Stretch-activated ion channels contribute to membrane depolarization after eccentric contractions

Area of Science:

• Muscle Physiology
• Cellular Electrophysiology

Background:

• Eccentric contractions are known to cause muscle damage.
• The underlying mechanisms of cellular changes post-contraction are not fully understood.

Purpose of the Study:

• To investigate the role of mechanosensitive or stretch-activated ion channels (SAC) in skeletal muscle response to eccentric contractions.
• To determine the ion channel activity responsible for prolonged membrane depolarization.

Main Methods:

• Measurement of resting membrane potentials and contractile function in rat tibialis anterior muscles.
• Exposure to single or multiple series of eccentric contractions.
• Assessment of ion permeability changes and effects of specific channel inhibitors.

Main Results:

• Eccentric contractions induced significant and prolonged (>24 h) membrane depolarization in muscle fibers.
• Depolarization magnitude correlated with the number of contractions.
• Increased Na(+) influx was the primary cause, indicated by altered Na(+)/K(+) permeability ratio and partial repolarization with Na(+) substitution.
• Stretch-activated ion channel (SAC) inhibitors (streptomycin, Gd3+) caused significant membrane repolarization.
• Amiloride and TTX did not significantly affect depolarization.

Conclusions:

• Eccentric contractions activate Na(+)-selective stretch-activated ion channels (SAC) in skeletal muscle.
• SAC activation leads to prolonged membrane depolarization due to increased cation conductance, primarily Na(+) influx.
• These findings elucidate a key cellular mechanism following eccentric exercise.