Acute mountain sickness (AMS) compromises health and work efficiency after rapid ascent. This study aimed to explore a low-altitude-data-based method for classifying AMS-susceptible young adults. Forty-four low-altitude residents (18-31 years) completed a step test at 50 m. Measurements included maximal oxygen uptake (V̇O2max), peripheral oxygen saturation at rest (re_SpO2), exercise (ex_SpO2), and recovery (rec_SpO2), heart rate at rest (re_HR), exercise (ex_HR), and recovery (rec_HR), and step index. Participants ascended to 3650 m within 6 h, and AMS was assessed using the 2018 Lake Louise Score (LLS). Associations with LLS were examined before k-means clustering. Neither re_SpO2 nor re_HR was significantly correlated with LLS, whereas non-resting-state variables (V̇O2max, ex_SpO2, rec_SpO2, ex_HR, rec_HR, and step index) were. Clustering using V̇O2max, ex_SpO2, rec_SpO2, and step index showed strong structure (silhouette coefficient = 0.767) and 93.18% agreement with LLS. Step index and ex_SpO2 showed the greatest between-cluster separation, followed by rec_SpO2 and V̇O2max. Exercise- and recovery-phase variables from a low-altitude step test may classify AMS susceptibility in young adults via unsupervised learning. Evaluated after rapid ascent to 3650 m, this noninvasive, low-cost, and practical approach shows potential for pre-ascent AMS susceptibility screening in healthy young adults.
This study examined whether cardiopulmonary exercise test (CPET) performance parameters are associated with chronic cancer-related fatigue in patients receiving immunotherapy checkpoint inhibitors (ICI) and healthy controls. Also, the differences in energy expenditure of steady-state cycling and gross efficiency were assessed during submaximal cycling efforts. This study involved patients (n = 19, 48 ± 13 years) receiving PD-1, PD-L1 checkpoint inhibitors and controls of similar age (n = 21, 49 ± 17 years). During the first visit, data on medical history, previous physical activity records, and CPET to voluntary exhaustion were collected. The second visit involved body composition assessment, the MFI-20 fatigue questionnaire, and 30-min steady-state cycling at 90% gas exchange threshold. There were no significant differences observed between the groups in age, stature, BMI, or resting blood pressure. Peak V̇O2 was 33% lower, and the group under ICI treatment had lower cycling efficiency (22.49% vs. 20.07%, p = 0.031), compared to controls. All self-reported fatigue items derived from MFI-20 were significantly higher in the ICI group compared to controls (p = 0.001). The regression analysis found no association between the self-reported general fatigue and data collected during CPET. Patients under ICI treatment reported higher levels of chronic fatigue, lower peak V̇O2, and reduced cycling efficiency. Interestingly, variables collected during CPET did not explain self-reported chronic fatigue, underlying the complexity of this phenomenon.
We tested whether there is a circadian variation in baroreflex function measured as sensitivity and effectiveness, and whether it aligned with circadian variations in systolic blood pressure (BP). Eleven healthy adults (24 ± 2 years; 4 males and 7 females) completed a 30-h circadian protocol incorporating five recurring, identical, 6-h cycles of 4-h standardized wakefulness and 2-h sleep opportunities. Spontaneous beat-to-beat BP (finger photoplethysmography) and R-R intervals (electrocardiogram) were recorded at rest for 10 min during each wakefulness period, to assess cardiac baroreflex sensitivity (BRS) and effectiveness index (BEI). Vascular endothelial function (VEF) was assessed as flow-mediated dilation of the brachial artery. Dim light melatonin onset was used as a circadian phase marker. Systolic BP exhibited a significant trough at ~1:40 am (p = 0.02). This trough closely aligned with the nocturnal peak of cardiac BEI that occurred at ~1 am (p = 0.02). BRS showed no significant variation. VEF exhibited a significant peak at ~10 am In healthy adults, the nocturnal peak in BEI is possibly aligned with the circadian trough in systolic BP. It remains to be determined whether shifting one would shift the other in a similar direction, and whether the alignment holds in people with disease.
Healthy aging is associated with a progressive decline in respiratory function and altered ventilatory mechanics, typically characterized on static physiological measurements. We aimed to evaluate the ventilatory response to exhaustive exercise across the age-span and hypothesized that aging would be associated with inefficient alterations that may be relevant in the etiology of breathlessness. We analyzed ventilatory data obtained from cardiopulmonary exercise tests performed in 526 healthy adults (aged 20-91 years; 52% female) from the COmPLETE cohort. Sample Entropy (SampEn) was used to quantify the irregularity of minute ventilation (V̇E), breathing frequency (Bf), and tidal volume (VT) time series. Age versus entropy relationships were assessed using penalized cubic splines, adjusting for sex, BMI, peak oxygen uptake, and FEV1. As a result, older age was associated with a progressive decline in peak oxygen uptake, V̇E, Bf, and VT (all p < 0.001). Ventilatory efficiency also decreased across the age span, evidenced by an increased VE/VCO2 nadir, and older adults demonstrated a tachypneic breathing pattern, with a higher Bf to V̇E ratio (p < 0.001). Contrary to our hypothesis, ventilatory SampEn remained stable through early adulthood but increased after the sixth decade (SampEn Bf p = 0.023; SampEn VT: p = 0.004; SampEn V̇E: p = 0.001). In conclusion, older age is accompanied by a shift in the ventilatory response to exercise, characterized by a mechanically constrained, frequency-dominant breathing pattern and diminished ventilatory efficiency. This is associated with increases in ventilatory irregularity that become most apparent after the sixth decade. Further work is needed to determine how these alterations relate to exertional breathlessness.
Acute muscle strain injuries belong to the most frequent sports injuries with high recurrence rates. Biopsies obtained from previously strain-injured muscles showed fat intra- and intermuscular, but quantification of fat content in the entire muscle volume following a strain injury has not been performed previously. The aim of the study was to evaluate fat fraction in the injured and the contralateral, uninjured muscle acutely, and 3- and 12-months after a strain injury. DIXON fat fraction was analyzed acutely after the injury, 3- and 12-months post injury in the injured and the contralateral, healthy muscle in 29 individuals with an ultrasound verified strain injury in either the calf or the hamstrings. There was a significant increase in fat content 3 and 12 months post injury in the injured, but not in the contralateral, uninjured muscles. There was a significant negative correlation between the increase in fat fraction and loss of muscle mass, and a significant positive correlation between the enlargement of the aponeurosis and the amount of fat in the injured muscles. Strain injuries lead to a rise in fat fraction in muscles from healthy, sports active individuals. The increased fat fraction appears permanent as fat accumulation in the muscle after the injury was not reversed after 12 months.
Insulin resistance (IR) contributes substantially to cardiovascular disease and type 2 diabetes mellitus, with increasing concern among people living with HIV (PLWH). However, sex-specific factors of IR in sub-Saharan Africa remain poorly understood. This study evaluated sex-specific associations between IR and clinical, metabolic, and inflammatory markers among adults with and without HIV in Zambia. A cross-sectional study was conducted among 233 adults in Zambia. Insulin resistance was assessed using the Homeostatic Model Assessment for Insulin Resistance (HOMA-IR). Sex-stratified multivariable linear regression models were used to identify factors associated with IR. Females had higher body mass index (26.9 vs. 23.5 kg/m2, p < 0.001), waist circumference (88.3 vs. 83.2 cm, p = 0.008), fasting insulin, and HOMA-IR compared with males. In the adjusted overall model, female sex was associated with higher HOMA-IR (β = 0.95, 95% CI: 0.06-1.84; p = 0.037), while HIV-positive status was associated with lower HOMA-IR (β = -1.54, 95% CI: -3.06 to -0.02; p = 0.046). Among males, hypertension was associated with higher HOMA-IR (β = 0.61; p = 0.019), whereas among females, HIV-positive status was inversely associated with HOMA-IR (β = -2.31; p = 0.049). Insulin resistance highlighted sex-specific patterns, with greater metabolic risk among females and distinct clinical factors among males. Future studies incorporating lifestyle and hormonal factors are needed to clarify these relationships.
Age-related changes in large-vessel biomechanics may contribute to neurovascular dysfunction and region-specific biochemical remodeling in the brain, with important implications for female health. This study investigated the impact of aging on neck vasculature and brain lipid biochemistry in female C57BL/6NHsd mice by comparing young (12 weeks; n = 10) and middle-aged (52 weeks; n = 10) cohorts using ultrasound imaging, histology, and mass spectrometry. In vivo ultrasound quantified carotid and jugular hemodynamics, including wall shear stress (WSS), circumferential cyclic strain (CCS), pulsatility index, and volumetric flow. Ex vivo assessments included spatial lipid mapping in vessels and brain, and histology staining to quantify elastin-to-collagen ratios. Middle-aged females exhibited reduced carotid systolic velocity, systolic WSS, and body weight-normalized carotid volumetric flow compared to young controls, while pulsatility index and CCS showed non-significant decreases. Histology revealed a reduction in the carotid elastin-to-collagen ratio, consistent with vascular remodeling. Lipidomic profiling identified age-dependent shifts in lipid headgroups, including decreases across multiple brain lipid classes, increased N-acylethanolamides, alongside increases in carotid cardiolipin and lysophosphatidylethanolamine. Hippocampal spectra showed clearer age-related separation than whole-brain analyses. Correlation analyses identified moderate to strong associations between vascular biomechanics and lipid features across tissues, supporting coordinated neurovascular and biochemical aging in female mice.
The growing accessibility of simulated altitude facilities (~13%-16% fraction of inspired oxygen [FIO2]) has expanded their use to broader recreational populations. Although acute normobaric hypoxia reduces arterial oxygen saturation and increases ventilatory and sympathetic responses, interindividual variability in dyspnea during hypoxic exercise remains poorly characterized. Twenty-two healthy individuals (24 ± 4 years, 50% female) completed one 90-min exposure at an altitude facility (FIO2 ≈ 15 ± 0.1%) that included an assessment of heart rate variability (autonomic activity), a vascular occlusion test (microvascular responsiveness), and submaximal cycling at 60% heart rate reserve. Vastus lateralis (VL) oxygen saturation and heart rate were measured throughout. Marked interindividual variability in dyspnea derived from the Multidimensional Dyspnea Profile was observed across the cycling protocol. While resting autonomic activity (all p > 0.326) and microvascular responsiveness (all p > 0.138) were not associated with dyspnea perception, greater VL deoxygenation was strongly correlated with dyspnea during cycling (all r > -0.558, all p < 0.007) with the interpretation unchanged when adjusted for wattage. Additionally, males exhibited higher dyspnea (p = 0.022) and greater VL deoxygenation (-32 ± 14% vs. -15 ± 18%, p = 0.022) compared to females. Combined, these findings highlight the importance of interindividual variability in dyspnea during hypoxic exercise and warrant further investigation into its functional implications.
Long COVID (post-acute sequelae of SARS-CoV-2 infection) affects approximately 5%-30% of survivors and is characterized by persistent fatigue, dyspnea, exercise intolerance, and cognitive impairment. We evaluated the immunological effects of supervised exercise in adults with long COVID. In this pre-specified exploratory substudy of the EXER-COVID randomized 2 × 2 crossover trial, participants completed a 6-week supervised exercise program (twice weekly) or usual care before crossing over after a 3-5 day washout. Plasma cytokines (IL-1β, IL-6, IL-10, TNF-α, MCP-1/CCL2, MIP-1α/CCL3, MIP-1β/CCL4, and IP-10/CXCL10) were measured by multiplex immunoassay. Immunophenotyping included 20 CD4+ and CD8+ T-cell subsets and five innate immune populations. Treatment effects were estimated using within-period change scores, with multiple testing controlled by the Benjamini-Hochberg procedure (false discovery rate < 5%). Five variables reached nominal significance before correction (two CD8+ T-cell subsets and IL-1β, IL-10, and MIP-1α), but none remained significant after adjustment. No changes were observed in innate immune populations, and no evidence of carryover was detected. Supervised exercise was not associated with significant immunological changes after correction for multiple comparisons, supporting the short-term immunological safety of moderate-intensity exercise in PESE-negative adults with long COVID (ClinicalTrials.gov: NCT04797871).
Acute cannabis use and its primary psychoactive constituent tetrahydrocannabinol (THC) can induce postural dizziness, indicating increased risk of orthostatic instability. However, it is unknown if vulnerabilities persist the morning after bedtime THC consumption. This study investigated the influence of bedtime THC consumption on cardiovascular variables during an orthostatic challenge. Nine individuals with no cannabis use and eight individuals who regularly use cannabis participated in a tilt table test associated with a 3-day in-laboratory stay. Participants underwent an acclimatization day, followed by a placebo dosing day, and a 10 mg THC dosing day. Placebo and THC pills were given 1 h before a participant's habitual bedtime, and the tilt table test was performed ~1 h upon awakening. Participants were instrumented with an electrocardiogram and an automated sphygmomanometer. Fluid intake and output were measured throughout the study. The morning after THC administration, individuals with no cannabis use reported a higher frequency of dizziness and exhibited a significant reduction in both diastolic blood pressure and heart rate reactivity to tilt (reactivity = tilt - baseline) compared to the morning after placebo. Our results indicate a potential increased risk for orthostatic instability the morning after cannabis consumption in individuals with no cannabis use history.
Abstract The deep fascia surrounds skeletal muscles and contributes to force transmission and mechanical coordination, but its response to denervation remains unclear. This study investigated morphological and transcriptional adaptations of the deep fascia following sciatic nerve denervation in mice. Male C57BL/6J mice ( n = 5–6/group) underwent unilateral sciatic nerve denervation or sham surgery. Fourteen days later, tibialis anterior (TA) muscle and overlying deep fascia (anterior crural fascia) were analyzed by histology and quantitative PCR. Denervation induced significant TA muscle atrophy with upregulation of inflammatory ( Il6 , p = 0.001), profibrotic ( Tgfb , p < 0.001), and extracellular matrix (ECM)–related genes ( Mmp2 , p = 0.006; Col3a1 , p = 0.005), and downregulation of regenerative factors ( Fgf2 , p < 0.001). Deep fascia thickness increased approximately 1.5‐fold ( p = 0.012) and was accompanied by elevated Il6 ( p < 0.001), Tgfb ( p = 0.035), Col1a1 ( p = 0.006), and Col3a1 ( p = 0.003) expression and a higher proportion of collagen type III ( p = 0.015). In conclusion, sciatic nerve denervation induces muscle atrophy and deep fascia thickening accompanied by extracellular matrix remodeling. These findings demonstrate coordinated yet tissue‐specific remodeling of skeletal muscle and deep fascia following sciatic nerve denervation.
Abstract Short‐term limb immobilization is known to impair muscle strength; however, its effects across distinct domains of motor function remain incompletely characterized. In this study, we assessed the effects of 72‐h of hand immobilization on motor functions in healthy adults. Twenty‐eight participants were randomized to an immobilization or control group and completed a motor test battery before and after the intervention. The battery assessed maximal and explosive strength, quantified as maximal voluntary contraction (MVC) force and rate of force development (RFD), fatigability during sustained maximal contractions, force steadiness during submaximal contractions, and manual dexterity. Immobilization induced domain‐specific impairments in motor performance. MVC force and RFD declined significantly following immobilization, indicating susceptibility of maximal and explosive strength to short‐term disuse. In contrast, no significant changes were observed in the selected parameters of fatigability during sustained maximal contractions, including the fatigue time constant and plateau force. Force steadiness showed a selective increase in relative force variability, whereas absolute force variability remained unchanged. Manual dexterity was not reduced from baseline, but immobilization attenuated the test–retest performance improvements observed in the control group and contralateral non‐immobilized hand. These findings demonstrate that hand immobilization induces task‐ and domain‐specific alterations in motor performance rather than a uniform decline, preferentially affecting motor domains that require high force production.
Abstract This study investigated the roles of the NLRP3 inflammasome in postoperative ileus (POI) pathogenesis. Male BALB/c mice were randomly divided into sham, POI, and MCC950 (NLRP3 inhibitor) groups. Intestinal motility was assessed 24 h postoperatively. RNA‐seq was performed. Histopathological changes were evaluated through H&E and immunofluorescence; CAT and POD activities in the intrinsic muscle layer were detected; Western blot was used to detect NLRP3, GSDMD‐N, cleaved caspase‐1, and p‐NF‐κB p65 expressions; ELISA was used to detect blood IL‐1β, TNF‐α, IL‐6, and IL‐10 levels. RNA‐seq analysis showed 152 differential genes in the POI group, including NLRP3. In intestinal tissue of the POI mice, NLRP3 expression and expressions of GSDMD‐N, cleaved caspase‐1, and p‐NF‐κB p65 increased. IL‐1β, TNF‐α, IL‐6, and IL‐10 levels increased, while CAT, POD, and SOD activities decreased. The postoperative small intestine advancement rate of POI mice was reduced. After MCC950 intervention, the pathological damage to intestinal tissue and the intestinal function were restored, and the small intestine advancement rate was improved. Meanwhile, MCC950 effectively inhibited the activation of the NLRP3 inflammasome. NLRP3 inflammasome activation drives the pathogenesis of POI and MCC950 can effectively alleviate intestinal injury.
Abstract Hypertensive disorders of pregnancy are associated with increased cardiovascular risk and arterial remodeling, further complicated by obesity. While carotid‐femoral pulse wave velocity remains the gold standard for arterial stiffness assessment, estimated PWV (ePWV) and carotid‐radial PWV (crPWV) offer practical alternatives. This study evaluated ePWV and crPWV in gestational hypertension (GH) and their association with asymmetric dimethylarginine (ADMA). Cross‐sectional analysis of 74 obese pregnant women (GH: n = 38; normotensive: n = 36). Lifestyle characteristics were assessed via WHO STEPS questionnaire. Seated blood pressure was measured and ePWV calculated. crPWV and augmentation index (AIx) were assessed using Complior Analyse. Serum ADMA was measured. Multivariable linear regression identified independent predictors of arterial stiffness, adjusting for central systolic blood pressure (cSBP), AIx, ADMA, and GH status. ePWV was significantly higher in the GH group (7.7 vs. 6.6 m/s; p < 0.001), while crPWV did not differ significantly ( p = 0.14). A significant correlation between ePWV and crPWV was observed ( r = 0.42; p < 0.001). ADMA did not differ between groups. cSBP and AIx independently predicted crPWV; GH status independently predicted ePWV. ADMA was not significantly associated with either marker. ePWV may serve as a practical, effective index for assessing vascular load in obese obstetric populations.
Abstract Vigorous exercise triggers signaling cascades that activate autophagy markers like the degradation of sequestosome 1 (p62) and accumulation of Light Chain 3 II (LC3II). Limited human data exist on autophagic responses across different local and systemic tissues and how training status affects these relationships. This study investigates the vigorous exercise‐induced changes in p62 and LC3II expression in peripheral blood mononuclear cells (PBMCs) and skeletal muscle between endurance‐trained and untrained men. Twelve men (endurance‐trained n = 7, untrained n = 5) completed 60 min of cycling at their second ventilatory threshold. Skeletal muscle biopsy samples and PBMCs were collected pre‐ and 3‐h post‐exercise and analyzed for p62 and LC3II protein expression. We found significant interaction effects of time and training status for p62 ( p < 0.001) and LC3II ( p = 0.002). In untrained men, p62 decreased in PBMCs (FC = 0.50 ± 0.14; p < 0.001) and skeletal muscle (FC = 0.57 ± 0.21; p < 0.001), while LC3II increased in both tissues (FC = 1.74 ± 0.79; p = 0.019 for PBMCs; FC = 1.69 ± 0.47; p = 0.033 for skeletal muscle). No changes were observed in endurance‐trained men (all p > 0.05). These results suggest that a bout of vigorous endurance exercise increased autophagy‐related markers in both skeletal muscle and PBMCs in the untrained men only, suggesting a diminished autophagic response in the trained men.
Abstract Striated muscle weakness and motor neuron (MN) death are associated with aging. These alterations affect both brainstem and spinal motor pools, including hypoglossal MNs innervating the tongue and lumbar MNs innervating the lower/hindlimbs. Both MNs and striated muscles exhibit type‐selective motor unit vulnerability, where larger MNs (likely fast fatigable motor units) and type IIx/b muscles are vulnerable to death and atrophy, respectively. These findings have been cemented in humans to some degree and in Fischer 344 and Wistar rats. However, MN survival in old age has not been evaluated in Sprague–Dawley rats. Here, in 6‐ (young) and 24‐month‐old (old) female and male Sprague–Dawley rats, we performed stereological MN counts on hypoglossal and lumbar MNs using 16 μm Nissl‐stained sections. We observed a 35% loss of hypoglossal and lumbar MNs in old age. Although mean MN somal surface areas were moderately reduced in hypoglossal and unchanged in lumbar MNs with age, frequency histogram analyses revealed a disproportionate loss of larger MN in old age hypoglossal and lumbar pools. These findings reveal reliable and robust observations of MN death in rats. This neurogenic aspect of neuromotor impairment with age may be a key driver of sarcopenia and frailty in the elderly.
Abstract Traumatic brain injury (TBI) is associated with cardiovascular dysfunction that worsens clinical outcomes, yet the underlying mechanisms are poorly understood. Clinical studies are limited by heterogeneity, highlighting the need for controlled experimental models. Controlled cortical impact (CCI) provides precise control of injury severity, and invasive pressure‐volume (PV) loop analysis allows detailed hemodynamic assessment. Adult male Wistar rats underwent sham operation or mild or severe CCI‐induced TBI. PV‐loop assessment and transthoracic echocardiography were performed at 8 or 24 h after TBI or sham. Serum epinephrine (EPI) and norepinephrine (NE) were quantified by ELISA. At 8 h post‐injury, mild TBI was associated with decreased E ES ( p = 0.013) and increased V 120 ( p = 0.016), accompanied by qualitative global hypokinesis on echocardiography. Severe TBI demonstrated decreased cardiac output ( p = 0.009) and stroke work ( p = 0.006), whereas load‐independent systolic indices were unchanged. At 24 h post‐injury, severe TBI exhibited persistent global cardiac dysfunction. Serum NE and EPI were similar to shams; however, the NE‐to‐EPI ratio was decreased 8 h after mild TBI ( p = 0.042). These findings suggest that TBI is associated with cardiovascular dysfunction that varies with injury severity; however, temporal characterization following mild TBI requires further study. Controlled experimental models provide a valuable platform for elucidating brain‐heart interactions after TBI.
Muscle atrophy caused by inactivity leads to declines in multiple physiological functions, including brain function. Although skeletal muscle is known to secrete extracellular vesicles (EVs) such as exosomes, how inactivity-induced muscle atrophy alters the properties and functions of these EVs remains unclear. In this study, we investigated the effects of cast immobilization-induced muscle atrophy on the microRNA (miRNA) profiles of skeletal muscle-derived EVs in mice, as well as their impact on transcriptome changes in brain neurons. Muscle atrophy induced by cast immobilization significantly altered the microRNA profiles of skeletal muscle-derived EVs, with 25 microRNAs upregulated and 2 microRNAs downregulated compared with controls. Moreover, treatment of brain neurons with EVs derived from atrophic skeletal muscle markedly changed neuronal mRNA expression profiles. Gene Ontology (GO) analysis revealed that upregulated mRNAs in EV-treated neurons were enriched in genes involved in the positive regulation of programmed cell death, including apoptosis. Consistently, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis demonstrated activation of apoptosis-related signaling pathways in brain neurons. These findings suggest that muscle atrophy-induced alterations in skeletal muscle-derived EVs may contribute to brain dysfunction by promoting apoptotic processes in brain neurons.
The hepatosplanchnic vascular response to isolated abdominal organ injury remains poorly defined. The aim of this review was to synthesize the available evidence on macrovascular hepatosplanchnic flow and organ-specific microvascular perfusion following isolated abdominal injury or surgery. PubMed/MEDLINE was searched through 11 May 2026 for human and animal studies reporting visceral hemodynamic changes after abdominal trauma, experimental injury, or surgery. Systematic-review methods included structured study selection, data extraction, and design-specific risk-of-bias assessment within a PRISMA-based scoping-review framework. Owing to heterogeneity, findings were synthesized narratively. Twenty-six studies were included: 14 human and 12 animal studies. Nineteen investigated pneumoperitoneum or elevated intra-abdominal pressure, four major abdominal surgery, and three other models. Perfusion reductions became more frequent with increasing pressure and were significantly more common at >15 than <10 mmHg (p = 0.031). Higher pressures also impaired compensatory mechanisms, including the hepatic arterial buffer response. After major surgery, portal and total hepatosplanchnic flow generally increased early postoperatively, while gastric mucosal perfusion deteriorated, indicating macro-microcirculatory dissociation. Only one study directly examined primary intra-abdominal injury and assessed microcirculation alone. Evidence remains indirect, heterogeneous, and methodologically limited. Studies combining serial macrovascular and organ-specific microvascular measurements are required to define the hepatosplanchnic response.
We evaluated acute (Study A) and chronic (Study B) effects of a novel breath-hold technique (BHT) protocol on performance in military personnel. In Study A, 11 healthy male participants completed either rest or a 40-min BHT before 15 min steady-state (SS) cycling at 80% V̇O2max and a 5-min time trial (TT). BHT acutely increased V̇O2 (200.3%, p = 0.005), produced a significant rise in hemoglobin (Hb; 3%, p = 0.030), and altered end-tidal oxygen (ETO2; 2.99%, p = 0.054), and lower end-tidal carbon dioxide (ETCO2; 12.1%, p = 0.065), reflecting changes in pulmonary gas exchange following breath-hold exposure, during rest. During SS, blood lactate was lower with BHT (-12.2%, p = 0.051; subsample n = 3). TT work was greater after BHT (84.4 ± 12.8 kJ vs. 78 ± 13.4 kJ; p = 0.019). In Study B, 48 United States Marine Corps Officer Candidates completed 3 weeks of BHT during training, with performance assessed via 3-mile run time. Run performance improved in both groups (BHT 7.2%; CON 4.9%). Hb concentration increased in BHT (4.3%; p = 0.037), but declined in CON (-6.6%). Pre-test arterial oxygen saturation (SPO2) was higher in BHT (97.7% ± 0.9% vs. 96.9% ± 1.6%; p = 0.03), while estimated partial pressures of arterial oxygen (PaO2) and carbon dioxide (PaCO2), used as indices of systemic gas exchange status, were similar between groups. These findings suggest that acute responses to BHT may translate into adaptations when repeated, supporting BHT as an adjunct to endurance training and warranting larger, mechanistic trials.
