Department of Clinical Medicine

Peripheral neuropathy is a common complication of diabetes most frequently presenting as a diabetic sensorimotor polyneuropathy (DSPN). Loss of muscle strength in patients with diabetes is believed primarily to be due to skeletal muscle atrophy highly related to the degree of DSPN with denervation of motor units, incomplete reinnervation, and consequently motor unit loss. Contrary to previous believes, emerging evidence suggests that motor nerve dysfunction is present already in early stages of DSPN with more widespread muscle impairments, which often go unnoticed in daily clinical practice. Advances in neurophysiological techniques, including nerve conduction studies (NCS) and motor unit number estimation (MUNE) methods, have documented that motor and sensory nerves are equally impaired in DSPN. Imaging modalities, including magnetic resonance imaging and ultrasonomyography, have enabled the assessment of muscle composition proving that muscle weakness in patients with DSPN is paralleled by muscle atrophy and fat infiltration. Compositional changes are found to be more pronounced distally in foot muscles and muscles of the lower leg. Yet, increased fat infiltration can be observed at thigh level even in patients with lesser degrees of DSPN. The importance of functional muscle deficits in patients with diabetes is emerging, including decreased muscle contractile properties with lower muscle power. Indeed, a larger decrease in muscle power has been observed in patients with diabetes and DSPN than the loss of muscle strength alone. Due to the highly dynamic movements needed, decrements in contractile muscle properties may further add to the functional deficits in activities of daily living. Muscle power seems to decrease in parallel with the occurrence of DSPN; however, decrements may be present even prior to DSPN. Large-scale studies indicate the presence of poor muscle quality, accelerated sarcopenia, and lower muscle strength, irrespective of DSPN, in patients with diabetes. Muscle dysfunction in patients with diabetes is a highly complex matter with emerging evidence emphasizing the effects of metabolic factors in addition to neuropathic deficits. The evident muscle dysfunction in diabetes is termed diabetic myopathy, which is increasingly apparent as an important factor for the overall health of patients with diabetes. Deteriorating muscle health, including muscle weakness, muscle quality, and reduced power, all contribute to postural instability, increased risk of falling, and ultimately increased mortality in patients with diabetes. No strategies exist directly addressing deficits in muscle function in patients with diabetes. Exercise, including aerobic, strength, and balance training, is observed to improve glycemic control and may directly improve the neuromuscular system and postpone the development of DSPN. Especially, training regimens of resistance training seem to directly improve muscle strength, volume, and quality. The optimal protocol for resistance training is still debated, with some evidence suggesting that high-intensity protocols emphasizing muscle power training may be the optimal intervention. Yet, it remains to be studied how patients with severe DSPN respond to long-term resistance training. Advances in neurophysiological techniques, imaging modalities, and dynamic muscle assessment are proving valuable in providing greater information and assessment of muscle dysfunction in patients with DSPN. Future research should aim to determine the independent implications of neuropathic and metabolic factors on functional muscle deficits and evaluate the effect of long-term exercise interventions on patients with DSPN.