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Related Concept Videos

Cross-bridge Cycle01:26

Cross-bridge Cycle

As muscle contracts, the overlap between the thin and thick filaments increases, decreasing the length of the sarcomere—the contractile unit of the muscle—using energy in the form of ATP. At the molecular level, this is a cyclic, multistep process that involves binding and hydrolysis of ATP, and movement of actin by myosin.
Smooth Muscle Contraction01:25

Smooth Muscle Contraction

Smooth muscle contraction is a complex process vital for various bodily functions, from maintaining blood vessel tension to facilitating the movement of food through the digestive tract. Unlike striated muscles, smooth muscle contraction begins more slowly and lasts longer.
The onset of contraction is triggered by an increase in calcium ions within the sarcoplasm, similar to the process in striated muscle. However, smooth muscles have a relatively smaller reservoir of the sarcoplasmic...
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.
Muscle Contraction01:10

Muscle Contraction

In skeletal muscles, acetylcholine is released by nerve terminals at the motor endplate—the point of synaptic communication between motor neurons and muscle fibers. The binding of acetylcholine to its receptors on the sarcolemma allows entry of sodium ions into the cell and triggers an action potential in the muscle cell. Thus, electrical signals from the brain are transmitted to the muscle. Subsequently, the enzyme acetylcholinesterase breaks down acetylcholine to prevent excessive muscle...
Muscle Contraction01:15

Muscle Contraction

The Role of Actin and Myosin in Non-muscle Cells01:10

The Role of Actin and Myosin in Non-muscle Cells

Actin and myosin or actomyosin filaments also play a significant role in cells other than those involved in muscle contraction (which occurs within the sarcomere of muscle cells). The mechanism of non-muscle cell contractile bundles was first observed in Dictyostelium and Acanthamoeba. In non-muscle cells, two bundles are commonly found: stress fibers and actomyosin adherence belts. These contractile bundles are smaller and less organized than the ones found in muscle cells. They  are held...

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Ex Vivo Assessment of Contractility, Fatigability and Alternans in Isolated Skeletal Muscles
14:02

Ex Vivo Assessment of Contractility, Fatigability and Alternans in Isolated Skeletal Muscles

Published on: November 1, 2012

Calpains, skeletal muscle function and exercise.

Robyn M Murphy1

  • 1Department of Zoology, La Trobe University, Melbourne, Victoria, Australia. r.murphy@latrobe.edu.au

Clinical and Experimental Pharmacology & Physiology
|October 2, 2009
PubMed
Summary
This summary is machine-generated.

Calpain-3, a muscle-specific protease, is activated 24 hours after eccentric exercise, suggesting its role in muscle repair. Ubiquitous calpains are not activated by exercise.

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Application of Chronic Stimulation to Study Contractile Activity-induced Rat Skeletal Muscle Phenotypic Adaptations

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Area of Science:

  • Muscle physiology and biochemistry
  • Enzymology
  • Molecular biology

Background:

  • Skeletal muscle contains ubiquitous (mu- and m-calpain) and muscle-specific (calpain-3) proteases involved in various cellular processes.
  • Calpain-3 deficiency causes limb-girdle muscular dystrophy Type 2A, highlighting its importance in muscle function.
  • Calpain activation is Ca(2+)-dependent, with activated forms indicating in vivo activity.

Purpose of the Study:

  • To investigate the activation patterns of mu-calpain and calpain-3 in skeletal muscle following different types of exercise.
  • To determine the physiological conditions leading to calpain-3 activation in skeletal muscle.

Main Methods:

  • Analysis of calpain activation states (autolysed vs. unautolysed forms) in skeletal muscle samples collected at various time points post-exercise.
  • In vitro studies exposing muscle fibers to controlled calcium concentrations and durations to mimic exercise-induced changes.

Main Results:

  • Neither mu-calpain nor calpain-3 were immediately activated after sprint, endurance, or eccentric exercise.
  • A significant portion of calpain-3, but not mu-calpain, was activated 24 hours post-eccentric exercise.
  • In vitro, calpain-3 activation occurred after prolonged exposure to elevated calcium levels (2-4x resting), consistent with post-eccentric exercise conditions.

Conclusions:

  • Eccentric exercise induces a delayed activation of calpain-3 in skeletal muscle.
  • The sustained, moderate increase in intracellular calcium following eccentric exercise is sufficient to activate calpain-3.
  • These findings support a role for calpain-3 in sarcomeric remodeling and muscle repair processes.