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Sun, V.

Publications and source records attributed to Sun, V..

2 recordsLinked to original sources

Acute caffeine ingestion differentially alters motor unit behaviour during submaximal and fatiguing contractions

Background: Caffeine is widely used as an ergogenic aid, yet its effect on neuromuscular function remains heterogeneous across exercise conditions. Although caffeine is known to enhance central nervous system excitability through adenosine receptor antagonism, the extent to which these effects modify spinal motor output remains unclear. Therefore, the present study aimed to characterise acute caffeine-induced alterations in neuromuscular properties during submaximal and sustained fatiguing contractions of the knee extensors. Methods: Seventeen healthy adults completed a randomised, placebo-controlled crossover study (3 mg/kg caffeine). Circulating serum caffeine concentrations were periodically quantified, while motor unit (MU) discharge behaviour, and delta F were derived from high-density surface electromyography. Statistical significance was set at p = 0.05. Results: No intervention effects were observed for MVC, force steadiness, or time to task failure (all p > 0.05). During graded contractions, vastus lateralis MU discharge rate was higher under caffeine (p < 0.001), and discharge variability was lower (p = 0.016). Recruitment and derecruitment thresholds were significantly greater under caffeine at 50% MVC (both p < 0.012), whereas paired MU analyses of delta F was unchanged (p = 0.083). During sustained contractions, caffeine altered fatigue-related trajectories of both MU discharge and discharge variability (intervention * phase interaction, p < 0.011). Conclusions: Acute caffeine ingestion alters motor unit behaviour without enhancing maximal force or fatigue resistance. These effects vary with contraction intensity and fatigue state but are not accompanied by a detectable change in discharge rate hysteresis in the vastus lateralis.

physiology↗

OPA1-dependent mitochondrial remodeling coordinates TCR signaling and metabolic adaptation during iNKT cell differentiation

Invariant natural killer T (iNKT) cells require mitochondrial metabolism for terminal effector development. We found iNKT cells express elevated levels of proteins regulating mitochondrial membrane dynamics, and identified Opa1, but not Drp1, as selectively required for iNKT cell differentiation. OPA1 deficiency disrupted mitochondrial cristae organization, reduced mitochondrial membrane potential, increased mitochondrial mass, and altered calcium homeostasis in iNKT cells. Bulk and single-cell transcriptomic analyses revealed impaired TCR-responsive gene expression, activation of mitochondrial stress adaptation and integrated stress response, enhanced glycolysis, and retention of immature differentiation features. SCENITH analysis demonstrated increased glycolytic dependence; LDHA became required in Opa1-deficient iNKT cells while dispensable for normal iNKT development, indicating compensatory glycolytic adaptation. EGTA in thymic organ culture partially restored NKT1 marker expression in Opa1-deficient cells. Co-deletion of Drp1 improved mitochondrial morphology, TCR signaling, stress and metabolic adaptation, and partially rescued iNKT cell differentiation, demonstrating that balanced mitochondrial dynamics coordinate mitochondrial function and terminal effector development.

immunology↗