Ageing is associated with impairments in muscle force-generating capacity and tendon mechanical properties, yet its effects on stretch-shortening cycle (SSC) function remain unclear. We combined in vivo ultrasonography with dynamometric and kinematic measurements to investigate the muscle-tendon mechanisms underpinning SSC performance in older adults. Fourteen young (28 ± 5 years) and fifteen older adults (67 ± 3 years) performed electrically evoked plantarflexion contractions on an isokinetic dynamometer. Pure shortening and stretch-shortening (SSC) contractions were performed at angular velocities of 60 and 150°·s-1. Ankle torque, muscle-tendon unit (MTU) force, fascicle force, fascicle and Achilles tendon (AT) length changes, muscle belly gearing, tendon gearing, and mechanical work were quantified. Older adults exhibited lower maximal plantarflexor force and AT stiffness than young participants (both P < 0.001). SSCs increased ankle torque, MTU force, and fascicle force in both groups, with a greater enhancement at the higher shortening velocity. The magnitude of SSC-induced force enhancement was similar between groups, with no significant age×SSC interactions for force-related variables. Older adults exhibited greater AT elongation and tendon gearing, but less fascicle shortening, smaller changes in pennation angle, and lower muscle belly gearing. AT mechanical work increased during SSCs in both groups, whereas fascicle work was reduced only in the young participants. These findings demonstrate no significant age-related differences in SSC-effect between populations despite marked reductions in maximal force-generating capacity. The comparable SSC-effect could be achieved through altered muscle-tendon interaction strategies characterised by greater AT compliance and modified fascicle behaviour. Ageing, therefore, seems to preserve SSC function while altering the distribution of mechanical work within the MTU.

Intervertebral disc degeneration (IVDD) is a leading global cause of chronic pain and functional impairment. The senescence of endplate chondrocytes (EPCs) associated with the IVDD cascade, with mitochondrial homeostatic imbalance serving as the central pathological key mediator. EPCs inhabit a physiological niche defined by hypoxia, limited nutrients, and high mechanical loads, requiring precise metabolic regulation and mitochondrial quality control. This review integrates recent advances in mitochondrial biology to clarify how organelle dysfunction promotes EPC senescence. We first analyze the metabolic shift from oxidative phosphorylation to glycolysis and its impact on extracellular matrix stability. We then examine the mechanisms by which mitochondrial reactive oxygen species activate the NLRP3 inflammasome and NF-κB pathways to drive the senescence-associated secretory phenotype. Furthermore, the review discusses how fusion-fission imbalance and mitophagy failure lead to the accumulation of damaged mitochondria, and how mito-nuclear communication facilitates epigenetic remodeling to sustain senescent transcriptional programs. Finally, we evaluate therapeutic interventions targeting mitochondrial homeostasis, including targeted antioxidants, NAD+ precursors, and mitochondrial transplantation. To address the delivery challenges of avascular cartilage, the potential of cartilage-penetrating nanocarriers and gene-editing technologies is also discussed. This review establishes a theoretical framework for developing etiology-based precision therapies for IVDD.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by large-scale network disruption. While static functional connectivity (sFC) has been extensively studied, dynamic functional connectivity (dFC) and its discriminative value across the AD spectrum remain insufficiently understood. In this study, resting-state functional magnetic resonance imaging (rs-fMRI) data from 174 participants in the Alzheimer's Disease Neuroimaging Initiative, including cognitively normal (CN, n = 44), subjective memory concern (SMC, n = 24), early mild cognitive impairment (EMCI, n = 46), late MCI (LMCI, n = 30), and AD (n = 30), were analyzed to assess group differences in sFC, dFC, and graph-theoretical metrics, as well as their associations with cognition. A BrainNetCNN model was further employed to evaluate the classification performance of sFC, dFC, and their combined features. The results revealed that sFC decreased across MCI stages but increased in AD, whereas dFC variability was predominantly reduced in the pre-dementia groups and increased in AD, particularly in frontal and temporal regions. Several static graph-theoretical metrics were significantly correlated with Mini-Mental State Examination (MMSE) scores, while dFC provided complementary information. In classification tasks, dFC showed higher accuracy than sFC in binary and five-class tasks, and their integration achieved the highest accuracy (CN vs. SMC: 89.6%; five-class: 82.7%). These findings suggest that dFC may provide complementary imaging information for characterizing stage-related network alterations and differentiating diagnostic groups across the AD spectrum.