There have been very many studies published on the effects of exercise, especially of endurance/aerobic exercise, in restoring the number, the quality and the activity of mitochondria, both in the skeletal muscles, the heart and in the brain neurons. As these are our highest energy demanding tissues. Continuing the discussion, here are articles on effects of exercise in restoring mitochondria. The second link addresses the benefits of strength (resistance) training. The details of the physiology are pretty dense in the first one, but you can appreciate the overall implications. Every "dose" of exercise counts.
Effects of Exercise on Mitochondrial Content and Function in Aging Human Skeletal Muscle
ncbi.nlm.nih.gov/pmc/articl...
"Skeletal muscle mitochondria are implicated with age-related loss of function and insulin resistance. We examined the effects of exercise on skeletal muscle mitochondria in older (age=67.3±0.6 yr) men (n=5) and women (n=3). Similar increases in (P<0.01) cardiolipin (88.2±9.0 to 130.6±7.5 μg/mU creatine kinase activity (CK)) and the total mitochondrial DNA (1264±170 to 1895±273 copies per diploid of nuclear genome) reflected increased mitochondria content. Succinate oxidase activity, complexes 2–4 of the electron transport chain (ETC), increased from 0.13±0.02 to 0.20±0.02 U/mU CK (P<0.01). NADH oxidase activity, representing total ETC activity, increased from 0.51±0.09 to 1.00±0.09 U/mU CK (P<0.01). In conclusion, exercise enhances mitochondria ETC activity in older human skeletal muscle, particularly in subsarcolemma mitochondria, which is likely related to the concomitant increases in mitochondria biogenesis."
Impact of Resistance Training on Skeletal Muscle Mitochondrial Biogenesis, Content, and Function
pubmed.ncbi.nlm.nih.gov/289...
"Synthesis of new mitochondrial reticular components (i.e., mitochondrial biogenesis) has profound effect on mitochondrial content and function. Mitochondrial biogenesis is reported to be attenuated with aging, prolonged inactivity, and/or chronic disease. While metabolic stressors inherent of exercise possess the ability to stimulate mitochondrial biogenesis. In accordance, metabolic stress inherent of endurance exercise has been demonstrated to stimulate mitochondrial biogenesis which, when repeated through prolonged training (i.e., endurance training), can accumulate into changes in mitochondrial content and function. Employment of animal models has improved our understanding on the molecular mechanisms underlying endurance exercise-induced mitochondrial biogenesis. Accordingly, alterations in intramuscular homeostasis (e.g., alterations in AMP, calcium, and reactive oxygen species) inferred by endurance exercise exert regulatory action on specific proteins involved in transcriptional regulation of mitochondrial biogenesis."
"With regards to resistance exercise, high-load resistance exercise has been demonstrated to stimulate myofibrillar protein accretion, which upon prolonged training (i.e., resistance training) can accumulate into muscle hypertrophy. However, the necessity of conducting resistance exercise with high loads has more recently been challenged by studies demonstrating that lower-load resistance exercise performed to volitional fatigue, is equally capable as high-load resistance exercise in stimulating muscle growth.
Interestingly, several studies also suggest that resistance exercise can stimulate myocellular signaling for mitochondrial biogenesis, albeit to a relatively lesser degree than endurance exercise, depending on training status and exercise principles employed. However, the impact of differentiated resistance exercise regimens on skeletal muscle mitochondrial adaptations remain rather overlooked, despite potential clinical significance. Such knowledge could be beneficial in the attempt to identify a therapeutic exercise-based strategy for concurrent effect on mitochondrial and myofribrillar adaptations."
So exercise, both aerobic and intense resistance (strength) training, can reverse much of the accumulated damage and restore mitochondrial content, quality and efficiency. But it does not correct all of it. There is still some inexorable decline in mitochondrial function and respiratory efficiency related to accumulated ROS damage to the genetic (both nuclear and mitochondrial genomes) and the physiologic machinery of energy production. Perhaps certain mitochondrial-specific antioxidants and nutrients can help to protect the mitochondria and slow the process of decline. That will be addressed in the next post on the topic. - Paul/MateoBeach
