# From twitch to relaxation: Obesity dysregulates muscle contractile function

**Authors:** L. Cesanelli, H. Degens, P. Minderis, D. Satkunskiene

PMC · DOI: 10.14814/phy2.70731 · 2026-02-15

## TL;DR

Obesity impairs muscle function by reducing force generation and slowing muscle contraction and relaxation in both mice and humans.

## Contribution

This study shows obesity causes slower muscle contractile kinetics and reduced force generation in both animal and human models.

## Key findings

- Obese mice had lower specific force and slower contraction-relaxation dynamics in EDL and SOL muscles.
- Obese men showed slower torque development and prolonged relaxation in plantar flexors during calf raises.
- Higher body mass to torque ratio in obese men contributed to slower muscle performance.

## Abstract

Obesity has been increasingly recognized not only as a metabolic disorder but also as a condition that impairs neuromuscular function, including strength relative to body mass. This translational study investigated whether obesity affects both force generation and contraction‐relaxation dynamics. In control (CN) and diet‐induced obese (OB) male mice, contractile properties of isolated extensor digitorum longus (EDL) and soleus (SOL) muscles were assessed in vitro. In parallel, plantar flexor performance was assessed in 25 normal‐weight (CN) and 25 class I obese (OB) sedentary men through maximal voluntary isometric contractions and a dynamic calf raise test. OB mice exhibited lower specific force and slower rates of force development and relaxation in both EDL and SOL (p < 0.05). In men, the lower rate of torque development and prolonged relaxation kinetics of the plantar flexors (p < 0.05), combined with a higher body mass to maximal voluntary isometric torque ratio (p < 0.05), contributed to slower calf raise phases in OB compared to CN men (p < 0.05). These findings reveal that obesity not only has a negative impact on the muscle force generating capacity but also induces slower muscle contractile kinetics.

## Linked entities

- **Diseases:** obesity (MONDO:0011122)
- **Species:** Mus musculus (taxon 10090), Homo sapiens (taxon 9606)

## Full-text entities

- **Genes:** MEF2A (myocyte enhancer factor 2A) [NCBI Gene 4205] {aka ADCAD1, RSRFC4, RSRFC9, mef2}, ADIPOQ (adiponectin, C1Q and collagen domain containing) [NCBI Gene 9370] {aka ACDC, ACRP30, ADIPQTL1, ADPN, APM-1, APM1}, RYR1 (ryanodine receptor 1) [NCBI Gene 6261] {aka CCO, CMYO1A, CMYO1B, CMYP1A, CMYP1B, KDS}, TTN (titin) [NCBI Gene 7273] {aka CMD1G, CMH9, CMPD4, CMYO5, CMYP5, EOMFC}, ADIPOR1 (adiponectin receptor 1) [NCBI Gene 51094] {aka ACDCR1, CGI-45, CGI45, PAQR1, TESBP1A}
- **Diseases:** muscle weakness (MESH:D018908), Achilles tendon rupture (MESH:D012421), drug abuse (MESH:D019966), fibrosis (MESH:D005355), metabolic and cardiovascular disorders (MESH:D024821), injury (MESH:D014947), inflammation (MESH:D007249), Tetanic contractions (MESH:C536214), muscle (MESH:D019042), mitochondrial deficits (MESH:D028361), metabolic disorder (MESH:D008659), knee or ankle injuries (MESH:D016512), OB (MESH:D009765), anterior knee or ankle pain (MESH:D046788), chronic obstructive pulmonary disease (MESH:D029424), fatigue (MESH:D005221), weight loss (MESH:D015431), tendinopathy (MESH:D052256), tetani (MESH:D013746), adiposity (MESH:D018205), muscle dysfunction (MESH:D009135)
- **Chemicals:** NaCl (MESH:D012965), fat (MESH:D005223), MgCl2 (MESH:D015636), CaCl2 (MESH:D002122), iron (MESH:D007501), carbohydrate (MESH:D002241), NaHCO3 (MESH:D017693), Ca2+ (-), KCl (MESH:D011189), calcium (MESH:D002118), glucose (MESH:D005947), CO2 (MESH:D002245), ATP (MESH:D000255), lipid (MESH:D008055)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606], Bos taurus (bovine, species) [taxon 9913]
- **Mutations:** C-23 C

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12907575/full.md

---
Source: https://tomesphere.com/paper/PMC12907575