ABSTRACT 【Background/Aim】Functional decline in the abdominal and external anal sphincter (EAS) muscles due to diabetic neuropathy (DN) can impair evacuation and continence mechanisms. However, the relationship between this decline and fecal excretion function remains unclear. This study investigates the effects of diabetes on the abdominal and EAS muscles, which are controlled by somatic nerves. 【Method】Type 1 diabetes was induced in 18 animals using streptozotocin (STZ), while 20 age-matched control animals were injected with a saline solution. We recorded rectal pressure and fatigability during stimulation of the nerves innervating the abdominal muscles, as well as the closing pressure and fatigability of the EAS muscle during nerve stimulation. Changes in each muscle type were analyzed. 【Results】The diabetic group exhibited lower rectal pressure output during abdominal muscle stimulation compared to the control group. Additionally, the diabetic group showed a slower decline in fatigability. No significant difference in anal closing pressure was observed between the diabetic and control groups during EAS muscle stimulation, nor were there significant differences in fatigability. In abdominal muscle fibers, the diabetic group experienced a decrease in type 2B fibers and an increase in type 2X fibers. No differences were observed in the EAS muscle between the diabetic and control groups. 【Discussion】Diabetes more significantly affects muscle strength in the abdominal muscles than in the EAS muscle, potentially causing an imbalance between reduced abdominal pressure, which aids defecation, and anal closure pressure, which aids in stool storage. This study reveals that in diabetic conditions, somatically innervated EAS muscles experience a slower decline compared to abdominal and limb muscles.

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【Purpose】The increasing global prevalence of diabetes necessitates the pursuit of innovative and effective glycemic management strategies, with a particular emphasis on the aging diabetic population. For elderly individuals with diabetes, implementing exercise therapy, a fundamental treatment approach, often poses challenges, thereby warranting the exploration of novel forms of exercise. This study aimed to evaluate blood glucose fluctuations in response to the administration of neuromuscular electrical stimulation (NMES) by utilizing an intermittent scanning continuous glucose monitor (isCGM) while considering patient’s skeletal muscle mass as well as the application intensity of NMES. 【Method】The participant was an 80-year-old female with a height of 145.9 cm, weight of 41.8 kg, body mass index of 19.6 kg/m2, and skeletal muscle mass index of 5.5 kg/m2. She was diagnosed with diabetes 37 years prior, with insulin therapy initiated 20 years ago. The HbA1c was 8.1%, with the following complications: weakened Achilles tendon reflexes bilaterally, bilateral medial malleolus vibratory sensation of 13 seconds, no subjective symptoms believed to be based on neuropathy, microalbuminuria (stage 2), no retinopathy, and no major vascular complications. NMES was applied with a low-frequency treatment device placed bilaterally on the quadriceps femoris and triceps surae muscles. Blood glucose fluctuations were monitored using an intermittent scanning continuous glucose monitoring (isCGM) device before, during, and after the NMES session. 【Results】No substantial changes were observed in blood glucose levels or physiological parameters during NMES. 【Discussion】The application of NMES in participants with low skeletal muscle mass suggests the possibility of inadequate glucose-lowering effects. This indicates the need to evaluate the individual's body composition and the method used to anticipate the glucose-lowering efficacy of NMES.

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[in Japanese]

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[in Japanese]

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[in Japanese]

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[in Japanese]

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