Experimental Physiology最新文献

Exercise and heat stress have been reported to independently provide benefits to brain health. We tested the hypothesis that 8 weeks of post-exercise local heating, passive local heating only, or exercise training only improves cognitive performance compared to a control group. Sixty young, healthy participants (n = 30 female, age: 23 [3] years) were randomised into one of four groups: control (CON), aerobic exercise (EX), local heating (HEAT), or combined heat and exercise (HEATEX). Participants completed supervised sessions three times per week for 8 weeks. Exercise sessions were completed at 70-75% of maximum heart rate on a cycle ergometer, and local heating sessions involved hot water immersion (42°C) of the feet (both 45 min duration). The HEATEX group performed both the EX and HEAT components sequentially in the same session (90 min total duration). Cognitive performance was measured at baseline and at the end of the 8-week intervention using the digit symbol substitution task (DSST) and the Stroop test. There was a main effect of time (P < 0.001) where DSST performance improved; however, there was no group effect (P = 0.089) or time by group interaction (P = 0.119). There was no effect of the interventions on Stroop cost (baseline: 90 [SD: 70] ms; post-intervention: 84 [SD: 70] ms; time by condition interaction P = 0.205). Similarly, there were no effects of the interventions on circulating plasma concentrations of brain-derived neurotrophic factor (interaction P = 0.189). Eight weeks of exercise training and/or local heating is not sufficient to improve cognitive performance in young, moderately fit individuals.

Cerebral blood flow (CBF) is essential for sustaining neuronal metabolism and cognitive performance; however, the precise relationship between perfusion and cognition remains unclear. Although ageing and disease are associated with progressive declines in CBF and cognitive impairment, the acute effects of altered CBF under environmental stressors have not been elucidated fully. The influence of environmental stress on cognitive function is likely to depend on the degree of stress (e.g., its intensity and duration). Therefore, it is necessary to carry out a systematic review of a large number of studies, and objective evidence is required to build a comprehensive dataset. This review summarizes research examining the effects of mild to moderate passive heat stress (an increase in core temperature of ∼1.0°C-1.5°C) and acute hypoxia on cognitive processing, as evaluated using electroencephalographic event-related potentials (EEG-ERPs), with the aim of facilitating future cross-experimental comparisons. During mild or greater hyperthermia, CBF decreases owing to blood flow redistribution and hypocapnia-induced by hyperventilation, whereas during hypoxia, CBF can either increase or decrease depending on the conditions (e.g., exposure time or intensity). To standardize comparisons, this review focuses on acute hypoxic exposures, during which CBF tends to decrease. Although it is undeniable that the content summarized here might be somewhat selective, it is hoped that this foundation will contribute to the future development of constructive and objective evaluations. Current evidence indicates that acute fluctuations in CBF are unlikely to predict cognitive outcomes. Rather, both heat and hypoxic stress appear to impair neural activity through mechanisms beyond perfusion alone.

We investigated the acute metabolic effects of two velocity-based resistance training (RT) protocols, differing in intra-set velocity loss (VL) thresholds, on postprandial substrate oxidation and glycaemic responses following a 75 g oral glucose tolerance test in individuals with excess body weight. A single-group, randomized, cross-over design was used, in which each participant completed three experimental conditions in random order: (1) control (rest); (2) RT with 20% velocity loss (VL20); and (3) RT with 40% velocity loss (VL40). Twenty-four participants (50% female; median body mass index 30.2 kg m^-2, interquartile range 27.9-34.1 kg m^-2) were included in the final analysis. Each RT session consisted of bilateral leg-press exercises at 55%-65% of one-repetition maximum performed in four sets with 3 min rest intervals, while monitoring repetition velocity. Baseline measurements were performed in the fasted state (1012 h) with participants in the supine position for 30 min, after the oral glucose load at 60 min, and during the experimental conditions at 120, 180, and 240 min. Primary outcomes were respiratory quotient, oxygen uptake, carbon dioxide output, resting energy expenditure and substrate oxidation rates. Secondary outcomes included blood glucose, lactate, heart rate, power output and repetition volume. VL40 elicited greater cardiovascular and metabolic stress, evidenced by elevated heart rate and lactate levels (p < 0.0001). Both RT protocols decreased postprandial respiratory quotient compared with control conditions, with VL40 producing a larger shift towards fat oxidation (time × conditions interaction p < 0.0001). The glucose area under the curve was significantly lower in VL40 than in VL20 or control conditions (p < 0.0001). These findings suggest that velocity-based RT acutely improves postprandial metabolism, with higher VL thresholds conferring superior fat oxidation and glycaemic regulation.

We evaluated the feasibility and efficacy of a 2-week training programme comprising resistance vibration exercise (RVE) without and with artificial gravity (AG). Participants (n = 24) were divided into three groups: (i) URVE: upright loaded squat exercise; (ii) HRVE: horizontal loaded squat exercise; and (iii) AGRVE: loaded squat exercise conducted on a short-arm human centrifuge. All participants followed the same protocol and were exposed to the same ground reaction force, whilst performing exercise comprising bilateral squats, triple extension squats and single/bilateral calf raises. Before and after the 2-week training period, we measured thigh and calf muscle strength with isokinetic dynamometry, muscular power with a jump test, volume with functional muscle magnetic resonance imaging, and body composition with dual-energy X-ray absorptiometry. All groups showed significant improvements in eight-repetition maximum squat strength (P < 0.0001, G > 0.80), whilst only the AGRVE group demonstrated a small effect in jump height (G = 0.26). The AGRVE group significantly increased knee extension and flexion maximum voluntary contraction (MVC), with no comparable changes in the HRVE or URVE groups. The AGRVE group increased total thigh muscle volume (P = 0.03), with notable hypertrophy in the vastus medialis, semitendinosus, and vastus intermedius muscles. These findings demonstrate that AGRVE is significantly superior to HRVE and URVE in enhancing knee MVC and thigh muscle volume, thus indicating that artificial gravity improves the outcome of resistance vibration exercise in ambulatory participants.

Due to a lack of technical capacity to directly visualise and quantify microvessels in the skin, little is known regarding regional and/or sex differences. We compared diameter, velocity, flow and density at four regional sites using a novel optical coherence tomography (OCT) approach. OCT and laser Doppler flowmetry (LDF) were performed on the back, forearm, foot and thigh in 30 healthy adults (15♂ 15♀; 31 ± 6years) at rest (33°C) and after 30 min of local heating (LH; 44°C). At baseline, larger diameter, speed, flow, density and LDF flux were recorded on the back than other sites (P < 0.017). In response to LH, the smallest changes in OCT-derived diameter were observed on the back (Δ12 ± 6 µm) and foot (Δ13 ± 6 µm vs. forearm 17 ± 5 µm; thigh Δ18 ± 5 µm, all P < 0.005 vs. foot, back). The back exhibited the smallest change in density (back Δ19 ± 7%, forearm Δ24 ± 5%, thigh Δ26 ± 6%, foot Δ26 ± 8%, P < 0.02 vs. back) whilst the foot exhibited the smallest changes in speed (foot Δ27 ± 14, back Δ58 ± 22, forearm Δ47 ± 17, thigh Δ48 ± 11 µm/s, P < 0.001 vs. foot) and flow (Δ135 ± 60, back Δ204 ± 76, forearm Δ212 ± 60, thigh Δ247 ± 51 µL/s, P < 0.001 vs. foot). When sites were grouped, males had larger baseline diameters (♂ 45 ± 3 vs. ♀ 42 ± 3 µm, P = 0.019) and flows (♂ 109 ± 20 vs. ♀ 93 ± 17 µL/s, P = 0.025) whilst females exhibited larger LH-induced changes in speed in the thigh (♀ Δ53 ± 10 vs. ♂ Δ43 ± 10 µm/s, P = 0.014) and density in the forearm (♀ Δ26 ± 4 vs. ♂ Δ21% ± 6%, P = 0.006). Regional differences exist in OCT-derived cutaneous microvascular diameter, speed, flow and density at baseline and in response to LH. Males showed larger cutaneous diameter and flow at baseline, while females exhibited larger changes in the speed and density outcomes in response to local heating.

Aldehyde dehydrogenase 2 (ALDH2) is a mitochondrial enzyme that plays an important role in aldehyde detoxification. A large percentage (30-50%) of the East Asian population carry a single point mutation in the ALDH2 gene (ALDH2*2 variant) that causes a severe reduction or lack of ALDH2 enzyme activity, and leads to disrupted cellular homeostasis due to the accumulation of toxic reactive aldehydes. The ALDH2*2 variant has been associated with several degenerative diseases, with evidence suggesting a link to cardiovascular disease, potentially mediated by endothelial dysfunction. This, however, remains to be confirmed. We aimed to investigate whether the ALDH2*2 variant is associated with impaired endothelial function in young, healthy East Asians. Twenty-two participants were genotyped and divided into non-carriers (ALDH2*1/*1; n = 12; 7 females and 5 males; age = 23 ± 3 years; height = 167.4 ± 8.7 cm; body mass = 60.1 ± 9.0 kg) and carriers (ALDH2*1/*2 and ALDH2*2/*2; n = 10; 8 females and 2 males; age = 24 ± 5 years; height = 162.6 ± 10.1 cm; body mass = 62.1 ± 9.7 kg) of the ALDH2*2 allele. Endothelial function was assessed via flow-mediated dilation (FMD) following current guidelines. Carriers displayed lower FMD, either absolute or relative, which was not statistically significant but approached significance (unpaired t-test) (FMD%: non-carriers = 10.2 ± 1.9% vs. carriers = 8.1% ± 3.1%, P = 0.079, effect size: Cohen's d = 0.82; FMD_abs: non-carriers = 0.32 ± 0.06 mm vs. carriers = 0.26 ± 0.09 mm, P = 0.082, effect size: Cohen's d = 0.78). In conclusion, our data seem to suggest that the ALDH2*2 variant impairs endothelial function even in young and healthy individuals without the presence of other stressor agents. Future studies with larger sample size are necessary to confirm our findings.

The endothelium plays a pivotal role in regulating cerebrovascular blood flow, and its dysfunction increases the risk of cerebrovascular disease. Endothelial shear stress, a primary mechanical stimulus for endothelial nitric oxide production, is a key modulator of vascular adaptation. In recent years, transient hypercapnia-induced flow-mediated dilation of the internal carotid artery (ICA-FMD) has emerged as a valuable in vivo approach for assessing cerebrovascular endothelial function in humans. This review first synthesizes methodological advances in ICA-FMD assessment, emphasizing the importance of transient carbon dioxide (CO₂) inhalation, normalizing ICA-FMD to the shear stress, and consideration of unique ICA haemodynamics. Second, it consolidates mechanistic insights and conditions for improving ICA-FMD, elucidating effective and ineffective strategies. Intermittent hypoxia-induced increases in shear stress improve ICA dilatory response, underscoring the pivotal role of shear rate. Although ICA blood flow during exercise has been extensively studied, data on shear rate during exercise are limited. Moderate-intensity leg cycling that avoids hyperventilation and elevates end-tidal CO₂ partial pressure increases ICA shear rate and augments post-exercise ICA-FMD, whereas higher-intensity exercise or small-muscle exercise fails to produce similar benefits. These observations suggest that a threshold shear stimulus may be required for post-exercise improvements in ICA-FMD. Future research should establish standardized methodologies, define the shear stimulus threshold, elucidate the time course of vascular adaptations, and extend investigations to populations at elevated cerebrovascular risk. Translating these mechanistic insights into clinical strategies has the potential to optimize cerebrovascular endothelial function and thereby contribute to the prevention of cerebrovascular diseases.