IT IS A TYPE OF AN EXCITABLE TISSUE
MUSCLES ARE THE MAIN EFFECTOR OF THE BODY.
ALSO KNOWN AS MOBILE TISSUE.
MUSCLES CONVERT DIFFERENT TYPES OF ENERGY IN CHEMICAL ENERGY.
THE MUSCLE FIBERS ARE UNSTABLE AND CAN GENERATE ACTION POTENTIAL.
PROPERTIES OF THE SKELETAL MUSCLE ARE AS BELLOW.
01) VOLUNTARY CONTROL
02) PHASIC MOVEMENTS
03) MULTI-NUCLEATED(NUCLEUS PRESENT ON THE PERIPHERY)
04) CALCIUM COMES FROM SARCOPLASMIC RETICULUM(S.R)
05) RMP IS -90mv.
06) TETANUS, TETANY. TATINIZATION ARE PRESENT.
07) SOMATIC NEVER SUPPLY
08) FATIGUE IS PRESENT
09) AEROBIC GLYCOLYSIS
10) TYPICAL NEUROMUSCULAR JUNCTION
11) CYLANDRICAL
12) A.T.P IS SOURCE OF ENERGY
13) HYPERTROPHY PRESENT
14) TRANSVERSE TUBULES PRESENT
15) SARCOMER PRESENT
PHYSIOLOGICAL ANATOMY OF SKELETAL MUSCLE
ONE FIBER CONTAIN MANY THOUSAND OF MYOFIBRILS
ONE MYOFIBRIL CONTAINS 1500 MYOSIN AND 3000 ACTIN FILAMENTS.
MYOSINS ARE THICK AND DARK COLORED FILAMENTS.
ACTINS ARE THIN AND LIGHT COLOR FILAMENTS.
SARCOMERE IS STRUCTURAL UNIT OF THE SKELETAL MUSCLE.
SARCOMERE CONTAINS MANY PROTION HAVING DIFFERENT COLORS
I-BAND(2 IN NUMBER) PRESENTADJACENT TO THE Z-LINE AND CONTAINS ONLY ACTIN FILAMENTS.
A-BAND(1 IN NUMBER) MAKE A BIG PORTION OF THE SARCOMERE CONTAINS SOME PORTION OF ACTIN AND ALL OF THE MYOSIN
FILAMENTS.
IN A-BAND A PORTION WHICH DO NOT HAVE ACTIN FILAMENTS CALLED H- BAND.
MID LINE WHICH HOLDS THE MYOSIN FILAMENTS CALLED M-LINE.
Z-LINE MAKES THE BOUNDERIES OF THE SARCOMERE.
MYOSIN GIVE RISE TO HOOK LIKE STRUCTURE CALLED "CROSS BRIDGE".
THESE CROSS BRIDGES WORKS FOR THE CONTRACTION BY BINDING THEIR HEADS ON ACTIN.
- "CNS" SEND MESSAGE TO "MOTOR
CORTEX" WHICH SEND THE MOTOR IMPULSES IN "SPINAL CORD".
- "SPINAL CORD" DELIVER THE IMPULSE TO
"ALPHA MOTOR NEURON" WHICH DELIVER IT TO THE "MOTOR
NERVE" OF THE SPECIFIC REGION.
- THROUGH "MOTOR NERVE" IMPULSE REACHES TO THE
PRESYNAPTIC MEMBRANE.
- TTHE ACTION POTENTIAL PROPAGATES BY ACTIVATING SODIUM
DEPENDENT CHANNELS ALONG THE AXON TOWARD THE SAYNAPTIC CLEFT.
- WHEN THE ACTION POTENTIAL REACHES THE MOTOR NEURON
TERMINAL AND CAUSES THE CALCIUM INFLUX THROUGH THE CALCIUM DEPENDENT
CHANNELS.
- IN PRESYNAPIC MEMBRANE IT CAUSES THE RELEASE OF THE
NEUROTRANSMITTER "ACETYLCOLINE" IN SYNAPTIC CLEFT WHICH BINDS
WITH RECEPTORS ON POST SYNAPTICS MEMBRANE.
- AFTER BINDING WITH RECEPTORS THERE IS OPENING OF
INTRINSIC SODIUM/POTASSIUM CHANNEL,
CAUSING SODIUM INFLUX AND POTASSIUM OUT FLUX WHICH
CAUSES THE "ACTION POTENTIAL".
- "ACTION POTENTIAL" THEN TRAVEL THROUGH OUT
THE FIBER.
- THIS ACTION POTENTIAL ACTIVATE THE SARCOPLASMIC
RETICULUM AND THIS ACTIVATION THUS RESULTS IN RELEASE OF THE CALCIUM IONS.
- CALCIUM BIND WITH TROPONIN-C WHICH PRESENT ON THE
ACTIN.THE TROPONIN THEN ALLOSTERICALLY MODULATES THE TROPOMYOSIN. NORMALLY
THE TROPOMYOSIN STERICALLY OBSTRUCT BINDING SITE FOR THE MYOSIN ON ACTIN
FILAMENT. ONE CALCIUM BINDS TO TROPONIN-C AND CAUSES CHANGE IN THE PROTEIN
OF THE TROPONIN THEN TROPONIN-T ALLOWS TROPOMYOSIN TO MOVE WHICH CAUSES
THE UNLOCKING THE BINDING SITE.
- MYOSIN BINDS TO UNCOVERED BINDING SITES ON ACTIN
FILAMENT.MYOSIN IS NOW STRONGLY BOUND WITH BINDING SITE OF ACTIN.
- THE RELEASE OF ADP & INORGANIC PHOSPHATE ARE
STRICTLY COUPLED THE THE POWER STROKE. THIS POWER STROKE WILL PULL THE
Z-BANDS TOWARDS EACH OTHER AND THUS CAUSE THE SHORTNING OF THE SARCOMERE.
- ATP WORKS FOR THE DETATCHMENT OF THE CROSS BRIDGES FROM
ACTIVE SITE OF ACTIN.
- NOTE IN THE ABSENCE OF ATP THERE WILL BE NO RALAXATION.
- RIGOR MORTIS IS ONE OF THE BEST EXAMPLE OF THAT.