Biophysics: muscle contraction

Muscle types:
- skeletal (striated) muscle
- smooth muscle (intestines, blood vessels, uterus)
- cardiac muscle (exclusively heart)
tendon

fascicle

fibre - myofibril

Scheme of skeletal muscle

sarcolemma myofibril
(bunch of myofilaments)
myofilament
T tubule

sarcoplasmic reticulum

terminal cysternae

Scheme of myofibril

synaptic button
synaptic vesicles

AChR’s postsynaptic folds

axon

end plate

myofibril
myofibril

Scheme of neuromuscular junction (end plate).

 Biophysics: muscle contraction

AC

terminal cysternae RR
DHPR
Ca++
Ca++

T tubule
sarcoplasm
ATP ADP

Dihydropyrydine receptor (DHPR) and ryanodine receptor (RR) co-

operate in the transmission of signal for Ca2+ release from sarcoplasmic
reticulum. To stop the muscle contraction calcium ions are removed from
sarcoplasm back to sarcoplasmic reticulum by the Ca2+–ATPase.

Sliding filaments model of muscle contraction: thin (actin) filaments slide

on thick (myosin) filaments. The length of sarcomere decreases from 2.4
µm (at rest) to less than 2 µm.

Calcium ions trigger contraction of muscle. Their presence is necessary

for binding between actin and myosin. Calcium ions must be removed
from sarcoplasm to stop actin-myosin binding and to finish the muscle
contraction.
actin

myosin
 Biophysics: muscle contraction

Sequence of elementary slide.

ATP binding

detachment of ADP ATP hydrolysis

detachment of Pi

Control of the calcium level in sarcoplasm:

• passive influx of calcium ions (mainly in cells using the mechanism of
slow resting depolarisation – heart muscle cells).
• calcium influx during the action potential (in cells using calcium
mechanism to generate action potential)
• Ca2+/Na+ exchange – calcium ions are transported out of the cell, the
transport is driven by the influx of sodium ions caused by the sodium
concentration gradient.
• active outward transport of calcium.
• intracellular stores of calcium: sarcoplasmic reticulum, nucleus,
mitochondria, calcium binding proteins.

Muscle force regulation.

Cardiac and skeletal muscles differ in the way of controlling the
contraction force. In cardiac muscle the inotropy (contractility) can be
changed while in skeletal muscle the force is regulated by the
recruitment of individual fibres.

Positive inotropic activity:

Factors increasing the calcium concentration in sarcoplasm increase the
strength of contraction. In cardiac muscle adrenalin and noradrenalin
(acting on β adrenergic receptors) modulate the time of calcium channel
opening and thus increase the amount of Ca2+ ions entering the muscle
cell.
Cardiac glycosides presumably influence the calcium concentration
inside the cell through the interference with the Na-K pump activity.
 Biophysics: muscle contraction

Higher Na+ intracellular concentration inhibit the sodium-calcium

exchange.

Negative inotropic activity:

Acetylcholine acts contrary to adrenalin and noradrenalin. It inhibits the
adenyl cyclase and by the lowering the intracellular concentration of
cAMP decreases the channel phosphorylation and opening time of
channel.
Calcium channel blockers (like verapamil) decrease the intracellular
calcium concentration.

Skeletal muscle – the strength of contraction depend on the number of

cells recruited for the contraction.
Motor unit – the muscle fibres innervated by the same neuron.

1 2 3

The muscle force depends on the number of number of motor units

recruited and on rate coding. Motor units are recruited according to the
size principle: small units first and larger later. The fast twitch units are
recruited for short efforts, the slow twitch units are recruited for
endurance activities.
Depending on the firing rate the individual twitches are accumulated and
muscle force increases.

Cardiac muscle cells: specialised in contraction or conduction of action

potential.

Cardiac conduction system

Cardiac conduction system is composed of several groups of muscle
cells providing appropriate activation of myocytes.
 Biophysics: muscle contraction

Bachmann’s bundle

Sinoatrial node
A-V (His) bundle

Atrioventicular node Left bundle branch

Purkinje fibres
Junctional fibres

Right bundle branch

Scheme of cardiac conduction system.

Cells of S-A node, A-V node and Purkinje cells can depolarise
spontaneously and therefore can act as cardiac pacemakers. The
inherent spontaneous rate of depolarisation is progressively slower from
the S-A node down to the Purkinje fibres. The rate of action potential
firing in S-A node is 78 min-1, in A-V node 50 min-1 and in Purkinje cells
30 min-1.

Cells of sinoatrial node are the primary pacemaker cells of the heart.
These cells are characterised as having no normal resting potential –
after the action potential the membrane potential successively increases
until the threshold potential is reached. This process is called
spontaneous depolarisation.

spontaneous depolarisation

Spontaneous depolarisation is a result of co-operation of several types of

channels. When the membrane potential (during repolarisation) reaches
–75 mV the cationic channels open and simultaneously the delayed
rectifying potassium channels close. In this situation the sodium influx
slowly increases the membrane potential until the threshold potential of
calcium T-channels is reached (-50 mV). Membrane depolarisation
 Biophysics: muscle contraction

caused by the opening of calcium T-channels activate calcium L-

channels and next action potential is generated.

Na

Ca 1

Ca 2

Action potentials of cardiac cells (pacemakers as well as normal

myocytes) are generated by calcium mechanism and therefore they differ
from action potential of neurons (sodium mechanism).

1
2

0 3

Phases of cardiac muscle cell action potential:

0 – depolarisation (sodium + chloride)
1 – peak (sodium inactivation + chloride)
2 – plateau (calcium L-type + potassium)
3 – repolarisation (calcium inactivation + potassium)
4 – resting

Action potentials along the cardiac conducting system are fired in

sequence providing the proper order of atrial and ventricular contraction.
In the atrioventricular node the propagation of action potential is delayed
for about 0.1 s (due to slow depolarisation of cells in this node).
In ventricles the depolarisation and repolarisation waves travel in
opposite directions: the last activated cells first become repolarised. The
ventricle depolarisation wave starts in interventricular septum and
propagated towards the apex of the heart. Then depolarisation runs back
along the outer edges of ventricles.
 Biophysics: muscle contraction

The rate of S-A node action potential firing can be regulated by factors
influencing the spontaneous depolarisation as well the action potential of
pacemaker cells.

Electrocardiography (ECG, EKG)

Electrocardiography is a diagnostic technique recording the electrical
activity of a heart by the electrodes placed on the surface of the human
body.
To establish the relation between the ECG recordings and electrical
activity of a heart the electrical model of heart must be constructed.

Heart as an electric dipole

The potential of electric field produced by a dipole can be described by a
following formula:

1  K 0 K1 K 2 
V (r ) =  + 2 + 3 + ... 
4πεε 0  r r r 

where K0, K1, K2 ... are moments of charge distribution and r is the
distance between the centre of charge distribution and point at which the
potential is calculated. For the heart the above formula can be simplified.
Since heart is not electrically charged K0 = 0 (K0 corresponds to the
charge of the considered object).
 Biophysics: muscle contraction

If localisation of the positive charge distribution centre is different from

localisation of the negative charge distribution centre the distribution is
then characterised by a dipole moment p = ql, where q is the sum of the
positive (or negative) charges and l is a distance between the possitive
and negative charges distribution centres. K1 is a projection of dipole
moment of the charge distribution on the direction of observation (r).

K1 = ql cosα = p cosα
p

α
K1 = p cosα
r
-

K2 and higher charge distribution moments in the V(r) formula can be

neglected since they are small comparing to K1. Thus for a heart
modelled as electric dipole the formula for potential can be written as:
1 p cos α
V (r ) =
4πεε 0 r 2

By measuring the potentials in two points (located in distances much

larger then the size of charge distribution) it is possible to calculate the
value of dipole moment p and to determine its orientation in the space.
In ECG examination potentials of at least three different points are
recorded.

ECG leads
For the ECG recording two different types of leads are used: unipolar
and bipolar.

mV mV

V1 0 V1 V2

unipolar bipolar
Unipolar leads measure the potential of a single electrode, bipolar leads
determine the voltage between two electrodes.
 Biophysics: muscle contraction

The reference electrode (zero potential) in unipolar ECG recording is

constructed according to Goldberger or Wilson method.

aV

Goldberger Wilson
The lower case “a” means augmented – the readings obtained by this
method has to be amplified to obtain signal amplitude identical as
bilpolar reading amplitude.
Modern ECG's utilize 12 leads which are composed of 6 limb leads and 6
precordial leads.
Limb leads are: I, II, III, aVR, aVL, and aVF. Limb leads are connected to
the points forming the Einthoven triangle.

- I +
- -
II III

+ +

I, II and III leads are bipolar. aVR, aVL and aVF are unipolar
(Goldberger) and their electrodes are located identically as I, II abd III.
Precordial leads are: V1, V2, V3, V4, V5 and V6 (Wilson).
 Biophysics: muscle contraction

Typical ECG recording consist of the following components:

- waves (deflections)
- complex (QRS)
- intervals
- segments
R

T
P

interval Q segment
S
complex

P wave represents the depolarisation of both atria.

PR interval represents atria to ventricular conduction time.
QRS complex represents depolarisation of ventricles.
T wave represents ventricular repolarisation.
In some recordings U wave is found (following the T wave). Interpretation
of U wave is not clear.
 Biophysics: muscle contraction

The electrical axis of the heart (in frontal plane) is determined using the
limb leads (I, II and III). The averaged QRS complex (sum of the Q, R, S
amplitudes or areas taken positive when wave has upward direction) of
each leads pair is presented as a vector on the corresponding direction.
The electric axis of the heart is the sum of two such vectors.

L - +R
- - -120
-90
-60
-150 -30

180 0

150 30
++ range of normal
F 120 60 axis positions
90

The third reading is not necessary since:

I = VL – VR,
II = VF – VR
III = VF – Vl.
Thus II = I – III.