Journal of applied physiology最新文献

This study investigated the effect of running in a hot environment compared with a temperate environment on exogenous carbohydrate oxidation, while maintaining a state of euhydration. Ten trained runners (24 ± 6 yr; 72.7 ± 8.3 kg; V̇o_2peak: 63 ± 6 mL/kg/min) completed two trials [100 min of steady state running at ∼65% V̇o_2peak in either a temperate (19°C; TEMP) or a hot environment (34°C; HOT)]. Water was provided every 20 min to replace ∼90% of body mass losses (TEMP: 0.8 ± 0.2 L; HOT: 1.7 ± 0.4 L). In each trial, participants consumed 60 g/h (bolus every 20 min) of a 35% dextrose solution enriched with [U-¹³C] glucose (145 ± 2 δ‰ vs. PDB). Expired breath (analyzed for ¹³C:¹²C) and blood samples were collected every 20 min during exercise. Average (40-100 min) and peak exogenous carbohydrate oxidation rates were 20% (HOT: 0.43 ± 0.09 vs. TEMP: 0.54 ± 0.12 g/min; P = 0.006) and 18% (HOT: 0.67 ± 0.10 vs. TEMP: 0.81 ± 0.11 g/min; P = 0.002) lower in HOT than in TEMP, respectively. Total carbohydrate oxidation (P = 0.111) was not significantly different between trials, resulting in a greater contribution from endogenous sources in HOT versus TEMP (2.10 ± 0.35 vs. 1.86 ± 0.30 g/min; P = 0.020). Gastrointestinal temperature and heart rate (P < 0.001) were greater in HOT. Even with adequate hydration, running in a hot environment reduced exogenous carbohydrate.NEW & NOTEWORTHY This study showed that exogenous carbohydrate oxidation is reduced by ∼20% during running in the heat, even while controlling fluid intake to maintain euhydration, highlighting that heat stress alone impairs exogenous carbohydrate use. These findings suggest a lower exogenous carbohydrate oxidation and a greater reliance on endogenous stores when exercising in the heat, independently of the effects of dehydration.

Surfactant protein B (SP-B) is essential for surface tension reducing function of pulmonary surfactant and alveolar unfolding processes during inspiration. SP-B is reduced early in acute lung injury. Hence, we hypothesize that 1) reduced SP-B expression increases susceptibility to ventilation-induced lung injury (VILI), and 2) deep inflations (DI) are protective against VILI. Conditional SP-B knockout mice were randomized into OFF (reduced SP-B) and ON groups (normal SP-B) and subjected to mechanical ventilation at zero end-expiratory pressure. Over 4 h of ventilation, either 4 or 16 DI were administered. Lung mechanics were recorded, and pulmonary structure was quantified by design-based stereology. Inflammatory cells and bulk RNA sequencing were measured in bronchoalveolar lavage (BAL) and tissue, respectively. No differences in inflammatory cells in BAL were detected between ON and OFF groups. During ventilation, alveolar derecruitment-related increase in elastance was most pronounced in OFF-4DI but reversible by DI so that lung mechanics did not worsen. Finally, volumes of the alveolar liquid lining layer and the intracellular surfactant were largest, whereas the surface area of the apical plasma membrane of type II pneumocytes was smallest in OFF-4DI, suggesting impaired surfactant secretion. A higher frequency of DI prevented these abnormalities. Electron microscopy revealed disorganized tight junctions between alveolar epithelial cells in OFF-4DI, which was linked with decreased expression of genes relevant to the apical junctional complex. Reduced SP-B resulted in a progressive increase in surface tension and a disturbed fluid balance without triggering definite VILI. Maintenance of residual surfactant function is highly dependent on DI in conditions of reduced SP-B levels.NEW & NOTEWORTHY Surfactant protein B (SP-B) is critical for efficient surfactant function in the lung. Reduced SP-B levels occur at an early stage of acute lung injury and impair alveolar unfolding. In this study, we demonstrate that mechanical ventilation of lungs with reduced SP-B levels does not trigger ventilation-induced lung injury but results in disbalance of alveolar fluid volume and increase in surface tension due to failure of surfactant maintenance. Deep inflations prevent these ventilation-induced effects.

Continuous bronchoscopy during exercise (CBE) allows assessment of large airway dynamics during ambulatory exercise; however, it is not yet clear whether the bronchoscope alters cardiopulmonary and ventilatory parameters. Accordingly, we aimed to evaluate the impact of bronchoscopy on parameters measured during cardiopulmonary exercise testing (CPET). Ten healthy participants (33% female) completed two randomized CPETs to exhaustion on a treadmill using an incremental protocol, with and without a bronchoscopy setup (5.0 mm bronchoscope inserted via a modified facemask). Breath-by-breath gas exchange and ventilatory data, including oxygen uptake (V̇o₂) and carbon dioxide output (V̇co₂), minute ventilation (V̇e), and respiratory exchange ratio (RER), were assessed between CPET conditions. Nine participants completed both CPET assessments to volitional exhaustion; one participant terminated the CPET-B test early due to scope-associated throat discomfort. Exercise duration was shorter (mean difference -52 s, P = 0.02) and heart rate (HR) values were lower (-7 beats/min, P = 0.001) in CPET-B compared with CPET. Peak exercise V̇e (median difference -13 L/min, P = 0.004) was lower during CPET-B, yet breathing frequency and tidal volume values did not differ between CPET conditions. No differences were found in peak exercise V̇o₂, V̇co₂, and RER values, nor parameters measured at an equivalent absolute duration (isotime). In healthy adults, performing CPET with bronchoscopy does not alter peak exercise oxygen uptake or carbon dioxide output but results in a lower overall minute ventilation, despite no differences in breathing frequency or tidal volume. It is likely these discrepancies arise due to slightly lower exercise duration in the CPET with bronchoscopy trials.NEW & NOTEWORTHY This study demonstrates that cardiopulmonary exercise testing with concurrent continuous bronchoscopy provides measurement of pulmonary gas exchange, ventilation, and visualization of large airway movement during vigorous exercise. Although oxygen uptake and carbon dioxide output were not altered during exercise with bronchoscopy, peak exercise ventilation and markers of effort were lower in these trials.

Physiological-based cord clamping (PBCC) involves aeration of the newborn lung before umbilical cord clamping. As the infant can continue to receive oxygen from the mother during PBCC, the dynamics of transplacental oxygen transfer are unknown, particularly following the onset of pulmonary gas exchange. We have investigated the effects of pulmonary ventilation with supplemental oxygen during PBCC on transplacental oxygen transfer in preterm lambs. Pregnant ewes and their fetuses (n = 8; 127 days of gestation; term 147 days) were instrumented with catheters and flow probes under general anesthesia to measure oxygen transfer across the placenta. Before umbilical cord clamping, lambs were intubated and mechanically ventilated with a fraction of inspired oxygen ([Formula: see text]) that increased every 10 min, from 0.21 to 0.5 and then 1.0. Data were analyzed using a mixed-effects analysis with a Holm-Šídák post hoc test. During PBCC, ventilation of lambs significantly decreased oxygen uptake across the placenta from 317.7 ± 15.0 to 166.5 ± 26.9 (P = 0.0028) and to 73.6 ± 34.3 mL/min/kg (P = 0.0009) at [Formula: see text] levels of 0.21 and 0.5, respectively. Ventilation with a [Formula: see text] of 1.0 reversed oxygen uptake across the placenta (-37.2 ± 14.0 mL/min/kg; P < 0.0001), resulting in oxygen transfer from lamb to ewe. In contrast, oxygen delivery to the lamb, via the umbilical vein, remained unchanged with increasing [Formula: see text] (P = 0.4485). During PBCC, pulmonary oxygen uptake by the newborn reduces oxygen uptake across the placenta, and when oxygen levels are in excess, the mother acts as an "oxygen sink," reducing the risk of hyperoxemia of the newborn.NEW & NOTEWORTHY This study investigated transplacental oxygen transfer during physiological-based cord clamping in preterm lambs. During physiological-based cord clamping, ventilating newborn lambs reduced oxygen uptake across the placenta and that ventilation with high oxygen (1.0 [Formula: see text]) reversed the oxygen gradient, resulting in newborn to mother oxygen transfer. Our findings indicate that the mother can act as an "oxygen sink" that protects the newborn from excess oxygen during physiological-based cord clamping.

Pregnancy at advanced maternal age (AMA, ≥35 yr) is increasingly common in developed countries. Delayed pregnancy may elevate the risk of adverse pregnancy outcomes, such as hypertensive disorders, potentially due to altered arterial structure and function or insufficient vascular adaptations during pregnancy. Therefore, this study aimed to characterize differences in maternal vascular and autonomic function across pregnancy and postpartum in healthy pregnant women of AMA compared with younger pregnant women by retrospectively analyzing data from 57 younger pregnant women (21-30 yr; 27 ± 3 yr) and 22 pregnant women of AMA (≥35 yr; 36 ± 1 yr). Arterial stiffness, remodeling, and endothelial function were assessed using carotid-femoral and carotid-brachial pulse wave velocity (cfPWV and cbPWV), carotid β-stiffness, carotid intima-media thickness (IMT), and brachial artery flow-mediated dilation (FMD) in the first, second, and third trimesters and postpartum (4-14 wk). Beat-to-beat blood pressure variability (BPV), cardiovagal baroreflex sensitivity (BRS), and heart rate variability (HRV) were also assessed. The AMA group exhibited higher cfPWV, cbPWV, β-stiffness, and IMT compared with the younger group during pregnancy (P ≤ 0.03), with cfPWV and cbPWV remaining higher in the postpartum period (P ≤ 0.01). The AMA group also had higher systolic BPV, lower BRS, and lower HRV compared with the younger group during pregnancy (P ≤ 0.04), with consistently lower BRS postpartum (P < 0.01). Blood pressure and FMD did not differ between groups throughout pregnancy and postpartum (P ≥ 0.27). These findings suggest that women of AMA have higher central arterial stiffness and altered autonomic function throughout pregnancy, which may contribute in part to increased risk of pregnancy complications.NEW & NOTEWORTHY This study assessed the impact of advanced maternal age (AMA) on vascular and autonomic function across all three trimesters. Compared with younger pregnant women, women of AMA exhibited higher arterial stiffness and greater carotid intima-media thickness, and impaired autonomic regulation throughout pregnancy, despite no significant difference in endothelial function. These observed differences may represent early subclinical changes in AMA women, which may bring them closer to a physiological threshold where complications may occur.

We investigated the effects of high altitude (HA) on postactivation potentiation (PAP) of the quadriceps muscles in 18 healthy adults (10 females). At sea level (SL; 300 m), and again after 1-2 and 11-13 days of residing at 3,800 m (HA1 and HA2, respectively), single electrical stimuli were delivered to the femoral nerve to quantify parameters of the resting twitch and the maximal compound muscle action potential (M_max), before and 2-300 s after a 10-s maximal voluntary contraction (i.e., the conditioning contraction). PAP was quantified by comparing peak force of twitches evoked after the conditioning contraction to the control twitch before it. On all days of testing, twitches were potentiated from 2 to 180 s (P ≤ 0.003). At SL, PAP was greater for males than females 2 and 15 s after the conditioning contraction (by 29.6% and 17.5%, respectively; P ≤ 0.005). For males, PAP was ∼19% lower at HA1 than SL (P ≤ 0.001), a deficit that persisted at HA2 (P = 0.001). Conversely, the magnitude of PAP did not change with HA for females (P ≥ 0.808). Finally, the M_max amplitude was greater at HA1 and HA2 compared with SL (P ≤ 0.039), with no difference between the sexes. From our findings, it can be suggested that mechanisms related to PAP of the quadriceps muscles are affected by HA (3,800 m) in healthy adult males but not females.NEW & NOTEWORTHY The capacity of the quadriceps muscles to become potentiated following a 10-s isometric maximal voluntary contraction became attenuated for males following 1-2 days of residing at 3,800 m above sea level and did not recover by 11-13 days. Conversely, for females, the magnitude of postactivation potentiation was unaffected by high altitude. Peak-to-peak amplitude of the maximal compound muscle action potential was augmented by high altitude for both males and females.

Phrenic long-term facilitation (pLTF) is a form of respiratory motor plasticity, expressed as a lasting increase in phrenic nerve activity following acute intermittent hypoxia (AIH). Whereas AIH also elicits ventilatory LTF (vLTF) in unanesthetized rats, concurrent hypercapnia (elevated background or episodic hypercapnia) is required for vLTF in humans. One major difference between rodent and human studies is the diurnal phase (nocturnal rats vs. diurnal humans). Diurnal phase regulates pLTF magnitude and mechanism; 15, 1-min hypoxic episodes elicit more robust pLTF in the rest (∼130%) versus active phase (∼30%) in rats. Thus, we assessed differences in pLTF elicited by acute intermittent hypercapnic-hypoxia (AIHH) versus AIH in mid-rest versus mid-active phase rats. In anesthetized, paralyzed, vagotomized, and ventilated male Sprague-Dawley rats (n = 7 per group), pLTF was assessed following moderate AIH (arterial Po₂ range 35-49 mmHg; 15, 1-min episodes) or AIHH (arterial Pco₂ range 46-50 mmHg) in the mid-rest (noon) and mid-active phases (midnight). In contrast to expectations, mid-rest phase pLTF 90-min post-AIHH (64 ± 45%) was less than that elicited by AIH (132 ± 93%; P < 0.001). As reported previously, AIH-induced pLTF was lower in mid-active (46 ± 47%; P = 0.050) versus mid-rest rats; however, AIHH-induced pLTF was not significantly different in mid-rest versus mid-active phase rats (37 ± 28%; P = 0.20), and there was no longer a significant difference between AIH versus AIHH in the active phase (P = 0.650). Thus, adding hypercapnia to an AIH protocol suppresses pLTF in anesthetized rats exclusively in the mid-rest, but not mid-active phase of the diurnal cycle. Possible mechanisms for hypercapnia and time-of-day effects are discussed.NEW & NOTEWORTHY Diurnal variations in acute intermittent hypoxia (AIH)-induced respiratory plasticity were evident in young, male rats, with robust phrenic long-term facilitation (pLTF) during their mid-rest phase and reduced pLTF during the mid-active phase. Surprisingly, adding hypercapnia (AIHH) suppressed pLTF during the mid-rest phase, with minimal impact during the mid-active phase. These results contrast with diurnal humans, where hypercapnia is necessary for ventilatory LTF, revealing species and time-of-day-dependent mechanisms that shape AIH efficacy.