SKELETAL MUSCLE PHYSIOLOGY

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.