AI Article Synopsis

  • - The study aimed to investigate how muscle damage in the knee extensors affects walking and running mechanics in healthy males, using eccentric exercises to induce damage.
  • - Significant muscle damage indicators, such as increases in creatine kinase (CK) and delayed onset muscle soreness (DOMS), were observed post-exercise, confirming the muscle damage took place.
  • - Kinematic analysis showed that muscle damage led to reduced knee-joint movement during walking and running phases, along with changes in pelvic rotation and tilt, possibly as a protective response to prevent further injury.

Article Abstract

To examine the effects of knee extensors muscle damage on walking and running biomechanics in healthy males. Muscle damage was caused by 60 (6x10) maximal eccentric knee flexions of both legs, selected in a random order, at an angular velocity of 1.05rad/s in 10 volunteers (mean age 20+/-1.0 years). Muscle damage indicators (creatine kinase (CK), lactate dehydrogenase (LDH), delayed onset muscle soreness (DOMS), eccentric and isometric (110 degrees knee flexion) peak torque), pelvic three dimensional (3D) orientation, as well as hip, knee and ankle-joint flexion/extension angles during gait (walking at 1.2m/s and running at 2.8m/s) were assessed pre- and 48h post-eccentric exercise. All muscle damage indicators revealed significant changes post- compared to pre-exercise data (P<0.05) confirming that muscle damage did occur. Kinematic analysis revealed that muscle damage significantly decreased the knee-joint angle range of movement at the stance and swing phases during walking (P<0.05) and running (P<0.05), respectively. These changes were accompanied by corresponding increases of pelvic rotation (P<0.05) and decrease of pelvic tilt (P<0.05). The present data demonstrate that damage of knee extensors result in changes of treadmill walking and running kinematics at both knee joint and pelvis. The fact that these alterations occur at different gait phases could be attributed to the speed of movement and to a self-protection mechanism to prevent further damage.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.gaitpost.2006.04.002DOI Listing

Publication Analysis

Top Keywords

muscle damage
20
damage indicators
8
damage
5
muscle
5
effects muscle
4
damage eccentric
4
eccentric exercise
4
exercise gait
4
gait biomechanics
4
biomechanics examine
4

Similar Publications

PrP Glycoprotein Is Indispensable for Maintenance of Skeletal Muscle Homeostasis During Aging.

J Cachexia Sarcopenia Muscle

February 2025

Department of Bioactive Material Sciences, Research Center of Bioactive Materials, Jeonbuk National University, Jeonju, Republic of Korea.

Background: The cellular prion protein (PrP), a glycoprotein encoded by the PRNP gene, is known to modulate muscle mass and exercise capacity. However, the role of PrP in the maintenance and regeneration of skeletal muscle during ageing remains unclear.

Methods: This study investigated the change in PrP expression during muscle formation using C2C12 cells and evaluated muscle function in Prnp wild-type (WT) and knock-out (KO) mice at different ages (1, 9 and 15 months).

View Article and Find Full Text PDF

Skeletal organoids.

Biomater Transl

November 2024

Organoid Research Center, Institute of Translational Medicine, Shanghai University, Shanghai, China.

The skeletal system, composed of bones, muscles, joints, ligaments, and tendons, serves as the foundation for maintaining human posture, mobility, and overall biomechanical functionality. However, with ageing, chronic overuse, and acute injuries, conditions such as osteoarthritis, intervertebral disc degeneration, muscle atrophy, and ligament or tendon tears have become increasingly prevalent and pose serious clinical challenges. These disorders not only result in pain, functional loss, and a marked reduction in patients' quality of life but also impose substantial social and economic burdens.

View Article and Find Full Text PDF

Use of Hemoadsorption and Continuous Venovenous Hemodialysis With Enhanced Middle Molecule Clearance in Drug-Induced Rhabdomyolysis.

Case Rep Crit Care

January 2025

Department of Anesthesiology and Intensive Care Medicine, Kreiskliniken Günzburg-Krumbach, Krumbach, Germany.

Drug-induced rhabdomyolysis has become increasingly prevalent due to the rising use of medications such as statins, antidepressants, and antipsychotics. These can lead to muscle cell destruction and the release of myoglobin, potentially causing kidney damage. Recent advancements include the use of CytoSorb hemoadsorption as a promising therapy to remove myoglobin and other potentially toxic substances from the bloodstream.

View Article and Find Full Text PDF

DNA damage is a driver of cancer formation, leading to the impairment of repair mechanisms in cancer cells and rendering them susceptible to DNA-damaging therapeutic approaches. The concept of "synthetic lethality" in cancer clinics has emerged, particularly with the use of PARP inhibitors and the identification of DNA damage response (DDR) mutation biomarkers, emphasizing the significance of targeting DDR in cancer therapy. Novel approaches aimed at genome maintenance machinery are under development to further enhance the efficacy of cancer treatments.

View Article and Find Full Text PDF

Backgrounds: Renal interstitial fibrosis (RIF) constitutes the ultimate pathological alteration in nearly all chronic kidney diseases (CKD). Mesenchymal stem cell conditioned medium (MSC-CM) exhibits an alleviating impact on renal fibrosis; however, the underlying mechanism remains unclear. The objective of this study was to explore whether MSC-CM regulates the expression of α-smooth muscle actin (α-SMA), Transforming growth factor-β1 (TGF-β1), Hypoxia-inducible factor-1α (HIF-1α), Nuclear receptor coactivators (NCOA1), and SRY-related high mobility (Sox9).

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!