Excessive training does not induce mitochondrial dysfunction or impair insulin signalling within skeletal muscle

Area of Science:

• Exercise Physiology
• Molecular Biology
• Metabolic Health

Background:

• Overtraining's impact on skeletal muscle mitochondrial function and glucose homeostasis is debated due to methodological challenges.
• Assessing mitochondrial bioenergetics alongside exercise-induced mitochondrial biogenesis is crucial for understanding overtraining's metabolic effects.

Purpose of the Study:

• To investigate skeletal muscle insulin signaling and mitochondrial bioenergetics following a 3-week overtraining protocol in highly trained endurance athletes.
• To determine if excessive training impairs mitochondrial function or induces insulin resistance in skeletal muscle.

Main Methods:

• A 3-week overtraining protocol was implemented in healthy, highly trained endurance athletes.
• Skeletal muscle proteomics, mitochondrial respiratory capacity, and insulin signaling (Akt phosphorylation) were assessed.
• Athletes were classified based on psycho-physiological performance into overreached and non-overreached phenotypes.

Main Results:

• Proteomics revealed increased proteins related to fatty acid metabolism and mitochondrial content post-overtraining.
• Mitochondrial respiratory capacity and H2O2 emission increased, indicating preserved oxidative phosphorylation.
• Despite increased oxidative stress, skeletal muscle insulin signaling (Akt phosphorylation) improved, showing no insulin resistance.
• Overreached athletes exhibited a blunted increase in proteins for cytoskeleton, glycogen metabolism, and protein translation.

Conclusions:

• Overtraining in highly active individuals stimulates mitochondrial biogenesis without impairing skeletal muscle mitochondrial oxidative capacity.
• Excessive training does not induce skeletal muscle insulin resistance; instead, insulin signaling appears improved.
• Specific proteome signatures characterize overreached athletes, with alterations in protein synthesis and metabolism pathways.