# Multimodal Rehabilitative Outcome Measures of Fatigue in Patients with Diabetic Neuropathy

**Authors:** Cira Fundarò, Dibo Mesembe Mosah, Fabio Plano, Roberto Maestri, Stefania Ghilotti, Pierluigi Chimento, Marina Maffoni, Monica Panigazzi, Guido Magistrali, Stefano Bruciamonti, Manuela Ravasio, Chiara Ferretti

PMC · DOI: 10.3390/brainsci16030298 · Brain Sciences · 2026-03-07

## TL;DR

This study evaluates how aerobic and resistance training affect fatigue in diabetic neuropathy patients using clinical and instrumental measures.

## Contribution

The study introduces a multimodal approach combining clinical and instrumental assessments to evaluate fatigue in diabetic neuropathy.

## Key findings

- Both aerobic and resistance training improved functional independence and fatigue perception in diabetic neuropathy patients.
- Instrumental sEMG analysis showed a physiological fatigue trend but no significant differences between training groups.
- Multimodal assessment effectively characterizes fatigue in diabetic neuropathy patients.

## Abstract

Background/Objectives: Diabetic neuropathy (DN), a common complication of type 2 diabetes mellitus, manifests as peripheral nerve dysfunction with symptoms such as fatigue. Although exercise effectively reduces fatigue in neuropathy patients, precise detection methods are crucial to elucidate the role of rehabilitation. Accordingly, this study aimed to evaluate fatigue in DN patients using a multimodal approach (clinical and instrumental) and to compare the efficacy of aerobic versus resistance training on fatigue parameters. Methods: Eligible DN inpatients admitted for rehabilitation at the Neuromotor Rehabilitation Unit of the IRCCS ICS Maugeri Institute of Montescano (PV) were enrolled. Inclusion criteria included age between 65 and 85 years and confirmation via the Michigan Neuropathy Screening Instrument (anamnestic section: ≥7; clinical section: ≥2.5). Patients with confounding orthopedic, neurologic, or unstable cardiopulmonary/diabetic conditions were excluded. Overall, 36 participants were randomized into two groups: 17 underwent aerobic training (treadmill), while 19 received resistance training (elastic bands), both as supplements to a standard rehabilitation program. Assessments at baseline and post-training comprised clinical measures (Borg CR10 scale, Functional Independence Measure (FIM) total and subitems, Six-Minute Walk Test (6MWT), fasting blood glucose) and instrumental evaluations (sEMG of the tibialis anterior muscle to analyze conduction velocity intercept, slope, and changes). Results: All patients completed the protocol without dropout or adverse events. Both groups demonstrated significant improvements in FIM scores and post-exercise perceived exertion over time. Instrumental sEMG analysis confirmed a physiological fatigue trend manifested as conduction velocity reduction, yet revealed no significant differences between groups. Conclusions: Multimodal assessment provides an effective means to characterize fatigue in DN patients. Both aerobic and resistance modalities enhance functional independence and fatigue perception. Its early identification enables clinicians to tailor rehabilitation strategies to overcome exercise barriers.

## Linked entities

- **Diseases:** Diabetic neuropathy (MONDO:0006626), type 2 diabetes mellitus (MONDO:0005148)

## Full-text entities

- **Genes:** SEMG1 (semenogelin 1) [NCBI Gene 6406] {aka CT103, SEMG, SGI, dJ172H20.2}, NGF (nerve growth factor) [NCBI Gene 4803] {aka Beta-NGF, HSAN5, NGFB}, BDNF (brain derived neurotrophic factor) [NCBI Gene 627] {aka ANON2, BULN2}, ZMYM2 (zinc finger MYM-type containing 2) [NCBI Gene 7750] {aka FIM, MYM, NECRC, RAMP, SCLL, ZNF198}
- **Diseases:** cardiopulmonary disorders (MESH:D006323), neuropathic symptoms (MESH:D001750), osteoarthritis (MESH:D010003), fractures of the lower limbs (MESH:D038061), cognitive frailty (MESH:D000073496), Diabetes (MESH:D003920), cardiovascular or gastrointestinal autonomic neuropathy (MESH:D005767), retinopathy (MESH:D058437), Neuropathy (MESH:D009422), breathlessness (MESH:D004417), hyperglycemic (MESH:D006944), neuromuscular junction disorders (MESH:D020511), muscle atrophy (MESH:D009133), DN (MESH:D003929), cognitive impairment (MESH:D003072), Parkinson's disease (MESH:D010300), sleep disturbances (MESH:D012893), fiber (MESH:D000071075), weakness (MESH:D018908), pain (MESH:D010146), nephropathy (MESH:D007674), demyelinating disease (MESH:D003711), T2DM (MESH:D003924), depression (MESH:D003866), diabetic peripheral neuropathy (MESH:D010523), diabetes complications (MESH:D048909), injury to (MESH:D014947), ulcers (MESH:D014456), infections (MESH:D007239), neuropathic (MESH:D009437), stroke (MESH:D020521), sensory disturbances (MESH:D012678), dyslipidemia (MESH:D050171), CV abnormalities (MESH:C564269), neuromuscular transmission failure (MESH:D051437), inflammation (MESH:D007249), lumbar and/or radiculopathy (MESH:D011843), autonomic dysfunctions (MESH:D001342), Fatigue (MESH:D005221), neurologic disorders (MESH:D009461), fissures (MESH:D003750), respiratory decompensation (MESH:D006333), hyperglycemia (MESH:D006943), hypertension (MESH:D006973), Distal symmetrical neuropathy (MESH:D008069), chronic (MESH:D002908), muscle soreness (MESH:D063806), hypoglycemic (MESH:C000721848), overweight (MESH:D050177), muscle fatigability (MESH:D009759), sensory (MESH:D009477), orthostatic hypotension (MESH:D007024), neuromuscular dysfunction (MESH:D009468), deficits in muscle strength (MESH:D009135), vascular dysfunction (MESH:D002561), deformities (MESH:D009140)
- **Chemicals:** alcohol (MESH:D000438), oxygen (MESH:D010100), glucose (MESH:D005947), Blood glucose (MESH:D001786), DPN (MESH:D009243)
- **Species:** Homo sapiens (human, species) [taxon 9606]
- **Mutations:** 2185 del 6

## Full text

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## Figures

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## References

104 references — full list in the complete paper: https://tomesphere.com/paper/PMC13023985/full.md

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Source: https://tomesphere.com/paper/PMC13023985