The barbell back squat is used widely across multiple sporting disciplines as part of strength and conditioning training. There are multiple training variations within performing a BBS. The hypothesis of this study was that bar positioning (high bar versus low bar), stance width (wide stance versus narrow stance), weight, and the number of repetitions completed (light weight - ten repetitions at 50% of maximum; heavy weight - three repetitions at 80% of maximum) can be manipulated for targeted training effects. The aim of the study was to quantify the effect squatting technique has on the activation of the rectus femoris, vastus medialis, vastus lateralis, biceps femoris, semitendinosus, gastrocnemius and gluteus maximus. Surface electromyography and kinematic data were recorded from eighteen healthy participants (twelve male, six female). Mean total area under the activation curve was compared for each muscle. Adopting a wide stance width showed increases in both peak and cumulative activation of the vastus medialis (p < 0.015). Squatting with increased weight showed increased cumulative activation of the vastus lateralis and semitendinosus (p < 0.041). An increased peak activation of the biceps femoris was observed when a high bar and wide stance technique was performed with a heavy weight compared to a light weight (p = 0.047). A narrow stance squat showed a 3.7° increase in peak knee flexion (p = 0.010) and a decrease of 8.2° of hip abduction (p < 0.001). A low bar position revealed increased hip flexion of 3.4° (p = 0.012). Overall, consistent muscle activations did not favour any combination of squat parameters. Athletes wishing to increase strength may choose one of several combinations of squat stance, bar positioning, and weight-to-repetition ratios, guided by what is most comfortable for the athlete.

The COVID-19 pandemic has generated widespread psychological distress worldwide, with fear emerging as a central emotional response; however, its role in shaping coping processes, particularly among female university students, remains unclear. The present study investigates the relationship between fear of COVID-19 and coping strategies in female university students, with a specific focus on the moderating role of various variables. Participants were 1000 female university students aged 21.5 (2.5) years, who completed a self-report questionnaire about levels of fear regarding COVID-19 and the coping strategies employed during the post-emergency phase. The result showed that fear of COVID-19 (FCV-19S) was positively related to coping with the outbreak (COS). Physical activity status and COVID-19 positive or negative experiences moderated the relationship between FCV-19S and COS. These findings suggest that individual characteristics such as sedentary lifestyle habits and firsthand infection experiences, may continue to shape COVID-19-related fear and coping responses even after the acute emergency phase has subsided. An intervention such as regular exercise that aims to develop and improve coping dynamics among people in response to new challenges posed by stressful events or public health crises, like COVID-19 infection, seems warranted.

Short-term heat acclimation (HA) induces cardiovascular and fluid-regulatory adaptations, but it's impact on markers of renal tubular injury and acute kidney injury risk (AKI) during exercise-heat stress remains unclear. Fourteen healthy endurance-trained male athletes were randomised to five days of isothermic HA (HOT; n = 7; 32 °C, 70% relative humidity; target core temperature ≥38.5 °C), or exercise in thermoneutral conditions (TEMP, n = 7). Heat stress tests (HST; 45 min cycling at 32 °C, 70% RH) were performed pre- and post-intervention. Blood biomarkers of kidney tubular stress (NGAL, KIM-1), fluid-regulation (copeptin, serum osmolality) and sympathetic activity (plasma normetanephrine) were measured at rest and immediately post-HST. HA reduced resting heart rate (-8 ± 5 bpm, p = 0.007, d = 1.0), increased plasma volume (+7.3 ± 5.1%, p = 0.022) and sweat loss (+500 ± 539 mL, p = 0.018, d = 1.1). Copeptin rose during the pre-intervention HST in both groups (HOT: + 11 ± 6; TEMP: + 12 ± 13 pmol·L ⁻ ¹, p < 0.05), but not post-intervention. NGAL increased only in TEMP during HST1 (+45 ± 29 μg·L ⁻ ¹, p = 0.030), while KIM-1 remained unchanged. No group x time interactions were observed for any biomarkers (p > 0.05). Five days of HA improved cardiovascular and thermoregulatory responses but did not alter renal stress markers or fluid-regulatory responses during exercise in the heat. These findings suggest short-term HA enhances heat tolerance but may not attenuate renal biomarker responses associated with early tubular stress under hot, humid conditions.

This narrative review aimed to summarize the consequences of hamstring tendon (HT) harvest for anterior cruciate ligament reconstruction (ACLR), with reference to tendon regeneration, knee flexor morphology, clinical assessment of knee flexion strength, and rehabilitation strategies for optimizing recovery. The available evidence suggests that the harvested semitendinosus (ST) and gracilis (GR) tendons regenerate in ∼70-86% of cases after ACLR. Despite tendon regeneration, ACLR with HT autograft results in morphological alterations in both the ST and GR. These changes include tendon elongation, proximal migration of the musculotendinous junction, muscle atrophy, shortened fascicles, and increased fatty infiltration, which may persist for several years after ACLR. Growing evidence also suggests that assessment of knee flexion strength after ACLR cannot rely on a single test position, and that knee flexion strength should be evaluated in both hip-flexed and hip-extended positions to provide a more comprehensive evaluation of the recovery. We propose that optimizing the recovery of knee flexion strength may benefit from a multifaceted approach: (1) early, symptom-guided initiation of isometric and low-load exercises to minimize early strength deficits, (2) progressive loading of the knee flexors across multiple hip-and knee-joint angles, including the seated leg-curl to promote a high ST activation, (3) subsequent incorporation of eccentric loading as part of progressive strengthening strategies, with the aim of enhancing ST and GR muscle volumes and fascicle lengths, and (4) strength assessments across multiple hip and knee-joint positions to monitor recovery, as testing in a seated position may underestimate residual deficits in the ST and GR.

Sarcopenia is an age-related progressive degenerative disorder of skeletal muscle characterized by declining muscle mass, strength, and function. Increasing evidence indicates that chronic low-grade inflammation plays an important contributory role in its pathogenesis. The inflammatory microenvironment contributes to sarcopenia through complex interactions involving cellular senescence, mitochondrial dysfunction, and sustained inflammatory signaling, forming a self-reinforcing pathological cycle within skeletal muscle. This review synthesizes current evidence on the molecular mechanisms underlying inflammation-driven sarcopenia, with particular emphasis on how inflammatory signaling disrupts protein turnover and satellite cell metabolism. In addition, exercise is examined as a precision "hormone-like" intervention tailored to different sarcopenia phenotypes, highlighting the distinct mechanisms through which resistance training, aerobic exercise, and combined training modulate the senescence-associated phenotype and inflammatory responses. The review further evaluates anti-inflammatory therapeutic strategies, including nutritional interventions, pharmacotherapy, and acupuncture. These approaches improve muscle health by restoring immune balance, enhancing mitochondrial function, modulating the gut-muscle axis, reducing oxidative stress, and promoting the clearance of senescent cells. Finally, emerging precision medicine frameworks and multi-omics strategies that may support individualized sarcopenia management are discussed. Overall, this review provides an integrated perspective on inflammatory signaling in sarcopenia and outlines potential therapeutic strategies targeting the inflammatory microenvironment, offering insights for future research and clinical management.

The Dual-Pathway Neuroprotection Hypothesis, recently proposed by Badea and colleagues, distinguishes voluntary from enforced exercise and links each to distinct neural pathways, moving beyond the unitary view of exercise as a homogeneous intervention. However, the hypothesis does not consider sex as a biological variable. Given that AD is a sex-biased disease affecting approximately 65-70% women, and that the neuroprotective effects of exercise are sexually dimorphic, we argue that sex may function as a critical moderator of this framework. We propose three testable predictions: (1) voluntary exercise's cortico-limbic effects may be potentiated in females through estrogen-BDNF signaling, but this effect may be constrained by menopausal status; (2) structured/supervised exercise may yield sex-divergent outcomes-with preliminary observations suggesting Aβ clearance in females versus neurotrophic upregulation in males-though evidence remains preliminary and derives from a limited number of heterogeneous studies; and (3) stress burden may reduce the net benefit of enforced exercise, but this will require direct testing. These predictions converge on a formal revision in which sex is not a confounder to be controlled for, but a core biological moderator that may moderate modality-specific neuroprotection. This extended model provides a hypothesis-generating framework for designing future sex-aware exercise studies in AD, but does not yet support sex-stratified clinical prescriptions. This framework is predominantly based on preclinical and indirect evidence from heterogeneous models, necessitating cautious interpretation and rigorous validation.

To identify which functional domains show the greatest improvement in patients with foot drop (FD) due to common peroneal nerve (CPN) injury treated with tibialis posterior tendon transfer (TPTT).

Retrieval-induced forgetting (RIF) refers to the phenomenon whereby selectively retrieving some information impairs later recall of related, non-retrieved information, often interpreted as reflecting inhibitory control processes during memory retrieval. Recent work suggested that acute aerobic exercise performed between repeated memory tests may preserve the RIF effect over time. The present study sought to directly replicate and extend this finding using a larger and more controlled experimental design. Healthy young adults (N = 372) completed a standard category-exemplar RIF task involving selective retrieval practice followed by two final test assessments. Between the two tests, participants were randomly assigned to one of five conditions that manipulated exercise exposure, duration, and order (exercise, standing control, or combined sequences). Exercise was performed on a treadmill at vigorous intensity (80% heart-rate reserve), whereas control conditions involved standing on a stationary treadmill. Replicating the classic RIF effect, recall for Rp- items was significantly lower than for Nrp- items. However, contrary to prior findings, acute exercise did not preserve RIF across the two tests. Instead, the magnitude of RIF decreased from the first to the second test across all groups, driven primarily by improved recall of previously suppressed items. These findings indicate that RIF can attenuate with repeated retrieval but fail to provide evidence that acute exercise acts to stabilize retrieval-induced forgetting.