People afflicted with metabolism-related diseases, from obesity and Type 1 diabetes to cancer, following recommended exercise programs could find that physical activity is not having the desired benefits if they are lacking in the protein p53. York researchers have found that the lack of this protein reduces the benefits of endurance exercise on skeletal muscles.
David Hood
“Since many different diseases, from obesity to cancer, implement exercise as part of the treatment strategy to improve health, it is important for us to understand what cellular changes are taking place with the onset of exercise,” says York Faculty of Health Professor David Hood, principal investigator of the study, along with Ayesha Saleem, the lead author on the paper, and Heather N. Carter.
The research looked at the importance of p53 in altering cell communication within muscles and found it is “a necessary protein for conveying cellular signals during endurance exercise”, says Saleem. “This finding enhances our understanding of the cellular communication system within muscle cells, and brings to light a specific protein that is necessary for promoting the positive benefits of exercise.”
The p53 protein, usually found inside the nucleus of the cell, normally serves to suppress cancer development. Exercise promotes the movement of p53 to the mitochondria where it plays a role in maintaining mitochondrial function by affecting the small amount of DNA found there. It has been shown previously that an absence of the protein could lead to a greater incidence of cancer and lower aerobic capacity.
Ayesha Saleem
“Our data indicate that after a single bout of exercise, lack of p53 protein in the muscle reduces and/or completely abolishes the activation of information signaling vital to translating the benefits of endurance activity into beneficial muscle adaptations,” says Hood, Director of the Muscle Health Research Centre and Canada Research Chair in Cell Physiology in the School of Kinesiology and Health Science.
Improvements in aerobic performance, endurance and metabolism, which come from regular endurance exercise training, are brought about by changes in the activation of molecules within each muscle cell. This includes the activation of multiple proteins which control cell signaling and communication pathways during exercise.
“A better understanding of the communication system that gets turned on with an acute bout of exercise is imperative for the future of exercise as a therapeutic tool in treating conditions like obesity, Type 2 diabetes, cardiovascular disease, and certain types of cancer,” says Hood.
Keeping these findings in mind when implementing exercise programs may assist in tailoring the exercise dosage to optimize the resulting adaptations. “This information also helps us understand one potential reason for the greater fatigability and lesser endurance capacity in cancer patients,” says Saleem.
The article, “p53 is Necessary for the Adaptive Changes in Cellular Milieu Subsequent to an Acute Bout of Endurance Exercise”, was published Feb. 1 in the American Journal of Physiology, Cell Physiology.