scholarly journals Altered Achilles tendon function during walking in people with diabetic neuropathy: implications for metabolic energy saving

2018 ◽  
Vol 124 (5) ◽  
pp. 1333-1340 ◽  
Author(s):  
M. Petrovic ◽  
C. N. Maganaris ◽  
K. Deschamps ◽  
S. M. Verschueren ◽  
F. L. Bowling ◽  
...  
Keyword(s):  
Peripheral Neuropathy ◽  
Achilles Tendon ◽  
Energy Saving ◽  
Diabetic Peripheral Neuropathy ◽  
Energy Savings ◽  
Metabolic Cost ◽  
Metabolic Energy ◽  
Diabetic Patients ◽  
Length Changes ◽  
Diabetes Patients

The Achilles tendon (AT) has the capacity to store and release elastic energy during walking, contributing to metabolic energy savings. In diabetes patients, it is hypothesized that a stiffer Achilles tendon may reduce the capacity for energy saving through this mechanism, thereby contributing to an increased metabolic cost of walking (CoW). The aim of this study was to investigate the effects of diabetes and diabetic peripheral neuropathy (DPN) on the Achilles tendon and plantarflexor muscle-tendon unit behavior during walking. Twenty-three nondiabetic controls (Ctrl); 20 diabetic patients without peripheral neuropathy (DM), and 13 patients with moderate/severe DPN underwent gait analysis using a motion analysis system, force plates, and ultrasound measurements of the gastrocnemius muscle, using a muscle model to determine Achilles tendon and muscle-tendon length changes. During walking, the DM and particularly the DPN group displayed significantly less Achilles tendon elongation (Ctrl: 1.81; DM: 1.66; and DPN: 1.54 cm), higher tendon stiffness (Ctrl: 210; DM: 231; and DPN: 240 N/mm), and higher tendon hysteresis (Ctrl: 18; DM: 21; and DPN: 24%) compared with controls. The muscle fascicles of the gastrocnemius underwent very small length changes in all groups during walking (~0.43 cm), with the smallest length changes in the DPN group. Achilles tendon forces were significantly lower in the diabetes groups compared with controls (Ctrl: 2666; DM: 2609; and DPN: 2150 N). The results strongly point toward the reduced energy saving capacity of the Achilles tendon during walking in diabetes patients as an important factor contributing to the increased metabolic CoW in these patients. NEW & NOTEWORTHY From measurements taken during walking we observed that the Achilles tendon in people with diabetes and particularly people with diabetic peripheral neuropathy was stiffer, was less elongated, and was subject to lower forces compared with controls without diabetes. These altered properties of the Achilles tendon in people with diabetes reduce the tendon’s energy saving capacity and contribute toward the higher metabolic energy cost of walking in these patients.

scholarly journals The Effects of Combined Exercise Training (Resistance-Aerobic) on Serum Kinesin and Physical Function in Type 2 Diabetes Patients with Diabetic Peripheral Neuropathy (Randomized Controlled Trials)

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Seyedeh Hoda Seyedizadeh ◽  
Sadegh Cheragh-Birjandi ◽  
Mohammad Reza Hamedi Nia
Keyword(s):  
Type 2 Diabetes ◽  
Peripheral Neuropathy ◽  
Exercise Training ◽  
Physical Function ◽  
Diabetic Peripheral Neuropathy ◽  
Diabetic Patients ◽  
Combined Exercise ◽  
Combined Exercise Training ◽  
Diabetes Patients

Diabetic peripheral neuropathy is one of the most common chronic complications of diabetics which causes nerve damage and muscle strength decrease in patients. This in turn results in imbalance leading to the diabetic patients’ daily activity disparity. The present investigation was conducted to specifically study the effects of combined training (resistance-aerobic) on serum kinesin-1 and physical function in type 2 diabetes patients with diabetic peripheral neuropathy. 24 diabetic neuropathic females were randomly to be selected out and divided into two experimental and control groups. The experimental group received resistance-aerobic training for 3 sessions during eight weeks. The exercise training included resistance exercises with 2-3 sets, 6-7 exercise stations, 8-12 repetitions (reps), and 3-5 minutes of rest in between the exercises, and the aerobic exercises contained 50-65% of heart rate reserve (HRR) for 3 minutes with 30 seconds of rest interval between sets and 5-10 repetitions. Results show that the serum kinesin-1 level and aerobic endurance declined after eight weeks of combined (resistance-aerobic) exercise training, but this decrease was not significant. The upper body strength increased but it was not significant, while the lower body showed a significant strength increase. With regard to the progressive nature of diabetic peripheral neuropathy, it seems that even the little changes resulting from the combined exercise training can be useful. Nevertheless, more research is required in this area.

scholarly journals Reducing monocarboxylate transporter MCT1 worsens experimental diabetic peripheral neuropathy

2020 ◽  
Author(s):  
Mithilesh Kumar Jha ◽  
Xanthe Heifetz Ament ◽  
Fang Yang ◽  
Ying Liu ◽  
Michael J. Polydefkis ◽  
...  
Keyword(s):  
Nervous System ◽  
Peripheral Neuropathy ◽  
Peripheral Nerve ◽  
Diabetic Peripheral Neuropathy ◽  
Peripheral Nerve Regeneration ◽  
Metabolic Energy ◽  
Monocarboxylate Transporter ◽  
Diabetic Patients ◽  
Wild Type ◽  
Monocarboxylate Transporter 1

AbstractDiabetic peripheral neuropathy (DPN) is one of the most common complications in diabetic patients. Though the exact mechanism for DPN is unknown, it clearly involves metabolic dysfunction and energy failure in multiple cells within the peripheral nervous system (PNS). Lactate is an alternate source of metabolic energy that is increasingly recognized for its role in supporting neurons. The primary transporter for lactate in the nervous system, monocarboxylate transporter-1 (MCT1), has been shown to be critical for peripheral nerve regeneration and metabolic support to neurons/axons. In this study, MCT1 was reduced in both sciatic nerve and dorsal root ganglia in wild-type mice treated with streptozotocin (STZ), a common model of type-1 diabetes. Heterozygous MCT1 null mice treated with STZ developed a more severe DPN compared to wild-type mice, as measured by greater axonal demyelination, decreased peripheral nerve function, and increased numbness to innocuous low-threshold mechanical stimulation. Given that MCT1 inhibitors are being developed as both immunosuppressive and chemotherapeutic medications, our results suggest that clinical development in patients with diabetes should proceed with caution. Collectively, our findings uncover an important role for MCT1 in DPN and provide a potential lead toward developing novel treatments for this currently untreatable disease.

scholarly journals Reduced Achilles Tendon Stiffness Disrupts Calf Muscle Neuromechanics in Elderly Gait

Gerontology ◽  
2021 ◽  
pp. 1-11
Author(s):  
Rebecca L. Krupenevich ◽  
Owen N. Beck ◽  
Gregory S. Sawicki ◽  
Jason R. Franz
Keyword(s):  
Older Adults ◽  
Achilles Tendon ◽  
Metabolic Cost ◽  
Calf Muscle ◽  
Metabolic Energy ◽  
Joint Work ◽  
Tendon Stiffness ◽  
Age Related ◽  
Ankle Muscle ◽  
Metabolic Energy Expenditure

Older adults walk slower and with a higher metabolic energy expenditure than younger adults. In this review, we explore the hypothesis that age-related declines in Achilles tendon stiffness increase the metabolic cost of walking due to less economical calf muscle contractions and increased proximal joint work. This viewpoint may motivate interventions to restore ankle muscle-tendon stiffness, improve walking mechanics, and reduce metabolic cost in older adults.

scholarly journals Sensory-Motor Mechanisms Increasing Falls Risk in Diabetic Peripheral Neuropathy

Medicina ◽  
2021 ◽  
Vol 57 (5) ◽  
pp. 457
Author(s):  
Neil D. Reeves ◽  
Giorgio Orlando ◽  
Steven J. Brown
Keyword(s):  
Peripheral Neuropathy ◽  
Diabetic Peripheral Neuropathy ◽  
Motor Nerve ◽  
Step Length ◽  
Falls Prevention ◽  
Motor Deficits ◽  
Falls Risk ◽  
Walking Gait ◽  
Risk Of Falls ◽  
Diabetes Patients

Diabetic peripheral neuropathy (DPN) is associated with peripheral sensory and motor nerve damage that affects up to half of diabetes patients and is an independent risk factor for falls. Clinical implications of DPN-related falls include injury, psychological distress and physical activity curtailment. This review describes how the sensory and motor deficits associated with DPN underpin biomechanical alterations to the pattern of walking (gait), which contribute to balance impairments underpinning falls. Changes to gait with diabetes occur even before the onset of measurable DPN, but changes become much more marked with DPN. Gait impairments with diabetes and DPN include alterations to walking speed, step length, step width and joint ranges of motion. These alterations also impact the rotational forces around joints known as joint moments, which are reduced as part of a natural strategy to lower the muscular demands of gait to compensate for lower strength capacities due to diabetes and DPN. Muscle weakness and atrophy are most striking in patients with DPN, but also present in non-neuropathic diabetes patients, affecting not only distal muscles of the foot and ankle, but also proximal thigh muscles. Insensate feet with DPN cause a delayed neuromuscular response immediately following foot–ground contact during gait and this is a major factor contributing to increased falls risk. Pronounced balance impairments measured in the gait laboratory are only seen in DPN patients and not non-neuropathic diabetes patients. Self-perception of unsteadiness matches gait laboratory measures and can distinguish between patients with and without DPN. Diabetic foot ulcers and their associated risk factors including insensate feet with DPN and offloading devices further increase falls risk. Falls prevention strategies based on sensory and motor mechanisms should target those most at risk of falls with DPN, with further research needed to optimise interventions.

scholarly journals Elastic energy savings and active energy cost in a simple model of running

2021 ◽  
Vol 17 (11) ◽  
pp. e1009608
Author(s):  
Ryan T. Schroeder ◽  
Arthur D. Kuo
Keyword(s):  
Elastic Energy ◽  
Energy Cost ◽  
Energy Savings ◽  
Mechanical Energy ◽  
Metabolic Cost ◽  
The Body ◽  
Metabolic Energy ◽  
Energetic Cost ◽  
Mass Model ◽  
Human Running

The energetic economy of running benefits from tendon and other tissues that store and return elastic energy, thus saving muscles from costly mechanical work. The classic “Spring-mass” computational model successfully explains the forces, displacements and mechanical power of running, as the outcome of dynamical interactions between the body center of mass and a purely elastic spring for the leg. However, the Spring-mass model does not include active muscles and cannot explain the metabolic energy cost of running, whether on level ground or on a slope. Here we add explicit actuation and dissipation to the Spring-mass model, and show how they explain substantial active (and thus costly) work during human running, and much of the associated energetic cost. Dissipation is modeled as modest energy losses (5% of total mechanical energy for running at 3 m s-1) from hysteresis and foot-ground collisions, that must be restored by active work each step. Even with substantial elastic energy return (59% of positive work, comparable to empirical observations), the active work could account for most of the metabolic cost of human running (about 68%, assuming human-like muscle efficiency). We also introduce a previously unappreciated energetic cost for rapid production of force, that helps explain the relatively smooth ground reaction forces of running, and why muscles might also actively perform negative work. With both work and rapid force costs, the model reproduces the energetics of human running at a range of speeds on level ground and on slopes. Although elastic return is key to energy savings, there are still losses that require restorative muscle work, which can cost substantial energy during running.

scholarly journals Albumin-Creatinine Ratio is More Diagnostic Sensitive than Cystatin-C in Assessment of Diabetic Peripheral Neuropathy

2018 ◽  
Vol 1 (3) ◽  
Keyword(s):  
Diabetes Mellitus ◽  
Peripheral Neuropathy ◽  
Cystatin C ◽  
Early Treatment ◽  
Diabetic Peripheral Neuropathy ◽  
Diabetic Patients ◽  
Creatinine Ratio ◽  
Serum Cystatin C ◽  
Albumin Creatinine Ratio

Background: Diabetic Peripheral neuropathy is one of the most common cardiovascular complications among diabetes mellitus patients and occurs in more than half of the population of diabetic patients world-wide. It is a common cause of foot ulcer, gangrene and amputation among diabetics. Thus, its prevention or early treatment can improve the quality of life of diabetic patients. In a bid to reduce it, various biochemical markers have been evaluated to enable early treatment and amelioration of diabetic neuropathy among diabetes mellitus patients. Aim: Evaluation of the diagnostic relevance of Cystatin-C versus Albumin-creatinine ratio in assessment of Peripheral neuropathy in diabetic type 2 subjects. Method: 102 type 2 DM subjects (66 females and 36 males) and 100 control subjects of same age range (40 – 80 years) were recruited for this study which includes 51 subjects with peripheral neuropathy and 51 subjects without peripheral neuropathy. Serum Cystatin-C, Microalbuminuria, Urine creatinine and HBA1c were analysed with standard methods. Results: Cystatin-C, Microalbuminuria, Albumin-creatinine ratio and Glycated haemoglobin were significantly elevated (P<0.05) in diabetic subjects compared to the control. Cystatin-C (ng/ml), microalbuminuria (mg/l), albumin creatinine ratio (mg/mmol) and HBA1c (%) is [105.52 ± 45.11; 90.07±20.29; 10.48 ± 4.82; 6.9±1.7] respectively. Microalbuminuria, albumin creatinine ratio showed significant increase (P<0.05) in subjects with peripheral neuropathy compared to those subjects without [92.11± 22.82; 35.70±16.35; 2.61±1.1; 6.38±1.79]. The ROC curve shows that Albumin-creatinine ratio showed significant (P<0.05) sensitivity to peripheral neuropathy [AUC=0.714] while Cystatin-C showed no significant (P<0.05) sensitivity to peripheral neuropathy complication [AUC=0.553]. Conclusion: Cystatin-C was found to be deranged in diabetics. However, Albumin-creatinine ratio showed more diagnostic sensitivity for peripheral neuropathy than Cystatin-C.

scholarly journals Diabetic Peripheral Neuropathy: Epidemiology, Physiopathology, Diagnosis and Treatment

2019 ◽  
Vol 7 (1) ◽  
pp. 35-48
Author(s):  
Nazma Akter
Keyword(s):  
Neuropathic Pain ◽  
Peripheral Neuropathy ◽  
Diabetic Peripheral Neuropathy ◽  
Clinical Evidence ◽  
Current Treatment ◽  
Diabetic Patients ◽  
First Line ◽  
Diabetic Neuropathic Pain ◽  
Current Treatment Regimen ◽  
Limb Proprioception

Diabetic peripheral neuropathy (DPN) is a common complication of both type 1 and type 2 diabetes. It affects over 90% of the diabetic patients. It is widely accepted that the toxic effects of hyperglycemia play an important role in the development of this complication, but several other hypotheses have been postulated. It is typically characterized by significant deficits in tactile sensitivity, vibration sense, lower-limb proprioception, and kinesthesia. Painful DPN has been shown to be associated with significant reductions in overall quality of life, increased levels of anxiety and depression, sleep impairment, and greater gait variability. DPN is often misdiagnosed and inadequately treated. Clinical recognition of DPN is imperative for allowing timely symptom management to reduce the morbidity associated with this condition. The management of diabetic neuropathic pain consists basically in excluding other causes of painful peripheral neuropathy, improving glycemic control as a prophylactic therapy and using medications to alleviate pain. First line drugs for pain relief include anticonvulsants, such as pregabalin and gabapentin and antidepressants, especially those that act to inhibit the reuptake of serotonin and noradrenaline. In addition, there is experimental and clinical evidence that opioids can be helpful in pain control, mainly if associated with first line drugs. Other agents, including for topical application, such as capsaicin cream and lidocaine patches, have also been proposed to be useful as adjuvant in the control of diabetic neuropathic pain, but the clinical evidence is insufficient to support their use. The purpose of this review is to examine proposed mechanisms of DPN, summarize current treatment regimen. A better understanding of the mechanisms underlying diabetic neuropathic pain will contribute to the search of new therapies. Delta Med Col J. Jan 2019 7(1): 35-48

scholarly journals Prognosis of Diabetic Peripheral Neuropathy via Decomposed Digital Volume Pulse from the Fingertip

Entropy ◽  
2020 ◽  
Vol 22 (7) ◽  
pp. 754
Author(s):  
Hai-Cheng Wei ◽  
Wen-Rui Hu ◽  
Na Ta ◽  
Ming-Xia Xiao ◽  
Xiao-Jing Tang ◽  
...  
Keyword(s):  
Logistic Regression ◽  
Peripheral Neuropathy ◽  
Diabetic Peripheral Neuropathy ◽  
Protective Factor ◽  
Binary Logistic Regression Analysis ◽  
Diabetic Patients ◽  
Frequency Noise ◽  
Baseline Measurement ◽  
Volume Pulse ◽  
Digital Volume Pulse

Diabetic peripheral neuropathy (DPN) is a very common neurological disorder in diabetic patients. This study presents a new percussion-based index for predicting DPN by decomposing digital volume pulse (DVP) signals from the fingertip. In this study, 130 subjects (50 individuals 44 to 89 years of age without diabetes and 80 patients 37 to 86 years of age with type 2 diabetes) were enrolled. After baseline measurement and blood tests, 25 diabetic patients developed DPN within the following five years. After removing high-frequency noise in the original DVP signals, the decomposed DVP signals were used for percussion entropy index (PEIDVP) computation. Effects of risk factors on the incidence of DPN in diabetic patients within five years of follow-up were tested using binary logistic regression analysis, controlling for age, waist circumference, low-density lipoprotein cholesterol, and the new index. Multivariate analysis showed that patients who did not develop DPN in the five-year period had higher PEIDVP values than those with DPN, as determined by logistic regression model (PEIDVP: odds ratio 0.913, 95% CI 0.850 to 0.980). This study shows that PEIDVP can be a major protective factor in relation to the studied binary outcome (i.e., DPN or not in diabetic patients five years after baseline measurement).

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