A research group in the Department of Immunology at the Graduate School of Biomedical and Health Sciences, Hiroshima University, has shown that the molecule CaMKIIγ/δ, which functions in skeletal muscle during exercise, supports the improvement of endurance through training.
Skeletal muscles adapt to repeated exercise by changing how they produce energy to sustain movement for longer periods. CaMKII is known to be activated during exercise and to receive calcium signals generated by muscle contraction, but its involvement in endurance and muscle energy metabolism was unclear.
This research group investigated the functions of CaMKII molecules by using mice lacking CaMKIIγ and CaMKIIδ, which are components of CaMKII that are highly active in skeletal muscle.
When mice lacking CaMKIIγ/δ in skeletal muscle alone and normal mice were subjected to 4 weeks of endurance training and compared, the normal mice showed an average improvement of approximately 25% in maximum running time after training. On the other hand, the running ability of the CaMKII-deficient mice hardly improved. Furthermore, the CaMKII-deficient mice showed impaired metabolic function, including reduced function of genes involved in energy production and glucose breakdown, an increase in mitochondria with disrupted internal membrane structures, and decreased oxygen consumption.
These results suggest that CaMKIIγ/δ is an important molecule that maintains mitochondrial structure and function, and supports the adaptation of energy metabolism necessary for endurance training.
This study suggests that CaMKIIγ/δ may be one of the "exercise effect switches" that activate muscle energy production during exercise and support improved endurance. This discovery provides a clue to understanding, at the molecular level, how exercise enhances physical fitness. Further research is needed to confirm whether the same mechanism works in human muscles, but in the future, it is expected that this will lead to the development of methods to further enhance the effects of exercise by utilizing the function of CaMKIIγ/δ, as well as the development of drugs and rehabilitation methods to maintain the exercise capacity of people who cannot exercise sufficiently due to aging or disease.
Paper information: [Molecular Metabolism] CaMKIIγ/δ contributes to mitochondrial metabolic adaptation in skeletal muscle during endurance training
