Myocardial infarction (MI) triggers a complex cascade of structural and functional alterations that frequently culminate in adverse cardiac remodelling and heart failure. Central to this process is the excessive production of reactive oxygen species (ROS), which disrupt mitochondrial function, impair calcium handling, and activate pro-apoptotic and pro-fibrotic pathways. Photobiomodulation (PBM) has emerged as a non-invasive therapeutic approach capable of modulating several key biological processes involved in post-infarction remodelling. Preclinical studies consistently demonstrate that PBM reduces infarct size, attenuates ventricular dilation, and improves both systolic and diastolic function. Through the absorption of red to near-infrared light by mitochondrial chromophores, particularly cytochrome c oxidase, PBM enhances cellular bioenergetics, modulates ROS production and activates redox-sensitive signalling pathways. These effects promote a shift from detrimental oxidative stress toward controlled ROS signalling and, in turn, facilitate cytoprotective, anti-inflammatory and pro-angiogenic responses. In addition, PBM promotes the mobilization of progenitor cells, contributing to tissue repair and microvascular restoration. Although still limited, the available clinical evidence suggests that PBM may confer modest improvements in cardiac function. However, variability in treatment protocols, delivery methods and study designs currently precludes definitive conclusions regarding its clinical efficacy. In summary, PBM represents a promising strategy for modulating oxidative stress after MI, integrating metabolic, redox and signalling pathways to attenuate cardiac remodelling. Further well-designed clinical studies are required to establish standardized protocols and to clarify its therapeutic potential in cardiovascular medicine.

Creatine monohydrate (CrM) supplementation has established benefits in exercising populations; however, its efficacy during disuse and subsequent rehabilitation remains unclear. This systematic review assessed the effects of CrM supplementation on muscle size, lean mass and muscle performance (strength, power, endurance) during periods of disuse and rehabilitation. PubMed, Scopus, Web of Science and Cochrane Library were searched from inception to March 2026 following PRISMA guidelines. Six randomised placebo-controlled trials were included (n = 118, mean ages: 15-24 years, disuse model: 1-2 weeks limb-immobilisation). Two studies reported comparable reductions in quadriceps cross-sectional area (CSA; assessed via CT or NMR imaging) between CrM and placebo during disuse (-5.6% vs. -5.5%; -11.0% vs. -9.4%), whereas two reported smaller reductions from CrM supplementation in lower-limb lean mass (-5.6% vs. -8.9%) or preserved upper-limb lean mass (0.9% vs. -3.7%) (assessed via bioelectrical impedance analysis (BIA) or dual energy X-ray absorptiometry (DXA)). These contrasting findings may reflect limitations of BIA/DXA, including hydration effects, rather than preservation of muscle tissue. Effects on muscle performance were inconsistent, with favourable findings from CrM supplementation in upper- but not lower-limb models. Four studies included recovery, three of which used resistance-based rehabilitation. Two reported greater increases with CrM supplementation across quadriceps CSA (21.3% vs. 14.3%), lower-limb lean mass (5.6% vs. 3.8%), power (52.2% vs. 35.2%) and strength (28.7% vs. 22.8%). Current evidence does not unanimously support CrM supplementation as an effective countermeasure to mitigate disuse-induced muscle atrophy, lean mass loss or declines in muscle performance. Whether CrM supplementation meaningfully influences rehabilitation following disuse, particularly in older adults and clinical populations at greater risk of disuse atrophy and incomplete recovery, warrants further investigation.

Experimental approaches that acquire maternal haemodynamics together with direct cardiac signals from more than one fetus remain limited. We developed a standardized in vivo method for simultaneous acquisition of maternal ECG, maternal arterial blood pressure and ECGs from two fetuses in anaesthetized late-gestation Sprague-Dawley rats. The platform combines custom-fabricated needle electrodes with conventional cardiovascular instrumentation and PowerLab/LabChart acquisition. Stable, analysable maternal arterial blood pressure, maternal ECG and dual-fetal ECG were maintained for ≤5 h. The recordings supported beat-to-beat ECG interval and heart rate variability analyses. Fetuses had lower heart rates and longer R-R intervals than dams, and fetal root mean square of successive differences (RMSSD), high-frequency power and standard deviation of RR intervals (SDRR) were lower than maternal values. As proof of recording responsiveness, maternal noradrenaline and verapamil administration produced readily resolved maternal haemodynamic changes together with time-aligned fetal heart rate responses. This protocol does not by itself demonstrate maternal-fetal cardiac coupling; rather, it provides synchronized high-resolution signals suitable for future analyses of dynamic maternal-fetal cardiovascular relationships and pharmacological responses.

This study aimed to determine the effects of acute ingestion of acetaminophen (ACT) on the magnitude of exercise-induced peripheral fatigue (ΔPtw) in patients with type 1 diabetes (T1D). In a randomized, placebo-controlled, double-blind design, 22 males (11 T1D and 11 control (CTR) completed 60 maximum voluntary contractions 60 min after ingesting 1 g of acetaminophen (ACT) or 1 g of placebo (PL) on two separate visits. Central and peripheral fatigue were assessed from pre- to post-exercise changes in quadriceps voluntary activation (ΔVA) and potentiated twitch force (ΔPtw), respectively. Critical torque (CT) was defined as the mean force produced during the final 12 contractions, and work performed (W') was computed as the impulse performed above CT. Maximal voluntary contraction (MVC), VA and Ptw decreased after exercise in both groups, with no significant difference between PL and ACT condition. Compared to PL, ACT increased root mean square/Mmax and CT values in the T1D (+21% and 8% respectively) and CTR groups (+40% and +19%; respectively), with significant lower effect in the T1D compared to the CTR group (P < 0.05). No significant effect of ACT was observed for W' in the T1D (+7%) and CTR groups (+4%) (P = 0.68). These findings indicate that acute ACT ingestion increased CT and muscle activation during the repeated-MVC protocol in both groups, although the magnitude of these responses was smaller in the T1D than the CTR group.

Chronic shiftwork can impair autonomic cardiovascular regulation and immune homeostasis. However, the interaction between occupational status and physical activity level in military police officers remains incompletely understood. This cross-sectional factorial study included 102 men stratified according to occupational status and physical activity level: physically active military police officers (PMP; n = 26), physically inactive military police officers (PMNP; n = 26), physically active civilians (CVP; n = 25) and physically inactive civilians (CVNP; n = 25). Quality of life, perceived stress, sleepiness, haematological parameters, cytokines and heart rate variability were assessed. Physical activity improved several Short-form questionnaire (SF-36) domains, particularly Physical Functioning and General Health. Military police officers demonstrated lower mean normal-to-normal intervals and lower high-frequency power than civilians, indicating differences in resting autonomic cardiovascular modulation associated with occupational status. Serum interleukin-10 concentrations were significantly lower in military police officers, whereas interleukin-2, interleukin-17 and interferon-γ did not differ significantly according to occupational status. Haemoglobin levels and platelet counts demonstrated significant occupational status × physical activity interactions. Perceived stress scores were lower in military police officers than in civilians. Chronic occupational exposure to shiftwork was associated with altered autonomic cardiovascular regulation and immune regulation in military police officers. Regular physical activity improved quality of life somewhat; however, several physiological alterations remained predominantly associated with occupational status, reinforcing the importance of occupational strategies targeting circadian health and physiological resilience. These findings highlight the physiological complexity of chronic shiftwork exposure in tactical occupational populations.

Intense unilateral muscle contractions evoke measurable activity within the contralateral neuroaxis, which can be detected with surface electromyographic activity in the resting homologous muscle. Physiological mirror activity (PMA), the unintentional increase in contralateral muscle excitation, has been implicated in cross-limb interactions and adaptations. Despite longstanding observations of PMA, it remains unknown whether this low-level muscle excitation influences local muscle metabolism. We addressed this question using a vascular occlusion test in 10 healthy adults. Surface electromyography and near-infrared spectroscopy-derived measures of tissue oxygen saturation and muscle oxygen consumption (m V . O 2) were obtained from the resting left forearm during vascular occlusion at rest and during fatiguing unimanual contractions. PMA in the contralateral resting arm was greater during fatiguing unimanual contractions than during rest (mean difference: 8.9%, 95% CI: 4.1 to 13.8). This increase was accompanied by a steeper rate of tissue oxygen desaturation (mean difference: -0.132% s[-] [1], 95% CI: -0.227 to -0.037) and greater m V . O 2 (mean difference: 0.188 mL O2 min[-] [1] 100 g[-] [1], 95% CI: 0.057 to 0.320). Greater PMA was associated with both a faster rate of oxygen desaturation (r = -0.85, 95% CI: -0.96 to -0.46) and greater m V . O 2 (r = 0.78, 95% CI: 0.28 to 0.94). These findings provide the first evidence that PMA is accompanied by increased local metabolic demand, consistent with a coupling between unintentional muscle excitation and oxygen extraction in the resting limb.

Pre-season training prepares soccer players for competition, but the longitudinal effects of friendly match exposure remain unclear. We investigated whether cumulative late pre-season match-play is associated with physiological adaptation in semi-professional players. Twenty-four male players from a randomly selected semi-professional team competing at national level were assessed at pre-season start, mid-pre-season and pre-competition. Measurements included body composition, physical performance, aerobic fitness and blood markers reflecting muscle damage, inflammation, hormonal status and haematological adaptation. Based on cumulative playing time across eight friendly matches, as determined by coaching staff, players were classified retrospectively into extended play (EP) or limited play (LP) groups. Controlling for mid-pre-season baseline, the EP group showed significantly lower pre-competition values for body mass (η p 2 = 0.276), body fat (η p 2 = 0.294) and 35 m sprint time (η p 2 = 0.129) and higher values for lower-limb power (dominant/non-dominant; η p 2 = 0.219-0.424), velocity at maximal oxygen uptake (η p 2 = 0.441) and at second ventilatory threshold (η p 2 = 0.708), serum glutamic-oxaloacetic transaminase (η p 2 = 0.296), myoglobin (η p 2 = 0.199), high-sensitivity C-reactive protein (η p 2 = 0.920), interleukin-6 (η p 2 = 0.893), tumour necrosis factor-α (η p 2 = 0.937) and red blood cell count (η p 2 = 0.190) (all P ≤ 0.038). Across all participants, total match-play time was correlated significantly with reductions in body fat (r = -0.47) and increases in lower-limb power (r = 0.44-0.67), second ventilatory threshold (r = 0.55) and inflammatory markers (r = 0.79-0.86) (all P ≤ 0.033). Greater friendly match-play exposure during pre-season was associated with favourable physiological adaptations and a more pronounced physiological and inflammatory response. These findings support friendly match-play as a meaningful physiological stimulus and highlight the importance of balancing match exposure with recovery during pre-season preparation.

Evaluation of aortic repair has traditionally prioritised perioperative safety, exclusion of the diseased segment and durability. As endovascular treatment expands to younger patients, attention is turning towards the biomechanical compatibility of prosthetic grafts with the native aorta. Native aortic compliance supports Windkessel function, whereas grafts create a compliance transition that may accelerate pulse-wave transmission, alter wave reflection and increase left-ventricular load. This narrative review distinguishes established evidence from emerging concepts after open surgical repair, endovascular aneurysm repair and thoracic endovascular aortic repair. Carotid-femoral pulse-wave velocity (cfPWV) is the accepted reference non-invasive measure of regional aortic stiffness; cardiovascular magnetic resonance (CMR)-derived segmental pulse-wave velocity and distensibility provide complementary information. Brachial-ankle pulse-wave velocity, the cardio-ankle vascular index, and augmentation index assess different territories or haemodynamic properties and are not interchangeable with cfPWV. Left-ventricular strain and mass are downstream cardiac outcomes. Clinical evidence generally reports increases in measured arterial-stiffness indices after endovascular repair, whereas findings after open repair are heterogeneous. Treatment length, landing-zone location, oversizing, anatomy and baseline vascular phenotype may be as important as graft fabric or stent-frame category. Conflicting comparisons of polyester and expanded polytetrafluoroethylene arise from small, non-randomised studies using non-equivalent endpoints and do not support a reliable ranking of commercial devices. Emerging 4D-flow CMR, simulation and compliant graft materials illustrate a shift from structural exclusion alone towards compliance-aware repair, but evidence of improved outcomes remains insufficient. Future studies should use standardised longitudinal stiffness, blood-pressure and cardiac assessments and relate biomechanical changes to hypertension, ventricular remodelling and cardiovascular outcomes.

Heat acclimation is increasingly used to induce haematological adaptations and enhance endurance performance. Although repeated hot-water immersion (HWI) has been shown to increase haemoglobin mass, the acute physiological responses that might underpin these longer-term adaptations remain poorly understood. This study investigated the 24 h time course of plasma volume (PV) and erythropoietin (EPO) responses following a single bout of HWI. Sixteen healthy adults (four females) completed a randomised crossover study comprising 45 min of HWI (40°C) and a time-matched control condition. Changes in PV were estimated from haemoglobin concentration and haematocrit, while serum EPO concentrations were determined using an ELISA. HWI induced a substantial contraction in PV immediately after immersion (-9.5%, 95% CI [-12.5, -6.5]; P < 0.001), accompanied by marked increases in tympanic temperature and thermal strain. However, PV returned to baseline within 12 h, and no subsequent PV expansion was observed. Serum EPO concentration was unaffected by time (P = 0.183), condition (P = 0.125) or the condition × time interaction (P = 0.309). Furthermore, changes in PV were unrelated to changes in circulating EPO in both the HWI (β = 0.07; [-1.3, 1.4]; P = 0.915) and control (β = 1.10; [-1.1, 3.3]; P = 0.326) conditions. These findings demonstrate that a 45 min bout of HWI induces a substantial but transient contraction in PV that is not accompanied by a measurable increase in circulating EPO within 24 h. Acute PV contractions following HWI therefore appear insufficient to stimulate a measurable erythropoietic response, suggesting that the haematological adaptations observed following chronic heat acclimation may instead depend upon sustained alterations in PV arising from repeated heat exposures.

Although the impact of obesity on the action of insulin has been studied extensively, little is known about how obesity affects the action of its counter-regulatory hormone, glucagon. The purpose of this study was to determine whether diet-induced obesity alters in vivo glucagon responsiveness, independent of insulin action. To study diet-induced obesity, C57BL/6J male mice were fed a normal chow diet or a Western diet for 16 weeks. Glucagon responsiveness was determined by assessing the blood glucose response to glucagon (25 µg/kg) while insulin secretion was inhibited by octreotide (1 mg/kg). Body composition was assessed by nuclear magnetic resonance spectroscopy. Insulin sensitivity was assessed by an insulin-assisted glucose tolerance test. As expected, the Western diet resulted in an increase in adiposity and a decrease in insulin sensitivity. Contrary to our initial hypothesis, diet-induced obesity increased glucagon responsiveness, as evidenced by significantly higher blood glucose levels following glucagon administration, resulting in a greater area under the curve in mice fed a Western diet compared with mice fed a normal chow diet. In a preclinical model of obesity and insulin resistance, our study indicates that the glycaemic response to glucagon is enhanced when insulin secretion is inhibited with octreotide, arguing against the idea of impaired glucagon responsiveness. Future studies can use this approach to identify alterations in glucagon signalling that might explain the enhanced glucose response to glucagon.

Pulsatility of the brain has been hypothesised to be linked to intracranial pressure (ICP), although the nature of this relationship remains poorly understood. We used a low-level expiratory resistance manoeuvre to characterise brain tissue pulsation (BTP) responses in a pilot healthy volunteer study. BTPs were measured using a transcranial tissue Doppler ultrasound prototype in 10 healthy volunteers at rest and during the manoeuvre. Measurements of mean arterial pressure (MAP), pulse pressure (PP), and heart rate (HR) were also recorded. One-way repeated-measures ANOVA compared changes between baseline, each phase of the manoeuvre, and recovery. Bulk BTP amplitude increased significantly during the initial phase compared with baseline (P = 0.004). A non-significant decrease was observed as the manoeuvre continued, with values decreasing below baseline during the late phase, followed by an increase above baseline during recovery. HR increased significantly during the late phase (P = 0.015). No significant changes were observed in MAP or PP. Bulk BTP amplitude demonstrated a dynamic response during low-level expiratory resistance, characterised by an initial increase followed by a non-significant decrease over the remainder of the manoeuvre. The physiological mechanisms underlying these observations remain uncertain. Future studies incorporating direct ICP measurements and complementary physiological monitoring are needed to clarify the relationship between BTPs and intracranial dynamics.

Creatine is among the most extensively studied and widely used nutritional supplements in sports and exercise science. Over the past two decades, however, interest has expanded well beyond skeletal muscle, driven by growing recognition of the central role played by the creatine-phosphocreatine system in cerebral bioenergetics. Experimental evidence indicates that creatine contributes to neuronal energy homeostasis, mitochondrial function, membrane stability and potentially neuroprotection. This has fuelled growing enthusiasm for the idea that creatine supplementation might enhance cognitive function and benefit individuals with compromised cerebral metabolism. Yet, despite strong physiological plausibility, clinical findings remain inconsistent and often difficult to interpret. In this review, it is argued that the gap between proposed mechanisms and available clinical evidence reflects two distinct challenges: biological constraints on cerebral creatine availability after supplementation, and persistent methodological weaknesses in the clinical literature. We contend that the central challenge for the coming decade is not to identify new mechanisms of creatine action in the brain, but to establish, unequivocally, whether measurable changes in cerebral bioenergetics translate into meaningful cognitive benefit - whether as enhanced performance in healthy individuals or as clinically significant improvement in patient populations.

Electronic cigarettes generate an aerosol by heating an e-liquid based on propylene glycol (PG) and/or glycerin (VG), with or without nicotine and flavourings. Their acute respiratory effects, particularly with respect to asthma, remain poorly defined. We exposed ovalbumin-sensitised female BALB/c mice, which were subsequently challenged with ovalbumin ('asthmatic') or saline ('non-asthmatic'), to one of four e-cigarette aerosols (PG or VG, each with 0 or 12 mg/mL nicotine) for 30 s. Airway resistance (Raw), tissue damping (G) and tissue elastance (H) were measured once/minute for 60 min using the forced oscillation technique. A second e-cigarette aerosol was given at the 30-min mark. Bronchoalveolar lavage (BAL) was taken for assessment of cellular inflammation. Group sizes were 4-9 mice (n = 53 for lung mechanics and 57 for BAL). All aerosols acutely increased Raw, G and H, and excipient was the dominant determinant. VG produced substantially larger increases than PG across most parameters and exposures (P < 0.0001, except airway resistance after the first exposure, P = 0.0569), responses approximately doubled after a second exposure, and allergic sensitisation augmented the repeated-exposure mechanical response. Nicotine was not required for these effects and, where significant, attenuated them. In BAL, granulocytic inflammation was confined to asthmatic mice and was greater with VG than PG. Acute e-cigarette aerosol exposure is not innocuous; e-liquid composition, especially the excipient, is a key determinant of acute respiratory effects independent of nicotine.