Journal of applied physiology最新文献

{"title":"Long-term exposure to moderate cold reduces incidence of reperfusion tachyarrhythmias in rats.","authors":"Pavel Vebr, Frantisek Galatik, Aneta Marvanova, Barbara Elsnicova, Daniela Hornikova, Marek Vecka, Sarka Spinová, Olga Novakova, Jitka M Zurmanova","doi":"10.1152/japplphysiol.00509.2025","DOIUrl":"10.1152/japplphysiol.00509.2025","url":null,"abstract":"<p><p>Recently, moderate cold acclimation (9°C; MCA) was found to exert cardioprotective effects by increasing resistance to ischemia-reperfusion (IR) injury and mitochondrial calcium overload in rats, but the effect of MCA on the incidence of IR arrhythmias is not known. The aim of this study was to determine whether MCA can induce an antiarrhythmic effect and, if so, to elucidate a possible mechanism. Adult male Wistar rats were acclimated (9°C) for short (1-3-10 days) and long-term (5 wk; CA) periods, followed by a 2-wk recovery period (24°C; CAR). The number of premature ventricular complexes (PVCs) and their duration after IR were determined. Left ventricular myocardium was analysed by western blotting, TLC & GC chromatography and immunofluorescence microscopy. We revealed that total reperfusion PVCs and tachyarrhythmia duration decreased even after CA, and accordingly, the antiarrhythmic n-3 PUFAs increased in cardiac membrane phospholipids, the n-6/n-3 PUFA ratio decreased. CA increased the distribution of connexin 43 (Cx43) in favor of end-to-end junctions and the expression of uncoupling protein 3 (UCP3) in mitochondria. These beneficial effects were lost after 2-wk recovery period CAR. Interestingly, the mitochondrial antioxidants superoxide dismutase (SOD2) and thioredoxin reductase (TRXRD2) were strongly upregulated exclusively after 1 day of cold exposure, whereas cytosolic TRXRD1 was downregulated. In conclusion, long-term MCA (5-wk) reduces the incidence of reperfusion arrhythmias, increases the proportion of antiarrhythmic n-3PUFAs in cardiomyocyte membranes, and has a positive effect on Cx43 distribution. By increasing the amount of UCP3 in mitochondria it may reduce the likelihood of free radical formation in mitochondria during reperfusion.<b>NEW & NOTEWORTHY</b> Moderate cold acclimation (CA) gradually reduces total reperfusion PVCs and tachyarrhythmia duration in rat myocardium, detectable after 5 wk and lost after a 2-wk recovery. Reduced n-6/n-3 PUFA ratio, protective Cx43 and UCP1 distribution, and increased GPX4 expression supports the antiarrhythmic effect elicited by CA. Mitochondrial antioxidants SOD2 and TXNRD2 are upregulated after just 1 day of exposure. The brown adipose tissue-to-body weight ratio increases during CA, and mitochondrial density exhibits an independent pattern of change.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"1156-1168"},"PeriodicalIF":3.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145130878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Maximal-effort knee-extension exercise impairs skeletal muscle oxidative capacity and V̇o₂ recovery in vivo.","authors":"Miles F Bartlett, Andrew P Oneglia, Delaney Davis, Sauyeh Zamani, Ashfaq Siddiqui, Mark D Ricard, Michael D Nelson","doi":"10.1152/japplphysiol.00517.2025","DOIUrl":"10.1152/japplphysiol.00517.2025","url":null,"abstract":"<p><p>In the present study, we examined how fatiguing exercise affects O₂-based measures of skeletal muscle oxidative capacity in vivo by measuring changes in the rate constant of muscle V̇o₂ recovery ([Formula: see text]). Healthy young adults completed isokinetic (120°·s^-1), maximal voluntary dynamic contractions (MVDCs) lasting 24 (baseline [Formula: see text]) and 240 s (postfatiguing exercise [Formula: see text]). Vastus lateralis [Formula: see text] was measured using near-infrared diffuse correlation spectroscopy (NIRS-DCS) via the conventional repeated arterial occlusion method (<i>part A</i>, <i>n</i> = 14) or a novel NIRS-DCS \"free-flow\" method (<i>part B</i>, <i>n</i> = 13). Pulmonary V̇o₂ (pV̇o₂), muscle V̇o₂ (mV̇o₂), and surface electromyography (sEMG) measures of muscle activation were also measured throughout the 240-s trial. Compared with the 24-s trial, [Formula: see text] following 240 s of MVDCs was impaired by ∼25% (<i>part A</i>; <i>P</i> = 0.005) and ∼16% (<i>part B</i>; <i>P</i> = 0.017). Moreover, both pV̇o₂ and mV̇o₂ rapidly increased to maximal levels, where they remained for the duration of the 240-s trial, despite sEMG activity and peak MVDC power declining. These results demonstrate that fatiguing exercise not only impairs O₂-based measures of skeletal muscle oxidative capacity, but also that mitochondrial O₂ consumption is uncoupled from power output and ATP demand during fatiguing exercise.<b>NEW & NOTEWORTHY</b> We measured rates of skeletal muscle V̇o₂ recovery ([Formula: see text]) at baseline and following fatiguing exercise using near-infrared diffuse correlation spectroscopy (NIRS-DCS). Regardless of whether [Formula: see text] was measured via the conventional repeated arterial occlusion method (<i>part A</i>) or a novel NIRS-DCS \"free-flow\" method (<i>part B</i>), fatiguing exercise impaired [Formula: see text] by ∼15%-25%. Because ATP demand rapidly declines post exercise, the slow [Formula: see text] recovery observed here suggests fatiguing exercise may uncouple the functional relationship between mitochondrial O₂ consumption and ATP synthase activity.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"1073-1089"},"PeriodicalIF":3.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145080830","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Critical role for scavenger receptor CD36 in microparticle-mediated neuroinflammation in a murine model of decompression sickness.","authors":"Abid R Bhat, Awadhesh K Arya, Zuha Imtiyaz, Su Xu, Stephen R Thom","doi":"10.1152/japplphysiol.00484.2025","DOIUrl":"10.1152/japplphysiol.00484.2025","url":null,"abstract":"<p><p>Blood-borne microparticles (MPs) play a role in several forms of brain injury, but how they interact with the vasculature and contribute to neuroinflammation is unknown. The scavenger receptor CD36 is expressed across various cell types and regulates inflammation, vascular function, and innate immunity. We hypothesized that CD36 mediates MPs-induced neuroinflammatory responses in a murine model of decompression sickness (DCS). Wild-type mice subjected to decompression and naïve mice injected with MPs from decompressed mice exhibited a 2.2 ± 0.5-fold elevation in perivascular MPs deposition, 2.8 ± 0.6-fold elevation of inflammatory MPs in blood and 2.4 ± 0.4-fold in cervical lymph nodes, 2.7 ± 0.6-fold increase in neutrophil activation, 2.0 ± 0.3-fold increased glymphatic flow, 3.1 ± 0.4-fold increased leakage of six megadalton dextran at the blood-brain barrier, and a doubling of inflammatory proteins in brain. These events failed to occur in CD36 knockout mice and those conditionally deficient in endothelial CD36 (FLOX). We conclude that inflammatory MPs interact with endothelial CD36 to mediate neuroinflammatory responses and vascular injury in DCS.<b>NEW & NOTEWORTHY</b> Elevated glymphatic flow, glial cell activation, increased circulating microparticles (MPs), and neutrophil activation due to decompression have been well documented in animal models. This report shows that filamentous (F)-actin expressing MPs produced postdecompression interact with endothelial CD36 driving a feed-forward neuroinflammatory cycle and inducing vascular injury.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"1112-1124"},"PeriodicalIF":3.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145130934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Revisiting hyper-resistance to muscle stretch in cerebral palsy: muscle hypo-extensibility is more of an issue than hyperreflexia.","authors":"Pedro Valadão, Jean-Michel Gracies, Francesco Cenni, Lynn Bar-On, Harri Piitulainen, Janne Avela, Taija Finni","doi":"10.1152/japplphysiol.00965.2024","DOIUrl":"10.1152/japplphysiol.00965.2024","url":null,"abstract":"<p><p>Hyper-resistance to passive muscle stretch is a common, debilitating symptom of spastic paresis. Although straightforward to assess, hyper-resistance is caused by a complex interaction of altered tissue properties, stretch hyperreflexia, and involuntary background muscle activation. Identifying the contribution of each underlying component causing hyper-resistance is of great significance for designing treatments. The aim of this study was to investigate the components contributing to ankle plantarflexors' hyper-resistance in spastic cerebral palsy. We compared ankle biomechanical and reflex variables during ankle plantarflexor stretches at various velocities in 15 individuals with mild spastic cerebral palsy (GMFCS I, age range: 9-22 yr, 10 males) versus 15 age- and sex-matched typically developing controls. In addition, we evaluated associations between biomechanical and reflex variables. The cerebral palsy group had a median 9° lower maximum passive dorsiflexion range of motion at slow stretch velocity (<i>P</i> = 0.001), a 9° lower stretch reflex threshold (<i>P</i> < 0.01) with higher stretch reflex response magnitude (<i>P</i> ≤ 0.001) for both soleus and medial gastrocnemius muscles, and higher peak torques at fast stretch velocities (<i>P</i> < 0.01). When normalized to the maximum passive range of motion, stretch reflex thresholds were not different between groups. Although hyperreflexia directly contributed to hyper-resistance, normalized stretch reflexes did not occur earlier in the stretch in individuals with cerebral palsy compared with typically developing controls, suggesting a direct influence of muscle hypo-extensibility on hyperreflexia. Treatments for hypo-extensibility are urgently needed, more so than treatments to reduce hyperreflexia. [Clinical trial prospectively registered in the International Standard Randomized Controlled Trial registry (No. 69044459)]<b>NEW & NOTEWORTHY</b> The difference in stretch reflex threshold angles as a measure of hyperreflexia between mild spastic cerebral palsy and typically developing groups was lost when normalized to the passive range of motion. Yet, in the cerebral palsy group, low stretch reflex thresholds correlated with high peak torques during stretches at fast velocities.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"1139-1147"},"PeriodicalIF":3.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145199517","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Eight weeks of running, but not stationary cycling, training attenuates the vestibulosympathetic reflex in healthy adults.","authors":"Chester A Ray, Christin Domeier, Charity L Sauder","doi":"10.1152/japplphysiol.00304.2025","DOIUrl":"10.1152/japplphysiol.00304.2025","url":null,"abstract":"<p><p>A possible mechanism for exercise training-induced orthostatic intolerance is attenuation of the vestibulosympathetic reflex (VSR) due to enhanced stimulation of the otolith organs during running. We tested the hypothesis that the VSR is attenuated after 8 wk of running, but not stationary cycling. Arterial blood pressure, heart rate, calf blood flow, and muscle sympathetic nerve activity (MSNA) were recorded in 37 healthy, sedentary subjects (14 males and 23 females, 25 ± 6 years old) during baseline and head-down rotation (HDR) before and after 8 wk of endurance training. Subjects were assigned to running or stationary cycling (<i>n</i> = 13 and <i>n</i> = 12, respectively) or served as controls (<i>n</i> = 12). HDR increased MSNA and decreased calf vascular conductance (CVC) significantly in all groups before training. In contrast, after training, the increase in MSNA was significantly attenuated during HDR in run-trained (before: Δ7 ± 5 vs. after: Δ3 ± 4 bursts/min, <i>P</i> = 0.032) but remained increased in cycle-trained (before: Δ5 ± 5 vs. after: Δ5 ± 3 bursts/min, <i>P</i> = 0.868) and control subjects (before: Δ4 ± 4 vs. after: Δ4 ± 6 bursts/min, <i>P</i> = 0.804). CVC did not decrease from baseline with HDR in run-trained but decreased in cycle-trained and controls after 8 wk (<i>P</i> < 0.02). These data suggest an attenuation of the VSR in run- but not stationary cycle-trained subjects. This is the first study to indicate that endurance running decreases the sensitivity of the otolith organs to changes in gravitational inputs.<b>NEW & NOTEWORTHY</b> Vestibular inputs contribute to blood pressure regulation. Endurance-trained runners have been reported to have lower orthostatic tolerance. We hypothesized that running endurance training would decrease MSNA responses to head-down rotation but not following stationary cycling endurance training. The vestibulosympathetic reflex, as measured by MSNA responses to head-down rotation, was attenuated in run- but not cycle-trained. This study supports the concept that the vestibulosympathetic reflex is diminished by physical activity that chronically enhances otolithic stimulation.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"1169-1174"},"PeriodicalIF":3.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145244635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Edward F. Adolph Distinguished Lecture. Protein and energy metabolism: a state of flux.","authors":"Benjamin F Miller","doi":"10.1152/japplphysiol.00762.2025","DOIUrl":"10.1152/japplphysiol.00762.2025","url":null,"abstract":"<p><p>Physiology processes are integrated, dynamic, and periodic and thus benefit from methods that capture their dynamic nature. Since we are often limited to discrete sampling points in physiological studies, many methods provide snapshots of a system. However, these snapshots can at times be limited in their ability to understand the underlying events. This article is a summary of my 2025 Adolph Lecture and discusses how tracers (particularly, stable isotopes) go beyond mere snapshots to provide important insight into dynamic events. The article is part review and part narrative that provides insight into my scientific journey and the thought process that went into the design of the highlighted studies. I primarily feature articles published in APS journals and note what insight the tracer-based measurements provide. I hope that the reader comes away with an appreciation of the complexity of physiological studies and why tracer-based studies are, in fact, mechanistic.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"1090-1100"},"PeriodicalIF":3.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145124516","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of riluzole on sevoflurane-induced gasping in adult mice.","authors":"Saki Taiji, Takashi Nishino, Hisayo Jin, Mayumi Hashida, Shiroh Isono","doi":"10.1152/japplphysiol.00347.2025","DOIUrl":"10.1152/japplphysiol.00347.2025","url":null,"abstract":"<p><p>The inhalation of a high sevoflurane concentration under hyperoxia induces gasping, similar to the breathing patterns observed during hypoxia-induced gasping in mice. This observation, coupled with the understanding that burster neurons in the pre-Bötzinger complex, which rely on a persistent sodium current, play a crucial role in generating hypoxia-induced gasping, led us to investigate whether sevoflurane-induced gasping could be triggered by activating this current within the brainstem. To this end, we evaluated the dose-dependent effects of intraperitoneal administration of riluzole, a blocker of persistent sodium channels, on sevoflurane-induced gasping in adult mice. We used ten trachealy intubated, spontaneously breathing, sevoflurane-anesthetized mice. Seven mice randomly received three doses of intraperitoneal riluzole (6, 12, and 18 mg/kg ip) with an interval of approximately 4 wk. The test trials to elicit the sevoflurane-induced gasping were conducted before and after administering each dose of riluzole by a sudden rise in inspired concentration of sevoflurane from 0.8 MAC (minimum alveolar concentration; 2.5%-2.7%) to 2 MAC (6.4%-6.6%). In the other three mice, the test trials for eliciting the hypoxia-induced gasping were performed before and after administering 18 mg/kg riluzole. The administration of the increasing dose of riluzole demonstrated an apparent and dose-dependent attenuation of sevoflurane-induced gasping. The administration of 18 mg/kg of riluzole completely abolished the hypoxia-induced gasping. These results indicate that sevoflurane-induced gasping, like hypoxia-induced gasping, could be generated by activating a persistent sodium current within the brainstem.<b>NEW & NOTEWORTHY</b> The inhalation of a high sevoflurane concentration induces specific ventilation similar to hypoxia-induced gasping. Riluzole is known to inhibit hypoxia-induced gasping dose-dependently by blocking persistent sodium channels. This study showed that riluzole dose-dependently attenuates sevoflurane-induced gasping in mice. Persistent sodium channels could be important in generating sevoflurane- and hypoxia-induced gasping.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"1148-1155"},"PeriodicalIF":3.3,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145182070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The impact of warm-up intensity and duration on maximal effort limited cardiopulmonary exercise testing parameters in healthy young adults.","authors":"Bastien Pedrosa, Chantal Daucourt, Vincent Gremeaux, Brian D Duscha, Brian J Coyne, William E Kraus, Davide Malatesta, Fabio Borrani, Aaron L Baggish, Daria Neyroud","doi":"10.1152/japplphysiol.00774.2025","DOIUrl":"https://doi.org/10.1152/japplphysiol.00774.2025","url":null,"abstract":"<p><p>The impact of warm-up protocols on peak oxygen uptake (V̇O_2-PEAK) during cardiopulmonary exercise testing (CPET) remains unclear. This study investigated the effect of warm-ups of different durations and intensities on V̇O_2-PEAK in healthy young adults during maximal-effort CPET cycle ergometry. Recreationally active participants (10 males, 4 females; 27 ± 4 years) performed five CPETs, each preceded by one of five randomized conditions: (i) no warm-up (NWU), (ii) short duration / low intensity (SD/LI) warm-up (5 min at 0.5 W/kg), (iii) long duration / low intensity (LD/LI) warm-up (10 min at 0.5 W/kg), (iv) short duration / moderate intensity (SD/MI) warm-up (5 min at 1 W/kg), and (v) a long duration / moderate intensity (LD/MI) warm-up (10 min at 1 W/kg). No significant differences were found in V̇O_2-PEAK, peak heart rate, maximal or submaximal power output across the different warm-up protocols (p > 0.05 for all comparisons), except for greater absolute HR and power output observed at the first ventilatory threshold (VT1) following SD/MI <i>vs.</i> NWU (p < 0.05). Participant ratings of warm-up protocols indicated a preference for shorter and/or lower-intensity warm-ups. Among healthy young adults, the inclusion of warm-up exercise prior to CPET has no significant effects on maximal exercise parameters. These findings question the necessity of warm-up prior to CPET and provide flexibility in CPET warm-up protocol selection in this population. Recapitulation of this study in alternative clinical and scientific populations is warranted.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145345366","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between aging and <i>in vivo</i> mitochondrial oxygen tension (mitoPO₂) and oxygen consumption (mitoVO₂) in healthy volunteers.","authors":"Calvin J de Wijs, Annika M van Smaalen, Lucia W J M Streng, Robert J Stolker, Egbert G Mik, Floor A Harms","doi":"10.1152/japplphysiol.00270.2025","DOIUrl":"https://doi.org/10.1152/japplphysiol.00270.2025","url":null,"abstract":"<p><p>The Cellular Oxygen METabolism (COMET^®) device provides validated bedside <i>in vivo</i> measurements of mitochondrial oxygen tension (mitoPO₂) and consumption (mitoVO₂). Because mitochondrial function has been shown in experimental <i>in vivo</i> and <i>ex vivo</i> studies to potentially alter with age, it is important to establish whether age itself influences these <i>in vivo</i> measurements. The aim of this single-center prospective observational study was to determine whether mitoPO₂ and mitoVO₂ values are influenced by age, thereby ensuring their validity for use across age groups. The aim of the study was not to evaluate COMET^® as monitor of aging. Using the COMET^® device, mitoPO₂ and mitoVO₂ were measured at the upper arm and sternum in 176 healthy participants aged 18-90 years. The mean arm mitoPO₂ was 75.3 ± 28.7 mmHg (mean ± SD), while the mean sternal mitoPO₂ was 65.8 ± 23.6 mmHg. Multivariable linear regression did not demonstrate a significant age-related change in mitoPO₂. Conversely, the mean arm mitoVO₂ was 6.37 ± 2.07 mmHgꞏs^-1, and the median sternal mitoVO₂ was 7.16 mmHgꞏs^-1 [IQR 5.63-9.17]. Multivariable linear models at both sites demonstrated a significant negative association between age and mitoVO₂. No significant sex differences were observed for either parameter. These findings reveal that while mitoPO₂ remains unaffected by age, mitoVO₂ shows a significant negative association with increasing age. This distinction suggests that mitoPO₂ can be interpreted independent of age, whereas mitoVO₂ requires age-informed consideration. By profiling healthy volunteers across four decades, we establish preliminary age-informed normative ranges for epidermal mitoPO₂ and mitoVO₂.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145337050","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypohydration Augments the Acute Increase in Urinary Biomarkers of Kidney Injury Following the 100-mile Western States Endurance Run.","authors":"Braxton A Linder, Soolim Jeong, Nina L Stute, Omar B El-Kurd, Joseph D Vondrasek, Andrew Pasternak, James R Bagley, Joseph C Watso, Zachary J Schlader, Matthew C Babcock, Gregory J Grosicki, Austin T Robinson","doi":"10.1152/japplphysiol.00289.2025","DOIUrl":"https://doi.org/10.1152/japplphysiol.00289.2025","url":null,"abstract":"<p><p><b>Purpose:</b> Ultra-endurance races may transiently increase acute kidney injury (<b>AKI</b>) risk, yet data on contributing factors are sparse. Therefore, we examined the acute effects of the Western States Endurance Run (<b>WSER</b>; [100 miles; 161 kilometers]) on urinary AKI biomarkers and kidney blood flow, while also assessing the influence of race pace and hydration status. <b>Methods:</b> Blood and urine samples were collected to assess urine specific gravity (<b>USG</b>), creatinine, and AKI risk (nephrin, neutrophil gelatinase-associated lipocalin <b>[NGAL]</b>, insulin like growth factor binding protein 7 [IGFBP7], tissue inhibitor of metalloproteinase 2 <b>[TIMP2]</b>, and IGFBP-7●TIMP-2). Renal blood velocity and conductance were measured via Doppler ultrasonography. <b>Results:</b> Pre and post measures were obtained from 36 runners (29Males/7Females, age: 44±9 years, mean finish time: 25:45:55). Urinary AKI biomarkers increased post-race, with nephrin, IGFBP7, and IGFBP7●TIMP-2 remaining elevated after indexing to creatinine (<i>p</i>s < 0.008). Hydration status declined, with only 8 of 35 runners remaining euhydrated post-race. Finishing euhydrated attenuated increases in urinary creatinine and creatinine-indexed IGFBP-7●TIMP-2 (<i>p</i>s ≤ 0.006). Faster race pace correlated with increases in USG (rho, ρ=0.338, <i>p</i>=0.048) and urinary creatinine (rho, ρ=0.443, <i>p</i>=0.010), but not with creatinine-indexed AKI biomarkers (<i>p</i>s ≥ 0.382). Kidney blood velocity and conductance were unchanged (<i>p</i>s ≥ 0.186). <b>Conclusion:</b> Finishing hydrated appears to help mitigate transient increase in kidney injury following an ultra-endurance race.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145337023","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}