Physiological Adaptations Research Articles

Introduction: Preeclampsia (PE), a leading cause of maternal morbidity and mortality, is associated with diastolic dysfunction and increased long-term cardiovascular risk. Mice lacking S-nitrosoglutathione reductase (GSNOR -/- ) recapitulate the clinical and molecular features of PE, including nitroso-redox imbalance. However, the mechanisms by which redox dysregulation impairs myocardial relaxation during pregnancy remain poorly defined. Hypothesis: GSNOR deficiency during pregnancy promotes oxidative stress-induced dysregulation of sarcomere protein phosphorylation, leading to altered Ca 2+ sensitivity and impaired cardiomyocyte relaxation. Methods: Ventricular cardiomyocytes were isolated from non-pregnant, late-pregnant (E17.5), and ascorbate-treated pregnant WT and GSNOR -/- mice (N=3–4 mothers/group). Ascorbate, a potent antioxidant, was delivered in drinking water. Sarcomere shortening, relaxation time (tt50%), and resting length were measured using IonOptix. Sarcomere length (SL)-[Ca 2+ ] hysteresis loops plotted SL vs. cytosolic [Ca 2+ ]. Western blots of heart lysates were assessed for total and phosphorylated (p) cardiac Troponin I (cTnI) and Myosin binding protein C (cMyBPC), oxidized (ox) CaMKII, and redox regulatory proteins including Xanthine oxidoreductase (XOR), transcription factor Nrf2, Catalase, Superoxide dismutase (SOD1/2). Results: In WT mice, pregnancy enhanced sarcomere relaxation (↓tt50% by ~18%), increased p-cTnI (1.8-fold), consistent with physiological adaptation. Pregnant GSNOR -/- mice failed to show these changes, exhibiting blunted sarcomere relaxation (tt50% unchanged) and incomplete re-lengthening (↓6%), increased total cMyBPC and reduced p-cMyBPC (~45%), indicating impaired cross-bridge cycling. SL-[Ca 2+ ] hysteresis was altered, suggesting disrupted Ca 2+ responsiveness. GSNOR -/- hearts also displayed reduced total CaMKII and higher ox-CaMKII level, and a 2.5-fold increase in XOR, a major ROS source, but suppressed antioxidant defenses (Nrf2, catalase, SOD 1/2). Ascorbate restored resting SL and contractile amplitude, but relaxation kinetics remained blunted. Conclusion: GSNOR deficiency impairs sarcomere relaxation via redox-sensitive suppression of cMyBPC phosphorylation, driven by XOR-mediated ROS and impaired antioxidant defense. This study is the first to mechanistically link nitroso-redox imbalance to sarcomere dysfunction in a model of PE and identifies redox-sensitive therapeutic targets to improve maternal cardiac function.

Background: Heart failure with preserved ejection fraction (HFpEF) frequently co-occurs with chronotropic incompetence (ChI), impairing the heart's ability to appropriately increase its rate during exertion. This combination causes significant functional impairment and diminished quality of life. While traditional moderate-intensity continuous training (MCT) yields limited cardiovascular improvements, high-intensity interval training (HIIT) – featuring alternating high-effort intervals and recovery – may offer superior benefits. Introduction: Although HFpEF and ChI are recognized as key drivers of declining function, the optimal rehabilitation strategy is debated. Emerging evidence indicates HIIT might improve peak oxygen uptake (VO2peak) and alleviate symptoms more effectively than MCT. This review synthesizes current evidence comparing the clinical effectiveness of HIIT versus MCT for improving outcomes in patients with HFpEF and ChI. Methods: A PRISMA-guided review searched PubMed, Embase, and Cochrane Library (2015–2025) for studies comparing HIIT vs. MCT in adults with HFpEF and ChI, reporting VO2peak or physiologic adaptation. Eligible designs included RCTs, meta-analyses, and mechanistic studies. Of 412 records, 28 full texts were reviewed; 8 met inclusion. Extracted data included study design, population, interventions, and outcomes. QoL was assessed using tools like the Kansas City Cardiomyopathy Questionnaire (KCCQ), evaluating social limits, function, and symptoms. Results: Eight studies met criteria: three RCTs, two meta-analyses, and three mechanistic reports. The TRAINING-HR trial (n=120) showed VO2peak gains of +2.3 mL/kg/min ( p <0.01) and improved QoL with HIIT. A 2025 meta-analysis (n=1,027) found greater VO2peak gains with HIIT (+1.7 mL/kg/min), though functional scores were similar. Mechanistic data linked HIIT to enhanced chronotropic response, autonomic flexibility, and vascular compliance. Across studies, HIIT showed consistent trends toward improved cardiopulmonary outcomes and tolerability. Limitations included short duration, small samples, and underrepresentation of older or multimorbid patients. Conclusion: Emerging data suggest HIIT may outperform steady regimens in improving VO2peak and physical capacity in HFpEF/ChI. Intermittent training improves performance, efficiency, and symptoms. While long-term effects remain unclear, findings support incorporating intensity-driven rehabilitation into care for this group.

Background: The autonomic nervous system dynamically adjusts cardiac regulation during cognitive challenges, reflecting the interplay between sympathetic and parasympathetic branches to support task performance. Objective: To investigate within-subject changes in heart rate variability (HRV) in healthy individuals transitioning from eyes-open resting baseline to performance of a visuo-spatial working memory task (VSWMT) with increasing cognitive demand. Methods: Thirty healthy control participants completed five-minute ECG recordings during eyes-open resting conditions and during VSWMT. HRV analysis included time-domain measures (SDNN, RMSSD, pNN50) and frequency-domain metrics (LF power, HF power, LF/HF ratio). Statistical analyses compared HRV indices between resting and task conditions within subjects. Results: Compared to baseline, controls exhibited significant increases in time-domain HRV parameter, SDNN, indicating enhanced parasympathetic modulation and greater beat-to-beat variability during task engagement. Frequency-domain analysis showed significant elevations in both LF and HF power (p < 0.05), with a stable LF/HF ratio, reflecting balanced sympathetic and parasympathetic activation. Total power of HRV increased significantly, supporting the notion of increased autonomic flexibility and adaptive regulation during cognitive load. Conclusion: Healthy individuals display robust autonomic modulation characterized by increased variability and balanced autonomic activity during visuo-spatial working memory demands. These physiological adaptations likely facilitate optimal cognitive function and resilience to stress during challenging mental tasks.

Introduction: Hibernation or aestivation involve physiologic and molecular adaptations across species that enhance survival under extreme conditions. These include reduced respiratory or heart rate and blood flow, resembling an ischemic state, but without any significant tissue damage. Similarly, the neonatal heart also exhibits protective adaptations against ischemia-reperfusion injury (IRI), resembling hibernation/aestivation. In contrast, adult non-hibernating mammals poorly tolerate ischemia-reperfusion, partly due to excess lactate and H + from anaerobic glycolysis, accelerating ATP depletion used to maintain intracellular pH, resulting in poor cardiac function. Hypothesis: We hypothesized that loss of the cardiac maturation RNA splicing factor RBFOX1 could promote a less mature (neonatal-like) cardiomyocyte state in adult mice, mimicking molecular changes seen during hibernation/aestivation, improving tolerance to IRI. Methods: We used the Alberta snail as a model for hibernation/aestivation and both male and female heart-specific RBFOX1 deficient mice to assess molecular signalling, along with IRI, utilizing the ex-vivo Langendorff working heart model with radiolabelled substrates to measure metabolic alterations. Results: We found increased circulating ketones in the hemolymph of aestivating snails, as well as decreased RBFOX1 levels and markers of less mature cardiomyocytes (i.e., decreased Hoxb13 and Meis1) in snail tissue. RBFOX1 deficient mice had normal cardiac function, but less mature cardiomyocytes, characterized by sarcomere disassembly, stemness marker expression, and increased mono-nucleated cardiomyocytes. Furthermore, RBFOX1-deficient cardiomyocytes had increased levels of glycolytic, ketone oxidation, and fatty acid oxidation rate-limiting enzymes as well as increased L-type Ca 2+ channels and sodium-hydrogen exchangers. These molecular metabolic changes resulted in an increase in baseline glycolysis rates for RBFOX1-deficient hearts, while after 20 minutes of global ischemia they had improved cardiac work recovery and increased post-IR glycolysis and ketone oxidation rates, while fatty-acid oxidation and glucose oxidation rates remained similar to control hearts. Conclusions: Loss of RBFOX1 appears to be an evolutionarily conserved mechanism in aestivating snails and non-hibernating neonatal mice that allows for improved tolerance to IRI through increased glycolysis, ketone oxidation and H + clearing in non-hibernating adult mice.

Case Presentation: An 87-year-old woman with atrial fibrillation, Parkinson’s disease and cardiovascular risk factors, presented to the ED with two weeks of progressive dyspnea and orthopnea. Chest X-rays from 2021 through 2023 showed progressive cardiomegaly, but there was no history of known heart failure or prior echocardiography. On admission, her labs showed proBNP was 3,474 pg/mL and troponin-I HS was 101 ng/L. TTE demonstrated a large right ventricular mass with near-complete cavity obliteration and reduced RV systolic function and normal LVEF. Cardiac MRI showed an 8.7 x 4.1 x 3.8 cm lobulated mass adherent to the myocardium, obstructing inflow and outflow tracts and creating pseudo-stenosis of the tricuspid and pulmonic valves. Despite markedly reduced RV stroke volume and compression, the patient was clinically stable, normotensive, and denied chest pain or syncope. She underwent right heart catheterization with biopsy, which confirmed intimal sarcoma, a rare and normally aggressive mesenchymal malignancy. She was deemed not to be a surgical candidate due to her comorbidities. She has otherwise been asymptomatic and will follow up with her oncologist in the outpatient setting. Discussion: This case demonstrates an extraordinarily rare intimal sarcoma of the right ventricle causing both inflow and outflow tract obstruction and severely reduced stroke volume, yet presenting with minimal clinical instability. The patient’s hemodynamic resilience, despite dramatic structural compromise, likely reflects chronic tumor progression, an uncommon occurrence in this otherwise aggressive tumor type. This has allowed for physiologic adaptation, reflected in her hemodynamic stability. The findings underscore the importance of correlating anatomic imaging with clinical and hemodynamic presentation, especially in elderly patients. Previous cardiomegaly without cardiac workup suggests missed opportunities for earlier detection. This case also emphasizes the role of multimodality imaging, histopathologic confirmation, and flexible, goal-concordant care planning in cardio-oncology. Cardiac MRI with the use of parametric mapping, perfusion and late gadolinium enhancement is a pivotal step in the evaluation of undifferentiated cardiac masses which can then be confirmed with biopsy. Intimal sarcoma should be considered in patients with unexplained RV dysfunction or intracardiac masses, even in the absence of systemic symptoms.

Background: Adolescence has been identified as a critical time point when physiological adaptations deviate into pathological cardiometabolic disease processes. Large-scale prospective evidence on the direct impact of increasing fat mass from adolescence with alterations in cardiac structure among apparently healthy adolescents is limited. Adolescent dyslipidaemia and elevated blood pressure (BP) have been established as independent predictors of premature cardiac damage. However, understanding the mechanism through which fat mass alters cardiac indices will be crucial for public health intervention and preventive cardiology. Purpose: To examine the longitudinal associations of total fat mass and trunk fat mass with progressive cardiac remodelling and examine the role of low-density lipoprotein cholesterol (LDL-c), systolic BP, and inflammation on the relationships. Methods: From the Avon Longitudinal Study of Parents and Children (ALSPAC), UK birth cohort, 1803 adolescents aged 17 years who had repeated dual-energy Xray absorptiometry-measured fat mass at ages 17 and 24 years clinic visits were included. Echocardiography at 17 and 24 years assessed left ventricular mass indexed for height 2.7 (LVM). Repeated-measure longitudinal multivariate-adjusted analyses were conducted with generalized linear mixed-effect models with identity links. Structural equation model causal mediation analysis assessed the proportion of the association between fat mass and cardiac mass during ages 17 to 24 years mediated by LDL-c, systolic BP, or high-sensitivity C-reactive protein (hsCRP). Results: Each unit increase of total fat mass from age 17–24 years ( β = 0.12g/m 2.7 [95% CI, 0.09 – 0.15], p<0.001) and trunk fat mass (0.23g/m 2.7 [0.18 – 0.28], p<0.001) were independently associated with increased LVM over the 7-year growth period. Increased LDL-c, systolic BP, and hsCRP partly mediated (7.9%, 10.6%, and 7.4% mediation, respectively) the longitudinal associations between increased fat mass and increased cardiac mass during growth from adolescence to young adulthood (Figure 1). Conclusions: Increased total and trunk fat mass in adolescence was associated with cardiac structural remodelling, partially explained by altered cardiometabolic and inflammatory indices. Trunk fat mass may have a two-fold worse deleterious effect on cardiac mass than total fat mass.

The human placenta serves as the predominant endocrine organ throughout pregnancy, assuming a central role in preserving endocrine homeostasis, facilitating maternal physiological adaptation, and safeguarding fetal well-being. Preeclampsia (PE), a multifaceted and systemic gestational complication, stands a primary contributor to maternal and perinatal morbidity and mortality. Defective placental development has been extensively acknowledged as the fundamental pathological foundation underlying this condition. Accumulating evidence has unveiled a disruption in the balance of steroid hormone production within placentas affected by early-onset PE (E-PE). Considerable endeavors have been undertaken to decipher the endocrine mechanisms driving E-PE. Recent investigations have illuminated a complex, multi-tiered regulatory system that governs placental steroidogenesis, encompassing epigenetic controls such as microRNAs (miRNAs) activity and metabolic flux-conjugated histone acetylation, post-translational modifications including O-linked β-N-acetylglucosamine (O-GlcNAc), as well as intricate endocrine feedback loops among steroids and other signaling molecules like melatonin. Notably, a growing body of evidence robustly supports a causal link between elevated placental testosterone (T0) synthesis and the onset of PE. Nevertheless, comprehensive studies exploring the endocrine pathophysiology of PE remain essential to illuminate novel therapeutic avenues for mitigating this adverse pregnancy outcome.

Background: Non-optimal temperatures have become silent amplifiers of cardiovascular(CV) risk, yet their impact on individuals <20 remains underrecognized. Children and adolescents possess limited physiological adaptability, making them especially vulnerable to environmental extremes. As global temperatures rise and climate resilience remains uneven, understanding the long-term influence of cold and heat exposure on CV health in the younger population is crucial for guiding future public health and climate policy. Method: Utilizing the Global Burden of Disease study 2021 framework to estimate the burden of CVD attributable to non-optimal temperature in individuals aged <20 years across 204 countries and territories from 1990-2021. The burden was calculated using population attributable fractions(PAFs), which quantify the proportion of CVD deaths,disability-adjusted life years(DALYs), and years of life lost(YLLs) linked to exposure to low and high temperatures(LT, HT) beyond the optimal temperature threshold. Estimates were stratified by age group, sex, year, and region. Result: Between 1990 and 2021, CVD deaths attributable to LT in youth declined from 4,762(95% UI: 3,900–6,015) to 1,790(1,458–2,290), while DALYs and YLLs showed parallel reductions from 395,310(320,864–504,340) to 142,752(114,672–185,052). Conversely, HT exposure saw an increase in burden: deaths rose by 18%, DALYs by 21%, and YLLs by 21%. Regionally, Sub-Saharan Africa exhibited the steepest increase in CVD deaths due to HT, surging by 101%, followed by a 37% rise in Central Europe, Central Asia, and Eastern Europe. Age-wise, the most pronounced increases in heat-related CVD deaths occurred in the 15–19 year group (+73%) and 10–14 year group (+34%), whereas younger age groups experienced a consistent decline. Despite higher historical burdens from cold exposure, the accelerating rise in heat-related mortality reflects a shifting climate-related threat among global youth. Conclusion: Over the last three decades, the burden of CVD attributable to non-optimal temperature in individuals under 20 has transitioned from being predominantly cold-driven to increasingly heat-driven—particularly in older pediatric age groups and certain geographic regions. This evolving epidemiological pattern underscores the urgent need for climate-resilient health systems, early-life cardiovascular monitoring, and targeted public health interventions to mitigate temperature-related health risks in the next generation.

Background: Pulse wave velocity (PWV) is a marker of arterial stiffness and cardiovascular risk. While conventionally measured using tonometry or oscillometric systems, recent advances suggest that photoplethysmography (PPG) derived features correlate with PWV, enabling estimation via wearables such as smart rings. Maternal cardiovascular adaptations during pregnancy, including systemic vasodilation and increased vascular compliance, follow a U-shaped trajectory. Compliance typically increases until the second trimester and then decreases toward term, a pattern observable through both PPG and PWV. This provides a test case for PPG-based PWV estimation. This study evaluates the accuracy of PPG-derived PWV (ePWV) and its ability to capture pregnancy-related physiological changes when monitored with a smart ring. Methods: Carotid-femoral PWV (cf-PWV) was measured simultaneously with Oura Ring PPG using the SphygmoCor XCEL system in a separate cohort of 300 healthy individuals. A model was trained on 200 participants using wearable-derived features and evaluated in the remaining 100. The model was then applied to an anomymised pregnancy dataset from 5,664 users of the third-generation Oura Ring who self-reported pregnancy. Night-time PPG signals were collected during sleep from one month before conception to six months postpartum. For each participant, a baseline was defined from the month preceding conception, and ePWV deltas were calculated as relative changes. Delta values were aligned to the observation period. Results: Validation of the ePWV algorithm against cf-PWV showed strong agreement (r = 0.76), with a mean difference of 0.210 m/s and SD of 0.999 m/s. ePWV followed the expected U-shaped pattern during pregnancy. A gradual decline was observed after conception, reaching a minimum near the end of the second trimester, followed by a steady rise into the third trimester. Additionally, ePWV peaked one week postpartum before returning to pre-pregnancy levels within six months. Conclusion: PPG-derived ePWV showed strong agreement with cf-PWV reference values enabling monitoring of arterial stiffness using wearable smart ring. In addition, the ePWV patterns captured pregnancy-related vascular adaptations, reproducing the U-shaped trajectory described in prior studies. These findings support the feasibility of wearables for scalable non-invasive monitoring of arterial stiffness in response to physiological adaptations.

Background/Significance: Exercise training induces physiological cardiac hypertrophy, mitochondrial biogenesis and myocardial function. In skeletal muscle, the transcriptional coactivator PGC-1α is a key orchestrator of these. The heart expresses abundant and exercise-responsive PGC-1α, but it is unclear whether this is necessary for cardiac adaptation to endurance training. Approaches: We utilize a genetic mouse model of cardiomyocyte PGC-1α deficiency along with somatic overexpression and knockdown of a PGC-1α related protein GDF15 using adeno-associated virus. We further utilize neonatal rat ventricular myocytes, human single nucleus RNA sequencing of patients with cardiomyopathies, and whole exome sequencing of human participants from the UK BioBank to address the relationship of PGC-1α with GDF15 and with cardiac dysfunction. Results: Wild-type and cardiomyocyte PGC-1α KO mice were subjected to voluntary wheel running for 5 weeks. Mice ran comparably over that time. Despite this, cardiomyocyte PGC-1α KO mice demonstrated no improvement in peak exercise capacity compared to WT mice (exercise work 33 J in WT vs 19 J in KO, p<0.001). Instead, PGC-1α KO mice demonstrated resting dilated cardiomyopathy after just 5 weeks of training (cardiac fractional shortening after training 60% in WT vs. 31% in KO, p<0.0001). Supporting this, extremely rare protein human genetic coding variants in PPARGC1A are associated with all-cause heart failure in the UK BioBank (RR 3.23, 95% CI 1.41-6.45, p=0.002). Cardiomyocyte PGC-1α-deficient trained hearts demonstrated absence of physiological hypertrophy (area 1170 vs. 555 μm 2 , p<0.0001) and markedly increased expression of the myomitokine GDF15 . GDF15 was secreted exclusively from cardiomyocytes but is not systemically elevated in PGC-1α-deficient mouse hearts. In cardiomyocytes, this occurs through the integrated stress response pathway, which is suppressed by PGC-1α overexpression. Cardiomyocyte-specific reduction of GDF15 preserves exercise tolerance, cardiac function, and exercise-induced cardiomyocyte hypertrophy in PGC-1α-deficient mice. We also find that cardiomyocyte PPARGC1A expression correlates with cardiomyocyte number and negatively with cardiomyocyte GDF15 expression in human cardiomyopathies through single nucleus RNA sequencing. Conclusions: Our data implicate cardiomyocyte PGC-1α as a vital enabler of physiological adaptation to endurance exercise through suppression of GDF15-mediated cardiac dysfunction.

Training not only enhances the athletic performance of horses but also improves cardiac structure and function, strengthens cardiovascular adaptability, and reduces the risk of cardiovascular diseases. However, the consequences of training on equine cardiac structure and function remain unclear. This study investigated the morphological, functional, genetic, and metabolic changes in the hearts of Yili horses divided into three groups: high athletic performance (agility group, AG), low athletic performance (ordinary group, OG), and untrained (untrained group, UN). The results showed remodeling of the cardiac structure and physiological adaptations in AG and OG compared to UN groups, with differences between AG and OG primarily in the left ventricle. To explore the molecular mechanisms underlying these phenotypic changes, transcriptomic and metabolomic analyses (particularly GO and KEGG pathway analyses) were performed to assess differences in gene expression and metabolite levels among the three groups. Our results show that miR-1842, miR-671, miR-106b and miR-18a were differentially expressed in the trained groups (AG group and OG group) compared with the control group that did not receive training. These regulatory factors would regulate PFKFB3 to affect the glycolytic activity mediated by HIF-1, there by promoting glycolysis and changing lactate level. This, in turn, would positively feedback to stabilize HIF-1, thus forming a closed loop for the reprogramming of myocardial energy metabolism. In the AG group, positive effects of cAMP signaling were noticeable. In conclusion, our findings offer new insights into physiological cardiac remodeling in Yili horses by highlighting genetic and metabolomic changes resulting from exercise training.

Ecotype-specific light intensity responses in Sargassum horneri: bloom-forming vs. benthic forms.

Dynamic response of partial nitritation-anammox systems to salinity stress with additional carbon input for stable nitrogen removal performance.

Cold exposure triggers distinct RNA editing, alternative splicing, and gene expression patterns in cold domestication pufferfish (Takifugu obscurus).

Bidirectional dynamics: A cross-lagged examination of physical exercise and loneliness in older adults.

A mechanistic investigation of the effects of lactic acidosis on myocardial contractility in the Neotropical fast-swimming freshwater fish Brycon amazonicus.

Global shark biodiversity is in decline, with numerous species facing extinction because of anthropogenic influence. Loss of species richness is expected to diminish trait diversity, encompassing ecological roles and physiological adaptations. We investigate whether the extinction of threatened species, as classified by the International Union for Conservation of Nature, drives morphological and ecological homogenization within Carcharhinus, a speciose genus of requiem sharks. We assembled a dataset of tooth morphology from 30 species and combined it with functional data such as diet, habitat, and body size. Simulated extinction scenarios, where species were sequentially removed from the highest to lowest threat level, revealed that the loss of threatened species would result in marked homogenization of morphology and ecology. Along this extinction trajectory, trait structures become increasingly depauperate, marked by contracting depth ranges and declining body-size diversity. Our results indicate that the diverse dental morphologies, shaped over millions of years, are at risk of disappearing—eroding the genus’s capacity to support varied ecological roles.

SUMMARYSalinity represents a major abiotic stressor that significantly impairs soybean growth and yield. Although jasmonic acid (JA) has been firmly established as a key regulator of plant defense against salt stress, the precise functions of lipoxygenase (LOX) genes responsible for initiating JA biosynthesis remain poorly defined. Here, a comprehensive genome‐wide analysis of the soybean LOX gene family was performed, and a detailed functional characterization of GmLOX6 was carried out. Subcellular localization confirmed that GmLOX6 is targeted to chloroplasts, while enzymatic assays demonstrated that it acts as a 13‐LOX enzyme with a strong preference for α‐linolenic acid as substrate. To clarify its role under salt stress, we generated both overexpression and CRISPR/Cas9‐mediated knockout lines of soybean. Phenotypic and molecular evaluations revealed that GmLOX6 facilitates JA production under salt stress, thereby contributing to enhanced JA accumulation. This elevation in JA levels was associated with improved salt tolerance through multiple physiological adaptations, including the activation of antioxidant enzymes for the detoxification of reactive oxygen species (ROS), enhanced Na+ extrusion to preserve ionic balance, and reinforced membrane stability. Moreover, GmRWP‐RK11 was identified as a transcriptional repressor of GmLOX6. Functional disruption of GmRWP‐RK11 via CRISPR/Cas9 conferred greater salt tolerance, further supporting its negative regulatory role. Collectively, these findings uncover a novel regulatory axis in which GmLOX6‐mediated JA biosynthesis enhances soybean resistance to salinity through modulation of ROS homeostasis and Na+ transport. These insights provide an expanded understanding of the transcriptional and biochemical mechanisms underpinning JA‐driven stress adaptation in soybean.

Adaptive hematological profiles and brain structure buffer depression in high-altitude healthy adults.

Blood flow restriction resistance training enhances athletic adaptations via distinct mechano-metabolic pathways. This review synthesizes evidence comparing three blood flow restriction resistance training modalities: Low-load resistance training with blood flow restriction (using 20%–30% of one-repetition maximum) prioritizes metabolic stress (lactate and hydrogen ion accumulation, cellular swelling), activating growth hormone (GH)/insulin-like growth factor 1 (IGF-1)/mechanistic target of rapamycin (mTOR) pathways to promote type I muscle fiber hypertrophy, making it suitable for joint-sparing rehabilitation scenarios. Supplemental blood flow restriction resistance training programs combine high-load tension (utilizing 75%–90% of one-repetition maximum) with additional blood flow restriction to produce an acute synergistic effect. This method enhances the recruitment of type IIa/x muscle fibers and prolongs mTOR phosphorylation. Combined blood flow restriction resistance training employs alternating cycles of high-load phases (70%–85% 1RM) and blood flow restriction phases (hypoxia-inducible factor 1-alpha (HIF-1α)-mediated angiogenesis), optimizing phosphocreatine resynthesis and neural drive to achieve specialization of type IIx muscle fibers. Periodized application requires matching modalities with training phases: combined blood flow restriction training for hypertrophy during the preparatory phase, supplemental blood flow restriction training for strength maintenance during the competitive phase, and low-load resistance training with blood flow restriction for active recovery. This mechanistic framework supports evidence-based blood flow restriction resistance training programming to maximize athletic adaptations while mitigating injury risk.