American journal of physiology. Regulatory, integrative and comparative physiology最新文献

{"title":"True or false: arterial stiffening in the seated position.","authors":"Amane Hori, Masaki Mizuno","doi":"10.1152/ajpregu.00008.2025","DOIUrl":"10.1152/ajpregu.00008.2025","url":null,"abstract":"","PeriodicalId":7630,"journal":{"name":"American journal of physiology. Regulatory, integrative and comparative physiology","volume":" ","pages":"R287-R288"},"PeriodicalIF":2.2,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063151","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":"Role of atrial natriuretic peptide and oxytocin in gastric emptying delay induced by right atrial stretch in rats.","authors":"Raimundo C Palheta, Moisés T B da Silva, Ana Débora N P Georgii, Camila M S Silva, Rômmulo C L Siqueira, Wagner L Reis, Silvia G Ruginsk, Lucila L K Elias, José Antunes-Rodrigues, Armênio A Santos","doi":"10.1152/ajpregu.00172.2024","DOIUrl":"10.1152/ajpregu.00172.2024","url":null,"abstract":"<p><p>Fluid volume and osmolality balance are maintained by complex neuroendocrine and liquid-salt intake behavior, cardiovascular and renal mechanisms, and gastrointestinal adjustments. Mechanical stretching of the right atrium [atrial stretch (AS)] enhances central venous pressure and heart rate while decreasing gastric emptying (GE) of liquid in rats. We evaluated the effect of AS on GE and plasma levels of atrial natriuretic peptide (ANP), oxytocin (OT), and corticosterone (CORT) to determine whether ANP contributes to the OT-mediated GE delay of liquids due to AS in awake rats. Initially, we performed thoracotomy followed by right appendectomy (AX) or sham thoracotomy. One week later, rats were randomly subjected to pretreatment with NaCl 0.15 M (control), atosiban (AT, OT-antagonist), anantin (ANT, ANP-antagonist), or dexamethasone (DEX). Afterward, 50 µL of AS was administered for 5 min or not (sham). Then, the rats were fed a test meal, and GE of liquids or solids was performed. The other animals were pretreated with NaCl 0.15 M, atosiban, anantin, or dexamethasone, followed by OT treatment for GE assessment. Compared with the sham group, 50 µL of AS decreased the GE of the liquid and solid test meals. This phenomenon was prevented by AT, ANT, DEX, and surgical procedures with AX. AS also increased plasma levels of ANP, OT, and CORT. In turn, oxytocin treatment decreased GE and increased plasma ANP, OT, and CORT levels, while AT, ANT, and DEX prevented OT-induced GE delay. Hence, AS delayed GE of liquid in rats, a phenomenon that involves oxytocinergic pathways and ANP activities.<b>NEW & NOTEWORTHY</b> We suggest a cardiogastric reflex with the participation of neuroendocrine mediators, which contributes to regulating liquid balance in the animal's body. Atrial natriuretic peptide and oxytocin are substances recognized for participating in diuresis and regulating the transit of liquids in the gastrointestinal tract in situations of cardiac volume overload, as was simulated with atrial stretching in the present experimental model.</p>","PeriodicalId":7630,"journal":{"name":"American journal of physiology. Regulatory, integrative and comparative physiology","volume":" ","pages":"R396-R407"},"PeriodicalIF":2.2,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143405184","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":"Catecholamine synthesis and secretion by adrenal chromaffin cells are reduced in deer mice native to high altitude.","authors":"Nicole A Pranckevicius, Angela L Scott, Aedan J Rourke, Ranim Saleem, Oliver H Wearing, Graham R Scott","doi":"10.1152/ajpregu.00194.2024","DOIUrl":"10.1152/ajpregu.00194.2024","url":null,"abstract":"<p><p>Hypoxia at high altitude can constrain aerobic metabolism and elicit physiological responses that are detrimental to health and fitness. Responses of the sympathoadrenal system are vital for coping with acute hypoxia but can become maladaptive with prolonged activation in chronic hypoxia. We examined how adrenal function is altered in high-altitude populations of deer mice (<i>Peromyscus maniculatus</i>), which have evolved to overcome chronic hypoxia in their native environment. High- and low-altitude populations were each born and raised in common laboratory conditions and then acclimated to normoxia or chronic hypoxia during adulthood. High-altitude mice exhibited lower plasma epinephrine concentrations than low-altitude mice in both normoxia and hypoxia. Primary cultures of chromaffin cells were used to examine the cellular mechanisms underlying differences in epinephrine secretion from the adrenal medulla. Chromaffin cells from high-altitude mice did not mount a diminished Ca²⁺ response to nicotinic stimulation, but cellular catecholamine stores were much lower in high-altitude mice than in low-altitude mice. Histological analyses of the adrenal gland showed that high-altitude mice did not have smaller adrenal medullae. Therefore, reductions in chromaffin cell catecholamine stores were the primary mechanism for lower secretion rates and circulating concentrations of catecholamines in high-altitude mice, which may help avoid sympathoadrenal overactivity in chronic hypoxia. Further exploratory analysis found that high-altitude mice have a larger adrenal cortex and higher plasma concentrations of corticosterone, which could reflect changes in stress responsiveness or metabolic regulation. Therefore, multiple evolved changes in the physiology of the adrenal gland may contribute to high-altitude adaptation in deer mice.<b>NEW & NOTEWORTHY</b> Prolonged activation of the sympathoadrenal system can become maladaptive in chronic hypoxia, but few previous studies have examined adrenal function in high-altitude natives. Comparing high-altitude versus low-altitude populations of mice, we show that high-altitude mice synthesize and store fewer catecholamines in adrenal chromaffin cells and thus have lower secretion rates and circulating concentrations of catecholamines in hypoxia.</p>","PeriodicalId":7630,"journal":{"name":"American journal of physiology. Regulatory, integrative and comparative physiology","volume":" ","pages":"R274-R286"},"PeriodicalIF":2.2,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063145","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":"TRPA1 channels modulate cutaneous vasodilation during exercise in the heat in young adults when NOS is inhibited.","authors":"Rei Hattori, Masanobu Kajiki, Tomomi Fujimoto, Tatsuro Amano, Glen P Kenny, Koichi Watanabe, Takeshi Nishiyasu, Naoto Fujii","doi":"10.1152/ajpregu.00269.2024","DOIUrl":"10.1152/ajpregu.00269.2024","url":null,"abstract":"<p><p>Nitric oxide synthase (NOS) is an important mediator of cutaneous vasodilation during exercise-heat stress. We recently reported that pharmacological activation of transient receptor potential ankyrin 1 (TRPA1) channel mediates cutaneous vasodilation via NOS-dependent mechanisms under nonheat stress-resting conditions. Here, we hypothesized that TRPA1 channel activation would contribute to cutaneous vasodilation during exercise in the heat via NOS-dependent mechanisms. To assess this response, we first conducted TRPA1 channel antagonist verification substudy (10 young adults and 5 women) wherein 1 mM ASP7663 (TRPA1 channel agonist) increased cutaneous vascular conductance (CVC; cutaneous blood flow divided by mean arterial pressure) and this response was blocked by ∼50% with 100 μM HC030031, a known TRPA1 channel antagonist. Subsequently, 12 young adults (5 women) completed two bouts of 30-min moderate-intensity cycling (45% of their predetermined peak oxygen uptake) in the heat (35°C). During the first exercise, CVC was evaluated at four dorsal forearm skin sites perfused with a 5% DMSO, whereas in the second bout, all sites were treated with either <i>1</i>) a 5% DMSO (control), <i>2</i>) 100 µM HC030031, <i>3</i>) 20 mM l-NAME, a nonselective NOS inhibitor, or <i>4</i>) combination of both. No between-site differences in CVC were measured during the first exercise (<i>P</i> > 0.182). During the second exercise, HC030031 alone had no effect on CVC relative to the control (all <i>P</i> > 0.104). Both l-NAME and HC030031 + l-NAME reduced CVC (all <i>P</i> < 0.001), with the combined treatment showing a greater reduction (all <i>P</i> < 0.001). We showed that TRPA1 channels mediate cutaneous vasodilation during exercise-heat stress only when NOS is inhibited.<b>NEW & NOTEWORTHY</b> We demonstrated that the administration of TRPA1 channel antagonist HC030031 only appears to attenuate cutaneous vasodilation during exercise in the heat when nitric oxide synthase (NOS) is inhibited. TRPA1 channels may function as a \"backup system\" to maintain cutaneous vasodilation when NOS-dependent vasodilation is compromised during exercise in the heat.</p>","PeriodicalId":7630,"journal":{"name":"American journal of physiology. Regulatory, integrative and comparative physiology","volume":" ","pages":"R319-R328"},"PeriodicalIF":2.2,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381549","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":"Endothelial dysfunction in middle-aged and older men with low testosterone is associated with elevated circulating endothelin-1.","authors":"Matthew C Babcock, Lyndsey E DuBose, Kerry L Hildreth, Brian L Stauffer, Wendy M Kohrt, Megan M Wenner, Kerrie L Moreau","doi":"10.1152/ajpregu.00218.2024","DOIUrl":"10.1152/ajpregu.00218.2024","url":null,"abstract":"<p><p>Low testosterone in middle-aged/older men contributes to accelerated vascular aging, including endothelial dysfunction. However, the mechanisms by which low testosterone affects endothelial dysfunction are not well understood. We sought to determine whether higher endothelin-1 (ET-1) levels are associated with reduced brachial artery flow-mediated dilation (FMD) in middle-aged/older men with low testosterone. Plasma ET-1 was quantified in 60 men categorized as young (<i>n</i> = 20, age = 30 ± 4 yr, testosterone = 510 ± 63 ng/dL), middle-aged/older with normal testosterone (<i>n</i> = 20, age = 59 ± 6 yr, testosterone = 512 ± 115 ng/dL), or middle-aged/older with low testosterone (<i>n</i> = 20, age = 60 ± 8 yr, testosterone = 265 ± 47 ng/dL). Endothelial function was determined via brachial artery FMD. Venous and arterial endothelial cells were harvested via endovascular biopsy in a subset of participants and stained for ET-1 expression. Middle-aged/older men with normal testosterone exhibited lower brachial artery FMD (5.7 ± 2.2%) compared with young men (7.3 ± 1.3%, <i>P</i> = 0.020), which was exaggerated in middle-aged/older men with low testosterone (4.0 ± 1.8%, <i>P</i> = 0.010 vs. middle-aged/older men with normal testosterone). Plasma ET-1 was not different between young (5.6 ± 0.9 ng/dL) and middle-aged/older men with normal testosterone (6.0 ± 1.4 ng/dL, <i>P</i> = 0.681) but was higher in middle-aged/older men with low testosterone (7.7 ± 2.8 ng/dL) compared with both groups (<i>P</i> < 0.001 vs. young men; <i>P</i> = 0.013 vs. middle-aged/older men with normal testosterone). There was no difference in venous (<i>P</i> = 0.616) or arterial (<i>P</i> = 0.222) endothelial cell ET-1 expression between groups. There was a significant inverse association between plasma ET-1 and FMD (<i>r</i> =-0.371, <i>P</i> = 0.004). These data suggest that the accelerated age-associated reduction in endothelial dysfunction in middle-aged/older men with low testosterone is related to higher circulating ET-1.<b>NEW & NOTEWORTHY</b> Middle-aged/older men with low testosterone have reduced vascular endothelial function compared with young and age-matched men with normal testosterone. In this manuscript, we demonstrate that men with low testosterone have higher plasma endothelin-1, which is associated with worse brachial artery flow-mediated dilation. The source of higher plasma endothelin-1 remains unknown; however, higher circulating endothelin-1 appears to be a mechanism contributing to reduced vascular endothelial function in men with low testosterone.</p>","PeriodicalId":7630,"journal":{"name":"American journal of physiology. Regulatory, integrative and comparative physiology","volume":" ","pages":"R253-R261"},"PeriodicalIF":2.2,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063147","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":"Metabolic fuel selection in rainbow trout: coping with intralipid infusion.","authors":"Giancarlo G M Talarico, Elie Farhat, Jan A Mennigen, Jean-Michel Weber","doi":"10.1152/ajpregu.00170.2024","DOIUrl":"10.1152/ajpregu.00170.2024","url":null,"abstract":"<p><p>The impact of hyperlipidemia on fuel selection has never been investigated in fish. This study quantifies how intralipid administration affects <i>i</i>) in vivo mobilization of lipids (lipolytic rate: <i>R</i>_a glycerol) and carbohydrates (hepatic glucose production: <i>R</i>_a glucose) in rainbow trout and <i>ii</i>) key proteins involved in the regulation of fuel metabolism that could explain changes in glycerol and glucose kinetics. Results show that intralipid triples lipolytic rate (from 2.5 ± 0.5 to 7.8 ± 1.1 µmol glycerol kg^-1·min^-1) and inhibits glucose production by 36% (from 7.3 ± 0.9 to 4.7 ± 0.4 µmol kg^-1·min^-1). The stimulation of lipolysis is probably driven by lipase activation (gene expression of hormone-sensitive lipase increases in muscle) or by mass action effect. Such a strong lipolytic response is quite surprising because baseline <i>R</i>_a glycerol is already particularly high in fish and is well known for its stability under a variety of stresses that have important effects in mammals. The reduction in trout <i>R</i>_a glucose is likely caused by a large decrease in glycogen mobilization because hepatic gluconeogenic pathway capacity may rise as a consequence of increases in gluconeogenesis gene transcript levels. In contrast to humans, which maintain steady glucose production in response to intralipid infusion, rainbow trout appears to overcompensate increased gluconeogenic capacity with a disproportionately large inhibition of glycogen breakdown. Overall, these intralipid-driven changes in glycerol and glucose kinetics allow fish to decrease their reliance on carbohydrates and amino acids by replacing them, in part, with fatty acids as metabolic fuels.<b>NEW & NOTEWORTHY</b> How do fish respond to an intralipid infusion (a soybean-derived emulsion used for parenteral nutrition of human patients)? In rainbow trout, intralipid administration triples the rate of lipid mobilization (lipolysis) and reduces hepatic glucose production by 36%. These changes in substrate fluxes allow fish to decrease their reliance on amino acids and carbohydrates by substituting them with fatty acids as metabolic fuels.</p>","PeriodicalId":7630,"journal":{"name":"American journal of physiology. Regulatory, integrative and comparative physiology","volume":" ","pages":"R306-R318"},"PeriodicalIF":2.2,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063167","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":"Do not sleep on vitamin D: vitamin D is associated with sleep variability in apparently healthy adults.","authors":"Meral N Culver, Braxton A Linder, Delaney E Lyons, Zach J Hutchison, Catherine L Garrett, Jessica N McNeil, Austin T Robinson","doi":"10.1152/ajpregu.00168.2024","DOIUrl":"10.1152/ajpregu.00168.2024","url":null,"abstract":"<p><p>Vitamin D is associated with sleep quality and duration, but it is unclear whether vitamin D status influences sleep variability. Therefore, we sought to determine whether vitamin D status was associated with sleep variability in healthy adults. We assessed objective sleep, including timing and duration standard deviation (SD) using the Philips Actiwatch Spectrum and subjective sleep quality using the Pittsburgh Sleep Quality Index (PSQI) in 130 adults. We measured plasma 25(OH)D concentration to assess vitamin D. We used one-way ANOVAs and Kruskal-Wallis tests to compare sleep in participants characterized as vitamin D deficient (<20 ng/mL), insufficient (21-29 ng/mL), and sufficient (>30ng/mL). We used covariate-adjusted linear regression to assess associations between vitamin D status and sleep metrics. We compared differences in \"low\" and \"high\" sleep variability based on vitamin D status using the Chi-squared test. There was an effect of vitamin D status on sleep timing SD (Kruskal-Wallis, <i>P</i> = 0.021) and sleep duration SD (Kruskal-Wallis, <i>P</i> < 0.001). There was an inverse association between vitamin D status with sleep duration SD (after covariate adjustment <i>R</i>² = 0.267, <i>P</i> < 0.001, deficient vs. sufficient <i>P</i> = 0.050, insufficient vs. sufficient <i>P</i> = 0.022). There was no effect of vitamin D status on objective sleep duration, efficiency, or PSQI scores (<i>P</i> > 0.05). We did not observe differences in \"low\" and \"high\" sleep timing SD based on vitamin D status (χ² = 5.43, <i>P</i> = 0.066), but we did for sleep duration SD (χ² = 22.4, <i>P</i> < 0.001). Our data indicate that individuals with poor vitamin D status exhibit greater objective sleep variability. Clinical Trial Registry: https://www.clinicaltrials.gov/; Unique identifiers NCT04334135, NCT04244604, and NCT04576338.<b>NEW & NOTEWORTHY</b> Our findings reveal that individuals with lower circulating vitamin D concentrations experience greater sleep variability compared with those with higher circulating concentrations. This supports the growing body of evidence suggesting an important link between vitamin D status and sleep health.</p>","PeriodicalId":7630,"journal":{"name":"American journal of physiology. Regulatory, integrative and comparative physiology","volume":" ","pages":"R262-R273"},"PeriodicalIF":2.2,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143051328","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":"Two-week paramedic hospital training augments blood pressure response to isometric handgrip exercise in healthy young men.","authors":"Amane Hori, Daisuke Kume, Ryuji Saito, Daisuke Hasegawa, Kenichi Suijo, Masaki Mizuno, Norio Hotta","doi":"10.1152/ajpregu.00258.2024","DOIUrl":"10.1152/ajpregu.00258.2024","url":null,"abstract":"<p><p>Persistent stressful situations can have detrimental cardiovascular effects; however, effects on the blood pressure (BP) response to exercise have not been fully examined. This study investigated the impact of a 2-wk stressful situation on the exercise pressor response. Eight healthy male university paramedic trainees underwent a 2-wk paramedic hospital training and a control period study. Pre- and postintervention, BP responses to the exercise test [2-min submaximal isometric handgrip (IHG) exercise followed by postexercise muscle ischemia (PEMI)] and cold pressure test (CPT) were assessed. A stress biomarker, salivary α-amylase (sAA) activity, significantly increased after hospital training (Pre: 8.8 ± 4.6; Post: 15.5 ± 7.3 kU/L; <i>P</i> = 0.036), whereas no significant changes were observed in the control period (Pre: 11.3 ± 3.6; Post: 10.4 ± 4.5 kU/L). Although no significant trial (hospital training vs. control)-by-intervention (pre- vs. post-2-wk period) interactions were detected in the mean arterial pressure (MAP) response to PEMI or CPT, a significant interaction in the MAP response to IHG exercise was noted (Δ48.9 ± 11.2 to Δ55.5 ± 9.1 mmHg, hospital training; Δ53.2 ± 14.1 to Δ51.2 ± 11.9 mmHg, control; <i>P</i> = 0.035). Consequently, changes in the sAA and MAP preintervention to postintervention showed a significant correlation (τ = 0.397, <i>P</i> = 0.036). Results showed that stressful paramedic hospital training augmented BP response to IHG exercise. This suggests that prolonged stressful situations increase pressor response to exercise, particularly in cases involving healthy young men.<b>NEW & NOTEWORTHY</b> Exposure to prolonged stressful situations augmented the blood pressure response to submaximal isometric exercise in healthy young men. This finding suggests that monitoring cardiovascular responses during exercise under chronic stress conditions could be important.</p>","PeriodicalId":7630,"journal":{"name":"American journal of physiology. Regulatory, integrative and comparative physiology","volume":" ","pages":"R242-R252"},"PeriodicalIF":2.2,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142998597","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":"No sex differences in performance and perceived fatigability during a self-paced endurance exercise performed under moderate hypoxia.","authors":"Julio S Hasegawa, Andre C Silveira, Rafael A Azevedo, Julio Cezar Schamne, Maria Urbana Pinto Brandão Rondon, Marcelo Papoti, Adriano Eduardo Lima-Silva, Michael S Koehle, Romulo Bertuzzi","doi":"10.1152/ajpregu.00145.2024","DOIUrl":"10.1152/ajpregu.00145.2024","url":null,"abstract":"<p><p>This study examined potential sex differences in performance and perceived fatigability during a whole body endurance exercise performed under normoxia or moderate hypoxia. Nine males and eight females cyclists performed a 4-km cycling time trial under normoxia or hypoxia conditions. Performance fatigability and its central and peripheral determinants were measured via pre- to post-exercise changes in maximal voluntary isometric contraction (IMVC), voluntary activation (VA), and potentiated twitch force (TwPt) of knee extensors, respectively. Perceived fatigability was characterized via a rating of perceived exertion (RPE). Time to complete the trial was longer in hypoxia than normoxia in females (482 ± 24 vs. 465 ± 21 s) and males (433 ± 30 vs. 408 ± 31 s) (<i>P</i> = 0.039). There was no effect of sex or condition (<i>P</i> ≥ 0.370) for the magnitude of decrease in IMVC (female: normoxia = -14.3 ± 4.4%, hypoxia = -11.8 ± 5.2% vs. male: normoxia = -13.1 ± 9.4%, hypoxia = -12.9 ± 9.8%), TwPt (female: normoxia = -34.4 ± 11.4%, hypoxia = -31.8 ± 18.9% vs. male: normoxia = -30.5 ± 17.9%, hypoxia = -31.9 ± 20.9%), and VA (female: normoxia = -0.5 ± 2.3%, hypoxia = -1.6 ± 1.6% vs. male: normoxia = 0.8 ± 2.2%, hypoxia = -0.5 ± 1.3%). RPE was higher in hypoxia than in normoxia for both groups (<i>P</i> = 0.002). In conclusion, moderate hypoxia similarly impairs performance and perceived fatigability development in females and males during a 4-km cycling time trial.<b>NEW & NOTEWORTHY</b> In this study, we showed that females and males develop a similar hypoxia-induced impairment in endurance performance, perceived and performance fatigability during a 4-km cycling time trial. These novel findings indicate that females and males regulate their power output similarly during a 4-km cycling time trial under moderate hypoxia, likely to avoid prematurely exacerbating metabolic disturbances and thereby reaching comparable levels of performance fatigability by the end of the task.</p>","PeriodicalId":7630,"journal":{"name":"American journal of physiology. Regulatory, integrative and comparative physiology","volume":" ","pages":"R352-R363"},"PeriodicalIF":2.2,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381453","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":"Life-threatening fentanyl overdose beyond medullary depression in breathing.","authors":"Annick Judenherc-Haouzi, Tristan Lewis, Amanda Reinhardt, Philippe Haouzi","doi":"10.1152/ajpregu.00238.2024","DOIUrl":"10.1152/ajpregu.00238.2024","url":null,"abstract":"<p><p>We sought to determine how the balance between O₂ delivery (Do₂) and O₂ consumption is altered by fentanyl during the initial and the most critical period following a bolus intravenous injection of high-dose fentanyl. We determined the acute changes in ventilation, gas exchange, and hemodynamic-including cardiac function-along with the acid-base and arterial blood gas status-in 27 unsedated rats, following an intravenous bolus injection of 150 µg/kg fentanyl. This injection produced an immediate coma and central apnea, followed by the emergence of a regular and sustained, yet very depressed, breathing pattern ∼2.5 min later. All rats displayed an instantaneous and profound decrease in Q̇c (from 295.7 ± 42.62 to 140.74 ± 74.96 mL/kg/min; <i>P</i> < 0.0001) resulting from abrupt bradycardia (from 333.3 ± 20.8 to 112.2 ± 36.4 beats/min; <i>P</i> < 0.05) with a transient decreased cardiac contractility, associated with very severe hypoxemia that persisted throughout the ensuing period of hypoventilation, for example, [Formula: see text] = 39.0 ± 18.4 mmHg; [Formula: see text] = 50.1 ± 26.2%, at 5 min. Do₂ was therefore immediately decreased by several folds; and the abrupt decrease in Q̇c was even more severe than the drop in oxygenation. Twenty-four rats survived; the three remaining animals presented a rapid cardiac arrest by pulseless electrical activity. Fentanyl overdose induces an instant decrease in Do₂, with a very early and predominant drop in Q̇c, out of proportion with the decrease in V̇o₂, a protective mechanism produced by hypoxemia. The relevance and translation of these findings to human hypoxic cardiac arrest are discussed.<b>NEW & NOTEWORTHY</b> Fentanyl overdose induces an instant decrease in arterial transport of O₂, with a very early drop in cardiac output, out of proportion of O₂ requirement. These results point to the prominent role of the cardiac (through bradycardia) and circulatory effects of fentanyl as major contributors to the lethality of a fentanyl overdose when apnea and hypoventilation-induced hypoxemia develop.</p>","PeriodicalId":7630,"journal":{"name":"American journal of physiology. Regulatory, integrative and comparative physiology","volume":" ","pages":"R408-R421"},"PeriodicalIF":2.2,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143447643","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}