Short-term bed rest-induced insulin resistance cannot be explained by increased mitochondrial H₂ O₂ emission

Area of Science:

• Exercise Physiology
• Mitochondrial Biology
• Metabolic Health

Background:

• Mitochondrial hydrogen peroxide (H2O2) is linked to diet-induced insulin resistance.
• The role of muscle disuse, such as from bed rest, in increasing mitochondrial H2O2 and insulin resistance is unclear.

Purpose of the Study:

• To investigate if short-term bed rest increases skeletal muscle mitochondrial H2O2 emission.
• To determine if increased mitochondrial H2O2 contributes to cellular redox stress and insulin resistance during bed rest.

Main Methods:

• Healthy males underwent a period of short-term bed rest.
• Hyperinsulinaemic-euglycaemic clamp assessed insulin sensitivity.
• Mitochondrial respiration and H2O2 emission were measured in skeletal muscle fibers.

Main Results:

• Bed rest reduced insulin sensitivity (glucose infusion rate) and impaired mitochondrial respiration.
• Maximal mitochondrial H2O2 emission showed a trend towards increase (P=0.053).
• H2O2 emission at resting ADP levels, the H2O2/O2 consumption ratio, and oxidative stress markers remained unchanged.

Conclusions:

• Short-term bed rest impairs mitochondrial ADP-stimulated respiration.
• Increased mitochondrial H2O2 emission does not appear to contribute to bed rest-induced insulin resistance.