New research has uncovered how mitochondria – the energy powerhouse of our cells implicated in devastating mitochondrial disease, type 2 diabetes, and cancers – respond to exercise training in unprecedented detail.
A joint study between the University of Melbourne and Victoria University, with collaborators at the German Diabetes Center, Monash University, and the Murdoch Children’s Research Institute, have successfully linked minutes of exercise to specific mitochondrial changes that support improved metabolism.
In work published in Nature Communications recently, the University of Melbourne’s Dr. Stroud from the School of Biomedical Sciences, and colleagues detail how they used state-of-the art equipment at the University of Melbourne’s Bio21 Molecular Science and Biotechnology Institute’s Mass Spectrometry and Proteomics Faculty to analyze in detail how our muscles respond to exercise.
While mitochondria are hugely important as they convert sugars, fats, and protein into energy used for muscle contraction, cell growth, and brain activity among other things, maintaining mitochondrial health is critical not just to various debilitating disease states where mitochondrial function is impaired, but also the quality of life of otherwise healthy people.
The team was able to discover ten times more mitochondrial proteins that respond to exercise training than documented in previous studies.
“Some 726 of the proteins were identified, of which 185 were altered with exercise, but we are most excited by the breadth of changes identified as well as the method we developed to detect these changes – previously, research groups have observed more mitochondria overall but didn’t assume much changed, by using our method we identified a previously unseen intricacy in changes,” Dr. Stroud said.
“We hope the method can now be applied to focused studies where we look at different types of exercise to elicit certain responses – for example increasing a certain function of mitochondria to counteract another function that may be defective in a patient with type 2 diabetes.”
The new findings challenge current exercise recommendations and highlight the well-documented therapeutic benefits of exercise training, and how it can be optimized by increasing the length of time that we exercise.
Professor David Bishop from Victoria University and former president of Exercise and Sport Science Australia said: “Regular exercise is an inexpensive therapeutic intervention that can improve our quality of life. As around 20 percent of people don’t get any health benefits following current exercise guidelines, our findings may lead to different exercise recommendations targeted to improving mitochondrial function. We really want this knowledge to help exercise and health professionals to design more personalized training interventions focused to specific conditions where mitochondrial function is implicated.”
Reference: “High-intensity training induces non-stoichiometric changes in the mitochondrial proteome of human skeletal muscle without reorganisation of respiratory chain content” by Cesare Granata, Nikeisha J. Caruana, Javier Botella, Nicholas A. Jamnick, Kevin Huynh, Jujiao Kuang, Hans A. Janssen, Boris Reljic, Natalie A. Mellett, Adrienne Laskowski, Tegan L. Stait, Ann E. Frazier, Melinda T. Coughlan, Peter J. Meikle, David R. Thorburn, David A. Stroud and David J. Bishop, 3 December 2021, Nature Communications.