Muscles and Muscle Tissue: Contraction, Metabolism, and Types of Muscle Contraction

Muscle Contraction and Relaxation

The Sliding Filament Mechanism

The sliding filament mechanism explains how muscle fibers contract by the interaction of thick and thin filaments within the sarcomere.

• Thick (myosin) and thin (actin) filaments slide past each other, shortening the sarcomere.

• Myosin heads pull on actin, causing the thin filaments to slide inward.

• Z discs move closer together, resulting in overall muscle contraction.

• Structural proteins transmit the force throughout the muscle, producing whole muscle contraction.

Changes in Sarcomere Bands During Contraction

• The I band and H zone decrease in size as the muscle contracts.

• The A band remains the same length.

The Cross Bridge Cycle

The cross bridge cycle describes the sequence of events that occur when myosin heads interact with actin filaments to produce muscle contraction.

1. Myosin head hydrolyzes ATP and becomes energized.

2. Myosin head binds to actin, forming a cross-bridge.

3. Myosin head pivots, pulling the thin filament toward the center of the sarcomere (power stroke).

4. As another ATP binds, the myosin head detaches from actin, and the cycle repeats.

Role of Calcium in Cross Bridge Cycling

• At low intracellular Ca2+ concentration:

  • Tropomyosin blocks active sites on actin.

  • Myosin heads cannot attach to actin; muscle fiber remains relaxed.

• At high intracellular Ca2+ concentration:

  • Ca2+ binds to troponin, causing a conformational change that moves tropomyosin away from myosin-binding sites on actin.

  • Myosin heads bind to actin, initiating contraction.

• When nervous stimulation ceases, Ca2+ is pumped back into the sarcoplasmic reticulum (SR), ending contraction.

Excitation-Contraction Coupling

Excitation-contraction (E-C) coupling is the process by which an action potential in the sarcolemma leads to muscle contraction.

• Transmission of the nerve impulse along the sarcolemma triggers the release of Ca2+ from the SR.

• Ca2+ initiates the sliding of filaments and sarcomere shortening.

Motor Neuron and Neuromuscular Junction (NMJ)

• Skeletal muscles are stimulated by somatic motor neurons.

• Axons of motor neurons branch and form neuromuscular junctions (NMJs) with muscle fibers.

Events at the Neuromuscular Junction

• Action potential arrives at the axon terminal.

• Voltage-gated Ca2+ channels open, causing exocytosis of acetylcholine (ACh) into the synaptic cleft.

• ACh binds to ligand-gated Na+ channels on the motor end plate, causing Na+ influx and muscle depolarization.

• Depolarization triggers Ca2+ release from the SR.

• ACh is broken down by acetylcholinesterase, terminating the signal.

Muscle Relaxation

• When stimulation ceases, Ca2+ is actively transported back into the SR (requires ATP).

• Tropomyosin re-blocks actin binding sites, inhibiting myosin-actin interaction and causing relaxation.

Rigor Mortis

• After death, Ca2+ floods the sarcoplasm, causing myosin and actin to bind.

• ATP is depleted, so myosin cannot detach from actin, resulting in muscle stiffness until tissue breakdown.

Muscle Metabolism

ATP Generation Pathways

Muscles derive ATP for contraction through three main pathways:

• Creatine phosphate (CP): Creatine kinase transfers a phosphate from CP to ADP, rapidly generating ATP (duration: ~15 seconds).

• Anaerobic glycolysis: Glucose is converted to pyruvic acid, yielding 2 ATP per glucose. Under low oxygen, pyruvic acid is converted to lactic acid (duration: ~2 minutes).

• Cellular (aerobic) respiration: Pyruvic acid enters mitochondria and is metabolized via the Krebs cycle and electron transport chain, producing 30–32 ATP per glucose (duration: several minutes to hours).

Muscle Metabolism at Different Activity Levels

• At rest: Muscles metabolize fatty acids and store glycogen.

• Light activity: ATP is generated aerobically from carbohydrates, lipids, or amino acids.

• Peak activity: Anaerobic metabolism predominates, producing lactic acid as a by-product.

Muscle Fatigue

Muscle fatigue is the inability to maintain force of contraction after prolonged activity.

• Causes include:

  • Inadequate Ca2+ release from SR

  • Depletion of CP, oxygen, and nutrients

  • Build-up of lactic acid and ADP

  • Insufficient ACh release at NMJ

  • Central fatigue (CNS changes)

Oxygen Debt (Excess Post-exercise Oxygen Consumption, EPOC)

• After exercise, heavy breathing continues to restore metabolic conditions.

• Extra oxygen is used to:

  • Replenish CP stores

  • Convert lactate to pyruvate

  • Reload O2 onto myoglobin

Types of Muscle Contraction

The Motor Unit

• A motor unit consists of one motor neuron and all the muscle fibers it innervates.

• Smaller motor units allow for finer control of muscle contraction.

• Muscle fibers from a motor unit are distributed throughout the muscle, so stimulation causes a weak contraction of the entire muscle.

Twitch Contraction

• A muscle twitch is a brief contraction of all muscle fibers in a motor unit in response to a single action potential.

• Phases:

  • Latent period

  • Contraction period

  • Relaxation period

Wave Summation and Tetanus

• Wave summation: A second stimulus triggers a stronger contraction before the first has relaxed.

• Unfused (incomplete) tetanus: Partial relaxation between stimuli; contractions build on each other.

• Fused (complete) tetanus: No relaxation between stimuli; sustained maximal tension.

Isotonic and Isometric Contractions

• Isotonic contraction: Muscle changes length while tension remains constant.

  • Concentric: Muscle shortens as it contracts (tension > load).

  • Eccentric: Muscle lengthens as it contracts (tension < load).

• Isometric contraction: Muscle develops tension but does not change length; no movement occurs.

Muscle Interactions

• Agonist (prime mover): Main muscle responsible for a movement.

• Antagonist: Muscle that opposes the action of the agonist.

• Synergist (fixator): Assists the agonist by adding force or reducing undesirable movements.

Comparison of Muscle Metabolism Pathways

Pathway	ATP Yield	Duration	By-products
Creatine Phosphate	1 ATP per CP	~15 seconds	Creatine
Anaerobic Glycolysis	2 ATP per glucose	~2 minutes	Lactic acid
Aerobic Respiration	30–32 ATP per glucose	Minutes to hours	CO2, H2O

Key Equations

• ATP generation from creatine phosphate: $\text{Creatine~phosphate} + \text{ADP} \xrightarrow{\text{creatine~kinase}} \text{Creatine} + \text{ATP}$

• Anaerobic glycolysis: $\text{Glucose} \rightarrow 2~\text{Pyruvic~acid} + 2~\text{ATP}$

• Aerobic respiration (overall): $\text{Glucose} + 6~\text{O}_2 \rightarrow 6~\text{CO}_2 + 6~\text{H}_2O + 30~\text{to}~32~\text{ATP}$

General Benefits of Muscle Exercise

• Weight control

• Improved muscle tone and posture

• Normalized blood sugar and insulin levels

• Improved circulation of blood and lymph

• Increased energy flexibility

Sample Questions and Answers

• True or False: An increase in sarcoplasmic Ca2+ starts thin filament sliding; a decrease stops it. True.

• True or False: During contraction, I bands and H zones diminish, A bands remain unchanged. True.

• In order for cross bridges to form, Ca2+ must: Bind to troponin, which moves tropomyosin (correct answer: B).

• Which is the correct sequence for muscle contraction? Motor neuron action potential → neurotransmitter release → muscle cell action potential → Ca2+ release from SR → ATP-driven power stroke → sliding of myofilaments (correct answer: A).

• Curare poisoning symptoms: Curare blocks ACh receptors, preventing muscle contraction, leading to paralysis.

• Anaerobic pathway yielding 2 ATP and 2 pyruvic acid: Glycolysis.

• If ATP production stops, myosin binds to actin but cannot detach, causing muscle rigidity (as in rigor mortis).

• In isotonic contraction, muscle changes length and moves the load (A).

• Complete tetanus involves development of maximum tension (B).

Additional info: This guide expands on the provided slides with definitions, explanations, and academic context for clarity and completeness.