Acute High-Intensity Exercise Impairs Skeletal Muscle Respiratory Capacity

Area of Science:

• Exercise Physiology
• Mitochondrial Biology
• Skeletal Muscle Metabolism

Background:

• The impact of acute, high-intensity exercise on mitochondrial respiratory complex function remains unclear.
• Understanding these effects is crucial for both healthy individuals and those in exercise rehabilitation programs.

Purpose of the Study:

• To comprehensively investigate electron transport chain (ETC) respiratory flux in skeletal muscle mitochondria.
• To compare mitochondrial function before and immediately after high-intensity aerobic exercise.

Main Methods:

• Skeletal muscle biopsies (vastus lateralis) were collected pre- and post-exercise (5-km time trial).
• Mitochondrial respiratory flux was measured using high-resolution respirometry in permeabilized muscle fibers.

Main Results:

• Oxidative phosphorylation capacity (state 3CI + CII respiration) significantly decreased post-exercise (27 to 17 ρm·mg·s).
• This reduction was mainly driven by diminished complex II-dependent respiration (state 3CII; 17 to 9 ρm·mg·s).
• Complex I respiration showed a non-significant trend downwards; Complex IV capacity and proton leak were unaffected.

Conclusions:

• Acute high-intensity aerobic exercise significantly inhibits skeletal muscle oxidative phosphorylation capacity and complex II function.
• This transient mitochondrial impairment may contribute to exercise-induced fatigue and initiate adaptive responses.