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Assessment of Murine Exercise Endurance Without the Use of a Shock Grid: An Alternative to Forced Exercise
Published on: August 14, 2014
Endurance exercise is protective for mice with mitochondrial myopathy
Tina Wenz1, Francisca Diaz, Dayami Hernandez
1Dept. of Neurology, Miller School of Medicine, Univ. of Miami, 1095 NW 14th Terrace, Miami, FL 33136, USA.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|March 17, 2009
Summary
Endurance exercise boosts mitochondrial function and extends lifespan in a mouse model of mitochondrial myopathy. This approach, by increasing PGC-1alpha and mitochondrial biogenesis, offers a potential therapeutic strategy for this inherited neurological disorder.
Area of Science:
- Biomedical Science
- Neurology
- Exercise Physiology
Background:
- Mitochondrial ATP-generating defects cause inherited neurological disorders with no current treatments.
- Peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha) modulation shows therapeutic potential in mitochondrial myopathy models.
- Endurance exercise is known to increase muscle PGC-1alpha levels.
Purpose of the Study:
- To investigate if endurance exercise provides therapeutic benefits in a mouse model of mitochondrial myopathy.
- To determine the effects of endurance exercise on PGC-1alpha levels, mitochondrial biogenesis, and oxidative capacity in affected muscle.
Main Methods:
- Male and female mice with cytochrome-c oxidase deficiency-induced mitochondrial myopathy were subjected to endurance exercise training.
- Phenotypical and metabolic changes were monitored in exercised mice, sedentary myopathy mice, and wild-type controls.
- PGC-1alpha levels, mitochondrial biogenesis, ATP levels, and antioxidant enzyme activity were assessed.
Main Results:
- Exercise significantly increased PGC-1alpha levels and mitochondrial biogenesis in the skeletal muscle of myopathy mice.
- Residual respiratory capacity and ATP levels were enhanced in exercised mice compared to sedentary controls.
- Endurance exercise delayed disease onset, prolonged lifespan, and induced antioxidant enzymes in the mouse model.
Conclusions:
- Endurance exercise effectively stimulates mitochondrial biogenesis and enhances residual oxidative phosphorylation in affected muscle.
- This approach offers a promising, non-pharmacological therapeutic intervention for mitochondrial myopathy.
- Stimulating mitochondrial function through exercise may represent a valuable strategy for treating patients with inherited mitochondrial disorders.
