Experimental Physiology最新文献

Our group previously showed that genetic or pharmacological inhibition of the cystine/glutamate antiporter, system x_c⁻, mitigates excitotoxicity after anoxia by increasing latency to anoxic depolarization, thus attenuating the ischaemic core. Hypoxia, however, which prevails in the ischaemic penumbra, is a condition where neurotransmission is altered, but excitotoxicity is not triggered. The present study employed mild hypoxia to further probe ischaemia-induced changes in neuronal responsiveness from wild-type and xCT KO (xCT^−/−) mice. Synaptic transmission was monitored in hippocampal slices from both genotypes before, during and after a hypoxic episode. Although wild-type and xCT^−/− slices showed equal suppression of synaptic transmission during hypoxia, mutant slices exhibited a persistent potentiation upon re-oxygenation, an effect we termed ‘post-hypoxic long-term potentiation (LTP)’. Blocking synaptic suppression during hypoxia by antagonizing adenosine A₁ receptors did not preclude post-hypoxic LTP. Further examination of the induction and expression mechanisms of this plasticity revealed that post-hypoxic LTP was driven by NMDA receptor activation, as well as increased calcium influx, with no change in paired-pulse facilitation. Hence, the observed phenomenon engaged similar mechanisms as classical LTP. This was a remarkable finding as theta-burst stimulation-induced LTP was equivalent between genotypes. Importantly, post-hypoxic LTP was generated in wild-type slices pretreated with system x_c⁻ inhibitor, S-4-carboxyphenylglycine, thereby confirming the antiporter's role in this phenomenon. Collectively, these data indicate that system x_c⁻ interference enables neuroplasticity in response to mild hypoxia, and, together with its regulation of cellular damage in the ischaemic core, suggest a role for the antiporter in post-ischaemic recovery of the penumbra.

Blood flow restriction (BFR) has been identified as a potential countermeasure to mitigate physiological deconditioning during spaceflight. Guidelines recommend that tourniquet pressure be prescribed relative to limb occlusion pressure (LOP); however, it is unclear whether body tilting or reduced gravity analogues influence LOP. We examined LOP at the leg and arm during supine bedrest and bodyweight suspension (BWS) at 6° head-down tilt (HDT), horizontal (0°), and 9.5° head-up tilt (HUT) positions. Twenty-seven adults (age, 26 ± 5 years; height, 1.75 ± 0.08 m; body mass, 73 ± 12 kg) completed all tilts during bedrest. A subgroup (n = 15) additionally completed the tilts during BWS. In each position, LOP was measured twice in the leg and arm using the Delfi Personalized Tourniquet System after 5 min of rest and again after a further 5 min. The LOP at the leg increased significantly from 6° HDT to 9.5° HUT in bedrest and BWS by 9-15 mmHg (Cohen's d = 0.7-1.0). Leg LOP was significantly higher during BWS at horizontal and 9.5° HUT postures relative to the same angles during bedrest by 8 mmHg (Cohen's d = 0.6). Arm LOP remained unchanged between body tilts and analogues. Intraclass correlation coefficients for LOP measurements taken after an initial and subsequent 5 min rest period in all conditions ranged between 0.91-0.95 (leg) and 0.83-0.96 (arm). It is advised that LOP be measured before the application of a vascular occlusion in the same body tilt/setting to which it is applied to minimize discrepancies between the actual and prescribed tourniquet pressure.

Female soccer players have been identified as presenting with low energy availability (LEA), though the prevalence of LEA may be overestimated given inaccuracies associated with self-reporting dietary intakes. Accordingly, we aimed to quantify total daily energy expenditure (TDEE) via the doubly labelled water (DLW) method, energy intake (EI) and energy availability (EA). Adolescent female soccer players (n = 45; 16 ± 1 years) completed a 9-10 day 'training camp' representing their national team. Absolute and relative TDEE was 2683 ± 324 and 60 ± 7 kcal kg^-1 fat free mass (FFM), respectively. Mean daily EI was lower (P < 0.01) when players self-reported using the remote food photography method (RFPM) (2047 ± 383 kcal day^-1) over a 3-day period versus DLW derived EI estimates accounting for body mass (BM) changes (2545 ± 518 kcal day^-1) over 7-8 days, representing a mean daily Δ of 499 ± 526 kcal day^-1 and 22% error when using the RFPM. Estimated EA was different (P < 0.01) between methods (DLW: 48 ± 14 kcal kg^-1 FFM, range: 22-82; RFPM: 37 ± 8 kcal kg^-1 FFM, range: 22-54), such that prevalence of LEA (<30 kcal kg^-1 FFM) was lower in DLW compared with RFPM (5% vs. 15%, respectively). Data demonstrate the potential to significantly underestimate EI when using self-report methods. This approach can therefore cause a misrepresentation and an over-prevalence of LEA, which is the underlying aetiology of 'relative energy deficiency in sport' (REDs). HIGHLIGHTS: What is the central question of this study? Do self-reported dietary intakes (via remote food photography method, RFPM) overestimate low energy availability (LEA) prevalence in female soccer players compared with energy intake evaluation from the doubly labelled water (DLW) method? What is the main finding and its importance? Estimated energy availability is greater with the DLW method compared with RFPM, such that the prevalence of LEA is greater when self-reporting dietary intakes. Accordingly, data demonstrate the potential to misrepresent the prevalence of LEA, an underlying factor in the aetiology of 'relative energy deficiency in sport' (REDs).

The use of acute carbon monoxide inhalation (COi) and hot water immersion (HWI) are of growing interest as interventions to stimulate erythropoietin (EPO) production. However, whether EPO production is further augmented when combining these stressors and whether there are sex differences in this response are poorly understood. Therefore, we measured circulating EPO concentration in response to acute COi and HWI independently and in combination and determined whether the responses were altered by sex. Participants completed three study visits—COi, HWI, and combined COi and HWI—separated by 1 week in a randomized, balanced, crossover design. Renal blood velocity was measured during all interventions, and carboxyhaemoglobin was measured during and after COi. Serum samples were analysed every hour for 6 h post-intervention for EPO concentration. HWI decreased renal blood velocity (46.2 cm/s to 36.2 cm/s) (P < 0.0001), and COi increased carboxyhaemoglobin (1.5%–12.8%) (P < 0.0001) without changing renal blood velocity (46.4–45.2 cm/s) (P = 0.4456). All three interventions increased peak EPO concentration from baseline (COi: 6.02–9.74 mIU/mL; HWI: 6.80–11.10 mIU/mL; COi + HWI: 6.71–10.91 mIU/mL) (P = 0.0048) and to the same extent (P = 0.3505). On average, females increased EPO while males did not in response to COi (females: 6.17 mIU/mL; males: 1.27 mIU/mL) (P = 0.0010), HWI (females: 6.47 mIU/mL; males: 2.14 mIU/mL) (P = 0.0104), and COi and HWI (females: 6.65 mIU/mL; males: 1.76 mIU/mL) (P = 0.0256). These data emphasize that combining these interventions does not augment EPO secretion and that these interventions may work better in females.

The objective was to assess if post-exercise ingestion of carbonated water in a hot environment ameliorates hypotension, enhances cerebral blood flow and heat loss responses, and positively modulates perceptions and mood states. Twelve healthy, habitually active young adults (five women) performed 60 min of cycling at 45% peak oxygen uptake in a hot climate (35°C). Subsequently, participants consumed 4°C carbonated or non-carbonated (control) water (150 and 100 mL for males and females regardless of drink type) at 20 and 40 min into post-exercise periods. Mean arterial pressure decreased post-exercise at 20 min only (P = 0.032) compared to the pre-exercise baseline. Both beverages transiently (∼1 min) increased mean arterial pressure and middle cerebral artery mean blood velocity (cerebral blood flow index) regardless of post-exercise periods (all P ≤ 0.015). Notably, carbonated water ingestion led to greater increases in mean arterial pressure (2.3 ± 2.8 mmHg vs. 6.6 ± 4.4 mmHg, P < 0.001) and middle cerebral artery mean blood velocity (1.6 ± 2.5 cm/s vs. 3.8 ± 4.1 cm/s, P = 0.046) at 20 min post-exercise period compared to non-carbonated water ingestion. Both beverages increased mouth exhilaration and reduced sleepiness regardless of post-exercise periods, but these responses were more pronounced with carbonated water ingestion at 40 min post-exercise (mouth exhilaration: 3.1 ± 1.4 vs. 4.7 ± 1.7, P = 0.001; sleepiness: −0.7 ± 0.91 vs. −1.9 ± 1.6, P = 0.014). Heat loss responses and other perceptions were similar between the two conditions throughout (all P ≥ 0.054). We show that carbonated water ingestion temporarily ameliorates hypotension and increases the cerebral blood flow index during the early post-exercise phase in a hot environment, whereas it enhances mouth exhilaration and reduces sleepiness during the late post-exercise phase.

Neck pain associated with helmet-wear is an occupational health problem often observed in helicopter pilots and aircrew. Whether aircrew helmet wearing is associated with physiological and biomechanical differences between sexes is currently unknown. This study investigated neuromuscular activation patterns during different helmet-wearing conditions. The helmet load was manipulated through a novel Helmet Balancing System (HBS) in healthy, non-pilot male and female participants (n = 10 each, age 19–45 years) in two phases. Phase A assessed the acute effects of helmet-wear on neck muscles activation during head movements. Phase B examined changes in muscle activity and cervical disc height after wearing a helmet for 45 min. In Phase A, muscle activity was similar between sexes in many movements, but it was higher in female participants when wearing a helmet than in males. The HBS reduced muscle activity in both sexes. In Phase B, female participants exhibited a greater level of muscular fatigue, and male participants’ cervical disc height was significantly decreased [5.7 (1.4) vs. 4.4 (1.5) mm, P < 0.001] after continuous wearing. Both sexes showed no significant change in muscle fatigue and disc height [male: 5.0 (1.3) vs. 5.2 (1.4) mm, P = 0.604] after applying HBS. These findings demonstrate sex-specific physiological and biomechanical responses to wearing a helmet. They may indicate different postural and motor control strategies, associated with different neck pain aetiologies in male and female aircrew, the knowledge of which is important to reduce or prevent musculoskeletal injuries associated with helmet wearing.