Journal of applied physiology最新文献

{"title":"Pathogenesis of fibrosis in patella-patellar tendon junction induced by jumping load in a rabbit model.","authors":"Haitao Liu, Xiaotian Liang, Haiwei Li, Lin Wang","doi":"10.1152/japplphysiol.00515.2024","DOIUrl":"10.1152/japplphysiol.00515.2024","url":null,"abstract":"<p><p>The mechanism of fibrosis at the patella-patellar tendon junction (PPTJ) was investigated using a rabbit overuse jumping model. Thirty-two female New Zealand White rabbits were randomly divided into control and jumping groups, and each group was further divided into four groups at 2, 4, 6, and 8 wk. The rabbit in the jumping group jumped 150 times/day, 5 days/wk. The PPTJ was removed at the corresponding time point and subjected to hematoxylin and eosin, safranin O, and immunohistochemical staining. Significant differences were observed in histological changes and fibrosis-related factors between the jumping and control groups (<i>P</i> < 0.01). Comparison within the jumping group indicated that the changes in the fibrocartilage zone thickness and proteoglycan area were pronounced at <i>week 6</i>; the expressions of transforming growth factor β (TGF-β1), Smad3, CTGF, α-SMA, COL-I, and COL-III peaked at <i>week 6</i> (<i>P</i> < 0.05). The jumping load can lead to morphological and fibrotic changes in the patella-patellar tendon junction, with peak changes occurring at <i>week 6</i>. The fibrosis in the patella-patellar tendon junction may be associated with increased secretion of TGF-β1 and Smad3 due to jump loading, which upregulates CTGF expression and thus promotes the synthesis of α-SMA, COL-I, and COL-III.<b>NEW & NOTEWORTHY</b> The temporal pattern of fibrosis in the patella-patellar tendon junction (PPTJ) was determined by observing changes in histology and fibrosis-related factors at different time points in an overused jumping rabbit model. The results revealed that <i>1</i>) the peak fibrotic changes in the PPTJ occurred at <i>week 6</i> of jump training; <i>2</i>) fibrosis in PPTJ may be associated with the changes in TGF-β1/Smad3. This study contributes to the development of targeted early interventions.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"378-388"},"PeriodicalIF":3.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142949323","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":"Ventilatory long-term facilitation at rest increases the feedforward contribution to subsequent exercise ventilatory responses.","authors":"Joseph F Welch, Brighton R Cretney, Gordon S Mitchell, George M Balanos","doi":"10.1152/japplphysiol.00737.2024","DOIUrl":"10.1152/japplphysiol.00737.2024","url":null,"abstract":"<p><p>The respiratory control system exhibits neural plasticity, adjusting future ventilatory responses based on experience. We tested the hypothesis that ventilatory long-term facilitation induced by hypercapnic acute intermittent hypoxia (AIH) at rest enhances subsequent ventilatory responses to steady-state exercise. Fourteen healthy adults (age = 27 ± 5 yr; 7 males) participated in the study. On <i>day 1</i>, pulmonary function testing was performed. On <i>days 2</i> and <i>3</i>, in a pseudorandomized counterbalanced order, participants were exposed to AIH or Sham; AIH consisted of 15, 1-min hypoxic episodes with 1.5-min room air intervals. Mild hypercapnia (end-tidal Pco₂ clamped ∼3 mmHg above baseline) was sustained throughout AIH and Sham and for 40 min after. Approximately 20-30 min later, participants performed continuous mild to moderate constant-load cycle exercise in room air at 30, 60, and 90 W for 5 min each. Inspired minute ventilation (V̇i) increased by 3.6 ± 1.2 L·min^-1 after AIH versus baseline and was significantly greater than Sham (<i>P</i> = 0.013), signifying the onset of ventilatory long-term facilitation. Although V̇i during subsequent steady-state exercise was not significantly different between AIH and Sham (<i>P</i> = 0.511), the slope of the relationship between V̇i and CO₂ production rate (i.e., the system gain) and the calculated feedforward exercise gain were significantly increased (<i>P</i> = 0.021 and <i>P</i> < 0.001, respectively). Consequently, end-tidal Pco₂ was regulated ∼1 mmHg lower across all exercise workloads after AIH versus Sham (<i>P</i> = 0.006). Thus, ventilatory plasticity induced at rest alters future ventilatory responses to mild or moderate steady-state exercise.<b>NEW & NOTEWORTHY</b> We demonstrate that by inducing ventilatory long-term facilitation (LTF) at rest, subsequent ventilatory responses to mild or moderate exercise are altered. When ventilatory LTF was induced via hypercapnic acute intermittent hypoxia, the feedforward contribution to exercise hyperpnea increased, accompanied by marginal increases in the overall system response and decreases in end-tidal Pco₂. Thus, respiratory motor plasticity at rest can \"spill over\" to other physiological states, including mild or moderate steady-state exercise.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"426-438"},"PeriodicalIF":3.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142949330","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":"Exploring the complex relationship between psychosocial stress and the gut microbiome: implications for inflammation and immune modulation.","authors":"Komal Marwaha, Ryan Cain, Katherine Asmis, Katya Czaplinski, Nathan Holland, Darly C Ghislaine Mayer, Jessica Chacon","doi":"10.1152/japplphysiol.00652.2024","DOIUrl":"10.1152/japplphysiol.00652.2024","url":null,"abstract":"<p><p>There is growing interest in understanding the complex relationship between psychosocial stress and the human gastrointestinal microbiome (GIM). This review explores the potential physiological pathways connecting these two and how they contribute to a proinflammatory environment that can lead to the development and progression of the disease. Exposure to psychosocial stress triggers the activation of the sympathetic nervous system (SNS) and hypothalamic-pituitary axis (HPA), leading to various physiological responses essential for survival and coping with the stressor. However, chronic stress in susceptible individuals could cause sustained activation of HPA and SNS, leading to immune dysregulation consisting of redistribution of natural killer (NK) cells in the bloodstream, decreased function of T and B cells, and elevation of proinflammatory cytokines such as interleukin-1, interleukin-6, tumor necrotic factor-α, interferon-gamma. It also leads to disruption of the GIM composition and increased intestinal barrier permeability, contributing to GIM dysbiosis. The GIM dysbiosis and elevated cytokines can lead to reciprocal effects and further stimulate the HPA and SNS, creating a positive feedback loop that results in a proinflammatory state underlying the pathogenesis and progression of stress-associated cardiovascular, gastrointestinal, autoimmune, and psychiatric disorders. Understanding these relationships is critical for developing new strategies for managing stress-related health disorders.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"518-535"},"PeriodicalIF":3.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142983465","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":"Acute selective serotonin-reuptake inhibition elevates basal ventilation and attenuates the rebreathing ventilatory response, independent of cerebral perfusion.","authors":"Jay M J R Carr, Jodie Koep, L Madden Brewster, Ayechew Getu, Jonah C Dizon, Declan Isaak, Andrew Steele, Connor A Howe, Philip N Ainslie","doi":"10.1152/japplphysiol.00751.2024","DOIUrl":"10.1152/japplphysiol.00751.2024","url":null,"abstract":"<p><p>Serotonin (5-HT) is integral to signaling in areas of the brainstem controlling ventilation and is involved in central chemoreception. Selective serotonin reuptake inhibitors (SSRIs), used to effectively increase 5-HT concentrations, are commonly prescribed for depression. The effects of SSRIs on the control of breathing and the potential influence of cerebral blood flow (CBF) have not been directly assessed. We hypothesized that a single SSRI dose in healthy adults would not impact resting ventilation, global CBF, or brainstem blood flow reactivity to CO₂ but would steepen the slope of the hypercapnic ventilatory response (HCVR). In 15 young, healthy adults (6 females, 25 [Formula: see text] 5 yr, 70 [Formula: see text] 10 kg, 172 [Formula: see text] 15 cm, 24 [Formula: see text] 4 kg/cm²), using a placebo-controlled, double-blind, randomized design, we assessed baseline cardiorespiratory and CBF (duplex ultrasound) responses to SSRI (40 mg citalopram), as well as to hyperoxic hypercapnic rebreathing (as an index of central chemoreception). Baseline measures of mean arterial pressure, heart rate, minute ventilation, CBF, and the pressures of end-tidal oxygen and carbon dioxide were all not influenced by SSRI. Likewise, the sum of blood flowing through both vertebral arteries (as an index of brainstem blood flow) during hypercapnia was also unchanged. In contrast, basal ventilation (during rebreathing following hyperventilation and during hyperoxia) was elevated from 9.5 [Formula: see text] 4.1 to 11.5 [Formula: see text] 5.5 L/min (interaction <i>P</i> = 0.023); and counter to our hypothesis, the central chemoreceptor-mediated ventilatory response to CO₂ was reduced following SSRI from 7.5 [Formula: see text] 5.3 to 5.1 [Formula: see text] 4.1 L/min/mmHg (interaction <i>P</i> = 0.027). The implications of these findings in health and pathology remain to be determined.<b>NEW & NOTEWORTHY</b> Acute inhibition of serotonin reuptake with citalopram diminishes the ventilatory response to hyperoxic hypercapnic rebreathing, possibly indicating decreased sensitivity of the central chemoreceptors and respiratory control centers. Additionally, ventilation during minimal chemoreceptor activation-i.e., following hypocapnia during hyperoxia-is elevated, perhaps signifying an increased tonic activity of the respiratory control areas. These changes appear to be independent of brainstem blood flow. These findings may have implications for antidepressant drug use.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"592-602"},"PeriodicalIF":3.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143005995","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":"Repeated hyperbaric oxygen exposure accelerates fatigue and impairs SR-calcium release in mice.","authors":"Heath G Gasier, Jack Kovach, Kris Porter","doi":"10.1152/japplphysiol.00723.2024","DOIUrl":"10.1152/japplphysiol.00723.2024","url":null,"abstract":"<p><p>Breathing hyperoxic gas is common in diving and accelerates fatigue after prolonged and repeated exposure. The mechanism(s) remain unknown but may be related to increased oxidants that interfere with skeletal muscle calcium trafficking or impaired aerobic ATP production. To determine these possibilities, C57BL/6J mice were exposed to hyperbaric oxygen (HBO₂) for 4 h on three consecutive days or remained in room air. Postfinal exposure, fatigue was determined by grip strength and run-to-exhaustion tests. Other measurements included indices of oxidant stress and antioxidant defenses, mitochondrial bioenergetics, caffeine-induced sarcoplasmic reticulum-calcium release, and <i>S</i>-nitrosylation of ryanodine receptor 1 (RyR1). Despite grip strength being unaffected by repeated HBO₂ exposure, mean running time was reduced by 50%. In skeletal muscle from HBO₂ exposed mice, superoxide production was significantly increased, resulting in elevated lipid and DNA (nuclear and mitochondrial) oxidation. Accompanying increased oxidant stress was a reduction in glutathione content and increased <i>Sod1</i> and <i>Hmox1</i> gene expression; <i>Ucp3</i> mRNA was reduced. Mitochondrial respiration, mitochondrial membrane potential, and NAD⁺/NADH were not influenced by HBO₂. In contrast, caffeine-induced sarcoplasmic reticulum (SR)-calcium release was reduced by 66% and <i>S</i>-nitrosylation of RyR1 was increased by 45%. Exposing mice to repeated HBO₂ increases oxidant stress that activates some antioxidant defenses. Mitochondrial function is not altered and could be related to decreased production of UCP3 that serves to maintain the electrochemical proton gradient. <i>S</i>-nitrosylation of RyR1 may promote SR-calcium leak and reduce content, a potential mechanism for repeated HBO₂-induced fatigue.<b>NEW & NOTEWORTHY</b> Breathing hyperoxic gas during prolonged and repeated dives causes fatigue but the mechanisms are unknown. Here, we show in mice exposed to repeated hyperbaric oxygen that running fatigue is accelerated and accompanied by increased skeletal muscle oxidant stress and reduced caffeine-induced sarcoplasmic reticulum (SR)-calcium release. The latter may be due to increased <i>S</i>-nitrosylation of ryanodine receptor 1 (RyR1) and be a mechanism for impaired physical performance after repeated oxygen diving.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"415-425"},"PeriodicalIF":3.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142894725","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 leg immobilization and recovery resistance training on skeletal muscle-molecular markers in previously resistance-trained versus untrained adults.","authors":"J Max Michel, Joshua S Godwin, Daniel L Plotkin, Mason C McIntosh, Madison L Mattingly, Philip J Agostinelli, Breanna J Mueller, Derick A Anglin, Nicholas J Kontos, Alexander C Berry, Marina Meyer Vega, Autumn A Pipkin, Matt S Stock, Zachary A Graham, Harsimran S Baweja, C Brooks Mobley, Marcas M Bamman, Michael D Roberts","doi":"10.1152/japplphysiol.00837.2024","DOIUrl":"10.1152/japplphysiol.00837.2024","url":null,"abstract":"<p><p>We sought to examine how resistance training (RT) status in young healthy individuals, either well resistance trained (T, <i>n</i> = 10) or untrained (UT, <i>n</i> = 11), affected molecular markers with leg immobilization followed by recovery RT. All participants underwent 2 wk of left leg immobilization via a locking leg brace. Afterward, all participants underwent 8 wk (3 days/wk) of knee extensor-focused progressive RT. Vastus lateralis (VL) ultrasound-derived thickness and muscle cross-sectional area were measured at baseline (PRE), immediately after disuse (MID), and after RT (POST) with VL muscle biopsies also being collected at these time points. Both groups presented lower ultrasound-derived VL size metrics at MID versus PRE (<i>P</i> ≤ 0.001), and values increased in both groups from MID to POST (<i>P</i> < 0.05); however, VL size increased from PRE to POST in UT only (<i>P</i> < 0.001). Mean and type II myofiber cross-sectional area values were greater at PRE and POST versus MID (<i>P</i> < 0.05), with T being greater than UT throughout (<i>P</i> ≤ 0.012). In both groups, satellite cell number was not affected by leg immobilization but increased in response to RT (<i>P</i> ≤ 0.014), with T being greater than UT throughout (<i>P</i> = 0.004). Total RNA (ribosome content) decreased (<i>P</i> = 0.010) from PRE to MID while total RNA and certain endoplasmic reticulum stress proteins increased from MID to POST regardless of training status. Immobilization-induced muscle atrophy and recovery RT hypertrophy outcomes are similar between UT and T participants, and the lack of molecular signature differences between groups supports these findings. However, results are limited to younger adults undergoing noncomplicated disuse.<b>NEW & NOTEWORTHY</b> Formerly trained and untrained individuals demonstrate similar atrophic responses to disuse while untrained individuals exhibited a greater hypertrophic response to subsequent resistance training. The molecular responses accompanying these changes were largely similar between groups and included increases in satellite cell content with resistance training and increases in ribosome biogenesis, which was largely driven by the formerly trained group.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"450-467"},"PeriodicalIF":3.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143006002","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":"Habitual preexercise caffeine supplementation prevents exercise training-induced attenuation of exercising systolic blood pressure and double product.","authors":"Kylee S West, Nate J Helwig, Laura E Schwager, Thomas W Hart, Anna C Zucker, Jacob S Venenga, Mark Flores, Nathaniel D M Jenkins","doi":"10.1152/japplphysiol.00874.2024","DOIUrl":"10.1152/japplphysiol.00874.2024","url":null,"abstract":"<p><p>We examined the effect of habitual preexercise caffeine supplementation on training-induced adaptations to exercising systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse pressure (PP), heart rate (HR), and double product (DP). Young women (means ± SD; 24 ± 7 yr) were randomized to a caffeine (120 mg) supplement (CAF; <i>n</i> = 17) or placebo (PLA; <i>n</i> = 16) group, completed 6 wk of high-intensity exercise training on three nonconsecutive days per week, and supplemented with CAF or PLA 30-60 min before exercise or else upon waking. Before (PRE) and after (POST) the intervention, SBP, DBP, and HR were measured and PP and DP were calculated, at rest and during fixed-power exercise at 50 and 75 W. Statistical analyses included three-way mixed-factorial ANOVAs with post hoc comparisons as necessary. Group × intensity × time interactions were observed for SBP (<i>P</i> = 0.0105) and DP (<i>P</i> = 0.003). SBP and DP increased with increasing exercise intensity at PRE and POST in both groups. However, although SBP and DP decreased PRE to POST at 50 and 75 W in PLA, SBP and DP did not change at any intensity from PRE to POST in CAF. An intensity × time interaction was observed for DBP (<i>P</i> = 0.006) indicating no change in resting DBP, but reductions from PRE to POST at 50 and 75 W that were independent of group. Main effects of intensity (<i>P</i> < 0.0001) and time (<i>P</i> = 0.03) were observed for HR, and a main effect of intensity was observed for PP (<i>P</i> < 0.0001). Habitual caffeine supplementation blunted training-induced reductions in exercising SBP and DP. Individuals may wish to avoid preexercise supplementation if seeking to maximize the BP-lowering benefits of exercise.<b>NEW & NOTEWORTHY</b> Habitual preexercise caffeine consumption prevented reductions in exercising systolic blood pressure and double product induced by 6 wk of high-intensity exercise in women. Therefore, our findings indicate that habitual preexercise caffeine supplementation may impede beneficial hemodynamic adaptations of exercise training in healthy, young women.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"358-365"},"PeriodicalIF":3.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142894724","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":"Daily blood flow restriction does not affect muscle fiber capillarization and satellite cell content during 2 wk of bed rest in healthy young men.","authors":"Thorben Aussieker, Cas J Fuchs, Antoine H Zorenc, Lex B Verdijk, Luc J C van Loon, Tim Snijders","doi":"10.1152/japplphysiol.00461.2024","DOIUrl":"10.1152/japplphysiol.00461.2024","url":null,"abstract":"<p><p>The present study assessed whether single-leg daily blood flow restriction (BFR) treatment attenuates the decline in muscle fiber size, capillarization, and satellite cell (SC) content during 2 wk of bed rest in healthy, young men. Twelve healthy, young men (age: 24 ± 3 yr; BMI: 23.7 ± 3.1 kg/m²) were subjected to 2 wk of bed rest, during which one leg was exposed to three times daily 5 min of BFR, whereas the contralateral leg received sham treatment [control (CON)]. Muscle biopsies were obtained from the m. vastus lateralis from both the BFR and CON legs before and immediately after 2 wk of bed rest. Types I and II muscle fiber size, myonuclear content, capillarization, and SC content were assessed by immunohistochemistry. No significant decline in either type I or type II muscle fiber size was observed following bed rest, with no differences between the CON and BFR legs (<i>P</i> > 0.05). Type I muscle fiber capillary density increased in response to bed rest in both legs (<i>P</i> < 0.05), whereas other muscle fiber capillarization measures remained unaltered. SC content decreased in both type I (from 7.4 ± 3.2 to 5.9 ± 2.7 per 100 fibers) and type II (from 7.2 ± 3.4 to 6.5 ± 3.2 per 100 fibers) muscle fibers (main effect of time <i>P</i> = 0.018), with no significant differences between the BFR and CON legs (<i>P</i> > 0.05). In conclusion, 2 wk of bed rest has no effect on muscle capillarization and decreases the SC content, and daily BFR treatment does not affect skeletal muscle fiber size and SC content in healthy, young men.<b>NEW & NOTEWORTHY</b> We recently reported that the application of daily blood flow restriction (BFR) treatment does not preserve muscle mass or strength and does not modulate daily muscle protein synthesis rates during 2 wk of bed rest. Here, we show that 2 wk of bed rest resulted in a decrease in satellite cell (SC) content. In addition, the BFR treatment did not affect muscle fiber size, capillarization, and SC content during 2 wk of bed rest.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"89-98"},"PeriodicalIF":3.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142769265","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":"Impact of acute sleep restriction on cerebrovascular reactivity and neurovascular coupling in young men and women.","authors":"Matthew J McDonald, Megan L Marsh, Sharon D Fears, Brian Shariffi, Jill A Kanaley, Jacqueline K Limberg","doi":"10.1152/japplphysiol.00648.2024","DOIUrl":"10.1152/japplphysiol.00648.2024","url":null,"abstract":"<p><p>Chronic exposure to shortened sleep is associated with an increased risk of Alzheimer's disease and dementia. Previous studies show insufficient (e.g., poor or fragmented) sleep impairs cerebrovascular reactivity to metabolic stress and may have a detrimental effect on the link between cerebral blood flow (CBF) and neural activity (i.e., neurovascular coupling, NVC). The purpose of this study was to examine the effect of acute sleep restriction on CBF in response to a metabolic (carbon dioxide, CO₂) and a cognitive stressor. We hypothesized sleep restriction (4-h time in bed) would attenuate CBF and NVC. Sixteen young adults (8 M/8 F, 28 ± 8 yr, 25 ± 3 kg/m²) completed two morning visits following a night of normal (7.38 ± 0.82 h) or restricted (4.27 ± 0.93 h, <i>P</i> < 0.001) sleep duration. Middle cerebral artery velocity (MCAv, transcranial Doppler ultrasound) was measured at rest and during <i>1</i>) 5 min of carbogen air-breathing and <i>2</i>) five trials consisting of a period of eyes closed (30 s), followed by eyes open (40 s) while being challenged with a validated visual paradigm (Where's Waldo). Baseline MCAv was unaffected by acute sleep restriction (control: 64 ± 14 cm/s; restricted 61 ± 13 cm/s; <i>P</i> = 0.412). MCAv increased with CO₂; however, there was no effect of restricted sleep (<i>P</i> = 0.488). MCAv increased in response to visual stimulation; the peak NVC response was reduced from control following restricted sleep (control: 16 ± 12%; restricted: 9 ± 7%; <i>P</i> = 0.008). Despite no effect of acute sleep restriction on resting CBF or the response to CO₂ in young men and women, NVC was attenuated following a night of shortened sleep. These data support an important role for sleep in NVC and may have implications for the development of neurodegenerative disease states, such as Alzheimer's and dementia.<b>NEW & NOTEWORTHY</b> Chronic exposure to shortened sleep is associated with an increased risk of Alzheimer's disease and dementia. We examined the effect of acute sleep restriction (4-h time in bed) on cerebral blood flow in response to a metabolic (carbon dioxide) and a cognitive stimulus. Despite no effect of acute sleep restriction on resting cerebral blood flow or the response to carbon dioxide in young men and women, neurovascular coupling was attenuated following a night of shortened sleep.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"282-288"},"PeriodicalIF":3.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142807154","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 extraction of neural strategies from the surface EMG: 2004-2024.","authors":"Dario Farina, Roberto Merletti, Roger M Enoka","doi":"10.1152/japplphysiol.00453.2024","DOIUrl":"10.1152/japplphysiol.00453.2024","url":null,"abstract":"<p><p>This review follows two previous papers [Farina et al. <i>Appl Physiol (1985)</i> 96: 1486-1495, 2004; Farina et al. <i>J Appl Physiol (1985)</i> 117: 1215-1230, 2014] in which we reflected on the use of surface electromyography (EMG) in the study of the neural control of movement. This series of papers began with an analysis of the indirect approaches of EMG processing to infer the neural control strategies and then closely followed the progress in EMG technology. In this third paper, we focus on three main areas: surface EMG modeling; surface EMG processing, with an emphasis on decomposition; and interfacing applications of surface EMG recordings. We highlight the latest advances in EMG models that allow fast generation of simulated signals from realistic volume conductors, with applications ranging from validation of algorithms to identification of nonmeasurable parameters by inverse modeling. Surface EMG decomposition is currently an established state-of-the-art tool for physiological investigations of motor units. It is now possible to identify large samples of motor units, to track motor units over multiple sessions, to partially compensate for the nonstationarities in dynamic contractions, and to decompose signals in real time. The latter achievement has facilitated advances in myocontrol, by using the online decoded neural drive as a control signal, such as in the interfacing of prostheses. Looking back over the 20 yr since our first review, we conclude that the recording and analysis of surface EMG signals have seen breakthrough advances in this period. Although challenges in its application and interpretation remain, surface EMG is now a solid and unique tool for the study of the neural control of movement.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"121-135"},"PeriodicalIF":3.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142687153","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}