Strength training affects lower extremity gait kinematics, not kinetics, in people with diabetic polyneuropathy.

Increased forefoot loading in diabetic polyneuropathy plays an important role in the development of plantar foot ulcers and can originate from alterations in muscle strength, joint moments and gait pattern. The current study evaluated whether strength training can improve lower extremity joint moments and spatiotemporal gait characteristics in patients with diabetic polyneuropathy. An intervention group receiving strength training during 24 weeks and a control group receiving no intervention. Measurements were performed in both groups at t=0, t=12, t=24 and t=52 weeks at an individually preferred and standardized imposed gait velocity. The strength training did not affect the maximal amplitude of hip, knee and ankle joint moments, but did result in an increase in stance phase duration, stride time and stride length of approximately 5%, during the imposed gait velocity. In addition, both groups increased their preferred gait velocity over one year. Future longitudinal studies should further explore the possible effects of strength training on spatiotemporal gait characteristics. The current study provides valuable information on changes in gait velocities and the progressive lower extremity problems in patients with polyneuropathy.

Lower leg muscle strengthening does not redistribute plantar load in diabetic polyneuropathy: a randomised controlled trial.

BACKGROUND: Higher plantar pressures play an important role in the development of plantar foot ulceration in diabetic polyneuropathy and earlier studies suggest that higher pressures under the forefoot may be related to a decrease in lower leg muscle strength. Therefore, in this randomised controlled trial we evaluated whether lower-extremity strength training can reduce plantar pressures in diabetic polyneuropathy. METHODS: This study was embedded in an unblinded randomised controlled trial. Participants had diabetes and polyneuropathy and were randomly assigned to the intervention group (n = 48) receiving strength training during 24 weeks, or the control group (n = 46) receiving no intervention. Plantar pressures were measured in both groups at 0, 12, 24 and 52 weeks. A random intercept model was applied to evaluate the effects of the intervention on peak pressures and pressure-time-integrals, displacement of center-of-pressure and the forefoot to rearfoot pressure-time-integral-ratio. RESULTS: Plantar pressure patterns were not affected by the strength training. In both the intervention and control groups the peak pressure and the pressure-time-integral under the forefoot increased by 55.7 kPa (95% CI: 14.7, 96.8) and 2.0 kPa.s (95% CI: 0.9, 3.2) over 52 weeks, respectively. Both groups experienced a high number of drop-outs, mainly due to deterioration of health status and lower-extremity disabilities. CONCLUSIONS: Plantar pressures under the forefoot increase progressively over time in people with diabetic polyneuropathy, but in this study were not affected by strength training. Future intervention studies should take this increase of plantar pressure into account and alternative interventions should be developed to reduce the progressive lower extremity problems in these patients. TRIAL REGISTRATION: This study was embedded in a clinical trial with trial number NCT00759265.

Increased forefoot loading is associated with an increased plantar flexion moment.

The aim of this study was to identify the cascade of effects leading from alterations in force generation around the ankle joint to increased plantar pressures under the forefoot. Gait analysis including plantar pressure measurement was performed at an individually preferred and a standardized, imposed gait velocity in diabetic subjects with polyneuropathy (n=94), without polyneuropathy (n=39) and healthy elderly (n=19). The plantar flexion moment at 40% of the stance phase was negatively correlated with the displacement rate of center of pressure (r=-.749, p<.001 at the imposed, and r=-.693, p<.001 at the preferred gait velocity). Displacement rate of center of pressure was strongly correlated with forefoot loading (r=-.837, p<.001 at the imposed, and r=-.731, p<.001 at the preferred gait velocity). People with a relatively high plantar flexion moment at 40% of the stance phase, have a faster forward transfer of center of pressure and consequently higher loading of the forefoot. This indicates that interventions aimed at increasing the control of the roll-off of the foot may contribute to a better plantar pressure distribution.

Lower extremity muscle strength is reduced in people with type 2 diabetes, with and without polyneuropathy, and is associated with impaired mobility and reduced quality of life.

AIM: The purpose of the present study was to distinguish the effects of both diabetes mellitus type 2 (DM2) and diabetic polyneuropathy (DPN) on mobility, muscle strength and health related quality of life (HR-QoL). METHODS: DPN patients (n=98), DM2 patients without DPN (DC) (n=39) and healthy subjects (HC) (n=19) performed isometric and isokinetic lower limb muscle strength tests. Mobility was determined by a timed up and go test (TUGT), a 6 min walk test and the physical activity scale for the elderly questionnaire. HR-QoL was determined by the SF36 questionnaire. RESULTS: DPN patients had moderate polyneuropathy. In both DPN and DC patients leg muscle strength was reduced by 30-50% compared to HC. Muscle strength was correlated with mobility tests, and reduced muscle strength as well as impaired mobility were associated with a loss of HR-Qol (all p<0.05). We did not observe major differences in muscle strength, mobility (except for the TUGT, p<0.01) and HR-QoL between diabetic patients with and without DPN. CONCLUSION: DM2 patients, with and without DPN, have decreased maximal muscle strength in the lower limbs and impaired mobility. These abnormalities are associated with a loss of HR-QoL. The additional effect of moderate DPN was small in our patients.

Calculation of plantar pressure time integral, an alternative approach.

In plantar pressure measurement, both peak pressure and pressure time integral are used as variables to assess plantar loading. However, pressure time integral shows a high concordance with peak pressure. Many researchers and clinicians use Novel software (Novel GmbH Inc., Munich, Germany) that calculates this variable as the summation of the products of peak pressure and duration per time sample, which is not a genuine integral of pressure over time. Therefore, an alternative calculation method was introduced. The aim of this study was to explore the relevance of this alternative method, in different populations. Plantar pressure variables were measured in 76 people with diabetic polyneuropathy, 33 diabetic controls without polyneuropathy and 19 healthy subjects. Peak pressure and pressure time integral were obtained using Novel software. The quotient of the genuine force time integral over contact area was obtained as the alternative pressure time integral calculation. This new alternative method correlated less with peak pressure than the pressure time integral as calculated by Novel. The two methods differed significantly and these differences varied between the foot sole areas and between groups. The largest differences were found under the metatarsal heads in the group with diabetic polyneuropathy. From a theoretical perspective, the alternative approach provides a more valid calculation of the pressure time integral. In addition, this study showed that the alternative calculation is of added value, along peak pressure calculation, to interpret adapted plantar pressures patterns in particular in patients at risk for foot ulceration.

Motor nerve decline does not underlie muscle weakness in type 2 diabetic neuropathy.

INTRODUCTION: Type 2 diabetes mellitus (DM2) patients may have decreased muscle strength. This decline can have multiple causes, among them diabetic polyneuropathy (DPN). We sought to determine the effect of nerve deterioration on muscle strength in DM2 patients with and without DPN. METHODS: Nineteen DM2 patients with DPN (DPN group), 15 DM2 patients without DPN (DC group), and 18 healthy subjects (HC group) were recruited. We determined motor and sensory nerve function of the lower extremity. Isometric dynamometry was performed to determine maximum torque of the ankle joint. RESULTS: The DPN group had significantly diminished nerve function and muscle strength (P < 0.05) compared with both other groups. Only muscle strength was lower in DC subjects compared with HCs. No significant correlations were found between nerve function and muscle strength. CONCLUSION: These results indicate that reduced ankle joint torque in DM2 patients with and without DPN is independent of the presence of disturbed nerve function.

Reduced glycaemic and insulinaemic responses following trehalose ingestion: implications for postprandial substrate use.

The proposed impact of slowly digestible sources of dietary carbohydrate in reducing the risk of developing obesity and related metabolic disorders remains unclear. The aim of the present study was to compare the postprandial metabolic response to the ingestion of glucose v. trehalose. We hypothesised that the reduced digestion and absorption rate of trehalose is accompanied by an attenuated glycaemic and insulinaemic response, leading to a less inhibited postprandial fat oxidation rate. In a randomised, single-blind, cross-over study, ten overweight subjects ingested two carbohydrate drinks (75 g carbohydrate equivalents of trehalose or glucose) following an overnight fast (08.40 hours) and together with a standardised mixed meal (12.30 hours; 25 % total energy content was provided as either glucose or trehalose). Blood samples were collected before ingestion and every 30 min thereafter for a period of 3 h; substrate use was assessed by indirect calorimetry and expired breath samples were collected. Ingestion of carbohydrates with a mixed meal resulted in a lower peak glucose response and a lower change in area under the curve (DeltaAUC) following trehalose when compared with glucose. Differences in peak insulin response and DeltaAUC were observed with trehalose when compared with glucose during the morning and afternoon. These differences were accompanied with a reduced carbohydrate oxidation after trehalose when ingested as a drink, whilst no significant differences in fat oxidation between drink were observed.

Reduced glycaemic and insulinaemic responses following isomaltulose ingestion: implications for postprandial substrate use.

The impact of slow digestible sources of dietary carbohydrate in reducing the risk of developing obesity and related metabolic disorders is unclear. The aim of the present study was to compare the postprandial metabolic response to the ingestion of sucrose v. isomaltulose. We hypothesised that the reduced digestion and absorption rate of isomaltulose would result in lower glycaemic and insulinaemic responses when compared with the ingestion of sucrose, leading to greater postprandial fat oxidation rates. In a randomised, single-blind, cross-over study, ten overweight subjects ingested two different carbohydrate drinks (sucrose and isomaltulose, 75 g carbohydrate equivalents) following an overnight fast (08.40 hours) and with a standardised meal (12.30 hours, 25 % of total energy content was provided as either a sucrose or isomaltulose drink). Blood samples were taken before ingestion and every 30 min thereafter for a period of 3 h, substrate use was assessed by indirect calorimetry and breath samples were collected. Ingestion of carbohydrates with a mixed meal resulted in a lower peak glucose and insulin response and a lower change in area under the curve (DeltaAUC) following isomaltulose when compared with sucrose. Together with the lower glucose and insulin responses, postprandial fat oxidation rates were higher (14 %) with isomaltulose when compared with sucrose when ingested with a mixed meal (P = 0.02). The attenuated rise in glucose and insulin concentrations following isomaltulose results in reduced inhibition of postprandial fat oxidation. The metabolic response to isomaltulose co-ingestion suggests that this may represent an effective nutritional strategy to counteract overweight-induced metabolic disturbances.