Contractions of  Skeletal Muscle

• Latent period - Interval between the AP in a muscle fiber and the initiation of contraction.
• Twitch - Single muscle contraction and relaxation produced by a single stimulus.

• Strength of a muscle contraction can be graded, or varied, depending on the number of muscle cells stimulated..

• Summation - The addition of 2 or more twitches as a result of rapidly repetitive stimulation, resulting in greater strength of contraction (tension) than is produced by a single contraction alone.
• Complete tetanus - Smooth, sustained maximal muscle contraction that occurs so rapidly that it does not have a chance to relax between stimuli.
• Fatigue - Inability to maintain muscle tension at a given level despite sustained stimulation.

          Possible causes of fatigue include: accumulation of extracellular K⁺, reduction of glycogen, increased lactic acid production, ATP depletion, and changes in the CNS (central fatigue).

• Types of contractions:

• Isotonic contraction - Contraction in which muscle tension remains constant as the muscle fiber length changes. As a result the muscle shortens.
• Isometric contraction - Contraction in which the development of tension occurs at constant muscle length.

• Isometric contractions can be converted to isotonic contractions and vice versa.

• Series-elastic component - The noncontractile portions associated with skeletal muscle that are arranged in series (e.g., tendons and other connective tissues). These must be pulled tight in order for muscle to shorten.

• Length-Tension Relationship - Relationship between the amount of overlap between the proteins actin and myosin and the tension developed by a sarcomere.  It states that maximum tension can be achieved when muscle is at its "ideal" resting length. Can be explained on the basis of the sliding filament mechanism.  This relationship applies to whole muscle as well.

• Neural control of skeletal muscle is mostly voluntary.
• Upper motor neurons are neurons in the brain that control the activity of the lower motor neurons.
• Lower (alpha) motor neurons are responsible for directly stimulating muscle contraction.  Cell bodies are located in the ventral horn of the gray matter of the spinal cord.
• Each muscle fiber receives a single axon terminal from the somatic motor neuron.
• Acetylcholine (ACh) is the neurotransmitter released from the motor neuron.
• Motor unit - A somatic motor neuron and all the muscle fibers that it innervates.
• When a motor neuron is activated, all of the muscle fibers innervated by that motor neuron are stimulated to contract in an all-or-none fashion.
• Fine neural control occurs when there are many small motor units involved (e.g., compare extraocular vs gastrocnemius muscles).

How can muscle tension be graded?

• Can adjust the # of fibers contracting within a muscle. (Recruitment of more or larger motor units)
• Can adjust the tension developed by each fiber. (Frequency of stimulation, length of fiber at onset of contraction, extent of fatigue, thickness of fiber)

• Recruitment - The stimulation of more and/or larger motor units in order to produce increasing strengths of muscle contraction.

Structural Basis of Contraction:

• There is a hierarchical arrangement of skeletal muscle which is also called striated or voluntary muscle.
• Muscle cells = fibers or myofibers
• Each fiber is made up of myofibrils which contain myofilaments = filaments.
• Each myofibril consists of longitudinally repeating units called sarcomeres, which span two Z lines (Z discs) and are the functional units of skeletal muscle.
• Striations are produced by alternating dark and light bands.

• A band - Dark band; contains thick filaments made up of myosin (protein) and some thin filaments. Myosin has small projections called cross bridges.
• I band - Light band; contains thin filaments made up of actin (protein); associated with this band are 2 other proteins, tropomyosin and troponin; spans 2 sarcomeres.
• H band - Lighter region in the center of the A band; no thin filaments.
• M line - Lies in the middle of the H band; anchor thick filaments.

Mechanisms of Contraction (Sliding Filament Mechanism or Theory):

• Sarcomeres shorten by decreasing the distance between Z lines.
• Thick and thin filaments remain the same length.
• A bands remain the same length, but successive bands move closer together.
• I bands decrease in length.
• H bands shorten as thin filaments are pulled toward the middle.

• Sliding of filaments is produced by the action of numerous cross-bridges that extend from the myosin toward the actin.
• At rest, the cross-bridges are not attached to actin.
• Cross bridge "heads" act as myosin ATPase enzymes that split ATP ADP + P_i. This activates the cross-bridge.
• When the activated cross-bridges attach to actin, they undergo a power stroke and in the process release P_i.
• At the end of the power stroke, a new ATP binds to the cross- bridge, allowing it to detach from actin and repeat the cycle. ADP is released when a new ATP binds to myosin.

• Inability of cross-bridges to detach from actin due to a lack of ATP is called rigor mortis.

• State of rigidity of muscle that occurs after death. Muscles remain in rigor until muscle proteins are broken down.

• Associated with actin are 2 other proteins called troponin and tropomyosin.

• Tropomyosin lies within a groove of actin molecules.
• Troponin is attached to tropomyosin.

• In a relaxed muscle, the position of tropomyosin in the thin filaments physically blocks cross-bridge binding to actin. Therefore, tropomyosin must be moved for the myosin to attach to actin.
• Binding of Ca²⁺ to troponin causes a conformational change that moves troponin and its attached tropomyosin out of the way so that the cross-bridges can attach to actin. This is followed by the power strokes and muscle contraction.

Excitation-Contraction Coupling:

• Ca²⁺ is stored within the terminal cisternae (= lateral sacs) of the sarcoplasmic reticulum (SR).
• Transverse (T) tubules - Narrow "tunnels" that are continuous with the cell membrane and conduct AP's deep into the muscle fiber.
• AP's in the T tubule stimulate Ca²⁺ release from the terminal cisternae.
• When AP's stop being produced, Ca²⁺-ATPase pumps in the SR actively transport Ca²⁺ and tropomyosin moves again to its inhibitory position.

1. AP's in a somatic motor neuron cause the release of acetylcholine at the neuromuscular (myoneural) junction.
2. ACh binds to nicotinic receptors on the motor end plate and produces an end-plate potential (epp).  EPP's can summate to produce an AP.
3. AP's are conducted across the sarcolemma (plasma membrane.)
4. T tubules conduct AP's deep into the muscle fiber.
5. AP's in the T tubule stimulate the release of Ca²⁺ from the terminal cisternae of SR.
6. Ca²⁺ attaches to troponin, causing a change in its structure.
7. Shape change in troponin causes tropomyosin to shift position in the actin filament, thus exposing binding sites for the myosin cross-bridges.
8. Myosin cross-bridges bind ATP (activating them), attach to actin, and undergo a power stroke that pulls the thin filaments over the thick filaments. ADP and P_i are released from the cross-bridge during the process.
9. Attachment of another ATP allows the cross-bridges to detach from actin and repeat the cross-bridge cycle over and over again as long as Ca²⁺ remains attached to troponin.
10. When AP's stop being produced, the SR actively accumulates Ca²⁺ and tropomyosin returns to its inhibitory position.

Note: See pages 186-187 (Acetylcholinesterase and Acetylcholine in the PNS) for additional information regarding the neuromuscular junction and learn the following terms: motor end-plate and end-plate potentials.

The neuromuscular junction is vulnerable to several chemicals such as:

Black widow spider toxin - Causes explosive release of ACh.

Botulinum toxin - Inhibits release of ACh.

Curare - Nicotinic ACh receptor blocker.

Nerve gas (e.g., Sarin) - Irreversibly inhibits acetylcholinesterase (AChE).

• Comes from ATP.
• ATP is required for cross bridge activity and for pumping calcium back into the SR by active transport.
• During sustained muscle contraction, ATP may be utilized faster than the rate at which it can be replenished.
• The immediate energy source tapped to replenish ATP is from creatine phosphate.

		Creatine kinase
Creatine phosphate	+ ADP		Creatine + ATP
(Phosphocreatine)
(Stored in resting muscle)

• Other sources of ATP

• Oxidative phosphorylation  

• Main source when O₂ is present (aerobic conditions.)
• Fueled by glucose or fatty acids.

• Glycolysis

• Main source when O₂ is not present (anaerobic conditions).
• Uses glucose obtained from blood or from glycogen.
• Can produce lactic acid (derived from pyruvic acid) in absence of O₂.

• Oxygen for muscle function is supplied by the bloodstream via hemoglobin and by myoglobin (a muscle pigment similar to hemoglobin that stores and releases oxygen to the muscles when required).

• Types of skeletal muscle fibers (Different types because our bodies use muscles for a wide variety of activities.)

• Slow-oxidative fibers - Useful for endurance events
• Fast-oxidative fibers - Useful for power and sprint events
• Fast-glycolytic fibers - Useful for power and sprint events

• Differ in speed of contraction (time required to reach maximum tension) and method of ATP formation.

Type of Fiber

Characteristic	Slow-Oxidative	Fast-Oxidative	Fast-Glycolytic
Myosin-ATPase Content	Low	High	High
Speed of Contraction = twitch rate	Slow	Fast	Fast
Resistance to Fatigue	High	Intermediate	Low
Myoglobin Content	High	High	Low
Color of Fiber	Red	Red	White

• How do muscles increase in size? Hypertrophy or hyperplasia?

Mechanism of Smooth Muscle Contraction

• Smooth muscle myosin is able to interact with actin only when myosin is phosphorylated (has a phosphate group attached to it).

Comparisons of Skeletal, Smooth and Cardiac Muscles

Characteristic	Skeletal	Smooth (Single-Unit*)	Cardiac
Location	Attached to bones	Walls of hollow organs	Heart
Mechanism of Contraction	Sliding Filament (SF)	SF	SF
Neural Control	Somatic NS, voluntary	ANS, involuntary	ANS, involuntary
Initiation of Contraction	Neurogenic	Myogenic	Myogenic (due to pacemaker)
Presence of myosin and actin	Yes	Yes	Yes
Striated	Yes	No	Yes
Presence of troponin and tropomyosin	Yes	Tropomyosin only (Doesn’t block actin binding site)	Yes
Presence of T tubules	Yes	No	Yes
Presence of gap junctions	No	Yes	Yes (at intercalated discs)
Uses calcium in contraction	Yes - From SR	Yes - From SR and ECF	Yes - From SR and ECF
Speed of Contraction	Fast or slow, depends on fiber type	Very Slow	Slow
Modified by hormones	No	Yes	Yes
Sarcoplasmic reticulum	Well-developed	Poorly developed	Moderately developed
L-T Relationship	Yes	No	Yes

*Single-unit smooth muscle - Some cells must be stimulated by an axon and the remaining cells are coupled to one another via gap junctions.

  Multiunit smooth muscle - Each cell must be stimulated by an axon.

ECF = extracellular fluid

 

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