Journal of applied physiology最新文献

Muscle sympathetic nerve activity (MSNA) responsiveness to mental stress is highly variable between individuals. Although stress perception has been posited as a contributor to the MSNA variability during mental stress, prior studies have been inconclusive. Furthermore, the importance of stress appraisal and coping on MSNA reactivity to mental stress has not been investigated. We hypothesize that appraisal of mental stress as a threat (i.e., perceived demands of stress exceed coping resources) versus a challenge (i.e., perceived coping resources sufficient for demands of stress) would be associated with greater MSNA reactivity. Twenty healthy adults (11 males, 9 females, 21 ± 3 yr, 23 ± 3 kg/m²) participated. Beat-by-beat blood pressure (finger plethysmography), heart rate (electrocardiography), and MSNA (microneurography) were recorded during a 10-min quiet rest followed by the Trier Social Stress Test (TSST). After each phase of the TSST (i.e., speech prep, speech, and mental arithmetic), participants reported threat versus challenge appraisal. Endorsement of a threat appraisal was positively associated with changes in MSNA burst frequency (r = 0.548, P = 0.018), burst incidence (r = 0.599, P = 0.009), and total MSNA (r = 0.697, P = 0.037) during the speech stress period. Moreover, increases in threat appraisal across tasks was associated with elevated MSNA burst frequency (r = 0.531, P = 0.023), incidence (r = 0.512, P = 0.030), and total MSNA (r = 0.727, P = 0.027) responsiveness. These findings support an association between stress appraisal processes and postganglionic sympathetic neural reactivity to psychosocial stress and may partially explain interindividual variability in MSNA responses to mental stress.NEW & NOTEWORTHY The present study investigated the association between stress appraisal and muscle sympathetic nerve activity (MSNA) reactivity to the Trier Social Stress Test. Appraisal of the stress task as a threat (i.e., perceived inability to cope with the demands of the task) was associated with exaggerated MSNA reactivity to mental stress in humans. Threat appraisal is associated with exaggerated sympathetic reactivity to stress, potentially underlying the commonly observed interindividual variability in MSNA responsiveness to mental stress.

Strength of vocal fold adduction has been hypothesized to be a critical factor influencing vocal acoustics but has been difficult to measure directly during phonation. Recent work has suggested that upper esophageal sphincter (UES) pressure, which can be easily assessed, increases with stronger vocal fold adduction, raising the possibility that UES pressure might indirectly reflect vocal fold adduction strength. However, concurrent UES pressure and vocal acoustics have not previously been examined across different vocal tasks. Doing so may offer insights into the potential use of UES pressure for relative quantification of the strength of vocal fold adduction and how this might contribute to vocal acoustics across different vocal tasks. We assessed UES pressure relative to vocal acoustics in 32 vocally healthy adults during sustained vowels, whispered sentences, and spoken sentences. Smoothed cepstral peak prominence (CPPs) and low-to-high spectral energy ratio (LHR) were derived from the acoustic signal. After controlling for resting UES pressure, age, and sex, we observed significant negative correlations between UES pressure and CPPs and a significant positive correlation between UES pressure and LHR. UES pressures were significantly higher during spoken sentences than whispered sentences and sustained vowels. Measuring UES pressure relative to vocal acoustics is a novel methodology for studying upper aerodigestive tract physiology during phonation and has the potential to enhance understanding of voice disruption in clinical populations. Clinical implications and considerations for implementation are discussed.NEW & NOTEWORTHY We identified relationships between upper esophageal sphincter (UES) pressures and vocal acoustics during phonation in vocally healthy individuals, potentially reflecting the influence of strength of vocal fold adduction and other phonatory factors on vocal acoustics. This methodology could lead to the development of a clinical and research tool that could provide insight into the strength of vocal fold adduction, a critical factor influencing voice quality that has historically been difficult to assess.

Reduced orthostatic tolerance is common following periods of bed rest that are associated with illness or surgery, putting individuals at higher risk for syncope and falls following hospitalization. Following menopause, mechanisms of female cardiovascular regulation change, which may be associated with sex-specific responses to orthostatic stress following bed rest. The purpose of our experiment was to investigate sex differences between healthy postmenopausal women and similar-age men (age: 55-65 yr) for their orthostatic tolerance and cerebrovascular responses to standing following bed rest. Twenty-two late-middle-aged adults (11 women) completed 14 days of head-down bed rest, with half of the participants being randomized into an exercise group that performed high-intensity exercise during bed rest. Supine-to-stand tests were performed before and ∼5 h after bed rest. Women had lower orthostatic tolerance than men after bed rest (bed rest × sex interaction: P = 0.004), without a protective effect of daily exercise. Both men and women were mildly hypocapnic while supine (main effect: P = 0.019) following bed rest and had lower middle cerebral artery blood velocity (MCAv) nadirs upon standing (main effect: P = 0.027). During the third minute of standing, both men and women had lower end-tidal Pco₂ (main effect: P < 0.001) and MCAv (main effect: P = 0.002) after bed rest, but only men had increased cerebrovascular resistance index (bed rest × sex interaction: P = 0.005) and only women were hypotensive (bed rest × sex interaction: P = 0.020) compared with pre-bed rest. Accordingly, lower MCAv of postmenopausal women and men while standing after bed rest was mediated by different factors.NEW & NOTEWORTHY Postmenopausal women had lower orthostatic tolerance than similar-age men while standing post-bed rest. Both sexes exhibited lower cerebral blood velocity nadirs upon standing; however, sex-specific interactions of the determinants of cerebral perfusion (i.e., Pco₂, cerebrovascular resistance index, and arterial pressure) were observed during prolonged standing after bed rest. These results indicate that postmenopausal women and men have different factors underlying reduced cerebral perfusion while standing after bed rest.

This review follows two previous papers [Farina et al. Appl Physiol (1985) 96: 1486-1495, 2004; Farina et al. J Appl Physiol (1985) 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.

The influence of peripheral antitussive drugs on spatiotemporal features of coughing has not been reported. We hypothesized that this class of compounds would alter the cough motor pattern, in part, by lengthening cough phases. Peripherally acting antitussives, 3-aminopropylphosphinic acid (3APPi, 5 mg/kg) and levodropropizine (Levo, 3 mg/kg) were injected intravenously in anesthetized spontaneously breathing cats (13 males, 2 females; 4.38 ± 0.19 kg). Spatio-temporal analysis of cough induced by mechanical stimulation of the trachea showed significant reductions in cough number and expiratory cough efforts after the administration of each drug. A significant reduction in inspiratory cough efforts occurred after Levo. Both drugs induced temporal changes in the cough motor pattern, including prolongations of inspiratory phase, inspiratory-expiratory transition, total cough diaphragm activity, and total cough cycle duration. Levo also significantly lengthened the expiratory phase of cough. A shortening of the overlap between diaphragm and abdominal activity and cough abdominal electromyogram (EMG) activity was observed after the administration of 3APPi. No significant changes in cardiorespiratory data were seen, with the exception of prolonged expiratory phase after 3APPi and lower blood pressure after Levo. Peripherally induced cough suppression is accompanied with changes in cough temporal characteristics that are not observed after the administration of centrally acting antitussives. The motor output produced by the cough central pattern generator differs significantly when coughing is perturbed by peripherally and centrally acting antitussives.NEW & NOTEWORTHY In a study on anesthetized cats, peripherally acting antitussives 3-aminopropylphosphinic acid (3APPi) and levodropropizine (Levo) significantly reduced cough number and expiratory efforts, with Levo also reducing inspiratory efforts. Both antitussives altered the cough motor pattern, extending various cough phases. 3APPi shortened diaphragm-abdominal activity overlap, whereas Levo decreased the respiratory rate. These changes contrast with those induced by centrally acting antitussives.

In high-intensity and sprint interval training, the frequency of contractions is typically higher compared with moderate-intensity continuous training, but it remains unclear whether this contributes to the effective increase in fatigue resistance mechanisms. Here, we investigated the role of contraction frequency in high-intensity training on endurance adaptations of mouse skeletal muscle. Male C57BL/6 mice were divided into groups based on high (0.25 s contraction every 0.5 s) and low (0.25 s contraction every 4.5 s) contraction frequencies, with either 360 contractions per session (Hi360 and Lo360) or 30 contractions per session (Hi30 and Lo30). The plantar flexor muscles were stimulated using in vivo supramaximal electrical stimulation, where all muscle fibers were maximally activated, every other day for 5 wk. In both the Hi360 and Lo360 groups, where force production declined to less than 40% of the initial value during the training session, muscle endurance, and mitochondrial content and respiratory capacity, were increased to a similar extent. In contrast, the rate of torque decline during the training session was more pronounced in the Hi30 group compared with the Lo30 group. In response, the Hi30 group, but not the Lo30 group, exhibited increased fatigue resistance and mitochondrial respiration, which was accompanied by increased peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) expression and an activation of AMP-activated protein kinase (AMPK)/unc-51-like autophagy activating kinase 1 (Ulk1) pathway. These data suggest that the frequency of contractions is a critical factor in determining the efficient enhancement of mitochondrial respiratory capacity and muscle endurance through high-intensity training, presumably due to promotion of mitochondrial quality control.NEW & NOTEWORTHY We investigated how training programs varying in contraction frequencies impact the endurance capacity of mouse skeletal muscle, using in vivo supramaximal electrical stimulation to ensure maximal activation of all muscle fibers. Increasing the frequency of contractions during high-intensity training led to increased fatigue resistance and mitochondrial respiratory capacity with fewer repetitions per training session, highlighting the pivotal importance of contraction frequency during exercise training in shaping endurance adaptations in skeletal muscle.

The aim of this study was to test whether combined physical exercise training of moderate intensity executed during the development of monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH) hinders the progression of pulmonary and right heart harmful functional and structural remodeling in rats. Wistar rats were injected with MCT (60 mg/kg) and after 24 h were exposed to a combined exercise training program: aerobic exercise (treadmill running-60 min/day; 60% of maximum running speed); and resistance exercise (vertical ladder climbing-15 climbs; 60% of maximum carrying load), on alternate days, 5 days/wk, for ∼3 wk. After euthanasia, the lung and right ventricle (RV) were excised and processed for histological, single myocyte, and biochemical analyses. Combined exercise increased the tolerance to physical effort (time until fatigue and relative maximum load) and prevented increases in pulmonary artery resistance (acceleration time (TA)/ejection time (TE)] and reductions in RV function [tricuspid annular plane systolic excursion (TAPSE)]. Moreover, in myocytes isolated from the RV, combined exercise preserved contraction amplitude, as well as contraction and relaxation velocities, and inhibited reductions in the amplitude and maximum speeds to peak and to decay of the intracellular Ca²⁺ transient. Furthermore, combined exercise avoided RV (RV weight, cardiomyocyte, extracellular matrix, collagen, inflammatory infiltrate, and extracellular matrix) and lung (pulmonary alveoli and alveolar septum) harmful structural remodeling. In addition, combined exercise restricted RV [nitric oxide (NO) and carbonyl protein (CP)] and lung [catalase (CAT), glutathione S-transferase (GST), and NO] oxidative stress. In conclusion, the applied combined exercise regime hinders the progression of pulmonary and right heart functional and structural harmful remodeling in rats with MCT-induced PAH.NEW & NOTEWORTHY This study reveals that combined exercise improves tolerance to physical effort, prevents increases in pulmonary artery resistance, and conserves the right heart function during the progression of pulmonary arterial hypertension. Our analyses show that combined exercise hinders harmful right ventricular and lung structural remodeling and oxidative stress, which reflects in the maintenance of right ventricular myocytes' contractile function by preserving the intracellular calcium cycling. An attenuated progression of the disease impacts positively on its prognosis.

Space agencies plan crewed missions to the Moon and Mars. However, microgravity-induced lumbopelvic deconditioning, characterized by an increased fat fraction (FF) due to reduced physical activity, poses a significant challenge to spine health. This study investigates the spatial distribution of FF in the lumbopelvic muscles to identify the most affected regions by deconditioning, utilizing a computer-vision model and a tile-based approach to assess FF changes. Twenty-four healthy individuals (8 F) were recruited, and automatic segmentation of the lumbopelvic muscles was applied before and after 59 days of head-down tilt bed rest (HDTBR + 59) and 13 days of reconditioning (R + 13). Axial Dixon sequence images were acquired from 3 T magnetic resonance imaging. FF in the lumbar multifidus (LM), lumbar erector spinae (LES), quadratus lumborum, psoas major, gluteus maximus (GMax), gluteus medius (GMed), and gluteus minimus (GMin) muscles from the upper margin of L1 vertebra to the inferior border of GMax muscle were automatically derived using a computer-vision model. Lumbar muscles were segmented into eight tiles (superficial and deep, lateral to medial), and gluteal muscles into regions (anterior/superior for GMed and GMin, superior/inferior for GMax). At HDTBR + 59, the deep centrolateral region at L5/S1 for LM (18.7 ± 15.7%, P < 0.001; d = 0.97) and the deep medial region at Upper L4 for LES (5.4 ± 5.9%, P < 0.001; d = 0.34) showed the largest increase in FF compared with baseline data collection. These regions did not recover at R + 13 (P < 0.05; d ≥ 0.25). These findings highlight the need to target deep fascicles of LM and LES in countermeasure strategies to mitigate microgravity-induced lumbopelvic deconditioning, optimizing spine health, and performance.NEW & NOTEWORTHY This study reveals novel insights into fat fraction changes in lumbopelvic muscles after 60 days of head-down bed rest and 13 days of reconditioning. Lipids increased in the deep regions of the lumbar multifidus (LM) and lumbar erector spinae (LES), particularly at lower vertebral levels, and persisted after reconditioning. These findings highlight the need to target deep fascicles of LM and LES in future countermeasures to mitigate microgravity-induced deconditioning and optimize spine health.

Hyperbaric oxygen (HBO) refers to pure oxygen with a pressure greater than 1 atmospheres absolute (ATA), and when the pressure is too high, it can cause convulsive attacks. Adenosine and dopamine have been shown to be closely associated with HBO-induced convulsion seizures, and their receptors exhibited a coexisting relationship of mutual antagonism on the membrane of nerve cells. We explored the influence of adenosine and dopamine interplay on the occurrence of oxygen convulsion. Rats were individually exposed to HBO of 6 ATA and treated with adenosine, dopamine, and their receptor modulators separately and jointly, with the latency of convulsion onset recorded. In addition, after administering adenosine to rats and exposing them to HBO for 30 min, the content of dopamine and its metabolites and the activity of enzymes related to their metabolism were measured. The results revealed that dopamine was effective in resisting convulsion (>60 min vs. 32.53 ± 5.31 min, P = 0.000), and low-dose adenosine partially counteracted its effect (>60 min vs. 28.18 ± 6.24 min, P = 0.002). The combined use of adenosine A1 and dopamine D1 receptor modulators significantly impacted the incidence of convulsion. The activation or inhibition of the A2A receptor had a particularly significant impact on convulsion, whereas modulating the D2 receptor did not affect their effects. The combination of A1 agonist and D2 agonist was highly effective in resisting convulsion (>60 min vs. 32.53 ± 5.31 min, P = 0.000). Exposure to HBO accelerated the metabolism of dopamine to its end products, which may be related to the enhanced activity of monoamine oxidase (MAO). Adenosine can inhibit MAO activity (0.0766 ± 0.0150 U/mg.prot vs. 0.1055 ± 0.0086 U/mg.prot, P = 0.004), maintaining a higher level of dopamine (1.820 ± 0.379 mg/g vs. 0.602 ± 0.087 mg/g, P = 0.000). The study demonstrated that dopamine plays a significant role in oxygen convulsion and adenosine can affect dopamine metabolism. The interaction between them can have a crucial impact on the occurrence of oxygen convulsion. The findings offer a novel perspective for further investigating the mechanism of oxygen convulsion and exploring effective preventive strategies.NEW & NOTEWORTHY The interaction between adenosine and dopamine is critically important in determining the incidence of oxygen convulsion. Simultaneous regulation of both adenosine and dopamine offers a superior approach to counteract oxygen convulsion, achieving a synergistic effect exceeding the sum of their individual impacts. These findings provide new directions and insights for future in-depth and systematic exploration of the pathogenesis of central nervous system oxygen toxicity.