Mechanics of Muscle Lecture notes



– Fatigue is exhaustion of muscle activity after some period of sustained muscle contraction (tetanus); it is the reason why we feel tired after exercise and it develop for different reasons.

– People are different in time to develop fatigue for a given activity, and that’s depends on energy producing machine in each person, for example if the person has low stores or low energy producing machine, he will develop Fatigue faster than who has high energy producing machine, and we mean by energy producing machine, all the ways that produce ATP e.g. oxidative phosphorylation pathway (need O2), glycolysis (no need for O2) which is anaerobic…etc.

– Athletics are training their muscle for better and longer time energy production, that’s why they do not develop Fatigue quickly like people who live inert  style.

– As we said Fatigue develops for one or both of two reasons:

1. Decrease in ATP that is available in muscle.

2. Decrease ACH in the neuromuscular junction (from increased rate of stimulation).

– The factors which produce maximum muscle tension are:

1.Increasing number of motor units that are active.

2.Increase length of muscle to optimum length (Lo).

3.Producing isometric contraction.

4.Increasing the rate of frequency of stimulation to produce tetanus.

5.Increasing number of myofibrils or muscle fibers.

And we can add the following point; amount of energy (ATP) that is available during contraction.

– When athletics train continuously, they are increasing the myofibrils and muscle fibers, for example, a person who can not lift 50Kg, after, let’s say 2years of training, he could lift this weight or more, because number of myofibrils and muscle fiber increased, and by this, produce more muscle tension during contraction.

– Now imagine two cases, in first case we apply electrodes (which produce frequent impulses of electricity) on nerve which supply muscle to stimulate muscle to contract frequently until reach tetanus, and in second case we apply these electrodes directly on muscle:

1.In first case we will make tetanus contraction until Fatigue begin, this period to develop Fatigue is short because there are two reasons for Fatigue;

  1. Decreased ACH in neuromuscular junction.
  2. Decreased ATP in muscle.

2.While in second case we stimulate muscle to tetanus contraction until Fatigue begin and now this period to develop Fatigue is longer than first case… Why? Because there is only one reason to develop Fatigue, which is decrease in ATP.

– The following figure show beginning of Fatigue after some period of tetanus contraction, followed by a period of rest, then again frequent stimulation to produce tetanus, but in second tetanus it will last for shorter period and Fatigue will begin sooner than first time, that’s because the energy (ATP) stores and production is decreased in second tetanus contraction.


Load – Velocity relationship:

· Load = force; the load applied to muscle during contraction to move it.

· We have two types of muscle tetanus contraction, to explain them, understand following.

· When you try to lift a pen or a book, you will make tetanus contraction and the muscle will produce tension that is the same of the object weight that you lifted, and the same principle if you lift (5) or (10) or (30) or (50) Kg, in all situations you will produce a muscle tension that is same of weight of object (to oppose gravity) and lift it, this condition of muscle tetanus contraction is called Isotonic contraction, as to say, same tension or force of the object weight, and notice…you lifted the object (you succeeded) and that’s mean there was shortening of muscle, in other word change in length of muscle, but, just notice that velocity of shortening decreases when the object weight increase (the load) referring to 20 or 30 or 50 Kg.

· But, if you try to lift (100) Kg or (200) Kg, you will make tetanus contraction, but the tension of muscle that developed is not enough to lift the weight, and you will continue contraction with out any movement of the object, that’s means no shortening happened or no change in length of muscle, as to say, the muscle is full contracting, but, still have the (same length) and this type of contraction is called Isometric contraction.

· In summary:

1.Isotonic contraction = contraction with same tension (weight) of object lifted and there is change in muscle length (shortening).

2.Isometric contraction = contraction with same length of muscle (no change in muscle length or no shortening).

· Don’t forget in Isotonic contraction; the more weight lifted (i.e. the load) the less velocity of shortening, and don’t forget in Isometric contraction there is maximum tension or strength that produced from tetanus muscle contraction. (I think you remember that Isometric contraction is one of situations that produce more or maximum muscle contraction tension or force).

Is there any relationship between Isometric and Isotonic contractions??… Yes there is… as follow:

· You may notice that when you try to lift or move heavy object you produce maximum contraction (tetanus), but, at early beginning (lets say during first seconds or fractions of first second) you couldn’t move the object (Isometric contraction), but, after a second (more or less) you move it and that is (Isotonic contraction) example on above: when you are alone to push a car, first, it doesn’t move (Isometric) but after awhile it will move some distance (Isotonic).

– We conclude from this, that the muscle contraction in response to a load will begin in Isometric and finish in Isotonic contraction, just notice that the time of Isometric contraction depends on the amount of load, the more load, the more time in Isometric contraction and you can expect if the load, for example, was (100) or (200) Kg you will spend all the time in Isometric contraction (no change in length) with out reaching isotonic contraction (because you couldn’t move the load).







Comparison between skeletal, smooth and cardiac muscles


Features of cardiac muscle:


1. Cardiac Muscle cells usual much smaller than skeletal, the cardiac cell has unique feature that they are branching between them, they are also striated muscles, they are present only in the heart forming hollow (مجوف) organ for pumping blood.

Note: striation = means has this arrangement of Actin & Myosin in the Sarcomere of skeletal muscle.

2. Cardiac cells are connected to each other electrically and mechanically.


* Cardiac cells are connected electrically because there is well organized structure between each two cell, called intercalated disc, that’s mean, when you stimulate a cell, all cells will be stimulated, and on the reverse of skeletal muscle cells which are separated electrically (each muscle fiber has terminal nerve supply).

* And they are connected mechanically, because they all contract in the same time and same tension [because there is NO Motor unit like that in skeletal muscle, where we can stimulate some muscle group in different (graded) tensions according to the frequency of stimulation].

3. Heart muscle has no nerve supply (to initiate contraction) because there is an area in the heart called SA Node that generate action potential continuously and spontaneously in a rate, but the heart has sympathetic and parasympathetic innervations that regulate heart function (not initiating contraction), sympathetic (stimulate), parasympathetic (inhibit) heart.

Note: the spontaneous generation of electricity is called autorhythmicity.

4. Mode of contraction of heart cells is only twitch type and there is no tetanus contraction.


You remember that twitch is single muscle contraction in response to single action potential, in heart, twitch is enough to generate sufficient tension to pump blood, because the duration of action potential in cardiac cells are long enough to produce long contraction duration, and no need for tetanus contraction to obtain good tension, in fact, if tetanus contraction happened (for some reason), this will be fatal because heart will continue in contraction without relaxation, and relaxation is necessary for refilling heart champers with blood, so; the heart will stop pumping.


i. The SA node that generate spontaneous action potentials is called (pace maker), and action potentials are transmitted in the heart by specialized cells in the heart, which allow fast transmission, called purkinje fibers.

ii. Some body may ask how can we adjust or (grade) the strength of contraction of heart as long as the cells are connected mechanically and there is no nerve supply that initiates contraction?? Answer is by change in length of cardiac cells, which is achieved by increasing the blood filling by increasing venous return (Frank – starling Low) and some other factors like Ca+2 level outside cell, autonomic nervous system, circulating (catecholamines), all these factors eventually affect Ca+2 concentration inside cardiac cells, these factors, if they increase muscle contraction tension (increase contractility) they are called positive inotropics (inotropic = contractility).

5. Source of Ca+2 that enter cardiac cell during contraction is from ECF and from Sarcoplasmic reticulum (Sarcoplasmic reticulum is not like that in skeletal muscle, in heart they are moderately developed).

* Notice: that in skeletal muscle we depend on Sarcoplasmic reticulum Ca+2 only.

Smooth muscle features:


1. Cells are usually shorter than skeletal, they are called smooth because there is no striation, as to say, no specially arrangement between Actin & Myosin like that in skeletal, but they are roughly aligned, Actin filaments is more in smooth muscles than that present in skeletal muscle.

2. They are present in hollow organs like GIT, blood vessels, urinary tract, and uterus.

3. They are two types:

A. multi-unit smooth muscle: as the name imply, the muscle cells are arranged in multi-unit; that’s mean, each cell is separated electrically, and mechanically, and this type of smooth muscle need nerve supply for initiating contraction (by sympathetic and parasympathetic) these autonomic nerves make synapse with each cell, and the neurotransmitter in sympathetic is (Noradrenalin) and for parasympathetic (ACH).

B. single-unit smooth muscle: whole muscle behave as one unit (mechanically and electrically), they have changing membrane potential periodically, once become near to threshold, and, once later become away from threshold (hyperpolarization), that’s mean their excitability is varying continuously (and this change in membrane potential spontaneously is called slow waves), action potentials are generated in (bursts) whenever the slow wave reach threshold.

* As we see there is no nerve supply that (initiate) contraction, instead of that, we have sympathetic & parasympathetic nerves that (regulate) the function of these single unit muscles (not initiating contraction), and these nerves are not making true synapses with each muscle, but, instead of, there is some bulges in the nerve terminals (and they are multiple) called varicosities, they secrete neurotransmitters (like noradrenalin in sympathetic and ACH in parasympathetic).

* Notice:

i. In multi unit there is synapse for each muscle.

ii. Factors that modify membrane excitability (in single unit) are: by autonomic system, local conditions (like stretching), and circulating hormones (i.e. catecholamines).

Note: in single-unit smooth muscle, stretching will elicit contraction

4. In smooth muscle in general they contract slowly (slow speed of shortening) because (ATP is splitted slowly) but, they can shorten for large distance (may exceed skeletal muscle)

5. Source of Ca+2 in smooth muscle is from ECF and little from Sarcoplasmic reticulum (Sarcoplasmic reticulum here is poorly developed). When the source of Ca+2 from ECF, it is called neurogenic Ca+2 (because the Ca+2 entered the cell in response to action potential that change permeability of cell membrane, making Ca+2 outside to enter, but, when the source of Ca+2 is from Sarcoplasmic reticulum that present (inside muscle), this Ca+2 is called Myogenic Ca+2 [i.e. from the stores of the muscle cell itself].

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