Paper

DISORDER AND ABNORMALITIES OF MUSCLE

Presented By :

          1.      Siska Mulyawati                     A 420 080 101

          2.      Nunung Rohmawati                A 420 080 121

          3.      Joko Purwanto                       A 420 080 122

          4.      Joko Purwanto                       A 420 080 135

          5.      Riskiati                                  A 420 080 136

          6.      Ginanjar Wismaji                    A 420 080 143

          7.      Sutar                                      A 420 080 146

DEPARTEMEN BIOLOOGI

TEACHER TRAINING AND EDUCATION FACULTY

MUHAMMADIYAH UNIVERSITY OF SURAKARTA

2010

PREFACE

Praise the presence of Allah SWT the Almighty, because of the abundance of grace,  we can complete the paper of "Disorder and Abnormalities of Muscle." The material of this paper in the form of the types of diseases and health disorders that affect muscle performance.

Preparation of this paper aims to fulfill the duties of the courses of Human Anatomy and Physiology. Also expected in the preparation of this paper can be a reference in reviewing about disorders and muscle disorders as well as techniques to overcome it.

There is no ivory that is not cracked, there is no perfect anything in this world. Likewise, this paper is still far from perfect, therefore constructive criticism and suggestions for preparing papers for a better future

                 Surakarta,    November 2010

                                Writer

 

CHAPTER I

INTRODUCTION

A.    Definition of Muscle

Muscle tissue consists of different cells, containing contractile proteins. Structural biology of this protein generates the pressure needed to cellular contraction, leading to movement between certain organs and body as one unit.

Muscle is a means of active motion because of the ability to contract. muscle shortens when it is contracted and elongated if relaxation. Muscle contraction occurs when muscles are doing the activities, whereas muscle relaxation occurs when the muscles are resting. Thus muscle memiliki3 characters, namely:

a.        Contractibility namely the ability of muscles to shorten and shorter than the original size, this happen if the muscle is doing the activity.

b.       Extentibility, namely the ability of muscles to elongate and longer than its original size.

c.       Elasticity, namely the ability of muscles to return to its original size.

Muscles are composed of two basic kinds of filaments, actin filaments and myosin filament. Thin actin filaments and myosin thick filament. Both filaments are preparing miofibril. Miofibril develop the muscle fibers and muscle fibers, muscle fibers make a muscle.

B.     Types of Muscle

In mammalian muscle tissue can be differentiated into 3 types based on morphological characteristics and functional and each muscle tissue has a structure appropriate to the role of that physiology.

a.       Smooth muscle (musculus nonstriata)

Smooth muscle is also called involuntary muscle or muscle tool in the (visceral muscle). Composed of smooth muscle cells - the cells are spindle-shaped smooth. Each - each cell has one core that is located in the middle. Smooth muscle contraction is not according to the will, but are supplied by autonomic nerves.

Smooth muscle found in the tools in the body, for example on:

1.      The walls of the digestive tract

2.       Respiratory Channels.

3.       Blood  vessel

4.      Urinary and genital

b.      Musculus Striata

Striated muscle is also called muscle fibers of skeletal muscle or latitude. This muscle works under consciousness. In striated muscle, that fibrils contain transverse lines dark (anisotropic) and light (isotrop) arranged criss-hose. Cylindrical cells and have many core. Skeletal muscles to contract quickly and have a rest period over and over - time. It has a collection of skeletal muscle fibers wrapped by fascia superfasialis. Combined muscle spindle-shaped and consist of parts:

1.       Ventricular, is the center of the bulge.

2.       Muscle fibers (tendons), is both ends of the shrink.

 Muscle tendon (tendon) is composed of connective tissue and are hard and tough. Based on how to attach to bones, tendons are distinguished as follows:

1.      Origin is a tendon attached to bone that has not changed his position when the muscles contract.

2.       Insersio a tendon attached to bone that moves when the muscle contracts.

 Continuously trained muscle will enlarge or hypertrophy, or the contrary if the muscles are not used (no activity) will be shriveled or atrophy.
The characteristic of striata Muscle:

3.        Consists of the muscles that are round, cylindrical

4.       There is sarcoplasma, sarcolema, myofibril

5.        The transverse lines on the disc anisotropic muscle.

6.       fibers (dark line) and Discus isotopes (light line).

7.        section nuclei more edge.

8.        conscious contractions, quickly and easily tired.

C. Cardiac Muscle

The location of the cell nucleus in the middle. Thus, the heart muscle called striated muscle that works not by the will.

·         Ability to contract rhythmically and continue.

·         The Discus interculatus.

·          There is anastomose / liaison

·         middle of the cell nucleus is oval

In physiological muscle can be divided into 2, namely:

1.       Voluantary / muscle conscious

2.      Involuantary / involuntary muscle

Muscle Function   

Muscle to contract because of the stimulation. Generally muscle to contract is not because one stimulus, but because a series of stimulus. The both of stimulus strengthen the first stimulus and second stimulus strengthen third stimulation. Thus, there was a maximum tension or tone. The maximum tonus continue - constantly called tetanus.

Nature of Working Muscle

The nature of the antagonist muscle work and synergistic distinguished as follows:

a. Antagonist

 Antagonist muscle contractions are labor movement opposite effect, for example:

1.       Extensor (straightening) and flexor (bending), such as triceps and biceps muscles.

2.       Abduktor (away from the body) and adductor (closer to the body) such as hand motion parallel to the shoulder and impeccable manners.

3.      Depresor (down) and adductor (upwards), for example motion ducked his head and looked up.

4.      Supinator (look up) and pronator (stomach), such as the palm of the hand motion and the motion of looking up the palms face down.

b.      Synergistic
Synergistic are the muscles that cause contractions in the direction of motion. Examples quadrate pronator teres and pronator quadratus .

Muscle Motion Mechanism

 From the results of research and observation by electron microscopy and X-ray diffraction, Hansen and Huxly (l955) said in the theory of muscle contraction called a model of sliding filaments. This model states that contraction is based the existence of two sets of filaments in the contractile muscle cells that form filaments of actin and myosin filament .. Stimuli received by acetylcholine causes aktomiosin shrink (contraction).

At the time of contraction, actin filaments slide between myosin into the H zone (zone H is the light between two dark bands). Thus the muscle fibers into a fixed length is shortened tire A (dark bands), while the tires I (bright band) and H zones increases short-time contraction.

 The tip of myosin can bind and hydrolyse ATP to ADP. Some energy is released by cutting the transfer of ATP to the myosin that changes shape to a high energy configuration. This high-energy myosin then binds to the specific position on actin to form cross bridges. Then the stored energy is released myosin, and myosin tip then rest with low energy, when this is happening relaxation. Relaxation is changing the point of attachment of myosin into myosin tail tip. Association between low-energy myosin and actin molecules break up when the new ATP joining the tip of myosin. Then the cycle was repeated again.

 Energy Sources for Muscle Motion

 ATP (Adenosin Tri Phosphate) is a major energy source for muscle contraction. ATP derived from oxidation of carbohydrate and fat. Muscle contraction is the interaction between actin and myosin that require ATP.
                      ATP ---- ADP P
Actin-myosin ------------------------- Aktomiosin
                             ATPase

       Fosfokreatin is a high-energy phosphate compounds are present in high concentrations in muscle. Fosfokreatin not be used directly as an energy source, but fosfokreatin can provide energy to the ADP.
                                     creatine
Fosfokreatin +ADP------------------Creatine + ATP
                               Phosphokinase

      In striated muscle fosfokreatin number more than five times the amount of ATP. Solving ATP and fosfokreatin to produce energy does not require free oxygen. Therefore, the phase of muscle contraction is often called anaerobic phase.

CHAPTER II

MUSCLE

A.    Disorder and Abnormalities of  Muscle

Muscle disorders in humans is one health disorder that can cause pain in sufferers. These musculoskeletal disorders can be caused by a wrong movement at the time or activity can also be caused by the accident. Here is a disorder in which normal muscle in humans:

1.      Strain

Strain is trauma to a muscle or tendon, usually caused by stretching of muscles or tendons that exceed normal limits. Strains can be accompanied by tissue tear or rupture. In the injured muscle or tendon inflammation that causes tissue to swell and ache. Penyernbuhan may take several weeks.

2.  SPRAIN (Java=Kesleo)

Sprain (sprain) is trauma to a joint, usually associated with ligament injury. In severe sprains, ligament. can be broken. Sprain can cause inflammation, swelling, and pain. Healing may take up to several weeks. The first phase of treatment made by RICE method, namely as follows:

a.        Rest, means that the patient should rest and protect the injured muscle area. If you feel pain during weight-bearing, use a crutch, and if you feel sick to move the injured part, protect with a splint or wooden splint.

b.      Ice, means to compress the injury with ice or something cold. Cooling can reduce swelling and reduce pain in the injury. This step should be done as soon as possible. Attach a cold cloth or ice wrapped on the injury for 20 minutes three times a day within the first 24 hours.

c.       Compress, means the press section to injury by using special bandages (ace bandage). This compression can reduce the swelling around the injury. Although this dressing should be neat, be sure that the bandage is not too tight because it can cause numbness, tingling, or even add to the pain.

d.      Elevation, the patient may have to raise as much as the injury is higher above the heart. For example if an injured ankle, try sleeping patient in a position later adopted or sustained ankle with a tool so that its position is higher than the heart. This technique refers to the principle of vessel related and useful to reduce swelling on the injury.

e.       The next step ,  therapy or massage and physiotherapy after treated with the RICE method for 2 x 48 hours, very help full.

3. Rabdomiolisis

Rabdomiolisis, also called mioglobinuria, is the existence of a number of hesar muscle protein, myoglobin, in the urine. Rabdomiolisis usually occurs after a major muscle trauma, especially injury involving muscle destruction. Running long-distance, certain infections are severe, and exposed to electric shock can cause extensive muscle damage and myoglobin excessive spending. Rabdomiolisis can cause kidney failure if myoglobin trapped in capillaries or kidney tubules.

4. Rigor mortis

Rigor rnortis (rigid body) is the stiffness or muscle contractions that occur several hours after death. Rigor mortis caused by reduction of ATP in muscle cells. In the absence of ATP bound to myosin heads, then the bridges cross the terbubung in muscle during and immediately after death can not be removed and the muscles to contract. In attempt to one day, muscle proteins are destroyed by local enzymes released by the cells that degenerate so that the back muscles relax.

5.      Atrophy

Atrophy is the decrease in the size of a cell or tissue. Atrophy of muscles can occur due to disuse of muscle or nerve terminated in accordance with that muscles. In muscle atrophy, miofibril size is reduced, although not actually atrophy, bone density can be reduced due to disuse of the bone or the presence of disease or metabolic deficiency. Atrophy due to disuse or lack of physical exercise. In most people, muscle atrophy caused by not using enough muscle. People who move jobs, medical conditions that limit their movement, or decreased activity levels can experience this disorder. In addition, the person who is bedridden people falam certain period of time may experience a decrease in muscle strength. Likewise, the astronauts away from Earth's gravity can experience this disorder, unable to lift weights or limited motion. An exercise program (under the guidance of a therapist or doctor) is recommended, including exercises in water to reduce the workload of the muscle.

6.       Dystrophy

Or muscular dystrophy Muscular dystrophy (MD) is a derivative of muscle diseases in which muscle fibers are very vulnerable to damage. Muscles, primarily voluntary muscles, become increasingly weak. At the final stage of muscular dystrophy, fat and connective tissue often replace muscle fibers. Some types of muscular dystrophy affects the heart muscles, involuntary muscles and other organs.

Signs and symptoms vary according to the type of muscular dystrophy. In general, the symptoms of muscular dystrophy include: muscle weakness, paralysis, resulting in fixations (contractures) muscles around the joints and lack of mobility. Many of the signs and specific symptoms vary from among the types of MD. Each different type of MD in the early days of contagion, symptoms appear in areas of muscular dystrophy.

There is currently no cure for any form of muscular dystrophy. Current treatment is designed to help prevent or reduce deformities in the joints and spine and to enable people with MD to stay moving long as possible. Treatment can include various types of physical therapy, drugs, devices and surgery.

7.    Muscle Fatigue

Muscle fatigue is the inability to maintain muscle power needed or expected. White muscle fibers more easily tired than red muscle fibers. In humans, one of you many ways in which information on muscle fatigue can be achieved by decreasing the peak voltage recorded in the group of muscles after contraction are very fast. The reduced peak muscle tension, can be taken some measure of fatigue. The possibilities of the meanings of fatigue:

·         Lack of intellectual performance.

·         Weak performance motor

·         Increased activity in the performance of electromyography.

·         The low frequency of EMG power spectrum

·         Failure to produce power.

The Perception is confusing:

·         The increase in an attempt to retain power.

·         Feeling uncomfortable or pain due to muscle activity.

·         Feeling weak / not able to generate power.

  Possible location and cause muscle fatigue, in the body, muscle or muscle group may experience fatigue, because failure of one or all of the terlabit neuromuscular mechanism in muscle contraction as an example, the failure of muscles to contract consciously, can occur because:

·         Neural muscle fibers in the muscle motor unit to transmit stimuli.

·         neuromuscular junction emit stimulations of the motor nerve to the muscle fibers

·         contractile mechanism itself to generate power

·         central nervous system, such as brain and spinal cord begin and radiate neurotimulation to the muscles.    

Most studies on local muscle fatigue at the neuromuscular junction shed, contractile mechanisms, and central nervous system. While a study of the possibility of motor nerves as the location and cause of fatigue is not so much.
Fatigue at the neuromuscular junction

According to Claman, HP, et al., (1979) and Komi, PV, et al., (1979) most evidence for and against that, local muscle fatigue caused by the failure of the neuromuscular junction. It seems common form of fatigue occurred in white muscle motor unit (Claman, HP, et al., 1979, and Komi, PV, et al, 1979), and fatigue may be the biggest part of the white muscle fibers compared with muscle fibers red. The failure of the neuromuscular junction to emit neurostimulation to muscle fibers is the biggest factor that causes a decrease in shipments of chemicals, acetylcholine from the nerve endings.

Fatigue and contractile mechanisms

Several factors are involved in the fatigue that is the contractile mechanism itself. Some of them are:

·         Accumulation of lactic acid

 The occurrence of muscle fatigue caused by the buildup of lactic acid has long been suspected. However, only recently people determine the relationship between the buildup of lactic acid in the intramuscular with decreasing peak voltage (a measure of fatigue).

If the ratio of lactic acid in red muscle and white muscle increases, the peak muscle tension decreases. So bias means that the magnitude of fatigue in white muscle fibers associated with the magnitude of their ability to form lactic acid.

The idea that lactic acid buildup in the accompanying fatigue process further strengthened by the fact that two physiological mechanisms by which lactic acid would hinder muscle function. Both these mechanisms depend on the effects of lactic acid in intra-cellular pH or hydrogen ion concentration (H) (Strauss, RH 1979).

 With the increase in lactic acid, the concentration of H increases and pH decreases. On the other hand, increasing the concentration of H ions hinder the process of excitation circuit, by decreasing the amount of Ca released from the sarcoplasmic reticulum and troponin binding capacity disruption. On the other hand, increased concentration of H ions also inhibit the activities of phosphofructokinase, a key enzyme involved in anaerobic glycolysis. Similarly slow glycolysis barriers, reducing the provision of ATP for energy.

•     Depletion of ATP and PC Storage

Because ATP is a direct energy source for muscle contraction, and a PC used to Resintesa ATP quickly, emptying of intracellular Fosfagen result in fatigue. How investigations on humans have been conclusion, that fatigue does not come from the low fosfagen within the muscle (FOX, EL1989). A similar conclusion has been obtained from the results of a study of frog muscle is cut in sartorius muscle.

For example, it has been reminded that during contraction activity, ATP concentration may be reduced miofibril region than in the whole muscle. Therefore, the ATP will be limited in contractile mechanisms, although only a moderate decrease of total ATP in the muscle. Another possibility is that the results in solving the energy of ATP less than the amount of ATP available within the limits for contraction muscle. (Holloszy, J.O., 1984 and DeVries, H.A., 1986).

The reason for this decrease may be associated with a higher concentration of H ions in small quantities to large within the intracellular, and is a major cause of the buildup of lactic acid (Stegemann, 1981).

•     Muscle Glycogen Depletion Deposit

  Just as with lactic acid and exhaustion, a causal relationship between the emptying of glycogen in muscle and  muscle fatigue could not be established firmly (Astrand, PO, 1986). Other factors associated with fatigue during a long training period (FOX, EL1989) is as follows:

a.        The low level / level of blood glucose, causing the emptying of the liver glycogen reserves.

b.      Local muscle fatigue caused by the emptying of muscle glycogen reserves.

c.       Drought (dehydration) and a lack of electrolytes, causing body temperature to rise.

BIBLIOGRAPHY

Clamann, H. P., and Broecker, K.T.: Relationship between force and fatigability og red and pole skeletal muscle in man. Am. J. Phys. Med.58 (2): 70-85, 1979.

Dubuque, lowa: Wm. C. Brown Publishers, 1989.

Fox, L. Edward., richard, W. Bowers, and Merle, L. Foss.: the Physiological Basis of Physical Eduction and athletics (edisi ke-4).

Junusul Hairy. Fisiologi Olahraga jilid 1. 1989. Jakarta: DepDikBud Direktorat Jenderal Pendidikan Tinggi Proyek Pengembangan Lembaga Pendidikan Tenaga Kependidikan.

Satriawan. 2009. Ganguan dan Penyakit pada Otot. (http://sukakita.com/web-blog/biologi-gangguan-sistem-gerak, diakses pada hari Sabtu, 20 November 2010)

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