Abstract

Dear Editor:
1. The investigators do not find this title misleading. Dr. Spielholz mistakes the purpose of exercise in young people compared with people with diabetes or many other populations with physical or metabolic impairments. Therapeutic exercise can be used to increase strength and endurance but in many cases is utilized to increase range of motion, to remove adhesions, or, in the case of people with diabetes, to improve glycemic control and maintain mobility. A treatment program is effective in just achieving better glycemic control; strength and endurance may not even be relevant. In a National Institutes of Health panel report presented at the American Diabetes Association's meeting about 4 years ago, the National Institutes of Health stated that to get a cardiovascular benefit in reducing heart disease, it only requires 20 min of brisk walking a week for most people. The American Diabetes Association, the Juvenile Diabetes Association, and European Association for the Study of Diabetes all recognize that the primary purpose of exercise in people with diabetes is to reduce medication and improve glycemic control. We are not trying to train an athlete with diabetes; efficacy is getting them moving. Because of the potential for hypoglycemic episodes, very low levels of exercise are usually recommended: enough to aid in balance and reduce sarcopenia and improve glycemic control. Because exercise is so infrequent in this population, muscle damage becomes a paramount issue. In this respect, Dr. Spielholz mistakes younger and diabetes populations and what efficacy really means for this population or, in fact, in many other therapeutic populations.
2. The study examined a young population with normal blood flow to assess, if indeed, delayed-onset muscle soreness (DOMS) in this group would have a similar response on muscle blood flow and inflammation as in the group with diabetes. It is no mistake that the two groups were compared; it was the study design. Using older subjects would be good to examine DOMS but would not allow us to examine what is normal without aging or diabetes impairments from people with diabetes. Certainly, future studies could look at various issues, including older people and age-matched people with diabetes to see the effect in diabetes versus aging; however, this was not the intended purpose of this study. Another point made by Dr. Spielholz is that these patients had good feeling of muscle pain, and therefore he states that the study did not accomplish its goals. The study used people with moderate to good glycemic control to test the correlation between pain and thermography. This was the study design. If you examine people with no feeling, there is no way to know if there is a correlation between thermography and tissue damage. You literally become the blind leading the blind. Future studies need to look at people with poor glycemic control, people with type 1 diabetes, and people with diabetes for many, many years. You need to start somewhere, and the best place to start is with people who have no impairments or some hypersensitivity to see if the tool worked; it did.
In summary, the study met the authors' goals, and future work can now progress on to the next steps with other diabetes and older populations. Exercise is a necessary tool, but if someone with severe diabetic polyneuropathies cannot feel the damage, too much exercise will induce more sarcopenia. Unlike chemical biomarkers, thermal imaging was reliable. Many studies have pointed to the unreliability of chemical biomarkers, especially in older people and people with diabetes where these markers can be consistently high at baseline before exercise; this technique had good correlation to damage.
