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Endurance training improves gastrocnemius mitochondrial function despite increased susceptibility to permeability
José Lumini-Oliveira1, José Magalhães, Cláudia V Pereira
1Research Centre in Physical Activity, Health and Leisure, University of Porto, Portugal.
Mitochondrion
|August 18, 2009
Summary
Endurance training improves gastrocnemius mitochondrial function but unexpectedly increases susceptibility to calcium-induced mitochondrial permeability transition pore (MPTP) opening in rats.
Area of Science:
- Exercise Physiology
- Mitochondrial Biology
- Cellular Respiration
Background:
- Endurance training is known to enhance mitochondrial function.
- The effect of training on the mitochondrial permeability transition pore (MPTP) remains less understood.
- Investigating MPTP opening is crucial for understanding cellular adaptation to exercise.
Purpose of the Study:
- To test if moderate endurance treadmill training improves gastrocnemius mitochondrial bioenergetics.
- To determine if training increases tolerance to calcium-induced mitochondrial permeability transition pore (MPTP) opening.
Main Methods:
- Adult male Wistar rats were divided into sedentary and trained groups.
- Trained rats underwent 14 weeks of treadmill running (60 min/day).
- Gastrocnemius mitochondrial function, including oxygen consumption and MPTP opening susceptibility, was assessed in vitro. Caspase-9 activity was measured.
Main Results:
- Endurance training significantly increased state 3 respiration and respiratory control ratio with both complex I and II substrates.
- Increased CCCP-induced uncoupled respiration was observed with succinate.
- Contrary to the hypothesis, trained rats showed increased susceptibility to calcium-induced MPTP opening and elevated caspase-9 activity.
Conclusions:
- Endurance training enhances gastrocnemius mitochondrial respiratory function.
- Training leads to mitochondrial and cellular alterations that increase susceptibility to calcium-induced MPTP opening.
- The findings suggest a complex interplay between exercise adaptation and mitochondrial stability.

