Medical Physiology

Exercise Physiology (1)

Gad El - Mawla A. Gad.Professor of Physiology

COLLEGE OF APPLIED MEDICAL SCIENCESKING SAUD UNIVERSITY

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Introduction:There are no normal stresses to which the body is exposed reaches the

stress of heavy exercise. If extremes of exercise are continued for slightly prolonged time, they may be fatal. Sports physiology is a study of the ultimate limits to which most of the body mechanisms can be stressed. To give an example; in a person who has high fever, the body metabolism increases to about 100 % above normal. By comparison, the metabolism of the body during a marathon race increases 2000 % above normal. We try to understand the changes which occur in the muscles during and after exercise. Also we try to know the effects of muscular exercise on different systems and organs of the body. And lastly we study the role of muscular exercise on health and welfare, as well as the role of muscular exercise in control and treatment of diabetes, hypertension, and obesity.

Neuro-muscular junction

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The skeletal muscle fibers are innervated by large myelinated nerve fibers (A alpha) that originate form the motor neurons located in either the spinal cord or the brain stem. Since the number of fibers in the muscle greatly exceeds the number of fibers in the motor nerve, each nerve fibers branches many times and stimulates a variable number of muscle fibers. Thus, a single motor neuron innervates many muscle fibers. A motor neuron, plus the muscle fibers supplied by it is called a motor unit. In the muscles which perform fine and delicate movements (e.g. eye muscles) only a few (less than 10) muscle fibers are supplied by one motor neuron, while in muscles used for coarse movements (e.g. gastrocnemius muscle) many muscle fibers (1000-2000) are supplied by a single neuron.

Functional anatomy of the neuro-muscular junction:Near the surface of the muscle, the motor nerve fiber loses its myelin

sheath and divides into many branches, each branch forms a junction with a single muscle fiber. The terminal branches of the axon are covered only by the cytoplasm and the cell membrane of the Schwann cells (the neurilemma) which fuses with the muscle membrane (the sarcolemma). The terminal part of the axon lies in a shallow groove on the surface of the muscle fiber.

The axon terminal (persynaptic terminal) contains small vesicles that carry acetylcholine which is the chemical transmitter at the neuromuscular junctions.The presynaptic terminals contain also a large number of mitochondria. These provide the metabolic energy for the synthesis of acetylcholine and also for the Na - K pumping mechanism that are necessary for the recovery process that follow the action potential.

The terminal part of the axon is separated from the muscle plasma membrane by a space known as the synaptic cleft.

The post-synaptic membrane is the plasma membrane of the muscle fiber under the terminal part of the axon; it is called the motor end plate. The surface area of this membrane is greatly increased by the presence of numerous folds of this membrane called the junctional folds. The post-synaptic membrane contains the receptors for the chemical transmitter acetylcholine (cholinergic receptors). These receptors are complex protein molecules that have a double functions. Each receptor has a binding site for acetylcholine and also acts as an ion

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channel. Normally, the receptor is not permeable to ions, but when acetylcholine is attached to the binding sites, Na+ and K+ ions can pass through the chemically activated channels according to their electrochemical gradients.

The membrane of the motor end plate contains also an enzyme called cholinestrase. This enzyme is essential for breaking down the acetylcholine to an inactive form once it has done its action.

Mechanism of neuro-muscular transmission:When a nerve impulse in a motor neuron reaches the axon terminal, it

opens the voltage sensitive Ca++ channels, and thus allowing the Ca++ ions to diffuse into the axon terminal. The increase in the intracellular Ca++ ion causes the synaptic vesicles that contain acetylcholine to move towards the membrane, fuse with it, and lastly to rupture and release their content into the synaptic cleft. Acetylcholine diffuses across the cleft to the postsynaptic membrane (motor end plate) where it combines with the specific binding sites on the receptor. When the binding occurs, the membrane channels becomes permeable to both Na+ and K+ ions at the same time. Because of the differences in electrochemical gradients across the membrane, more Na+ move in, than K+ moves out, producing a local depolarization of motor end plate known as the motor end plate potential.

Mechanism of neuro-muscular transmission

The end plate potential causes small local currents which depolarize the adjacent muscle plasma membrane to the threshold level for generation of an action potential. This action potential propagates on both sides of the motor end plate to the whole length of the muscle fiber leading to its contraction. After

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passage of the action potential, the muscle membrane repolarizes and returns to its resting potential.

Once, acetylcholine produces its action, it is rapidly hydrolyzed by the cholinestrase enzyme into choline and acetic acid. Choline is actively taken up by the presynaptic terminal, where it is utilized again in the formation of acetylcholine which re-fills the vesicles. Degradation of acetylcholine is necessary to prevent it from causing multiple muscle contractions.

Properties of neuro-muscular transmission:1) One way (unidirectional) conduction:

Neuromuscular transmission occurs only from the nerve to the muscle and not in the opposite direction because the chemical transmitter acetylcholine is present only in the terminal parts of the nerve fiber ( presynaptic terminals) and not in the muscle (postsynaptic membrane) and there is a synaptic cleft in between them.

2) There is a delay in conduction:

Electrical recording shows that, there is a delay of about 0.5 m.sec between the nerve impulse reaching the neuromuscular junction and the action potential generated in muscle. This delay is due to the time needed for the release of acetylcholine from the presynaptic terminals, its diffusion across the synaptic cleft and its combination with the receptors which open the channels leading to diffusion of ions and depolarization of the motor end plate.

3)Neuro-muscular transmission readily shows fatigue:

Fatigue is caused by rapid repeated stimulation of the motor nerve which leads to depletion of the acetylcholine vesicles. O2 lack facilitates the onset of fatigue because it decreases the metabolic reactions needed to reform acetylcholine.

4) Effect of drugs:

A. Drugs which stimulate neuro-muscular transmission

1. By direct action: Acetylcholine (exogenous):

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It is not used clinically because it is rapidly destroyed by cholinestrase enzyme. Methacholine, carbacol and nicotine, have the same effect of acetylcholine but they are not destroyed by cholinestrase enzyme or are destroyed very slowly. These drugs produce contraction of the muscles which may persist for many minutes to several hours i.e. produce spasm.

2. By indirect action; anti-cholinestrases:

These drugs increase neuro-muscular transmission by inhibiting the action of cholinestrase enzyme which normally destroys acetylcholine after producing its action. Inhibition of cholinestrase enzyme leads to accumulation of acetylcholine at the motor end plate which causes strong and prolonged contraction of the muscle. Anti-cholinestrases are of two types:

a) Reversible: These drugs combine temporarily with cholinestrase enzyme e.g. eserine (physostigmine) and prostigmine (neostigmine). These drugs are used in treatment of a disease known as myasthenia gravis.

b) Irreversible: These chemical substances combine strongly and for a long time with cholinestrase enzyme e.g. di-isoprophyl flurophosphate (DFP). It is a dangerous substance used in war (nerve gas) which kills by producing massive inhibition of the cholinestrase enzyme. This leads to accumulation of acetylcholine causing persistent contraction (spasm) of all muscles including the respiratory muscles. This causes asphyxia and death.

B) Drugs which block neuro-muscular transmission

1. Pre-synaptic block: by inhibiting the release of acetylcholine from the pre-synaptic terminals. It is produced by:

Hemicholiniums: this drug interferes with uptake of choline and therefore acetylcholine becomes depleted.

Botulinum toxin: It is an extremely deadly poison produced by bacteria (clostridium botutinum) present in spoiled food. The toxin interferes with synthesis or release of acetylcholine. Poisoning with this toxin results in muscle paralysis and death.

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2. Post-synaptic block: by preventing the action of acetylcholine on the motor end plate. It is produced by:

Competitive neuro-muscular blockers (e.g. curare) which combines with the cholinergic receptors in the motor end plate preventing the action of acetylcholine. Anticholinestrases (e.g. prostigmine) can overcome the blocking action of curare.

Depolarizing neuro-muscular blockers (e.g. succinylcholine) which produces initial stimulation of the motor end plate due to depolarization, then blocking by maintaining this state of depolarization. So, it produces initial muscular twitches followed by muscle relaxation.

Neuro-muscular blockers are used clinically to produce muscular relaxation during surgical operation and to reduce movements during electroconvulsion treatment of psychotic patients.

5) Effect of ions:

- Ca++ ions help neuro- muscular transmission by causing rupture of the acetylcholine vesicles. Decrease Ca++ ions near the axon terminal will prevent the release of acetylcholine and therefore decreases transmission.

- Mg++ ions inhibit neuro-muscular transmission by stabilizing the acetylcholine vesicles. Excess Mg++ ions will prevent the release of acetylcholine and therefore decreases transmission.

- K+ ions have anticurare action on the motor end plate.

MUSCLE6

Muscles are machines for converting stored chemical energy into mechanical energy (work) and heat. Muscles constitutes 50% of the body weight (40% skeletal muscles and 10% smooth muscles and cardiac muscle).

There are three types of muscles; skeletal muscles, smooth muscles and cardiac muscle. They differ in structure (histologically) in location (anatomically), in functions (physiologically) and in innervations (neurologically).

Skeletal muscles (Somatic, voluntary or striated muscles)

These muscles are usually attached to the skeleton (skeletal muscles). Their contraction moves the body (soma) or part of it (somatic muscles). Contraction of these muscles is under voluntary control (voluntary muscles). These muscles appear striated under the microscope (striated muscles).

Functions of the skeletal muscles:1. They move the body as a whole or part of it e.g. one limb.

2. They maintain the body posture by their tonic contraction and muscle tone.

3. Heat production from skeletal muscles represents about 50% of the metabolic rate during rest and increased very much during muscular exercise. The activity of skeletal muscles play a very important role in the control of body temperature.

Functional histology:

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Nearly all skeletal muscles are attached to bones by means of tendons. A tendon is composed of dense, white, fibrous (inelastic) connective tissue fibers, surrounded by loose connective tissue. The fibers of the tendon are fixed to sarcolemma of the muscle fibers. The connective tissue around the tendon continues around the muscle to from a sheath known as epimysium (epi = above, my = muscle). From the outer sheath, connective tissue extends into the muscle dividing it into fasiculi. Each fasiculus is surrounded by its own sheath known as perimysium (peri = around). The muscle fasiculus is composed of many muscle fibers (myofibers) surrounded by connective tissue called endomysium. The endomysium is continuous with the sarcolemma, which is a thin sheath formed of glycoprotein.

The tight connection between the cell membranes and the surrounding connective tissue structures make the force developed by the muscle contraction to be transmitted effectively to the tendons.

The muscle fiber (myofiber):Skeletal muscle is made up of thousands of muscle fibers. The muscle fiber

is the structural unit of the skeletal muscle. It is an elongated, multinucleated cell. The muscle fiber is about 10-100 m in diameter and vary with the length of the muscle. In many muscles, the fibers run from one end to the other. However, in other muscles (large muscles) the muscle fibers run obliquely and inserted in the connective tissue sheath which surrounds the muscle.

The muscle fiber is surround by two membranes, the outer is called the sarcolemma and the inner is the plasma membrane (true cell membrane). Tubular extensions of the sarcolemma called transverse tubules (T tubules) extend deep into the muscle fiber (at the junction of the A and I bands). The lumen of the T tubules is continuous with the extracellular fluid around the muscle fibers. The T tubules have the following functions.

1. They increase the surface area of the sarcolemma many folds.

2. They help in movement of ions and other substances into and out of the cell.

3. They allow the depolarization wave to pass rapidly inside the muscle fiber to activate deep myofibrils.

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The muscle fiber (myofiber) consists of several hundred myofibrils (fibril = little fiber) which are surrounded by a cytoplasm known as the sarcoplasm. The sarcoplasm contains the usual cytoplasmic organelles; sarcosomes (mitochondria), sarcoplasmic (endoplasmic) reticulum which extends between the myofibrils, Golgi apparatus, ribosomes and glycogen granules. The sarcosomes are located beneath the plasma membrane and also between and parallel to the myofibrils.

Sarcoplasmic reticulum and T tubules.

The sarcoplasmic reticulum is a network of anastomosing longitudinal tubules which run parallel to the myofibrils. These longitudinal tubules extend the length of the sarcomere and are closed at each end. The dilated ends of the tubules are called the terminal cisternae. A group of the T tubule and two terminal cisternae on either sides is called a triad. The sarcoplasmic reticulum has the following functions:

1.It helps in longitudinal distribution of fluids, ions and substances synthesized within the sarcoplasm or mitochondria.

2.Terminal cisternae releases calcium ions during muscle contraction and store it during muscle relaxation.

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The myofibril:The myofibrils are about 1 m in diameter and extend from one end of the

muscle fiber to the other giving the muscle fiber its longitudinal striation. The myofibrils are divided into functional units called sarcomers (little muscles) by transverse sheets of protein called Z lines or discs.

The muscle fiber contains myofibrils which are composed of sarcomeres

Each myofibril is composed of filaments (myofilaments), thick and thin filaments formed of contractile proteins. The thick filaments contain the contractile protein myosin while the thin filaments contain the contractile protein actin as well as two other proteins, troponin and tropomyosin.

The thick and thin filaments are arranged in a special manner causing the myofibrils to have alternate light and dark bands. These bands give the skeletal muscle fiber its characteristic transverse striation under the light microscope. The dark bands are called A bands (Anisotropic), where as the light bands are called I bands (Isotropic). Z lines (discs) cross the center of each I band and divide the myofibril into smaller units (sarcomeres; a sarcomere is the part of the myofibril present between the 2 Z discs).

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The thick filaments are located in the middle of each sarcomere, producing the dark A band. In contrast, each sarcomere contains two sets of thin filaments, one at each end. One end of each thin filament is attached to the Z disc, where the other end overlaps a part of the thick filaments. The I band contains only the thin filaments that do not overlap the thick filaments. The Z disc present in the middle of the I band. The function of the Z disc is to connect the ends of the thin filaments from one myofibril to another attaching the myofibrils to each other across the muscle fiber.

The H zone is a relatively lighter zone in the center of the A band where the thick and thin filaments do not overlap. It corresponds to the space between the ends of the thin filaments. In the center of the H zone, there is a narrow dark line, known as the M line. It is produced by proteins that bind all the thick filaments in a sarcomere together. Thus, neither the thick nor the thin filaments are free floating, since the thin filaments are attached to the Z disc and the thick filaments are linked together by the M line.

The space between adjacent thick and thin filaments is bridged by projections known as cross-bridges. These are parts of myosin molecules that extend from the surface of the thick filaments towards the thin filaments. The head of cross-bridges act as ATPase and contain a binding site for actin and another binding site for ATP. During contraction, these cross-bridges make contact with the thin filaments and exert force on them.

Excitation contraction coupling: (mechanism of muscle contraction):

It is the process by which an action potential initiates the muscle contraction. Excitation contraction coupling involves the following steps:

1. Propagation of the action potential and release of Ca++ ions:

Propagation of the action potential in the motor nerve leads to production of an end plate potential which results in generation of an action potential at the adjacent areas of the motor end plate. This action potential spreads on both sides of the motor end plate and excites the whole muscle fiber. The action potential spreads along the T tubules which extend deep into the muscle fiber causing release of Ca++ ions from the terminal cisternae (calcium-filled sacs) of the sarcoplasmic reticulum. The released Ca++ ions diffuse rapidly to the region of the thick and thin filaments.

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2. Binding of the cross-bridges between the thick (myosin) and thin (actin) filaments:

Note: The thin filament is formed of two chains of actin molecules which wind around each other. In each actin molecule there is a binding site for myosin. These binding sites are covered by tropomyosin (a thin filament protein which coils around the actin chain). The position of tropomyosin is controlled by another protein known as troponin. The troponin molecule contains binding sites for Ca++ ions (troponin C) and tropomyosin (traponin T).

The action potential leads to release of Ca++ ions (first step) which combine with traponin molecules. Combination of Ca++ ions with traponin on the thin filament causes the tropomyosin to move away from its blocking position and thus exposing the binding sites present on actin molecules. Cross bridges from the thick (myosin) filaments combine with the binding sites on the actin.

N.B. Myosin is a complex protein consisting of a head (the cross-bridge) and a long tail

Action potential leads to release of Ca++

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3. Cross-bridge cycling which results in sliding of the thin filaments across the thick (myosin) filaments:

Cycling of cross-bridges occurs by the following steps:

a. Binding: Cross-bridges on the thick filament bind to actin.

b.Bending: Binding of the cross bridges leads to release of energy stored in myosin (ATP by ATPase) producing angular movement of the cross bridges i.e. bending of the crossbridges and sliding of the thin filaments across the thick filaments.

c.Detachment: Detachment of the cross-bridges from the thin filaments which needs energy derived also from ATP.

d.Return to original position: The cross bridge returns to its original position and another cycle can occur by binding to another actin molecule and so on.

Cross-bridge cycling occurs so long as Ca++ ions combine with troponin. This leads to sliding of the thin filaments towards the center of the sarcomere approximating the Z lines (discs) from each other (the sarcomers become shorter). The width of the I bands decrease and the H zones become narrower but the width of the A bands do not change.

Cross-bridge cycling.

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4. Relaxation occurs when Ca++ ions are transported into the sarcoplasmic reticulum by an active process using ATP and Ca-ATPase.

The active Ca++ pump is located in the membranes of the sarcoplasmic reticulum. Removal of Ca++ ions makes troponin to return to its original state which causes trapomyosin to move back and cover the binding sites on actin. Thus, the cross bridge cycles stop causing the thin filaments to slide back again to their original position and the sarcomere to return to their original length.

Changes occurring as a result of muscle contraction:I. Electrical changes:

Initiation and conduction of action potentials in the skeletal muscles are similar to that produced in the nerve fibers except for quantitative differences in timing and magnitude:

- Resting membrane potential in the skeletal muscle fibers is –90 m.v (in the nerve fibers –70 m.v).

- In the skeletal muscles, the firing level is reached at -50 m.v. i.e. after 40 m.v. depolarization (in the nerve it is at -55 m.v. i.e. after 15 m.v. depolarization).

- The magnitude of the spike potential in the skeletal muscles is 130 m.v. , from –90 m.v. to +40 m.v. (in the thick myelinated nerve fibers it is 105 m.v., from –70 m.v. to + 35 m.v.).

- Duration of the action potential in the skeletal muscles is 3-5 m. sec (in the thick myelinated nerve fibers 0.5 – 1 m.sec).

- The duration of the negative and positive after potentials are relatively longer in skeletal muscles than in nerve fibers.

- The velocity of conduction of the action potential on the surface of the muscle fibers is 3-5 meters/sec (in the thick myelinated nerve fibers it reaches up to 120 met/sec).

II. Excitability changes:

The excitability changes which occur in the muscle are identical to those which occur in the nerve. Thus, once the action potential is produced in the muscle, the excitability passes in the following phases: Absolute refractory

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period, relative refractory period, supernormal phase of excitability, subnormal phase of excitability.

III. Metabolic (chemical) changes:

A) During contraction: Energy of contraction is derived from ATP which is considered the immediate and only source of energy in this process. The head of myosin (cross bridges) contain ATPase enzyme which catalyses the hydrolysis of ATP. ATP ADP + P (phosphoric acid) + Energy.

Metabolic reaction during contraction.

ATP is rapidly reformed from ADP by the addition of phosphate group from creatine phosphate (Cr~P) (a high energy phosphate compound). ATP and Cr~P represent the stored energy which can be utilized rapidly by the muscle.

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The high energy phosphate storage in the muscle is sufficient to allow the muscle to contract only 50-100 times.

To maintain muscle contraction, a steady supply of energy is derived from the following sources:

◘ Anaerobic oxidation of glucose (or muscle glycogen):

Glucose ( ms glycogen ) 2 Pyruvic. Acids + 2ATP

During sever exercise, when the muscle is doing work at faster rate than the blood can supply O2 and nutrients, the muscle depends on local glycogen stores and anaerobic glycolysis to meet its energy requirements. The pyruvic acid produced is converted into lactic acid which diffuses out of the muscle and accumulate in the blood.

The advantage of anaerobic glycolysis is that it is able to supply ATP at a high rate and within a short time.

The disadvantage of anaerobic glycolysis is that it provides only small amounts of high energy phosphate ( 2 ATP molecules from each molecule of glucose). So, anaerobic glycolysis is rapid but not economic.

◘ Aerobic oxidation of glucose and free acids:

BI. Glucose + 6O2 6CO2 + 6H2O + 38ATP

Free fatty acids + O2 CO2 + H2O + ATP

At low or moderate levels of activity, ATP is produced by the aerobic oxidation of blood glucose or free fatty acids (carried by the blood from the adipose tissues). Aerobic oxidation of glucose or fatty acid produces great amount of high energy phosphate (38 ATP for each molecule of glucose), but the process is relatively slow.

Most muscles contain a mixture of cells, some adapted to use anaerobic glycolysis which can supply ATP very rapidly (but not economic), and others adapted to use aerobic metabolism (economic) which is relatively delayed.

◘ In exhausted muscles, there is an emergency mechanism for the supply of ATP. This is done by combining two ADP molecules to reform one ATP molecule and one AMP (Adenosine Mono-phosphate) molecule.

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ADP + ADP ATP + AMP

B) During recovery:At the end of muscular activity, the energy stores in the muscle (ATP, Cr-P

and muscle glycogen) are depleted and lactic acid is increased in blood. Recovery occurs by removal of lactic acid and regeneration of the energy stores.

a) Part of the lactic acid is oxidized into CO2 and H2O. The energy produced from this oxidation is used for reformation of ATP and by turn Cr-P.

Lactic acid Pyruvic acid CO2+ H2O + ATP

ATP + creatine Cr-P + ADP

b) The other part of the lactic acid diffuses to the blood stream and then to the liver where it is converted into blood glucose (through the Cori cycle which is the reverse of glycolysis). Muscles take glucose from the blood stream and changes it into muscle glycogen.

At the end of recovery the energy stores in the muscle (ATP, Cr~P and muscle glycogen) are reformed again, and the lactic acid is removed.

Metabolic reactions during recovery

IV. Thermal changes:

During contraction, the heat production in the muscle is markedly increased (about 100-1000 times) compared with the heat production during rest. During contraction, 40-50% of the energy liberated as a result of hydrolysis

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of ATP is converted into work. The remaining 50-60% of the energy is liberated as heat at the onset of and during contraction of the muscle. The heat production from the muscle during contraction occurs in two phases:

A) Initial heat: which includes:

1. Activation heat:

It is a very rapid heat production which starts before any shortening has occurred. It results from release of Ca++ from the terminal cisternae, binding of Ca++ to troponin protein, movements of cross-bridges towards the binding sites on the thin filaments, and active reuptake of Ca++ by the sarcoplasmic reticulum which requires ATP and starts immediately after Ca++ release.

2. Shortening heat:

The heat production during isotonic contraction (the muscle shorten) is greater than the heat production during isometric contraction (contraction without shortening). The difference represents the heat produced by the process of shortening (cross-bridge cycling). Shortening heat is proportional to the degree of shortening.

3. Work heat:

If the muscle performs work, additional heat is liberated which is proportional to the work done.

B) Delayed (recovery) heat:

It is the heat liberated from the muscle after its relaxation. Delayed heat results from the metabolic reactions needed to reform the energy stores in the muscle (ATP, Cr-P and muscle glycogen) and to remove lactic acid. Delayed heat is nearly equals to the initial heat, and it continues for about 30 minutes after the end of muscle contraction.

V. Mechanical changes:

There are two types of muscle contraction:

1. Isotonic (same tension) contraction:

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This type of contraction occurs when the muscle contracts against a light or moderate load. This contraction leads to shortening of the muscle and movement of the load. Thus a work is done (work = weight of the load x distance of movement). In this type of contraction, the mechanical efficiency of the muscle (percentage ratio of the work done to the total energy expenditure) is maximum (40-50%). The tension inside the muscle increases at first, then maintained constant during the major part of contraction (isotonic)

Force velocity relationship:When the muscle contracts isotonically (against a movable load), the

velocity of shortening is inversely proportional to the weight of the load. If the muscle is unloaded, it shortens with maximum velocity. As the weight of the load increases, the velocity of shortening decreases. When the load reaches a maximum, the muscle contracts without shortening i.e. contracts isometrically.

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Force velocity relationship

2. Isometric (same length) contraction:

This type of contraction occurs when the muscle contacts against a heavy load. The muscle does not shorten i.e. contracts without change in length (isometric), and the load does not move. So, no work is done and the mechanical efficiency is zero i.e. all the energy is converted to waste heat. The tension inside the muscle is markedly increased .

Isotonic and isometric contraction

Mechanism of isometric contraction:The muscle is supposed to be composed of 2 components, a contractile

components (sarcomers) and elastic components; one in series with the contractile components, and a second elastic element in parallel with the two components. The parallel elastic element present in the sarcolemma and the series elastic element may be present in the tendon, connective tissues or in the corssbridges (in the hinge regions of the myosin).

When the muscle contracts against a heavy load (isometric contraction), the contractile components shorten, in the same time the elastic components are stretched to the same degree. So, the length of the muscle remains constant, but its tension is markedly increased.

N.B. The muscles in body can contract both isometrically and isotonically, but most contractions are actually a mixture of the two. Example, during walking or

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running, the muscles of the leg contract isometrically to keep the limbs stiff when the leg hits the ground and isotonically to move the limb.

Length tension relationship:The tension developed during the isometric contraction depends on the

length of the muscle during experiments. A maximum tension is obtained when the length of the muscle is nearly equals to the resting length of the muscle in the body (optimal length). The tension decreases when the length of the muscle is longer or shorter than the normal body length (optimal length) At optimal length (when the sarcomere length is 2.0-2.2 m) there is a maximum number of cross bridges connecting the thick and thin filaments. At lengths longer or shorter than the optimal length the degree of overlap between the thick and thin filaments decreases and the number of cross-bridge between the thick and thin filaments also decreased leading to decreased contraction i.e. decreased tension.

Effects of stimulation of skeletal muscle by a single stimulus:

The response of the muscle depends on:

A) Intensity of the stimulus:

- Subminiml (subthreshold) stimuli: are ineffective i.e. produce no contraction.

- Minimal (threshold) stimulus: produces weak contraction which results from stimulation of the most excitable muscle fibers.

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- Superminimal (superthreshold) stimuli: produce contractions which increase in magnitude according to the intensity of the superminimal stimulus. These stimuli produce contraction of more muscle fibers.

- Maximal stimulus produces maximal contraction because all muscle fibers are stimulated.

- Supermaximal stimuli, produce no further increase in magnitude of contraction.

Simple muscle twitch:

A single maximum stimulus produces a single brief contraction followed by relaxation known as simple muscle twitch. It consists of the following:

Simple muscle twitch

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1. Latent period:It is the time between stimulation of the nerve and beginning of contraction.

2. Contraction phase:During this phase, the muscle shorten and performs work (move the lever).

3. Relaxation phase:During this phase the muscle relaxes and returns to its original length.

B) Conditions of the muscle which affect the response:

(Factors affecting the simple muscle twitch)

1) Type of the muscle:

Skeletal muscles contain mainly two types of muscle fibers.

a) Slow (red) muscle fibers (type I):

These muscle are adapted for long slow contractions which maintain the body posture (support the body against gravity) e.g. back muscles, soleus muscle etc. These muscles have a relatively longer latent period, contract slowly and relax slowly. The duration of the simple muscle twitch is about 100 m. sec

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Duration of S.M.T. of different types of muscles

These muscles are red because they contain the respiratory pigment myoglobin which facilitates the uptake of O2 from the blood stream. These muscles are composed of muscle fibers which are of small diameter, contain much mitochondria (aerobic oxidation) and surrounded by numerous blood capillaries (red fibers). Slow (red) muscles do not show fatigue because:

- They are slowly contracting i.e. use ATP at a slow rate.

- These muscles are richly supplied with blood which is able to supple them with O2 and nutrients (glucose and free fatty acids).

- These muscles are adapted to use aerobic oxidation (contain much mitochondria, myoglobin and blood capillaries) which provides much energy (38 ATP molecules for each molecule of glucose).

b) Fast (pale) muscle fibers (type II):

These muscles are adapted for fine and rapid movements e.g. extra ocular muscles. These muscles have a short latent period, contract rapidly and relax rapidly. The duration of the simple muscle twitch is less than 10 m. sec.

These muscles are composed of muscle fibers which are larger in size and contain much more sarcoplasmic reliculum and glycogen granules. The myoglobin is absent and there are few blood capillaries (pale fibers) and few mitochondria.

Fast (pale) muscles are adapted to use anaerobic glycolysis (absent myoglobin, few mitochondria, few blood capillaries and more sarcoplasmic

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reticulum and glycogent granules). So, these muscles are able to produce ATP rapidly and at high rates but quickly fatigued once their glycogen stores are depleted.

c) A third type of muscle fibers (intermediate type; fast oxidative) are present. These fibers share the characteristics with each of the other two types. They have high ATPase activity like the fast (anaerobic) fibers and high oxidative capacity like the slow (aerobic) fibers. They contract more rapidly than the slow fibers and can maintain contraction for a longer period of time than the fast fibers.

Most muscles of the body are composed of a mixture of the three types of muscle fibers e.g. gastrocnemius muscle (duration of simple muscle twitch 30 m. sec). The muscles which react very rapidly are composed mainly of the fast fibers while the muscles which maintain contraction for long periods of time without fatigue are composed mainly of the slow fibers.

Types of muscle fibers: Pale fast and slow red fibers.

2) Temperature of the muscle:

Warming of a muscle leads to a stronger contraction than normal, together with shortening of all phases of the simple muscle twitch. The effects of warming are due to acceleration of the metabolic reactions needed to provide energy for muscle contraction. Also, warming decreases the viscosity of the muscle and therefore facilitates the process of contraction. During muscular exercise the muscle temperature rises which makes contraction stronger and more rapid. Cooling of the muscle produces the opposite effects.

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Effect of temperature ca S.M.T (W = warm, N = normal, C = cold

3) Fatigue of the muscle:

Rapid and repeated simulation of the muscle leads to muscle fatigue which is manifested by decrease in strength of contraction and prolongation of all phases of the simple muscle twitch specially the relaxation phase. Relaxation becomes incomplete i.e. contracture.

Effect of fatigue on S.M.T.

Contracture is a state of sustained muscle contraction which occurs when the muscle become extremely fatigued. It is due to depletion of ATP which is important for muscle relaxation.

In isolated muscles, fatigue occurs rapidly because:

- Fatigue of the excitation contraction coupling mechanism (fatigue of neuromuscular transmission, changes in the membrane permeability and failure of cross-bridge cycling due to decreased ATP).

- Decreased active transport of Ca++ ions into the sarcoplasmic reticulum.

- Decreased energy stores inside the muscle (ATP, Cr-P and glycogen).

- Accumulation of metabolites e.g. CO2 and lactic acid.

- Decreased O2 supply.

- Decreased pH of the muscle cells.

- Electrolyte disturbance.

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Inside the body, muscle fatigue is delayed because:

- The circulatory system plays a very important role in supplying the muscle with O2 and nutrients and in removing the metabolites from the muscle.

- The CNS regulates the muscle contraction so that not all the muscle fibers are contracted at the same time, but instead, there is alternation between contracted and relaxed muscle fibers.

- Hormones (e.g. adrenaline, nor-adrenaline, glucocorticoids, thyroxin and insulin) delay onset of fatigue because these hormones regulate the metabolic rate, glycogen stores, blood pressure and excitability of the nervous system.

4) Initial lesngth of the muscle:

The strength of the muscle contraction is directly proportional to the initial length of the muscle, within limit. This is known as Starling’s law which is applied also to the cardiac muscle and smooth muscles.

If the muscle is stretched, its initial length is increased and the resulting contractions are increased. If the muscle is over stretched, the muscle contraction becomes weaker.

This is proved by muscle loading. If the weight attached to the tendon of the muscle is supported during relaxation and does not pull on the muscle except when the muscle starts to shorten, the contraction is called after loaded i.e. the muscle is loaded after the contraction starts. On the other hand, when the load pulls the muscle during relaxation and increases its length, the contraction is called preloaded. A preloaded muscle gives stronger contraction than after loaded muscle provided the weight does not overstretch the muscle.

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Contraction of preloaded muscle is stronger than after loaded muscle.

5) Size of the muscle:

The strength of the muscle is determined mainly by its size. Thus, the athlete who has hypertrophied his muscles through an exercise training program will have increased muscle strength because of increased muscle size. The maximal contractile force is 2.5 – 3.5 Kg. / cm2 of muscle cross-sectional area.

6) Age of the muscle:

The maximal strength of the muscles decreases with increasing age. It is due to an unavoidable effect of aging and the typical decrease in physical activity that often accompanies getting older?. It is apparent that strength training remains highly effective in maintaining muscular strength throughout life. However, after about age 60, strength levels fall more rapidly, independent of training. This is probably influenced by the marked hormonal changes. Both testosterone and growth hormone appear to decline more dramatically after about age 60. Reduction in the circulating concentration of these hormones will result in a shift in the balance between muscle protein synthesis (anabolism) and protein breakdown (catabolism). The decreased strength is due to atrophy of muscle fibers. It is important to notice that with strength training, the maximal strength of a 60 year old can exceed that of his untrained sons! And, several

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studies have demonstrated that strength gains are possible even at 90 years old. So it is never too late to begin a strength training program.

Effects of stimulation skeletal muscle by two successive stimuli:

The response of the muscle to the two successive stimuli depends on the time interval between the two stimuli.

-If the second stimulus falls during the latent period of the first twitch, it will produce no response because the second stimulus falls during the absolute refractory period of the first stimulus.

-If the second stimulus falls during the contraction phase of the first twitch, the muscle responds by more contraction giving a stronger contraction (higher twitch) with more prolonged duration.

-If the second stimulus falls during the relaxation phase of the first twitch, the muscle will contract again given another twitch i.e. a curve with two peaks.

-If the second stimulus falls immediately after the end of relaxation phase of the first twitch, the muscle will contact again giving another twitch which is bigger than the first twitch. The second stimulus finds the muscle in a better physiological condition (more warm and more Ca++ ions are present inside the muscle fiber.

Effect of two successive stimuli

Effects of stimulation of skeletal muscle by several successive stimuli:

The response of the muscle to several successive stimuli depends on the frequency of stimulation:

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Effect of several successive stimuli.

If the frequency of stimulation is low, so that the stimuli fall immediately after the relaxation phases of the preceding twitches, separate twitches will be obtained, the first few contractions gradually increase in strength. This condition is known as the stair case phenomenon. The cause of this phenomenon is that

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the second stimulus finds the muscle in a better physiological condition (more warm, and more Ca ++ ions are present inside the muscle fibers). The third and fourth stimuli find the muscle in a more and more better conditions producing increasing contraction up to a certain limit where there is no further increase in contractions.

If the frequency of simulation is increased so that the stimuli fall during the relaxation phases of the preceding twitches, colonus or incomplete tetanus is obtained. Colonus means rapid repeated contractions of the muscle.

If the frequency of stimulation is further increased, so that the stimuli full during the contraction phases of the preceding twitches, a complete tetanus is obtained. Tetanus means a continuous contraction which results from fusion of successive contractions produced by the rapid successive stimulation. These stimuli cause persistent release of Ca ++ ions which lead to continuous contractions. The tension developed during a complete tetanus is about 4 times that developed by a simple muscle twitch. Tetanus is the common type of muscle contraction which occurs in the human body.

The frequency of stimulation needed to produce tetanus depends on the duration of the simple muscle twitch. It is around 20-60 times per second for most skeletal muscles. The longer the duration of the twitch, the lower the frequency of stimuli needed.

The minimal frequency needed to produce complete tetanus depends on:

1. Type of the muscle: Slow (red) muscle which have a longer contraction phase needs a less frequency of stimulation to produce tetanus.

2. All factors that lengthen the contraction phase lower the minimal frequency needed to produce tetanus e.g. cooling, fatigue, decrease O2 supply, decrease blood supply and decrease Ca++ ions.

3- Anticholinestrases (e.g. prostigmine) prolong the contraction phase by preventing hydrolysis of acetylcholine. Stimulation of the motor nerve leads to accumulation of acetylcholine at the motor end plate producing tetanus.

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The power of the muscle: The power of the muscle is a measure of the amount of work which the

muscle can perform in a given period of time. This is determined by:

- The strength of muscle contraction.

- The velocity of muscle contraction.

- The number of muscle contractions in each minute.

The muscle power is measured in Kilogram-meter ( Kg-m) / minute. A muscle which can lift a kilogram weight to a height of 1 meter in 1 minute is said to have a power of 1 Kg-m/min. The maximum power can be done by all muscles in the body of a highly trained athlete with all the muscles working together is the following:

- First 10 to 15 seconds 7000 Kg-m/min.

- Next 1 minute 4000 Kg-m/min.

- Next half hour 1700 Kg-m/min.

Thus a person has the capability of an extreme power surge for a short period of time, such as during a 100 meter dash which can be completed within the first 10 seconds, where as for long-term endurance events the power output of the muscles is only one fourth that produced during the initial power surge.

Endurance in muscular exercise:Endurance is the final measure of muscle performance. This depends on the

nutritive support for the muscle – more than anything else – on the amount of glycogen stored in the muscle before the start of exercise. A person on high carbohydrate diet stores far more glycogen in muscles than a person on either a mixed diet or a high fat diet. So, endurance is greatly enhanced by a high carbohydrate diet. When athletes run at speeds typical for marathon race, their endurance is measured by the time that they can sustain the race until complete exhaustion is approximately the following:

■ High carbohydrate diet 240 minutes.■ Mixed diet 120 minutes.■ High fat diet 85 minutes.

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The corresponding amounts of glycogen stored in the muscles are the following:

◘ High carbohydrate diet 33 grams / Kg. of muscle.

◘ Mixed diet 17.5 grams / Kg. of muscle.

◘ High fat diet 6 grams / Kg. of muscle.

Energy Systems in Sport and Exercise:The same basic metabolic systems are present in muscles as in all other

parts of the body. However, special quantitative measure of the activities of the three metabolic systems are important in understanding the limits of muscular activity. These are:

1-Phosphagen system: ) ATP and Creatine-Phosphate (

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◘ Adenosine Triphosphate ( ATP ):

The basic source of energy for muscle contraction is ATP, which has the following formula: Adenosine-PO3 ~ PO3 ~ PO3 . The bonds attaching the 2 phosphate radicals are high energy phosphate bonds. Each of these bonds stores about 11,000 calories of energy per mole of ATP. Removal of first phosphate converts the ATP into ADP ( adenosine diphosphate ), and removal of the second coverts this ADP into AMP ( adenosine monophosphate ).

Unfortunately, the amount of ATP present in the muscles is sufficient to sustain maximal muscle power for only 5 or 6 seconds, may be enough for a 50 meter dash. Therefore, it is essential that new ATP be formed continuously. This is done through the Creatine-Phosphate.

◘ Creatine-Phosphate:

It is a chemical compound which has a high energy phosphate bond, with the following formula: Creatine ~ PO3. The high energy phosphate bond of Creatine-Phosphate has more energy than the bond of ATP. Therefore, the Creatine-Phosphate can provide enough energy to reform ATP. Muscles contain 2 – 3 times as much Creatine-Phosphate as ATP.

Transfer of energy from Creatine-Phosphate to ATP occurs within a small fraction of a second. So, all the energy stored in Creatine-Phosphate is readily available for muscle contraction, just as is the energy stored in ATP.

ATP and Creatine-Phosphate can provide maximal muscle power for a period of 10 – 15 seconds, both are enough for 100 meter run. Thus, the energy from the Phosphagen system is used for maximal short brusts of muscle power.

2-Anaerobic system: ) Glycogen – lactic acid system (The stored glycogen in the muscle is hydrolyzed into glucose and the

glucose then utilized for energy. Glucose is split into 2 pyruvic acids, and the energy is released to form 2 ATP molecules.

Glucose ( ms glycogen ) 2 Pyruvic. Acids + 2ATP

During sever exercise, when the muscle is doing work at faster rate than the blood can supply O2 and nutrients, the muscle depends on local glycogen stores and anaerobic glycolysis to meet its energy requirements. The pyruvic acid

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produced is converted into lactic acid which diffuses out of the muscle and accumulate in the blood.

The advantage of anaerobic glycolysis is that it is able to supply ATP at a high rate and within a short time. The disadvantage of anaerobic glycolysis is that it provides only small amounts of high energy phosphate ( 2 ATP molecules from each molecule of glucose). So, anaerobic glycolysis is rapid but not economic.

When there is insufficient O2, most of pyruvic acid is converted into lactic acid, which then diffuse out of the muscle into the interstitial fluid and blood.

Anaerobic glycolysis can form ATP molecules about 2.5 times as rapidly as can the aerobic oxidation of glucose. It can provide 30 to 40 seconds for maximal muscle activity in comparison of 10 to 15 seconds provided by the Phosphagen system.

3-Aerobic system: Aerobic oxidation of glucose and fatty acids leads to release of excess

amounts of energy which are used to reform ATP.

BI. Glucose + 6O2 6CO2 + 6H2O + 38ATP

Free fatty acids + O2 CO2 + H2O + ATP

At low or moderate levels of activity, ATP is produced by the aerobic oxidation of blood glucose or free fatty acids (carried by the blood from the adipose tissues). Aerobic oxidation of glucose or fatty acid produces great amount of high energy phosphate (38 ATP for each molecule of glucose), but the process is relatively slow.

Most muscles contain a mixture of cells, some adapted to use anaerobic glycolysis which can supply ATP very rapidly ( but not economic ), and others adapted to use aerobic metabolism ( economic ) which is relatively delayed.

In comparing the aerobic, anaerobic and Phosphagen systems, the relative maximal rates of ATP utilized are the following:

- Aerobic system 1 M of ATP / min.

- Anaerobic system 2.5 M ATP / min.

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- Phosphagen system 4 M ATP / min.

On the other hand, when comparing the systems for endurance, the relative values are the following:

- Phosphagen system 10 – 15 seconds.

- Anaerobic system 30 – 40 seconds.

- Aerobic system unlimited time ( as long as nutrients last )

Thus, Phosphagen system is utilized by the muscle for power surges, anaerobic system gives the muscle extra power during intermediate races ( as 200 to 800 meter runs ), and aerobic system is required for prolonged athletic activity.

Energy systems used in various sports:

◘ Phosphagen system: 100 meter dash, jumping, weight lifting, and diving.

◘ Phosphagen and anaerobic systems: 200 meter dash.

◘ Anaerobic system mainly: 400 meter dash, 100 meter swim, 800 – 1,500 meter dash, 200 – 400 meter swim, and boxing.

◘ Aerobic system: 10,000 meter skating, marathon run, and Jogging ( 42.2 Km.)

Performance in athletic events is determined by how rapidly the athlete can recover strength between surges of activity, and in general this means how rapidly the energy systems can recover.

Effects of exercise on skeletal muscles:Forceful muscular activity over a prolonged period causes muscle to

increase in size as the number of myofibrils within the muscle fibers increases. Increase in muscle size, called hypertrophy, occurs only if the muscle contracts to at least 75 % of its maximum tension.

Prolonged muscular exercise improves muscular strength, muscular endurance, and flexibility. Muscular strength is the force a muscle can exert against a resistance in one maximal effort. Muscular endurance is judged by the ability of a muscle to contract repeatedly or sustained a contraction for an

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extended period. Flexibility is tested by observating the range of motion about a joint.

As muscular strength improves, the overall size of the muscle, as well as the number of muscle fibers and myofibrils in the muscle, increases. The total amount of protein, the number of capillaries, and the amount of connective tissue, including tissue found in tendons and ligaments, also increase. Physical training with weights can improve muscular strength and endurance in all adults, regardless of their age. Over time, increase muscle strength promotes strong bones.

Muscles which are not used or which are used for only very weak contractions decrease in size, or atrophy. Atrophy can occur when a limb is placed in a cast or when the nerve supply of the muscle is damaged. If nerve stimulation is not restored, muscle fibers are gradually replaced by fibrous tissue.

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