Distinguishing gastrocnemius and soleus muscle function is relevant for treating gait disorders in which abnormal plantarflexor activity may contribute to pathological movement patterns. Our objective was to use experimental and computational analysis to determine the influence of gastrocnemius and soleus activity on lower limb movement, and determine if anatomical variability of the gastrocnemius affected its function. Our hypothesis was that these muscles exhibit distinct functions, with the gastrocnemius inducing limb flexion and the soleus inducing limb extension. To test this hypothesis, the gastrocnemius or soleus of 20 healthy participants was electrically stimulated for brief periods (90 ms) during mid- or terminal stance of a random gait cycle. Muscle function was characterized by the induced change in sagittal pelvis, hip, knee, and ankle angles occurring during the 200 ms after stimulation onset. Results were corroborated with computational forward dynamic gait models, by perturbing gastrocnemius or soleus activity during similar portions of the gait cycle. Mid- and terminal stance gastrocnemius stimulation induced posterior pelvic tilt, hip flexion and knee flexion. Mid-stance gastrocnemius stimulation also induced ankle dorsiflexion. In contrast mid-stance soleus stimulation induced anterior pelvic tilt, knee extension and plantarflexion, while late-stance soleus stimulation induced relatively little change in motion. Model predictions of induced hip, knee, and ankle motion were generally in the same direction as those of the experiments, though the gastrocnemius's results were shown to be quite sensitive to its knee-to-ankle moment arm ratio.
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http://dx.doi.org/10.1016/j.jbiomech.2014.07.007 | DOI Listing |
Diabetes Obes Metab
January 2025
Department of Endocrinology, First Hospital of Shanxi Medical University, Taiyuan, China.
Metabolic syndrome-related diseases frequently involve disturbances in skeletal muscle lipid metabolism. The accumulation of lipid metabolites, lipid-induced mitochondrial stress in skeletal muscle cells, as well as the inflammation of adjacent adipose tissue, are associated with the development of insulin resistance and metabolic dysfunction. Consequently, when antidiabetic medications are used to treat various chronic conditions related to hyperglycaemia, the impact on skeletal muscle lipid metabolism should not be overlooked.
View Article and Find Full Text PDFInt J Exerc Sci
December 2024
Longwood University, Farmville, Virginia, USA.
Unlabelled: To investigate the effects of differing treadmills on impact acceleration and muscle activation.
Methods: 15 males and 7 females (27.8 ± 7.
Diabetes Obes Metab
January 2025
National Engineering Research Center for Biomaterials, College of Biomedical Engineering, Sichuan University, Chengdu, Sichuan, People's Republic of China.
Aim: To achieve glucose-activated transcriptional regulation of insulin analogue in skeletal muscle of T1D mice, thereby controlling blood glucose levels and preventing or mitigating diabetes-related complications.
Materials And Methods: We developed the GANIT (Glucose-Activated NFAT-regulated INSA-F Transcription) system, an innovative platform building upon the previously established intramuscular plasmid DNA (pDNA) delivery and expression system. In the GANIT system, skeletal muscle cells are genetically engineered to endogenously produce the insulin analogue INSA-F (Insulin Aspart with Furin cleavage sites).
Skelet Muscle
January 2025
Department of Anesthesia and Critical Care, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Background: Duchenne muscular dystrophy (DMD) is a prevalent, fatal degenerative muscle disease with no effective treatments. Mdx mouse model of DMD exhibits impaired muscle performance, oxidative stress, and dysfunctional autophagy. Although antioxidant treatments may improve the mdx phenotype, the precise molecular mechanisms remain unclear.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Chromosome Biomedical Engineering, School of Life Science, Faculty of Medicine, Tottori University, 86 Nishi-cho, Yonago, Tottori, 683‑8503, Japan.
Duchenne muscular dystrophy (DMD) is an X-linked recessive disorder caused by mutations of the dystrophin gene, which spans 2.4 Mb on the X chromosome. Creatine kinase (CK) activity in blood and titin fragment levels in urine have been identified as biomarkers in DMD to monitor disease progression and evaluate therapeutic intervention.
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