Experimental Physiology最新文献

Established methods of measuring functional residual capacity (FRC) involve sophisticated equipment and elaborate procedures. Here we present a new method based on CO₂ rebreathing that has a simple fast procedure and only requires end-tidal CO₂ monitoring. Ten healthy subjects with diverse anthropometric and respiratory parameters were studied in the sitting position. Reference FRC (RefFRC) and tidal volume (TV) were measured with a Cosmed Quark PFT/DLCO unit using the single-breath methane dilution technique in combination with spirometry. Rebreathing through an external dead space of precisely known volume and recording the rising end-tidal CO₂ value of the first two breaths allows the determination of effective lung volume (ELV) and the calculation of FRC. Two sets of measurements were made on each subject 15 min apart. Bland-Altman analysis of a comparison between FRC and RefFRC showed a mean bias of 0.04 L, with limits of agreement (LoA, 95% CI) of -1.24 to +1.32 L and a percentage error (PE) of 0.54. When the mean value of two observations from a subject (meanFRC) was compared to RefFRC we obtained a mean bias of -0.08 L, LoA (95% CI) of -0.88 to +0.72 L and PE of 0.23. The FRC data obtained demonstrate good absolute accuracy. An average of repeated measurements improves precision indicating that a criterion for exchangeability with the reference method can be met. The simplicity of the equipment and the procedure could make this method attractive in the pre-operative and the post-operative settings, as well as in out-of-hospital applications.

Jamal, L., Michelant, L., Delanaud, S., Hugueville, L., Mazet, P., Lévêque, P., Baz, T., Bach, V., & Selmaoui, B. (2024). Autonomous nervous system responses to environmental-level exposure to 5G's first deployed band (3.5 GHz) in healthy human volunteers. Experimental Physiology, 109(12), 2122–2133. https://doi.org/10.1113/EP092083

The original article should have included a section titled ‘Funding information’, with the following text:

‘This project has received funding from the European Union's Horizon Europe research and innovation programme under grant agreement No 101057262. Views and opinions expressed are however those of the authors only and do not necessarily reflect those of the European Union or the Health and Digital Executive Agency. Neither the European Union nor the granting authority can be held responsible for them.’

We apologize for this error.

The aim of this study was to determine whether inflammatory and vascular responses to passive heating differ between the early follicular phase (EFP) and the mid-luteal phase (MLP) of the menstrual cycle. Ten healthy, naturally menstruating females (26 ± 3 years of age; body mass index 21.4 ± 1.9 kg/m²) were assessed during EFP and MLP. Participants underwent 60 min whole-body passive heat exposure (71°C ± 2°C, dry heat) in both phases. Outcomes included body temperature, interleukin-6, interleukin-1 receptor antagonist and plasma nitrite concentrations, cutaneous vascular conductance, blood pressure, arterial stiffness and perceptual responses. Rectal temperature and mean skin temperature increased during heat exposure but did not differ between EFP and MLP. Likewise, heat exposure increased interleukin-6, interleukin-1 receptor antagonist and plasma nitrite concentrations, with no differences between menstrual cycle phases. However, brachial (EFP, 75 ± 4 mmHg vs MLP, 72 ± 5 mmHg; p = 0.040) and central (EFP, 75 ± 4 mmHg vs MLP, 72 ± 5 mmHg; p = 0.042) mean arterial pressures were higher in EFP than in MLP at 40 min of heat exposure. Additionally, arterial stiffness declined more in EFP (-13% ± 7%) than in MLP (-5% ± 6%; p = 0.019) from the end of heat exposure to 30 min into recovery. Perceptual responses, including thermal sensation and comfort, were similar between menstrual cycle phases, but skin wetness perception was heightened during EFP. In conclusion, the inflammatory and plasma nitrite responses to passive heating did not differ between EFP and MLP. However, some vascular function and perception parameters were affected by the menstrual cycle phase.

The global prevalence of obesity and related metabolic disorders has spurred interdisciplinary research to develop new intervention strategies. Current research is increasingly focusing on the exercise-induced browning of white adipose tissue and the mechanisms by which it improves energy metabolism. Creatine, as the primary carrier of high-energy phosphate bonds within cells, is gaining attention for its role in the metabolic reprogramming of adipose tissue. This review aims to clarify the synergistic regulatory mechanisms between exercise and creatine metabolism, and introduces an innovative 'skeletal muscle-adipose creatine metabolic axis' model. Exercise may upregulate the expression of the creatine transporter in skeletal muscle by activating the AMP-activated protein kinase/peroxisome proliferator-activated receptor γ coactivator 1-α signalling pathway, enhancing phosphocreatine shuttle kinetics, and thereby increasing energy metabolism efficiency. Concurrently, exercise-induced exosomes or miRNAs from skeletal muscle may regulate the futile creatine cycle in adipose tissue and activate non-uncoupling protein 1-dependent thermogenic pathways, thus alleviating obesity conditions. This model not only reveals the multi-organ cross-talk mechanism mediated by exercise in lipid metabolism regulation but also provides a theoretical basis for creatine metabolism-targeted obesity interventions.

Central blood volume (CBV) reduction challenges circulatory and respiratory homeostasis, particularly during the initial compensatory phase (0-2 min), when rapid physiological adaptations occur. In this study, we examined dynamic cardiorespiratory responses to CBV reduction using lower-body negative pressure (LBNP) in 11 healthy young males. Participants completed three standardized 2 min LBNP trials at -45 mmHg, with respiratory variables assessed via flow measurement and breath-by-breath gas analysis, while cardiovascular parameters and cerebral blood flow were monitored using ECG, blood pressure and transcranial Doppler ultrasonography. During LBNP exposure, thoracic admittance, an indicator of CBV reduction, decreased by 13.4% (p < 0.001), indicating significant CBV reduction. Following rigorous statistical correction for multiple comparisons, time-course analysis revealed that mean blood pressure decreased temporarily during the initial phase (0-30 s), whereas heart rate increased progressively (16.4%, p < 0.001). End-tidal $P_{C{O}_2}$ showed a consistent reduction (5.9%, p < 0.001), whereas minute ventilation and middle cerebral artery mean blood velocity showed no significant changes after statistical correction (-9.3% and -5.0%, respectively, p > 0.05). Exploratory correlation analysis revealed a significant negative correlation between mean blood pressure and tidal volume during the initial phase only (r = -0.78, p = 0.004). Cross-correlation analysis suggested temporal patterns between respiratory and cerebrovascular responses, with respiratory changes preceding cerebrovascular adjustments by 10-20 s. These findings, along with individual variability, suggest rapid cardiorespiratory and cerebrovascular interactions during orthostatic stress, demonstrating dynamic cardiovascular and respiratory responses with distinct temporal patterns that provide insights into physiological mechanisms maintaining homeostasis during gravitational stress.

The pre-hearing mouse cochlea undergoes critical periods of spontaneous Ca²⁺-dependent activity that spreads across non-sensory supporting cells and inner hair cells (IHCs). These signals have been shown to regulate not only the refinement of neural circuits along the auditory pathway towards functional maturity, but also the maturation of the hair cells into sensory receptors. Although the origin and interplay of these Ca²⁺ signals during cochlear development have recently been investigated in live mice, the impact of anaesthesia on in vivo functional measurements was not explored. Here, we investigate the effects of different anaesthetic regimes (ketamine and xylazine; 2.5% isoflurane; and 1.0%-1.5% isoflurane with the sedative acepromazine) that provided an effective unconsciousness to perform the surgery and Ca²⁺-imaging recordings from the intact cochlea of live mice. The IHCs, supporting cells and spiral ganglion neuron terminals onto the IHCs showed spontaneous Ca²⁺-dependent activity under all anaesthetic regimes, with a few significant differences observed between conditions. Calcium waves from supporting cells synchronized the activity of IHCs. Moreover, we found that the endocochlear potential, which is crucial for cochlear function, was unaffected by the different anaesthetics. However, low concentrations of isoflurane produced the most stable recordings of vital physiological signs in mice, including heart rate and breathing rate. Although all anaesthetic regimes tested appeared to be suitable for performing Ca²⁺ imaging from the cochlea of pre-hearing live mice, a low concentration of isoflurane (1.0%-1.5%), combined with the pre-anaesthetic sedative acepromazine and oxygenation, represents the most suitable approach to maintain a stable and long-lasting depth of anaesthesia.

Exercise limitation is a cardinal feature of fibrotic interstitial lung disease arising from pulmonary gas exchange, respiratory mechanical and cardio-circulatory abnormalities. More recently, it has been recognized that impairment in locomotor muscle function (e.g., reduced muscle mass/strength or heightened fatigability) might also play a relevant contributory role. Exercise training as part of pulmonary rehabilitation is the most effective intervention to improve exercise tolerance, dyspnoea and quality of life in patients with fibrotic interstitial lung disease. Given that exercise training has modest effects on exertional ventilation, breathing pattern and respiratory muscle performance, improvement in locomotor muscle function is a key target for pulmonary rehabilitation in these patients. In the present narrative review, we initially discuss whether the locomotor muscles of patients might be exposed to negative risk factors. After offering corroboratory evidence on this matter (e.g., oxidative stress, inflammation, hypoxia, physical inactivity and medications), we outline their effects on skeletal muscle mass and functional properties. We finish by addressing the potentially beneficial effects of rehabilitative exercise training on these muscle-centred outcomes, providing perspectives to facilitate or optimize the muscle benefits derived from this intervention. This narrative review, therefore, provides an up-to-date outline of the rationale for rehabilitative approaches focusing on the locomotor muscles in this patient population.

Dynamic resistance exercise (RE) produces sinusoidal fluctuations in blood pressure that are mirrored by middle cerebral artery blood velocity (MCAv). However, whether lower- or upper-body RE elicits a differential cerebrovascular response has not yet been examined. We investigated the cerebrovascular response to lower-body RE versus upper-body RE in 15 healthy untrained individuals (12 females and 3 males; mean ± SD; age 25 ± 6 years, height 179 ± 10 cm, weight 71 ± 15 kg and body mass index 24 ± 6 kg/m²). Participants completed four sets of 10 paced repetitions (15 repetitions/min) of unilateral leg-extension exercise and unilateral bicep-curl exercise at 60% of predicted one-repetition maximum (leg extension 30 ± 9 kg and bicep curl 7 ± 3 kg). Beat-to-beat blood pressure, bilateral MCAv and partial pressure of end-tidal carbon dioxide were measured throughout. Within-exercise mean arterial blood pressure (MAP) and mean MCAv were averaged across the set. Additionally, zenith, nadir and zenith-to-nadir difference in MAP and mean MCAv for each repetition were averaged across each set. Baseline measures preceding each set were not different for all dependent variables, with no significant interaction differences observed (all p > 0.161). The mean MCAv within exercise decreased across sets (set effect p < 0.001), but MAP did not (p = 0.071). No interaction effects were observed for any dependent variables (all p > 0.06), However, there was a zenith-to-nadir difference in mean MCAv (p = 0.008), although post hoc tests revealed no significant difference between exercises (all p > 0.078). There were no differences in the cerebrovascular and cardiovascular responses to lower- and upper-body RE, with similar sinusoidal fluctuations in MAP and MCAv_mean present during both exercises.