
%T' synthesis also stop( this is oxidative 'hosphorylation.
%naeroic 9espiration
+. 'yruvate at the end of glycolysis is reduced to lactate and the
oxidised form of N%& is regenerated.
,. %naeroic respiration allo"s glucose to e ro2en do"n
partially to ma2e a small amount of %T'.
-. 8actate uilds up in the muscles and as it accumulates the p?
of the cell falls inhiiting the en3ymes that catalyse the
glycolysis reactions.
.. 8actate can e converted ac2 to pyruvate and is oxidised
directly to caron dioxide and "ater via the 5res cycle thus
releasing energy to synthesis %T'.
/. This excess oxygen reBuirement is called the oxygen det and
is needed to fuel the oxidation of lactate.
1. Some lactate could e converted into glycogen and stored.
0lectrical Ampulses of the ?eart
1. $ave of excitation :electrical impulse; from S%N spreads
across atria "alls causing them to contract.
2. Ampulses pass to the ventricles via the %CN.
3. The impulse is delayed at the %CN for D.+- seconds.
4. Ampulses pass do"n the pur2yne fres and undle of ?is to
the apex of the heart.
5. The impulses spread up"ards through the ventricle "alls and
cause contraction of the ventricles.
6. Elood is sBuee3ed into the arteries.
0C* Trace 0xplanation
#' $ave: depolarisation of the atria( leading to atrial contraction.
#'9 Anterval: the time ta2en for impulses to e conducted from
the S%N across the atria to the ventricles through %CN.
#F9S Complex: the "ave of depolarisation resulting in
contraction of the ventricles.
#T $ave: repolarisation of the ventricles during heart)s relaxation
phase.
Nervous Control of ?eart 9ate
+. Stimulation of the sinoatrial node y the sympathetic nerve
causes an increase in heart rate.
,. Ampulses from the vagus nerve slo" do"n heart rate.
-. Cardiovascular control centre detects accumulation of
caron dioxide and lactate in the lood( reduction of
oxygen and increased temperature.
.. !echanical activity in muscles and joints is detected y
sensory receptors in muscles and impulses are sent to the
Cardiovascular control centre these changes result in
higher heart rate.
Anhalation
1. Centilation centre sends nerve impulses every ,#- seconds to
the external intercostal muscles and diaphragm muscles.
2. Eoth these sets of muscles contract causing inhalation.
0xhalation
+. %s the lungs inGate stretch receptors in the ronchioles are
stimulated.
,. Stretch receptors send inhiitory impulses ac2 to the
ventilation centre.
-. Ampulses to the muscles stop and muscles relax stopping
inhalation and allo"ing exhalation.
.. 0xhalation is caused y the elastic recoil of the lungs and y
gravity helping to lo"er the ris.
/. 9emaining air in the lungs mixes "ith ne" inhaled air to
prevent stagnant air lingering "ithin the lungs.
1. Anternal intercostal muscles only contract during deep
exhalation.
Controlling reathing rate and depth
+. % small increase in lood caron dioxide concentration causes
a large increase in ventilation.
,. Caron dioxide dissolves in the lood plasma ma2ing caronic
acid.
-. Caronic acid dissociates into hydrogen ions and hydrogen
caronate ions therey lo"ering the p? of the lood.
.. Chemoreceptors sensitive to hydrogen ions are located in the
ventilation centre of the medulla olongata.
/. They detect the rise in hydrogen ion concentration.
1. Ampulses are sent to other parts of the ventilation centre.
4. Ampulses are sent from the ventilation centre to stimulate the
muscles involved in reathing.
6. Chemoreceptors in the aorta and carotid artery are stimulated
y changes in p? resulting from changes in caron dioxide
concentration.
7. Chemoreceptors monitor the lood efore it reaches the rain
and send impulses to the ventilation centre.
'eptide ?ormones
+. 9elatively small molecules( peptide hormones cannot pass
through cell memranes easily ecause they are charged.
,. They ind to a receptor on the cell memrane "hich activates
another molecule in the cytoplasm called a second
messenger.
-. The functional second messenger rings aout chemical
changes in the cell directly or indirectly afecting gene
transcription.
Steroid ?ormones
+. Steroid hormones are formed from lipids and have complex
ring structures.
,. The hormone passes through the cell surface memrane and
inds directly to a receptor molecule "ithin the cytoplasm.
-. =nce activated the hormone#receptor complex rings aout
characteristic responses resulting from its efect on
transcription.
Transcription Factors
+. *enes are s"itched on and of y successful formation and
attachment of the transcription initiation complex to the
promoter region.
,. *enes remained s"itched of y failure of the transcription
initiation complex to form and attach to the promoter region.
-. This is due to the asence of protein transcription factors or
the action of repressor molecules.