Mitochondria and Exercise

📖 Literature Information and Japanese Abstract Translation

Impact of aging and lifelong exercise training on mitochondrial function and network connectivity in human skeletal muscle

[Background/Objective] Aging is accompanied by a decline in skeletal muscle metabolism, but this can be delayed by physical activity. Furthermore, in mouse skeletal muscle, both lifelong exercise training and short-term exercise training have been shown to prevent age-related fragmentation of the mitochondrial network. However, it is not yet clear whether lifelong endurance exercise training exerts similar effects in human skeletal muscle. Therefore, the purpose of this study was to examine the effects of volume-dependent lifelong endurance exercise training on mitochondrial function and network connectivity in elderly human skeletal muscle.

[Methods-Results]
■ Mitochondrial oxygen consumption
・Complex I+II-linked ADP-stimulated respiration was approximately 1.5 times higher in highly trained elderly subjects than in untrained elderly and trained elderly subjects (p < .05), and maximal respiration differed overall between groups.
・Intrinsic complex I-linked and intrinsic complex I+II-linked ADP-stimulated respiration did not differ between young untrained subjects and elderly untrained subjects, but were ~40%–60% lower in highly trained elderly subjects than in young untrained and elderly untrained subjects (p < .05).

■ Mitochondrial activity and content
・Vastus lateralis CS activity (μmol - min-1 - mg-1 protein) did not differ between young untrained subjects and elderly untrained subjects, but was ~2.5 times higher in highly trained elderly subjects compared to untrained subjects and trained elderly subjects (p < .05).
・Content of complex I (subunit NDUFB8), complex II (subunit SDHB), complex III (subunit UQCRC2), complex IV (subunit MTCO1), and complex V (subunit ATP5A) were all found to be higher in the vastus lateralis of highly trained elderly subjects than in young untrained, elderly untrained, and elderly trained subjects (p < .05).
・Total OXPHOS protein (sum of the five complexes) was similar in untrained young subjects and untrained elderly subjects, but was ~1.6 times higher (p < .05) in highly trained elderly subjects than in untrained and trained elderly subjects.

■ Mitochondrial network
・The proportion of MHC II-positive fibers in skeletal muscle was similar among young untrained, elderly untrained, elderly trained, and highly trained elderly subjects, but the proportion of MHC I-positive fibers was higher in elderly trained and highly trained elderly subjects than in young untrained or elderly untrained subjects (p < .05).

🌱 So What?: What did I find interesting?

When I first read it, I thought, 'Is this true!? What is this text!?'
But now, I am connecting the dots.
High-intensity training really does increase mitochondria, densifies the network structure, and enhances oxygen consumption.
This study I read today showed that with beautiful diagrams.

Mitochondria are waiting for our motivation.

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