Excessive Exercise Training Causes Mitochondrial Functional Impairment and Decreases Glucose Tolerance in Healthy Volunteers

Summary by Utah Sports and Wellness

Exercise training positively affects metabolic health through increased glucose regulation:

Mitochondria are the primary source of cellular ATP synthesis.
The size and function of the mitochondrial pool are vital for metabolic health and muscular function.
Mitochondrial capacity is a strong proxy for metabolic function and health.
In many pathological states, mitochondria display a reduced ability to respond to nutrient supply.

Acute exercise increases the total Nrf2 protein within minutes:

Nfr2 is the master regulator of several hundred genes involved in the antioxidant defense.
Exercise training has proven to be a powerful tool to act as a preventative treatment against many metabolic disorders by stimulating glucose uptake.
Extreme amounts of exercise have been associated with negative effects on cardiac health.
In competitive sports, it is established exercise improves performance, whereas too much training leads to staleness and reduced performance.
There is a bell-shaped relationship between exercise training load and mitochondrial function.

These authors also note:

After the recovery phase, when training load is drastically reduced, performance peaks.
Mitochondrial function is an important determinant of insulin sensitivity.
Mitochondrial impairment is associated with impaired glucose tolerance.
Also assessed were the continuous blood glucose profiles in world-class endurance athletes. They had impaired glucose control compared with a matched control group.