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Related Concept Videos

Relaxation of Skeletal Muscles01:29

Relaxation of Skeletal Muscles

The period of muscle contraction primarily influences the duration of stimulation at the neuromuscular junction (NMJ), the presence of free calcium ions in the sarcoplasm, and the availability of energy or ATP to support contractions.
When an action potential reaches the axon terminal, it depolarizes the membrane and opens voltage-gated sodium channels. Sodium ions enter the cell, further depolarizing the presynaptic membrane. This depolarization causes voltage-gated calcium channels to open.
Depolarizing Blockers: Mechanism of Action01:28

Depolarizing Blockers: Mechanism of Action

Depolarizing blockers act on skeletal muscle fibers' membranes and induce their depolarization. Most depolarizing blockers have two quaternary N+ atoms that bind the nicotinic acetylcholine receptors and cause neuromuscular blockade within minutes.
Succinylcholine is the most commonly used depolarizing blocker. Chemically, it constitutes two molecules of acetylcholine joined together by an acetate methyl group. They act on the receptors in the same way as acetylcholine. Because succinylcholine...
Antihypertensive Drugs: Potassium-Sparing Diuretics01:28

Antihypertensive Drugs: Potassium-Sparing Diuretics

Liddle syndrome is a genetically inherited form of hypertension characterized by the overactivity of epithelial sodium channels in the nephron, the functional unit of the kidney. This heightened activity leads to increased sodium reabsorption and excessive excretion of potassium. To counteract this, potassium-sparing diuretics such as amiloride are used. They function by blocking these sodium channels, thereby reducing the influx of sodium into the epithelial cells and minimizing the loss of...
Neuromuscular Junction And Blockade01:29

Neuromuscular Junction And Blockade

The site of chemical communication between a motor neuron and a muscle fiber is called the neuromuscular junction (NMJ). The end of the motor neuron at the NMJ divides into a cluster of synaptic end bulbs. The cytoplasm of these bulbs consists of synaptic vesicles enclosing acetylcholine molecules, the principal neurotransmitter released at the NMJ. The region opposite the synaptic bulb that ends in the muscle fiber is called the motor end plate, which has acetylcholine receptors. Within the...
Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacological Actions01:27

Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacological Actions

Nondepolarizing neuromuscular blockers prevent the membrane depolarization of muscle cells and inhibit muscle contraction. These are usually administered with anesthetics to achieve complete muscle relaxation. Upon administration, these drugs first block the small, rapidly contracting muscles of the face and hands, followed by the larger muscles of the trunk and the intercostal muscles. The diaphragm is the last muscle to be affected.
Although all competitive neuromuscular blockers are designed...
Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action01:17

Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action

Nondepolarizing neuromuscular blockers induce paralysis by competitively blocking nicotinic acetylcholine receptors at the muscle end plate. Examples include pancuronium, mivacurium, vecuronium, and rocuronium. These quaternary ammonium derivatives are administered intravenously, are poorly absorbed, and are excreted via the kidneys.
Competitive antagonists prevent acetylcholine from binding to its receptor, inhibiting membrane depolarization. Without conformational changes or intrinsic...

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Application of Chronic Stimulation to Study Contractile Activity-induced Rat Skeletal Muscle Phenotypic Adaptations
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Stretch-activated ion channel blockade attenuates adaptations to eccentric exercise.

Timothy A Butterfield1, Thomas M Best

  • 1Division of Athletic Training, Department of Rehabilitation Sciences, College of Health Sciences, University of Kentucky, Lexington, KY, USA. tim.butterfield@uky.edu

Medicine and Science in Sports and Exercise
|January 8, 2009
PubMed
Summary

Stretch-activated ion channel (SAC) function is crucial for skeletal muscle adaptation to eccentric exercise. Blocking SAC function reduces but does not eliminate the repeated bout effect (RBE), indicating partial SAC dependence.

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Area of Science:

  • Muscle physiology
  • Mechanobiology
  • Exercise science

Background:

  • The repeated bout effect (RBE) describes skeletal muscle's increased resistance to damage after prior exercise.
  • Stretch-activated ion channels (SACs) are mechanosensitive channels in the muscle membrane.
  • The role of SACs in mediating RBE adaptations is not fully understood.

Purpose of the Study:

  • To investigate if SAC function is essential for the RBE in skeletal muscle.
  • To determine if blocking SACs with streptomycin abrogates muscle's adaptive resistance to eccentric exercise.
  • To test if abrogating the RBE is due to a lack of functional adaptations like increased torque or hypertrophy.

Main Methods:

  • Twelve rabbits underwent 12 eccentric exercise bouts over 4 weeks.
  • Rabbits received daily injections of streptomycin (SAC blocker) or sham injections.
  • Biomechanical parameters, muscle hypertrophy, and torque-angle relationships were assessed.

Main Results:

  • Blocking SAC function eliminated expected adaptive responses in biomechanical parameters.
  • An acquired RBE was still observed, but it was attenuated compared to controls.
  • Functional adaptations associated with the RBE were dependent on intact SAC function.

Conclusions:

  • Sarcolemmal SACs are critical for functional adaptations following eccentric exercise.
  • Despite blocking SACs, some degree of RBE was still present in chronically exercised muscles.
  • The signaling cascade for RBE adaptations during eccentric exercise relies on intact SAC function.