A new literature review finds that about one in five people with type 2 diabetes do not respond favorably to exercise…
Exercise benefits most, but not all, individuals with type 2 diabetes (T2D). The beneficial effects are well studied, but why some individuals do not respond favorably to exercise training is largely unexplored. It is critical to treatment and prevention strategies to identify individuals with T2D that have a blunted metabolic response to exercise and investigate the underlying mechanisms that might predict this “programmed response to fail.”
The researchers carried out a systematic review of classic and contemporary primary reports on clinical human and animal exercise studies. They referenced unpublished data from their previous studies, as well those of collaborators. Genetic and epigenetic components and their associations with the exercise response were also examined.
As evidence of the exercise resistance premise, the researchers found that supervised exercise training results in substantial response variations in glucose homeostasis, insulin sensitivity, and muscle mitochondrial density, wherein approximately 15–20% of individuals fail to improve their metabolic health with exercise. Classic genetic studies have shown that the extent of the exercise training response is largely heritable, whereas new evidence demonstrates that DNA hypomethylation is linked to the exercise response in skeletal muscle. DNA sequence variation and/or epigenetic modifications may, therefore, dictate the exercise training response.
Studies dedicated to uncovering the mechanisms of exercise resistance will advance the field of exercise and T2D, allowing interventions to be targeted to those most likely to benefit and identify novel approaches to treat those who do not experience metabolic improvements after exercise training.
J Clin Endocrinol and Metab. November 20, 2014. Dr Natalie A Stephens (Translational Research Institute for Metabolism and Diabetes, Florida Hospital, Orlando and Sanford Burnham Medical Research Institute, Orlando) and Dr Lauren M Sparks (Sanford Burnham Medical Research Institute) http://press.endocrine.org/doi/pdf/10.1210/jc.2014-2545