Diabetic neuropathy and exercise -
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Clinics 63 , — Prevention of foot ulcers in the at-risk patient with diabetes: A systematic review. Download references. The authors would like to thank Full Professor Ana Claudia Latronico Xavier for supporting us with a database of diabetic patients at Hospital das Clínicas, Faculty of Medicine, University of São Paulo.
The funders had no role in the design, execution, interpretation, or writing of the study and did not have any authority over any study activity or in the decision to submit the report for publication.
Physical Therapy, Speech and Occupational Therapy Department, Faculdade de Medicina, Universidade de São Paulo, Rua Cipotânea, Cidade Universitária, São Paulo, São Paulo, , Brazil.
Renan L. Monteiro, Jane S. Ferreira, Érica Q. Silva, Ronaldo H. Cruvinel-Júnior, Jady L. Department of Biological Science and Health, Federal University of Amapá, Macapá, Brazil.
Department of Rehabilitation Medicine, Amsterdam Movement Sciences, Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands.
You can also search for this author in PubMed Google Scholar. All authors have made substantial contributions to the manuscript. and I. were responsible for the conception and design of the study; R.
and R. were responsible for data acquisition and data processing; R. were responsible for data analysis and interpretation; R. were responsible for drafting the paper; I. and S. revised the manuscript critically. All authors read, provided feedback and approved the submitted version.
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The original online version of this Article was revised: The original version of this Article contained errors in Table 2. As a result, in the Supplementary Tables file, Table 1 contained the same errors. Open Access This article is licensed under a Creative Commons Attribution 4.
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Vincent, A. Figure 6. Group analyses of the effect of exercise on median sensory nerve evoked electrodiagnostic parameters. Data shown are the median, interquartile range, and minimum—maximum range of latency, amplitude, and calculated conduction velocity elicited from antidromic stimulation of median sensory nerves at entry into the study baseline , immediately following intervention, and again at week post-intervention of responding patients, as indicated.
Figure 7. Group analyses of the effect of exercise on tibial nerve evoked electrodiagnostic parameters. Data shown are the median, interquartile range, and minimum—maximum range of latency, amplitude, and calculated conduction velocity elicited from antidromic stimulation of tibial nerves at entry into the study baseline , immediately following intervention, and again at week post-intervention of responding patients, as indicated.
Figure 8. Group analyses of the effect of exercise on peroneal nerve evoked electrodiagnostic parameters. Data shown are the median, interquartile range, and minimum—maximum range of latency, amplitude, and calculated conduction velocity elicited from antidromic stimulation of peroneal nerves at entry into the study baseline , immediately following intervention, and again at week post-intervention of responding patients, as indicated.
Qualitative improvement in sensory electrodiagnostic studies included the presence of sural sensory nerve action potentials that had been absent in the prior baseline evaluation. Table 5A. Table 5B. By comparison, two of the three sedentary patients who underwent repeat testing showed a progressive loss of epidermal nerve fiber density with a third having no detectable levels of epidermal nerve fiber density at baseline.
Marked small-fiber neurologic deficits within this patient population were also evident from quantitative sensory testing studies. At entry into this study, patient responses to vibration stimuli were nearly negligible Table 6. By comparison, patient responses to a cooling sensation were varied range, 13—21 JND whereas responses to the onset of heat pain were delayed range 19—20 JND.
Exercise intervention, regardless of type, did not significantly alter patient perception of vibration, cooling, or heat-pain Table 6. Forty-five subjects with long-standing type 2 diabetes mellitus and length-dependent distal symmetric polyneuropathy were randomized to a week clinical trial conducted to determine whether a structured aerobic-, isokinetic strength-, or combined aerobic—isokinetic strength exercise intervention program, compared with sedentary controls, would alter peripheral nerve function.
Exercise, regardless of type, neither improved or impaired sensory or motor nerve electrodiagnostic findings across or within groups when analyzed parametrically. Non-parametric analyses of composite electrodiagnostic findings of individual responses supported a modest beneficial effect of exercise, however, on sensory nerve function.
Importantly, the beneficial effect of exercise on sensory nerve function was even more evident following the intervening post-intervention interval. In contrast, exercise did not elicit any detectable benefit to tibial or peroneal motor nerves. Three of six patients that had undergone exercise intervention exhibited a marked improvement in epidermal nerve fiber density.
Compared to baseline values within groups, and compared with sedentary values across groups, neither aerobic-, isokinetic strength-, or the combination of aerobic—isokinetic strength exercise intervention significantly altered metabolic or hemodynamic findings in this chronic diabetic patient population.
Patients that underwent aerobic- or the combined aerobic—isokinetic strength exercise intervention demonstrated an increase in treadmill test duration that was sustained over the week post-intervention period. Aerobic exercise intervention alone elicited a significant and sustained improvement in overall perceived SFV physical, but not mental, component score.
While many clinical trials Pan et al. Previous studies suggest that the beneficial effects of structured exercise intervention programs on diabetes management are primarily realized through improved insulin sensitivity and blood glucose control Boule et al.
Improved glycemic control, leading to lower HbA 1 c levels, is also associated with reduced onset and progression of microvascular retinopathy and nephropathy and neuropathic complications Diabetes Control and Complications Trial Research Group et al.
In our experience, a week-on week-off course of exercise, regardless of type, did not significantly alter HbA 1 c levels in well-managed glycemic controlled patients with long-standing diabetes. Given that HbA 1 c levels reflect an average glycemia over several months Sacks et al.
The acute effect of exercise on glycemic control was not, however, sustained by either a week course of structured exercise or following a week post-intervention period. The observed effect of acute exercise on blood glucose levels was therefore transient and most consistent with a rapid short-lived skeletal muscle dependent GLUT4-mediated mechanism of glycemic control Stanford and Goodyear, While short-term moderately intense structured exercise programs, such as the ones used in this study, do little to sustain acute-exercise induced effects on glycemic control, more extensive and prolonged structured programs of physical activity may be necessary to even modestly alter the progression of diabetes in patients with established disease Gregg et al.
This, however, may not necessarily be the case for diabetes associated vascular complications. Beyond glycemic control, structured exercise intervention programs are thought to improve vascular endothelial function by increasing endothelial-derived nitric oxide NO bioavailability Green et al.
Early studies have shown that a short-term 4-week program of physical activity increases agonist-induced endothelium-dependent vasodilatory capacity and average peak flow velocity in patients with stable coronary artery disease Hambrecht et al. Endothelial dysfunction culminating in macro- and microvascular damage plays a key role in the initiation of diabetes associated complications.
Peripheral nerves of long-standing diabetic patients show extensive microvascular pathology, including basement membrane thickening, loss of pericyte investment, as well as endoneurial endothelial cell hyperplasia, which strongly correlates clinically with nerve function deficits.
Secondary to reduced nerve blood flow and increased endoneurial vascular resistance, ischemia and hypoxia are considered the two most prevailing pathophysiological mechanisms by which chronic diabetes alters peripheral nerve function Nakuda, Given that exercise improves vascular endothelial function, we speculated that an increase in endoneurial blood flow elicited by exercise may afford a measure of protection against further ischemic insult to affected peripheral nerve fibers.
All subjects randomized to this study had clinical and electrodiagnostic findings consistent with length-dependent distal symmetric polyneuropathy.
Marked small-fiber neurologic deficits within this patient population were evident from quantitative sensory testing studies. In comparison to sensory nerve fibers, motor nerve fibers examined were not as affected, which perhaps contributed to the relatively positive quality of life measures indicated at baseline and throughout this study on the standardized SFV health survey questionnaire.
In those patients where electrodiagnostic responses were initially measurable, exercise, regardless of type, had no statistically significant beneficial or detrimental effects on motor nerve electrodiagnostic findings nor on sensory nerve studies as parametrically analyzed within and across experimental groups.
Similarly, exercise intervention did not significantly alter patient perceptions of vibration, cooling, or heat-pain as determined by quantitative sensory testing. Aerobic exercise did, however, improve subject treadmill endurance times as well as overall physical component scores, supporting a modest clinical benefit for aerobic exercise in the management of the diabetic neuropathic patient.
When analyzed in this manner, a week structured exercise program was found to elicit a modest, statistically significant, beneficial effect on sensory nerve fiber function. During the intervening week post-intervention period, even more individuals that had undergone exercise showed improvement on electrodiagnostic findings.
When analyzed in an identical non-parametric manner, exercise elicited neither a beneficial or detrimental effect on motor nerve function. In addition to these qualitative electrodiagnostic analyses, 12 randomized subjects volunteered to be biopsied for determination of epidermal nerve fiber density.
These findings infer a restorative effect of exercise on this population of small sensory nerve fibers. The selective effect of exercise on sensory nerve fiber function is not without precedence and may be related to localized increased production by sensory ganglia of numerous neurotrophic BDNF, NGF, NT-3 and related factors Cooper et al.
This program was well-tolerated by our patients with no exercise-related adverse events encountered. Despite its intensity, there were no immediate or sustained effects of aerobic-, isokinetic strength-, or the combination of aerobic—isokinetic strength training, compared to sedentary controls, on peak patient achieved oxygen uptake.
This sample of well-managed glycemic controlled chronic diabetic patients appeared rather resistant to metabolic change and neither benefited or were detrimentally harmed by performing regular-interval exercise intervention.
The lack of exercise-improved cardio fitness encountered in this patient population may have limited the impact on our primary electrodiagnostic and secondary quality of life outcome measures in this study.
Subjecting diabetic individuals to a more rigorously intense exercise training program is not recommended due to elevated risk of exacerbating associated retinopathic, nephropathic, and neuropathic diabetic complications.
Alternatively, extending the length of time patients are subjected to exercise lifestyle intervention beyond 12 weeks of training may prove beneficial to cardio fitness as well as allowing endoneurial vascular remodeling to alleviate ischemic damage to affected peripheral nerves.
As with all randomized clinical trials, this single-site study is not without limitations. Our small sample size coupled with variable electrodiagnostic findings with this chronic patient sample unavoidably limited the statistical power of this study.
Since it is well known that exercise improves glycemic management, this study was specifically designed to address and identify whether a specific type of exercise would improve peripheral nerve function among patients exhibiting tight glycemic control.
Enrolled patients were therefore clinically well-managed, which may have buffered or masked any exercise-dependent direct effects on peripheral nerve function. The length of time patients were subject to exercise intervention 12 weeks, Fisher et al. Longer durations of intermittent exercise may prove more effective at improving peak metabolic parameters among chronic diabetic patients while eliciting endoneurial changes that enhance regenerative repair of distal peripheral nerve fibers.
Although our patient sample was comprised of sedentary subjects, we advocated throughout this study lifestyle modifications that included increased physical activity in compliance with recommended standard of care. An objective measure of each patients daily physical activity level, similar to that of HbA1c, would have proved a useful means of normalization.
A structured aerobic exercise program is recommended as a safe well-tolerated adjunctive therapy for the management of diabetic patients with long-standing distal symmetric polyneuropathy. In most patients, a week course of physical exercise, regardless of type, does not appear to adversely alter sensory or motor nerve electrodiagnostic findings.
In a subset of patients, a short-term structured program of exercise may selectively improve sensory nerve fiber function. Large-scale exercise lifestyle intervention trials are warranted to further evaluate the impact of aerobic exercise on nerve function in diabetic neuropathic patients. This study was carried out in accordance with the recommendations of the Edward Hines Jr.
VA Hospital human studies subcommittee with written informed consent from all subjects. All subjects gave written informed consent in accordance with the Declaration of Helsinki. The protocol was approved by the Edward Hines Jr. VA Hospital human studies subcommittee. ES, MF, and EC conceived, designed, and implemented the study, participated in data analyses and data interpretation, and contributed to the writing of the original manuscript.
CMM was the nurse clinical coordinator for this study. CJ, JB, and CM was the exercise electrophysiologist technicians responsible for training subjects randomized to respective training groups.
MF was the neurologist responsible for conducting and collecting all primary outcome neurological EMG data. ES was the principal investigator responsible for overseeing and conducting all administrative aspects of this study and conducting QST measurements.
This work was supported by grants [BR and BR I01 RX ] from the Department of Veterans Affairs Rehabilitation Research and Development Service. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
The authors wish to express their sincere admiration and appreciation to the Veterans that volunteered to participate in this study.
The authors are grateful to Ms. Louise Corzine and Drs. Nicholas Emanuele and Lonnie Edwards for their unwavering devotion toward providing the highest standards of care to our participating Veterans and for their invaluable insight and assistance with administrative oversight.
FIGURE S1 Exercise does not alter SFV patient self-reported subscale scores. Indicated subscale scores are expressed as a percentage of weighted score Supplementary Table S1 determined at entry into the study baseline , immediately following intervention, and again at week post-intervention, as indicated.
TABLE S3 Relative effect of exercise type on self-reported health status using the SFV questionnaire. Abbott, C.
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Diabetic neuropathic pain DNP is Caffeine pills for increased metabolism common disease Diabetic neuropathy and exercise affects the daily lives nekropathy diabetic patients, and its incidence exeecise is Diabetic neuropathy and exercise high worldwide. At present, drug and exercise therapies are common treatments for DNP. Drug therapy has various side effects. In recent years, exercise therapy has received frequent research and increasing attention by many researchers. Currently, the treatment of DNP is generally symptomatic. We can better select the appropriate exercise prescription for DNP only by clarifying the exercise mechanism for its therapy. Disbetic you neuropaathy to Diabetic neuropathy and exercise Anti-cancer organizations about neruopathy safely with specific diabetes complications, check out the list below. It is also annd to talk to your healthcare team. Very strenuous activity, heavy lifting or straining, isometric exercises, exercise in extreme heat or cold. Beneficial Activities Moderate activity such as walking, daily chores, gardening, fishing. Moderate dynamic lifting, stretching. Activity in moderate climate. Very strenuous activity, heavy lifting or straining and isometric exercise.
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