Journal of Applied Physiology

Abstract Purpose: MyotonPRO (MTP) and time-harmonic elastography (THE) are increasingly used to assess muscle mechanical properties, yet they operate on fundamentally different physical principles. MTP measures composite MTP stiffness (N/m) through surface oscillations, while THE quantifies intrinsic shear modulus (THE stiffness, kPa) via propagating shear waves. This study aimed at systematically compare MTP and THE measurements in the vastus lateralis muscle across different contraction intensities and examine how the skin layer and subcutaneous fat (SLSF) thickness influence their relationship. Methods: Twenty-six healthy adults (15 males, 11 females; age 25 [SD 4] years) underwent MTP and THE measurements of the vastus lateralis at rest and during isometric contractions at 15% and 30% maximal voluntary contraction (MVC). Effects of contraction intensities on tissue properties were assessed using univariate analyses of variance with repeated measures. Associations between the different outcomes of THE and MTP technologies were explored using Pearson's correlations and partial correlation coefficients separately for each contraction intensity with adjustment of the SLSF thickness of participants. Results: Both technologies detected contraction intensity-dependent stiffening across all outcomes (p < 0.001). THE stiffness increased from 5.3 [1.2] kPa at rest to 15.6 [6.1] kPa at 30% MVC; THE wave attenuation increased from 0.83 [0.19] to 1.42 [0.36] s/m while MTP stiffness increased from 337.3 [49.3] N/m at rest to 529.4 [160.7] N/m at 30% MVC. Correlations between modalities were weak and condition-dependent. THE wave attenuation did not significantly correlate with any MTP outcome across conditions. Conclusion: MTP and THE detect contraction-induced stiffening through fundamentally different physical mechanisms and should not be regarded as interchangeable. Their correlation is modest at rest and breaks down (or reverses) during active contraction, with subcutaneous fat as a key modifying factor. Clinical trial number: Not applicable.

Background: Exercise-based cardiac rehabilitation (CR) improves peak oxygen uptake ([V]O2peak) in patients with coronary heart disease (CHD); however, whether women and men exhibit similar adaptations across the steps of O2 transport remains unknown. We aimed to compare the ventilatory and circulatory determinants of [V]O2peak changes between women and men with CHD following a structured exercise training program. Methods: A total of 28 women (27%) and 75 men (73%) with CHD, matched for age, body mass index, and [V]O2peak (% predicted), underwent maximal cardiopulmonary exercise testing (CPET) before and after 12 weeks of CR. [V]O2peak and minute ventilation ([V]E) were measured breath by breath. Heart rate and cardiac output ([Q]c)were assessed non-invasively using impedance cardiography. Exercise efficiency ({Delta}[V]O2/{Delta}W), alveolar ventilation ([V]A), ventilatory efficiency (OUES), O2 pulse, arteriovenous oxygen content difference (C(a-[v])O2) and gross muscular efficiency (W) were calculated using standard equations. Mixed model analyses (sex x time) were used to compare training-induced changes between sexes. Results: At baseline, values of [V]O2peak (absolute and normalized by fat free mass), [V]E, [V]A, O2 pulse, C(a-[v])O2, {Delta}[V]O2/{Delta}W, W were significantly lower in women than in men with CHD (group effect, p<0.01). [V]O2peak normalized by fat-free mass improved similarly in both sexes after CR (p<0.0001, no significant sex x time interaction). Pulmonary convection ([V]E, [V]A), ventilatory efficiency (OUES), circulatory convection ([Q]c, cardiac index, O2 pulse), and peripheral gross muscular efficiency (W) all improved similarly after CR in women and men (effect sizeXtime effect, p<0.05, no significant group x time interaction). The prevalence of responder categories did not differ between sexes (p=0.826). Conclusion: Women and men with CHD demonstrated equivalent O2 transport phenotype adaptations after CR, with comparable improvements across the O2 transport chain (pulmonary, circulatory, and peripheral determinants of [V]O2peak).

This study examined the utility of HRV detrended fluctuation analysis alpha-1 (DFA1) to assess readiness-to-train and exercise durability under varying acute training loads. Nineteen trained cyclists completed two 20-minute time-trials (TT) under rested and fatigued conditions. DFA1 was measured during a standardized warm-up (WU), 20-min TT, and standardized cool-down (CD). Power output (PO) and DFA1 responses were compared across conditions, and associations with performance and fitness (W/kg) were examined. DFA1 values declined with increasing WU and CD exercise intensity (p<0.001) and were significantly attenuated following the 20-min TT (p<0.001). While DFA1 profiles did not differ significantly between rested and fatigued conditions, lower pre-TT DFA1 was associated with reduced TT performance (p=0.022; r=0.55), suggesting relevance to training readiness. Additionally, an 18% decline in DFA1 between 10- and 20-min during the TT (p=0.031), and lower post-TT values at matched intensities were observed (p<0.001), indicating physiological perturbation from the 20-min TT. Fitter participants exhibited lower DFA1 values during the 20-min TT (p<0.001; r=-0.77), suggesting a greater capacity to sustain physiological stress. While DFA1 is responsive to exercise intensity and stress, offering potential to assess training readiness and durability, more robust fatigue protocols are needed to validate DFA1 as training load monitoring tool.

BackgroundThe cardiovascular (CV) benefit of CPAP in OSA remains debated and its effects on new OSA-related CV risk markers are unclear. We aimed to quantify short-term CPAP effects on these markers along with vascular and autonomic phenotypes. MethodsIn a 2-week withdrawal study, patients on long-standing effective CPAP took part in three visits (V1-V3: on/off/back-on CPAP) with overnight polygraphy followed by vascular and autonomic phenotyping. Co-primary endpoints included endothelial function assessed by flow-mediated dilation (FMD) and baroreflex sensitivity (BRS), hypoxic burden (HB), pulse wave amplitude drop index (PWADi) and spontaneous-PWADi (excl. apnoea-triggered drops), and event-related heart-rate response ({Delta}HR). Between-visit differences were tested in adjusted mixed models, with visit or within-participant changes in AHI/HB as fixed effects. ResultsIn 42 participants (61{+/-}10 years, 83% male), CPAP withdrawal reinstated OSA (medians [IQR] V1 to V3: AHI 3.9[1.5, 8.8] to 33.4[19.5, 42.1] to 4.0[2.0, 8.8] events/h, HB 4.3[1.1, 8.7] to 51.3[19.7, 83.7] to 2.0[1.2, 6.5] %{middle dot}min/h, p<0.001) and increased total PWADi (mean{+/-}SD 42.25{+/-}18.73 to 50.22{+/-}17.77 to 41.29{+/-}17.14 drops/h, p<0.001), while spontaneous PWADi decreased as respiratory-events recurred (-1.17 drops/h per 10 events/h, p=0.015) along with FMD (3.7{+/-}1.9% to 3.2{+/-}2.5% to 4.2{+/-}2.7%, V2 vs V3 p=0.047). {Delta}HR and BRS were stable across visits. ConclusionShort-term CPAP re-initiation improved endothelial function (FMD), with no significant effects on autonomic measures (BRS, {Delta}HR) or structural vascular indices. This supports a temporal dissociation between rapidly reversible exposure metrics (AHI, HB) and slower dynamics of autonomic markers. Changes in spontaneous PWADi suggests that it may track physiological CPAP benefits beyond indices driven primarily by respiratory-event frequency.

BackgroundChronic exposure to high-altitude hypoxia imposes sustained cardiovascular stress, yet hemodynamic adaptation among healthy high-altitude dwellers is heterogeneous and remains poorly characterized. This study aimed to identify distinct hemodynamic phenotypes in a healthy high-altitude population using unsupervised machine learning and to evaluate their association with multi-system subclinical target organ damage. MethodsThis cross-sectional study enrolled 694 healthy adults permanently residing at [&ge;]3300 m on the Qinghai-Tibet Plateau. Unsupervised K-means clustering was performed on nine hemodynamic variables, including peripheral and central blood pressures, augmentation index (AIx), pulse pressure amplification ratio (pPP/cPP), and systolic pressure amplification (pSBP-cSBP). Differences across phenotypes in carotid intima-media thickness (IMT), estimated glomerular filtration rate (eGFR), left ventricular mass index (LVMI), and pulse wave velocity (PWV) were assessed using one-way ANOVA with Bonferroni-corrected post-hoc tests. ResultsThree distinct hemodynamic phenotypes were successfully identified. The C2 (Balanced Adaptation) phenotype (n = 245) demonstrated the most favorable hemodynamic profile, characterized by the lowest blood pressure and augmentation index (AIx) values, along with the highest peripheral-to-central pulse pressure ratio (pPP/cPP). The C1 (Vascular Stress) phenotype (n = 267) presented with normal peripheral systolic blood pressure (125.9 {+/-} 11.3 mmHg) but exhibited markedly elevated wave reflection indices, including the highest heart rate-adjusted augmentation index (AIx@HR75: 31.9 {+/-} 9.7%) and the lowest pPP/cPP ratio (1.29 {+/-} 0.08). The C3 (High-Load Decompensation) phenotype (n = 182) displayed significantly elevated blood pressures and the greatest overall hemodynamic load. Regarding target organ damage, a clear gradient was observed across the three phenotypes. The C3 phenotype showed the highest carotid intima-media thickness (IMT: 1.162 {+/-} 0.23 mm) and left ventricular mass index (LVMI: 69.18 {+/-} 40.73 g/m{superscript 2}). Conversely, the C2 phenotype exhibited the highest estimated glomerular filtration rate (eGFR: 97.38 {+/-} 16.38 mL/min/1.73m{superscript 2}) and the lowest IMT (0.994 {+/-} 0.26 mm). The C1 phenotype consistently displayed intermediate values for all organ damage indicators. After Bonferroni correction, all pairwise comparisons for LVMI and pulse wave velocity (PWV) reached statistical significance (all P < 0.05). ConclusionsHealthy high-altitude individuals manifest three distinct hemodynamic phenotypes arrayed along a cardiovascular risk continuum. The novel Vascular Stress (C1) phenotype represents a "masked" high-risk state characterized by normal peripheral blood pressure but elevated arterial stiffness and wave reflection, challenging sole reliance on brachial pressure for risk assessment. This phenotype-based stratification provides a framework for precision prevention and early intervention in high-altitude populations.

EMG-based muscle force predictions are often inaccurate following active muscle stretch or shortening because of residual force enhancement (rFE) or depression (rFD), respectively, which can alter the neural drive to a muscle. However, the extent of neural drive modulation due to rFE or rFD remains unknown, making it difficult to correct EMG-based force predictions. Therefore, seventeen participants performed dorsiflexion contractions at 20 and 40% of maximum voluntary torque (MVT) in three conditions: stretch-hold, shortening-hold, and fixed-end reference (REF) conditions. The ankle dorsiflexion torques and angles were matched using dynamometry to the REF condition over a 10-s steady state following a 1-s 25{degrees} stretch or shortening, during which we recorded and decomposed tibialis anterior individual motor unit action potentials from high-density surface EMG recordings to gain insights into neural drive. Normalized EMG amplitudes were 2% lower following stretch and 1 or 3% higher following shortening relative to REF at 20 versus 40% MVT (p[&le;].008), respectively. Discharge rates (DRs) from 19 matched motor units per person on average obtained via DEMUSE and MUedit were similar (p=.871). Following stretch and shortening, DRs were [~]1 Hz lower (p[&le;].004) and 0 (p=.966) to 1 Hz higher relative to REF (p=.003), respectively. More unique motor units were also detected following shortening versus REF and in REF versus following stretch. These findings indicate that to account for rFE or rFD, neural drive is respectively decreased or increased via reduced or additional motor unit recruitment and DR modulation, with a contraction-intensity specific discharge rate modulation following active shortening.

IntroductionCardiopulmonary exercise testing (CPET) quantifies exercise limitation and helps differentiate cardiovascular dysfunction from deconditioning in patients with exertional dyspnoea. In mild pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH), traditional CPET oxygen delivery parameters may not adequately distinguish cardiac limitation. We evaluated whether oxygen pulse (O2 pulse) kinetics and the ratio of ventilation-carbon dioxide slope to peak oxygen uptake (VEVCO2/peakVO2) improve identification of cardiovascular limitation and prognostication. MethodsWe retrospectively analysed 289 consecutive patients referred for CPET. Patients were categorised into pre-capillary PH, no PH, or "unclassified" PH based on haemodynamics. O2 pulse slopes were calculated across exercise phases, and qualitative curve patterns were classified. VEVCO2/peakVO2 was derived from standard CPET parameters. Logistic regression assessed predictors of cardiac dysfunction (peak O2 pulse <65% predicted). Survival was evaluated using Kaplan-Meier and Cox regression analyses. ResultsPre-capillary PH patients demonstrated more impaired aerobic capacity and ventilatory efficiency than those without PH. Abnormal O2 pulse patterns (early plateauing or down-sloping) were associated with shallower slopes, lower peak O2 pulse, and greater chronotropic index. A work-phase O2 pulse slope < 0.40 identified impaired oxygen delivery but was not independently predictive in multivariable analysis. VEVCO2/peakVO2 independently predicted cardiac dysfunction (OR 3.9 [2.6-6.2], p < 0.001) and showed strong discrimination (AUC 0.83). VEVCO2/peakVO2 [&ge;] 2.7 independently predicted mortality (HR 13.6, 95% CI 3.8-48.5, p<0.001) outperforming peak O2 pulse and VE/VCO2 slope. ConclusionO2 pulse kinetics, particularly a work-phase slope < 0.40 and plateauing or decreasing trajectories, are associated with cardiac dysfunction in patients with pre-capillary PH. VEVCO2/peakVO2 appears to be a marker of cardiovascular limitation and mortality and may aid differentiation between cardiac dysfunction and deconditioning in this population when conventional CPET parameters are inconclusive.

ObjectivesTo determine whether early functional severity at presentation explains variability in return to sport (RTS) after ankle sprain in young athletes, compared with sprain subtype and injury mechanism. DesignRetrospective cohort study. MethodsAthletes aged [&le;]22 years with acute ankle sprains were identified from a prospectively maintained institutional database. Surgically treated cases were excluded. Functional severity at presentation was classified into three grades based on the ability to continue sports participation and ambulate immediately after injury. Injury mechanisms were categorized as high-energy deceleration (HED) or non-HED. RTS was analyzed as time to return and as prolonged RTS ([&ge;]4 weeks). Multivariable logistic regression was performed to identify factors independently associated with prolonged RTS. ResultsA total of 437 cases were included. Median RTS was 2.0 weeks (interquartile range, 0.0-4.0), and prolonged RTS occurred in 33.0% of cases. RTS duration increased stepwise with greater functional severity (p < 0.001). In multivariable analysis, functional severity was strongly associated with prolonged RTS (Grade 2: adjusted odds ratio [OR], 3.58; 95% confidence interval [CI], 2.07-6.19; Grade 3: adjusted OR, 24.53; 95% CI, 10.67-56.43; p < 0.001), and age was also independently associated (adjusted OR, 1.19 per year; 95% CI, 1.11-1.27; p < 0.001). Sprain subtype and injury mechanism were not independently associated with RTS after adjustment. ConclusionsEarly functional severity at presentation is the primary determinant of RTS after ankle sprain in young athletes. Apparent differences related to sprain subtype and injury mechanism are largely explained by initial functional impairment.

Given its well-documented effects on human physiology, hypoxia has garnered increasing interest for its potential to enhance specific adaptations to exercise. However, the molecular response of skeletal muscle to exercise under normobaric hypoxia remains poorly understood. To address this gap in knowledge, ten healthy young males completed a crossover study in which exercise in hypoxia was compared to exercise in normoxia matched by either absolute or relative intensity. This design allowed us to identify shared transcriptomic responses across all three conditions, as well as changes that were specific to exercise intensity or hypoxic exposure. Skeletal muscle biopsies were collected before, immediately after, and at 3 and 24 hours following each exercise session, with RNA sequencing performed to assess changes in gene expression. Following exercise, a greater number of differentially expressed genes were observed in hypoxia compared to normoxia at 24 h post-exercise. This hypoxia-specific response involved the downregulation of multiple mitochondrial pathways and appears to be regulated by a transcriptional network comprising both positive and negative regulators of HIF-1 activity. These findings highlight the ability of normobaric hypoxia to influence exercise-induced gene expression and suggests that it may promote distinct molecular adaptations in skeletal muscle following longer-term training.

ObjectivesThis study aimed to compare exercise-induced changes in serum and salivary concentrations of cardiac troponin-I (cTnI) in athletes during and after a marathon. MethodsThirty-six male runners were recruited. Eighteen participants in group 1 completed a marathon (42.195 km), while eighteen participants in group 2 did not undergo this exercise. Blood and saliva samples were collected at twelve different time points and then analyzed for cTnI using an immunoassay. ResultsBiphasic cTnI release into the circulation was observed during and after the marathon. Moreover, a similar pattern of biphasic cTnI elevation was found in saliva. In group 1, salivary and serum concentrations of cTnI first peaked after 60 min of exercise (0.67{+/-}0.08 ng/mL and 0.76{+/-}0.07 ng/mL), decreased slightly towards the end of the marathon (0.40{+/-}0.06 ng/mL and 0.46{+/-}0.06 ng/mL), and then reached a second, higher peak 4 h post-exercise (0.72{+/-}0.09 ng/mL and 0.82{+/-}0.09 ng/mL), returning to baseline by 48 h after marathon completion (0.16{+/-}0.04 ng/mL and 0.18{+/-}0.04 ng/mL). In group 2, there were no time-dependent changes in cTnI concentrations in both saliva and serum. Deming regression and Passing-Bablok regression demonstrated that there was proportional agreement between salivary and serum levels of cTnI in both groups at all twelve time points. The Bland-Altman method revealed that there was a negative differential bias but no proportional bias in the data. ConclusionsDocumenting a similar, biphasic pattern of cTnI elevations in saliva and serum during and after the marathon provides a reliable non-invasive alternative without requiring a blood draw.

BackgroundQuadriceps weakness may reduce sagittal plane shock absorption during landing, shifting load toward the frontal plane and increasing knee abduction moment (KAM), a biomechanical risk factor for anterior cruciate ligament (ACL) injuries. PurposeThe purpose of this study was to evaluate the association between isokinetic quadriceps strength and peak KAM during drop vertical jump landing in adolescent athletes. Study DesignSecondary analysis of previously collected data. MethodsHealthy adolescent athletes completed quadriceps strength testing using an isokinetic dynamometer and a biomechanical assessment during a drop vertical jump task. Quadriceps strength was quantified as peak concentric torque and the peak external KAM was calculated during the landing phase on the dominant limb. Both strength and KAM were normalized to body mass. Linear regression was used to examine the association between normalized quadriceps strength and peak external KAM on the dominant limb. ResultsThe association between quadriceps strength and peak normalized KAM on the dominant limb was not statistically significant ({beta} = -0.053 (95% CI [-0.137 to 0.030]), F(1,119) = 1.62, R2 = 0.013, p = 0.206). Quadriceps strength explained only 1.3% of the variance in peak KAM, indicating a negligible association between these variables in this cohort. DiscussionQuadriceps strength was not associated with peak normalized KAM during landing, suggesting that frontal-plane knee loading during a drop vertical jump is not meaningfully explained by maximal concentric quadriceps strength alone. KAM appears to be driven more by multi-joint movement strategy and neuromuscular coordination than by the capacity of a single muscle group.

BackgroundCalcitonin gene related peptide (CGRP) hyperpolarizes pulmonary arterial smooth muscle cells (SMCs) and endothelial cells (ECs) through PKA-dependent activation of KATP channels. CGRP can diminish the severity of pulmonary fibrosis (PF), however, the effects on vascular signaling were poorly defined. We hypothesized that hyperpolarization to CGRP would be augmented in a mouse model of PF. MethodsPF was induced in male and female C57BL/6 mice by intratracheal delivery of bleomycin (3 wk), with saline used as control (sham). Pulmonary arteries (PAs; 100-150 {micro}m diameter) were cannulated and pressurized to 16 cmH2O, and endothelial tubes were studied in complementary experiments to eliminate the influence of SMCs. Membrane potential (Vm) was recorded continuously using intracellular microelectrodes. Responses were also evaluated in isolated lungs preconstricted with U46619 ([~]10 mmHg). ResultsPF led to greater indices of PH in males vs. females. Isolated lungs and PAs from male PF mice had enhanced vasodilation and hyperpolarization of Vm to CGRP, although no effect was observed in females. The greater vasodilation and hyperpolarization of SMCs to CGRP in males persisted in endothelium-disrupted PAs and during treatment with L-NAME indicating that ECs are not required for greater responsiveness to CGRP. With no effect on resting Vm, inhibition of KATP channels or PKA significantly attenuated hyperpolarization of SMCs and ECs, attenuated vasodilation to CGRP in PAs, and eliminated differences between groups in males. Direct activation of PKA, but not KATP, evoked greater Vm hyperpolarization and vasodilation in PF vs. sham PAs and lungs. Although no difference in sensory nerves was observed in fibrotic mice, perivascular nerve stimulation evoked greater vasodilation in PAs. ConclusionsIn a mouse model of PF, CGRP-dependent hyperpolarization of pulmonary arterial SMCs and ECs is augmented through increased PKA-dependent activation of KATP channels leading to increased vasodilator sensitivity.

BackgroundPreserving muscle function is essential for maintaining independence during aging, but muscle force-generating capacity is not commonly measured clinically due to a lack of accessible, sensitive tools. Magnetic resonance imaging (MRI) provides gold-standard measures of muscle volume and microstructure, which reflect force-generating capacity, while dynamometry quantifies peak joint moments during voluntary contraction. Both modalities are time-consuming and costly, so clinical and large-scale studies often rely on low-fidelity measures such as the time to complete the five times sit-to-stand test (5xSTS). OpenCap, a tool for quantifying musculoskeletal dynamics from smartphone videos, may provide an accessible and more informative approach to assessing muscle function. We evaluated whether OpenCap-derived knee extension moments during chair rise relate to MRI-based measures of quadriceps muscle volume and microstructure, using dynamometry as a comparator. MethodsNineteen healthy adults of various ages (63.2% female, 57.8 {+/-} 15.4 y, 30-78 y) underwent quadriceps MRI, dynamometry, and 5xSTS time with concurrent OpenCap data collection. Using MRI, we computed quadriceps volume and radial diffusivity (a measure related to fiber size). We standardized these features and summed to create a composite MRI score, reflecting muscle quantity and quality. We estimated peak knee extension moment using OpenCap during chair rise and via both isometric and isokinetic dynamometry. We compared OpenCap kinematics (torso angle) and dynamics (knee moment), 5xSTS time, and dynamometry to MRI measures of muscle function using linear regression; false discovery rate was controlled using the Benjamini-Hochberg procedure. ResultsThe OpenCap-derived knee extension moment was associated with quadriceps muscle volume (r=0.63, p=0.014) and radial diffusivity (r=0.61, p=0.016). Peak knee extension moments measured by both isometric and isokinetic dynamometry were correlated with muscle volume (r=0.66-0.75, p=0.002-0.009), but not with radial diffusivity (r=0.04-0.52, p=0.054-0.91). Both OpenCap and isokinetic dynamometry showed their strongest associations with the composite MRI score (r=0.77, p=0.002 and r=0.73, p=0.002, respectively). 5xSTS time and a kinematic feature (torso angle) were not associated with any MRI-derived measures (r=-0.16-0.35, p=0.22-0.97). ConclusionsSmartphone video-based joint moments associate with muscle size and microstructure, unlike time or kinematic features. OpenCap offers a scalable assessment of muscle force-generating capacity that can be conducted rapidly without specialized equipment, enabling higher-fidelity assessments of muscle function in the clinic and in large-scale studies where imaging and dynamometry are impractical.

Hypoxemia occurs in intermittent forms, such as obstructive sleep apnea, and in continuous forms, such as at high altitude, and is increasingly recognized as a modulator of cardiometabolic risk. Although hypoxemia alters postprandial glucose and lipid metabolism, its effects on ketone bodies remain unclear. Using a randomized crossover design, we examined whether six hours of normoxemia or intermittent hypoxemia (15 hypoxemic cycles/hour targeting [~]85% peripheral oxyhemoglobin saturation with 100% medical-grade nitrogen) alters plasma {beta}-hydroxybutyrate (BHB) concentrations in 12 young adult females (mean [SD]: 21 [3] years) following a high-fat meal (33% of estimated daily energy requirements; 59% of calories from fat). In a follow-up session, a subset (n = 8) completed six hours of continuous hypoxemia (fraction of inspired oxygen [~]12.0% in a normobaric chamber). Postprandial data were analyzed using baseline-adjusted linear mixed-effects models, with Bonferroni post hoc tests. A time x condition interaction (P = 0.010) indicated that BHB concentrations at 360 minutes were higher during continuous hypoxemia (0.247 mmol/L; 95% CI: 0.218-0.275) than normoxemia (0.176 mmol/L; 95% CI: 0.153-0.200; PBonferroni = 0.029) and intermittent hypoxemia (0.163 mmol/L; 95% CI: 0.139-0.186; PBonferroni = 0.002), representing increases of 13.0% and 14.2% in estimated marginal means, respectively. This response was accompanied by higher postprandial plasma glucose and triglyceride concentrations during continuous hypoxemia than during normoxemia and intermittent hypoxemia (PBonferroni [&le;] 0.002), despite similar plasma insulin and non-esterified fatty acid responses across conditions (P [&ge;] 0.081). These findings indicate that continuous hypoxemia increases late postprandial plasma BHB concentrations in young adult females. New FindingsO_ST_ABSWhat is the central question of this study?C_ST_ABSWhat are the effects of normoxemia, intermittent hypoxemia, and continuous hypoxemia on plasma {beta}-hydroxybutyrate (BHB) concentrations in young adult females after a high-fat meal? What is the main finding and its importance?Compared to normoxemia, young adult females showed higher postprandial plasma BHB concentrations during continuous hypoxemia, but not during intermittent hypoxemia, despite similar changes in plasma concentrations of two main regulators of BHB production (non-esterified fatty acids and insulin) across experimental conditions. These findings suggest that continuous hypoxemia modifies postprandial BHB concentrations through mechanisms not fully explained by circulating non-esterified fatty acids or insulin concentrations alone.

ObjectiveTandem cycling requires a coordinated effort between the pilot and the stoker. Previous research suggests that randomly paired tandem cyclists produce lower power output than when cycling solo. This study examined how a cyclists individual ability and their position on the tandem (pilot or stoker) affects pair performance, when partners are either closely matched or differ substantially in solo cycling capacity, as this might be relevant for training and selection. MethodsTwenty-three trained cyclists completed three 10-minute time trials: solo, equal-capacity tandem ([&le;]25 W difference in solo performance), and unequal-capacity tandem ([&ge;]40 W difference). Mean power output, heart rate, cadence, and rating of perceived exertion (RPE) were recorded. Positions (pilot or stoker) were counterbalanced. Linear mixed-effects models assessed effects of capacity and position. ResultsRelative to solo cycling, equal-capacity tandem pairs revealed lower power output (-3.9%), lower heart rate (-2.3%), and lower RPE (-11.5%). Unequal-capacity tandems differed from solo only in heart rate (-2.7%). Stokers produced lower power relative to solo (-5.3%) and relative to pilots (-3.7%) and reported lower RPE relative to solo (-13.9%), while pilots matched their solo power at a lower heart rate (-2.9%). Cadence did not differ across conditions. Total tandem power averaged 95.6% of combined solo power, and differences in partner capacity did not significantly affect combined power output. ConclusionThis study provides the first known experimental data on how partner matching affects individual and combined power output in tandem cycling. Equal- and unequal-capacity tandem pairs showed similar performance. Lower power and RPE among stokers suggest reduced engagement or a redistribution of effort between riders. These findings highlight that effective tandem performance depends on physiological capacity and rider position on the tandem, but not on the difference in capacity between partners.

Mass is a fundamental aspect of muscle contractile function, yet the inertial effects of inactive muscle mass is generally neglected in modeling and not quantified in studies on small muscles or isolated fibers. However, during submaximal contractions, inactive muscle tissue may take longer to be accelerated by active fibers, and may be subject to prolonged deceleration, both of which may potentially reduce force development and work output. We sought to test if inactive tissue mass imposes an inertial penalty on muscle performance, using in situ sinusoidal work-loop experiments on rat plantaris muscles. Regional fascicle dynamics, measured across supramaximal and submaximal levels of activation, showed that decreasing activation significantly reduced fascicle strain and increased both shortening and lengthening latency. Contrary to our predictions, however, reductions in work, beyond those explained by decreased fascicle strain, were negligible. Normalized work did not decline disproportionately relative to force, suggesting no clear inertial penalty on work at this muscle size. Our findings suggest that while inactive muscle mass influences the dynamics of submaximal contractions, its impact on work during submaximal contractions at small muscle sizes is limited.

Objectives To examine the acute effects of a single bout of high-intensity interval training (HIIT) on fetal blood flow distribution during the third trimester of pregnancy. Methods Thirty-four healthy pregnant participants (mean age 31.6 years, standard deviation (SD) 4.1; gestational week 33.8 (SD 0.4) completed eight 30-second high-intensity cycling work-bouts interspersed with 2-minute rest periods. Fetal heart rate (FHR), maternal blood pressure, and Doppler-derived blood flow indices in the middle cerebral artery, umbilical artery and vein, and ductus venosus were assessed before and after exercise. We estimated fetal liver blood flow and the ratio of umbilical vein flow to ductus venosus. Maternal heart rate (HR) and FHR were recorded throughout exercise. Paired t-tests compared pre- and post-exercise values. Results No significant changes were observed in fetal blood flow indices or distribution following exercise. Average maternal HR and FHR during the work-bouts were 158 bpm (SD 16) and 152 bpm (SD 12), respectively. Following HIIT, maternal systolic blood pressure increased by 5 mmHg (95% CI 1 to 8, p=.014), maternal HR by 22 bpm (95% CI 15 to 28, p<.001), and FHR by 13 bpm (95% CI 10 to 17, p<.001). We recorded 16 instances of FHR above normal range during HIIT. Conclusion A single HIIT session in late pregnancy increased maternal blood pressure and HR and transiently elevated FHR but did not affect fetal blood flow indices or distribution. Brief episodes of fetal tachycardia were observed but appeared to be clinically insignificant. Future research should investigate the effects of repeated HIIT exposure during pregnancy.

This cross-sectional derivation and internal validation study aimed to develop and internally validate a clinical triage scoring system (CTSS) for field-based identification of collegiate athletes requiring priority intervention for lumbopelvic-hip (LPH) dysfunction. A total of 864 collegiate athletes (mean age 21.3 {+/-} 2.4 years; 80.8% male) were recruited from 10 universities. Participants underwent standardized assessments including demographic characteristics, clinical history, and LPH functional testing. Using an expert-adjudicated binary reference standard (priority intervention vs self-management), a multivariable logistic regression model was developed to derive the weighted CTSS. Model performance was evaluated using discrimination, calibration, and decision curve analysis (DCA), and internal validation was performed using 1,000 bootstrap resamples. Of the 864 participants, 463 athletes (53.6%) were classified as requiring priority intervention. The final 14-factor CTSS comprised 12 positive-weight predictors, such as localized LPH pain, muscle weakness, and higher body mass index, and 2 negative-weight predictors, positive Lasegues sign and hamstring weakness, which functioned served as safety-related modifiers. The model demonstrated acceptable discrimination (AUROC = 0.851, 95% CI: 0.824-0.876), with minimal optimism (optimism-corrected AUROC = 0.842) and excellent calibration (calibration slope = 1.000; calibration intercept = 0.000). A total score of [&ge;]9 was identified as the optimal threshold, yielding a sensitivity of 84.4% and specificity of 71.8%. DCA showed greater net benefit than treat-all and treat-none strategies across clinically relevant threshold probabilities (20%-50%), with a net benefit of 0.319 at a 50% threshold probability. The CTSS may provide a pragmatic field-based triage tool to support early identification of athletes who may require priority intervention, although external validation is needed before broader implementation in sports medicine settings.

Walking speed is widely used to assess gait recovery following stroke, yet it provides limited insight into how walking performance is mechanically organized. This study examined how center-of-mass (COM) work organization and propulsion-support coupling vary across walking speeds in individuals with post-stroke hemiparesis to distinguish recovery of gait organization from recovery of limb-level mechanical function. Eleven individuals with post-stroke hemiparesis performed treadmill walking across speeds ranging from 0.2 to 0.7 m/s while ground-reaction forces were recorded. Limb-specific COM power and work were computed using an individual-limbs framework, and interlimb asymmetry in net and positive work, along with the propulsion-support ratio (PSR), were quantified. A qualitative transition in gait organization was observed: at lower walking speeds, COM power exhibited a simplified two-phase pattern, whereas at higher walking speeds (approximately [&ge;]0.5 m/s), a structured four-phase COM power pattern emerged, including identifiable push-off and preload phases. Despite this recovery of gait organization, interlimb work asymmetry remained elevated and paretic PSR remained reduced across all speeds, indicating persistent limb-level mechanical deficits. These findings demonstrate that increases in walking speed and the emergence of typical COM power structure reflect recovery of gait organization rather than restoration of underlying limb-level mechanical capacity. Consequently, walking speed alone is insufficient to characterize gait recovery after stroke, and biomechanically informed measures of COM work organization and propulsion-support coupling provide complementary insight by distinguishing organizational recovery from limb-level mechanical recovery.

Background: Quadriceps strength and landing mechanics are two modifiable factors associated with anterior cruciate ligament (ACL) injury risk. Collecting detailed biomechanical data is an arduous task. Identifying a relationship using more easily measured variables, such as quadriceps strength, would offer value for athlete counseling and injury prevention programs. Although quadriceps weakness has been associated with altered landing strategies in ACL-reconstructed (ACLR) individuals, this relationship is less clear in healthy athletes. Purpose: To investigate the association between isokinetic quadriceps strength and peak knee flexion angle during a vertical drop jump in healthy adolescent athletes. Study Design: Secondary analysis of previously collected data. Methods: Healthy adolescent athletes had their dominant leg quadriceps strength measured using an isokinetic dynamometer at 60{degrees}/s from 0-90{degrees} of knee flexion. Landing mechanics were assessed during a vertical drop jump using three-dimensional motion capture synchronized with force plates. Pearson correlation was used to evaluate the association between quadriceps strength and peak knee flexion angle during landing, with statistical significance defined as p < .05. Results: There was a weak negative correlation between quadriceps strength and peak knee flexion angle (p = .017, R = -.22 [-.04, -.38]), suggesting that stronger athletes achieved greater knee flexion angles. Discussion: Greater quadriceps strength was associated with increased peak knee flexion angles during landing; however, the weak correlation suggests that strength explains only a small portion of the variability in landing mechanics. These findings deviate slightly from prior literature in healthy populations but are consistent with studies demonstrating that greater quadriceps strength is associated with achieving greater peak knee flexion in ACLR patients. Accordingly, quadriceps strengthening should remain a key component of multifactorial ACL injury prevention programs.