Passive mechanical properties of adipose tissue and skeletal muscle from C57BL/6J mice.

Skeletal muscle and adipose tissue are characterized by unique structural features finely tuned to meet specific functional demands. In this study, we investigated the passive mechanical properties of soleus (SOL), extensor digitorum longus (EDL) and diaphragm (DIA) muscles, as well as subcutaneous (SAT), visceral (VAT) and brown (BAT) adipose tissues from 13 C57BL/6J mice. Thereto, alongside stress-relaxation assessments we subjected isolated muscles and adipose tissues (ATs) to force-extension tests up to 10% and 30% of their optimal length, respectively. Peak passive stress was highest in the DIA, followed by the SOL and lowest in the EDL (p < 0.05). SOL displayed also the highest Young's modulus and hysteresis among muscles (p < 0.05). BAT demonstrated highest peak passive stress and Young's modulus followed by VAT (p < 0.05), while SAT showed the highest hysteresis (p < 0.05). When comparing data across all six biological specimens at fixed passive force intervals (i.e., 20-40 and 50-70 mN), skeletal muscles exhibited significantly higher peak stresses and strains than ATs (p < 0.05). Young's modulus was higher in skeletal muscles than in ATs (p < 0.05). Muscle specimens exhibited slower force relaxation in the first phase compared to ATs (p < 0.05), while there was no significant difference in behavior between muscles and AT in the second phase of relaxation. The study revealed distinctive mechanical behaviors specific to different tissues, and even between different muscles and ATs. These variations in mechanical properties are likely such to optimize the specific functions performed by each biological tissue.

Myostatin dysfunction is associated with reduction in overload induced hypertrophy of soleus muscle in mice.

The aim of the study was to investigate if myostatin dysfunction would promote the gain in muscle mass and peak isometric force (P0 ) of soleus muscle (SOL) in response to functional overloading (FO) after ablation of the gastrocnemius muscle. Fifteen male Berlin high (BEH) mice homozygous for the compact mutation causing dysfunction of myostatin and 17 mice with the corresponding wild-type allele (BEH+/+) were subjected to FO of SOL for 28 days at the age of 14 weeks. Compared with BEH+/+ mice, SOL of BEH was heavier (mean ± SD, 13.5 ± 1.5 vs 21.4 ± 1.8 mg, respectively, P < 0.001). After FO, SOL mass increased relatively more in BEH+/+ than BEH strain (34.9 ± 11.5 vs 17.7 ± 11.9%, respectively, P < 0.01). P0 fell (P < 0.01) only in BEH strain, which also showed an increase (P < 0.01) in optimal muscle length. Specific P0 became even more depressed in BEH compared with BEH+/+ strain (8.4 ± 1.4 vs 10.8 ± 1.3 N/g, respectively, P < 0.001). Phosphorylation p70 S6 kinase did not differ between the strains. In summary, myostatin dysfunction impairs adaptation of SOL muscle to high functional demands.