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Abstract Background Electrical muscle stimulation (EMS) induces involuntary muscle contraction. Several studies have suggested that EMS has the potential to be an alternative method of voluntary exercise; however, its effects on cerebral blood flow (CBF) when applied to large lower limb muscles are poorly understood. Thus, the purpose of this study was to examine the effects of EMS on CBF, focusing on whether the effects differ between the internal carotid (ICA) and vertebral (VA) arteries. Methods The participants performed the experiments under EMS and control (rest) conditions in a randomized crossover design. The ICA and VA blood flow were measured before and during EMS or control. Heart rate, blood pressure, minute ventilation, oxygen uptake, and end-tidal partial pressure of carbon dioxide (PETCO2) were monitored and measured as well. Results The ICA blood flow increased during EMS [Pre: 330 ± 69 mL min−1; EMS: 371 ± 81 mL min−1, P = 0.001, effect size (Cohen’s d) = 0.55]. In contrast, the VA blood flow did not change during EMS (Pre: 125 ± 47 mL min−1; EMS: 130 ± 45 mL min−1, P = 0.26, effect size = 0.12). In the EMS condition, there was a significant positive linear correlation between ΔPETCO2 and ΔICA blood flow (R = 0.74, P = 0.02). No relationships were observed between ΔPETCO2 and ΔVA blood flow (linear: R = − 0.17, P = 0.66; quadratic: R = 0.43, P = 0.55). Conclusions The present results indicate that EMS increased ICA blood flow but not VA blood flow, suggesting that the effects of EMS on cerebral perfusion differ between anterior and posterior cerebral circulation, primarily due to the differences in cerebrovascular response to CO2.

When exposed to ambient temperatures that cause thermal discomfort, a human’s behavioral responses are more effective than autonomic ones at compensating for thermal imbalance. These behavioral thermal responses are typically directed by an individual’s perception of the thermal environment. Perception of the environment is a holistic amalgamation of human senses, and that in some circumstances, humans prioritize visual information. Existing research has considered this in the specific case of thermal perception, and this review investigates the state of the literature examining this effect. We identify the frameworks, research rationales, and potential mechanisms that underpin the evidence base in this area. studied behaviors. Our review identified 31 experiments, comprising 1392 participants that met the inclusion criteria. Methodological heterogeneity was observed in the assessment of thermal perception, and a variety of methods were employed to manipulate the visual environment. However, the majority of the included experiments (80%) reported a difference in thermal perception after the visual environment was manipulated. There was limited research exploring any effects on physiological variables (e.g. skin and core temperature). This review has wide-ranging implications for the broad discipline of (thermo)physiology, psychology, psychophysiology, neuroscience, ergonomics, and behavior.

NEW FINDINGS What is the central question of this study? To what extent do hypoxia-induced changes in the peripheral and central respiratory chemoreflex modulate anterior and posterior cerebral oxygen delivery, with corresponding implications for susceptibility to acute mountain sickness? What is the main finding and its importance? We provide evidence for site-specific regulation of cerebral blood flow in hypoxia that preserves oxygen delivery in the posterior but not the anterior cerebral circulation, with minimal contribution from the central respiratory chemoreflex. External carotid artery vasodilatation might prove to be an alternative haemodynamic risk factor that predisposes to acute mountain sickness. ABSTRACT The aim of the present study was to determine the extent to which hypoxia-induced changes in the peripheral and central respiratory chemoreflex modulate anterior and posterior cerebral blood flow (CBF) and oxygen delivery (CDO2 ), with corresponding implications for the pathophysiology of the neurological syndrome, acute mountain sickness (AMS). Eight healthy men were randomly assigned single blind to 7 h of passive exposure to both normoxia (21% O2 ) and hypoxia (12% O2 ). The peripheral and central respiratory chemoreflex, internal carotid artery, external carotid artery (ECA) and vertebral artery blood flow (duplex ultrasound) and AMS scores (questionnaires) were measured throughout. A reduction in internal carotid artery CDO2 was observed during hypoxia despite a compensatory elevation in perfusion. In contrast, vertebral artery and ECA CDO2 were preserved, and the former was attributable to a more marked increase in perfusion. Hypoxia was associated with progressive activation of the peripheral respiratory chemoreflex (P 0.05). Symptom severity in participants who developed clinical AMS was positively related to ECA blood flow (Lake Louise score, r = 0.546-0.709, P = 0.004-0.043; Environmental Symptoms Questionnaires-Cerebral symptoms score, r = 0.587-0.771, P = 0.001-0.027, n = 4). Collectively, these findings highlight the site-specific regulation of CBF in hypoxia that maintains CDO2 selectively in the posterior but not the anterior cerebral circulation, with minimal contribution from the central respiratory chemoreflex. Furthermore, ECA vasodilatation might represent a hitherto unexplored haemodynamic risk factor implicated in the pathophysiology of AMS.

We examined the acute impact of both low- and high-glycemic index (GI) breakfasts on plasma brain-derived neurotrophic factor (BDNF) and dynamic cerebral autoregulation (dCA) compared with breakfast omission. Ten healthy men (age 24 ± 1 yr) performed three trials in a randomized crossover order; omission and Low-GI (GI = 40) and High-GI (GI = 71) breakfast conditions. Middle cerebral artery velocity (transcranial Doppler ultrasonography) and arterial pressure (finger photoplethysmography) were continuously measured for 5 min before and 120 min following breakfast consumption to determine dCA using transfer function analysis. After these measurements of dCA, venous blood samples for the assessment of plasma BDNF were obtained. Moreover, blood glucose was measured before breakfast and every 30 min thereafter. The area under the curve of 2 h postprandial blood glucose in the High-GI trial was higher than the Low-GI trial ( P < 0.01). The GI of the breakfast did not affect BDNF. In addition, both very-low (VLF) and low-frequency (LF) transfer function phase or gains were not changed during the omission trial. In contrast, LF gain (High-GI P < 0.05) and normalized gain (Low-GI P < 0.05) were decreased by both GI trials, while a decrease in VLF phase was observed in only the High-GI trial ( P < 0.05). These findings indicate that breakfast consumption augmented dCA in the LF range but High-GI breakfast attenuated cerebral blood flow regulation against slow change (i.e., the VLF range) in arterial pressure. Thus we propose that breakfast and glycemic control may be an important strategy to optimize cerebrovascular health.

We investigated genecology and ecophysiological mechanisms of the polymorphism of leaf trichome density of Leptospermum recurvum Hook. f. (Myrtaceae) in the deglaciated summit zone above 3, 000 m a.s.l. of Mt. Kinabalu, Borneo. Various phenotypes with variable foliar trichome densities occurred sympatrically in the same population, and the composition of coexisting phenotypes varied substantially among populations. We conducted a common garden experiment by sowing seeds from multiple maternal trees of different leaf trichome densities. We found a significant relation between pubescence of maternal trees and offspring, which indicated that leaf trichome density had a genetic basis. Microsatellite analysis revealed that there was no barrier to gene flows among phenotypes or among populations, and very low neutral genetic differentiation among populations with high gene flows for both directions of phenotypes. The soils in the sites dominated by pubescent trees were significantly more desiccated than in the sites dominated by glabrous trees during a short drought. Glabrous trees had a significantly greater mortality rate than pubescent trees after an intensive El Niño drought (13.7 vs. 3.9%) in the same sites where both phenotypes occurred sympatrically. Pubescent individuals demonstrated a significantly greater photosynthetic water-use efficiency than glabrous individuals. El Niño droughts could cause large difference in soil moisture among sites and that a greater desiccation stress removed glabrous phenotypes as one end of divergent natural selection to form pubescent populations. These results implied that the process shaping the phenotypic polymorphisms involved strong gene flows combined with ongoing divergent selection.

Purpose: Cognitive performance appears to be impaired during high-intensity exercise, and this occurs concurrently with a reduction in cerebral blood flow (CBF). However, it is unclear whether cognitive impairment during high-intensity exercise is associated with reduced CBF. We tested the hypothesis that a reduction in CBF is responsible for impaired cognitive performance during high-intensity exercise.Methods: Using a randomized crossover design seventeen healthy males performed spatial delayed-response (DR) and Go/No-Go tasks in three conditions [Exercise (EX), Exercise+CO2 (EX+CO2), and a non-exercising Control (CON)]. In the EX and EX+CO2, they performed cognitive tasks at rest and during 8-mins of moderate and high-intensity exercise. Exercise intensity corresponded to ~50% (moderate) and ~80% (high) of peak oxygen uptake. In the EX+CO2, the participants inspired hypercapnic gas (2% CO2) during high-intensity exercise. In the CON, they performed the cognitive tasks without exercise. Results: Middle cerebral artery mean velocity (MCAv) increased during high-intensity exercise in the EX+CO2 relative to the EX [69.4 (10.6) cm.s-1, vs. 57.2 (7.7) cm.s-1, P < 0.001]. Accuracy of the cognitive tasks was impaired during high-intensity exercise in the EX [84.1 (13.3) %, P < 0.05] and the EX+CO2 [85.7 (11.6) %, P < 0.05] relative to rest [EX: 95.1 (5.3) %, EX+CO2: 95.1 (5.3) %]. However, no differences between the EX and the EX+CO2 were observed (P > 0.10). These results demonstrate that restored CBF did not prevent cognitive impairment during high-intensity exercise. Conclusion: We conclude that a reduction in CBF is not responsible for impaired cognitive performance during high-intensity exercise.

Virtual reality (VR) technology combined with exercise, called VR exercise, is believed to have beneficial effects on mood; but VR factors contributing to improved mood remain ambiguous. The purpose of this study was to examine the effect of visual flow speed on psychophysiological responses (i.e., physiological responses, ratings of perceived exertion or RPE, and mood) to immersive VR exercise in a simulated natural environment. Eighteen male participants ( Mage =23.1, SD = 1.9 years) cycled an ergometer at 80 watts for 5 minutes on three separate occasions while watching a first-person VR movie through VR goggles at three different speeds of visual flow, corresponding to 7.5 km.h−1, 15 km.h−1, and 22.5 km.h−1. The order of the three speeds was randomized in a counterbalanced design. We measured heart rate, oxygen uptake, minute ventilation, respiratory rate, and cadence during the exercise, and we recorded ratings of perceived exertion (RPE) and mood immediately after the exercise. We evaluated mood states with the Two-Dimensional Mood Scale. One-way repeated measures analysis of variance or the Friedman test revealed no significant effects on any physiological variables, RPE or cadence as a result of altered visual flow speed during VR exercise ( p > .05). However, speed of visual flow significantly influenced participant ratings of Vitality ( p = 0.01) and Pleasure ( p = 0.02), with the faster speed resulting in a more positive mood state. As these findings showed that VR exercise with faster visual flow induced positive mood states, we recommend faster visual flow to induce better mood states in VR exercise.

The handgrip exercise, a small muscle exercise, is useful for exercise therapy, particularly in the elderly and bedridden patients. The isometric handgrip (IHG) exercise has been utilized in training programs to reduce resting blood pressure; however, the acute effects of the IHG exercise on cognitive performance are not fully understood. The present study aimed to investigate the effect of an intermittent IHG exercise protocol with short exercise duration, which minimizes the arterial blood pressure response to exercise, on cognitive performance. Twenty-two young healthy subjects performed the intermittent IHG exercise protocol, which consisted of 30-s IHG and 45-s recovery × 16 trials; the exercise intensity of the IHG exercise was 30% of the maximal voluntary contraction. Cognitive performance was evaluated before and after the exercise with the Go/No-Go and memory recognition tasks. Specifically, the reaction time (RT) and performance accuracy were measured. The intermittent IHG exercise protocol did not change the RT or performance accuracy of either the Go/No-Go task (P = 0.222 and P = 0.260, respectively) or the memory recognition task (P = 0.427 and P = 0.245, respectively). These findings suggest that the intermittent IHG exercise protocol with short exercise duration may not provide enough stimulation to improve cognitive performance despite being useful as a safe exercise therapy in the elderly and in patients with cardiovascular disease.

Previous studies have reported that even a single bout of dynamic exercise improves cognitive performance. However, the acute effect of the interval handgrip (HG) exercise protocol, which is effective in reducing resting blood pressure, on cognitive performance is poorly understood. Cognitive performance was assessed in 17 young healthy subjects before and after a resting control (e.g., time control) and the interval HG exercise (Exercise), which consisted of four trials of 2-min HG exercise at 25% of maximum voluntary contraction with 3-min recovery in between each trial. Mean arterial blood pressure (MAP) and middle cerebral artery blood velocity (MCA V) were measured continuously throughout the experiment. Memory recognition and executive function were assessed using memory recognition and Go/No-Go tasks, respectively. During interval HG exercise, MAP and mean MCA V increased from the resting baseline condition (both P < 0.049) and returned to the resting baseline levels during recovery after the interval HG exercise (both P = 1.000). The reaction time and performance accuracy of the memory recognition task did not change in either the time control condition or Exercise condition (P = 0.514 and P = 0.414 respectively). However, the changes in reaction time of Go/No-Go task from the baseline in Exercise condition was significantly shorter than that in time-control condition (P = 0.004) without affecting performance accuracy (P = 0.482). The results of the present study show that an acute interval HG exercise could improve the processing speed in executive function despite no post-exercise improvement in hemodynamic parameters in young healthy subjects. These findings suggest that the interval HG exercise is a useful exercise mode that can be expected to have a positive effect on the processing speed in executive function regardless of cardiovascular adaptation to exercise.

PurposeFindings concerning the effects of exhaustive exercise on cognitive function are somewhat equivocal. The purpose of this study was to identify physiological factors that determine executive function after exhaustive exercise.MethodsThirty-two participants completed the cognitive tasks before and after an incremental exercise until exhaustion (exercise group: N = 18) or resting period (control group N = 14). The cognitive task was a combination of a Spatial Delayed-Response (Spatial DR) task and a Go/No-Go task, which requires executive function. Cerebral oxygenation and skin blood flow were monitored during the cognitive task over the prefrontal cortex. Venous blood samples were collected before and after the exercise or resting period, and blood catecholamines, serum brain-derived neurotrophic factor, insulin-like growth hormone factor 1, and blood lactate concentrations were analyzed.ResultsIn the exercise group, exhaustive exercise did not alter reaction time (RT) in the Go/No-Go task (pre: 861 ± 299 ms vs. post: 775 ± 168 ms) and the number of error trials in the Go/No-Go task (pre: 0.9 ± 0.7 vs. post: 1.8 ± 1.8) and the Spatial DR task (pre: 0.3 ± 0.5 vs. post: 0.8 ± 1.2). However, ΔRT was negatively correlated with Δcerebral oxygenation (r = −0.64, P = 0.004). Other physiological parameters were not correlated with cognitive performance. Venous blood samples were not directly associated with cognitive function after exhaustive exercise.ConclusionThe present results suggest that recovery of regional cerebral oxygenation affects executive function after exhaustive exercise.

Acute exercise has been demonstrated to improve cognitive function. In contrast, severe hypoxia can impair cognitive function. Hence, cognitive function during exercise under severe hypoxia may be determined by the balance between the beneficial effects of exercise and the detrimental effects of severe hypoxia. However, the physiological factors that determine cognitive function during exercise under hypoxia remain unclear. Here, we examined the combined effects of acute exercise and severe hypoxia on cognitive function and identified physiological factors that determine cognitive function during exercise under severe hypoxia. The participants completed cognitive tasks at rest and during moderate exercise under either normoxic or severe hypoxic conditions. Peripheral oxygen saturation, cerebral oxygenation, and middle cerebral artery velocity were continuously monitored. Cerebral oxygen delivery was calculated as the product of estimated arterial oxygen content and cerebral blood flow. On average, cognitive performance improved during exercise under both normoxia and hypoxia, without sacrificing accuracy. However, under hypoxia, cognitive improvements were attenuated for individuals exhibiting a greater decrease in peripheral oxygen saturation. Cognitive performance was not associated with other physiological parameters. Taken together, the present results suggest that arterial desaturation attenuates cognitive improvements during exercise under hypoxia.

Exercise intensity from stretching is very low, making it well suited to varied populations, including physically inactive people. We tested the hypothesis that acute stretching would improve cognitive function and improved mood states in physically inactive people. We asked 19 physically inactive young participants to perform the Stroop task and complete the short form of Profile of Moods Scale before and after 10 minutes of whole body stretching using yoga techniques and poses (stretching condition) versus a resting period. In the stretching condition, we observed decreases in Tension–Anxiety, Depression–Dejection, Anger–Hostility, Fatigue, and Confusion scores on the Profile of Moods Scale (all p values

Acute moderate intensity exercise has been shown to improve cognitive performance. In contrast, hypoxia is believed to impair cognitive performance. The detrimental effects of hypoxia on cognitive performance are primarily dependent on the severity and duration of exposure. In this review, we describe how acute exercise under hypoxia alters cognitive performance, and propose that the combined effects of acute exercise and hypoxia on cognitive performance are mainly determined by interaction among exercise intensity and duration, the severity of hypoxia, and duration of exposure to hypoxia. We discuss the physiological mechanism(s) of the interaction and suggest that alterations in neurotransmitter function, cerebral blood flow, and possibly cerebral metabolism are the primary candidates that determine cognitive performance when acute exercise is combined with hypoxia. Furthermore, acclimatization appears to counteract impaired cognitive performance during prolonged exposure to hypoxia although the precise physiological mechanism(s) responsible for this amelioration remain to be elucidated. This review has implications for sporting, occupational, and recreational activities at terrestrial high altitude where cognitive performance is essential. Further studies are required to understand physiological mechanisms that determine cognitive performance when acute exercise is performed in hypoxia.

Key points DNA methylation may play an important role in regulating gene expression in skeletal muscle to adapt to physical activity and inactivity. Neuronal nitric oxide synthase (nNOS) in skeletal muscle is a key regulator of skeletal muscle mass; however, it is unclear whether nNOS expression is regulated by DNA methylation. We found that 1 week of cast immobilization increased nNOS DNA methylation levels and downregulated nNOS gene expression in atrophic slow-twitch soleus muscle from the mouse leg. These changes were not detected in non-atrophic fast-twitch extensor digitorum longus muscle. Twelve hours of cast immobilization decreased nNOS gene expression, whereas nNOS DNA methylation levels were unchanged, suggesting that downregulation of nNOS gene expression by short-term muscle inactivity is independent of the DNA methylation pattern. These findings contribute to a better understanding of the maintenance of skeletal muscle mass and prevention of muscle atrophy by epigenetic mechanisms via the nNOS/NO pathway. Abstract DNA methylation is a mechanism that controls gene expression in skeletal muscle under various environmental stimuli, such as physical activity and inactivity. Neuronal nitric oxide synthase (nNOS) regulates muscle atrophy in skeletal muscle. However, the mechanisms regulating nNOS expression in atrophic muscle remain unclear. We hypothesized that nNOS expression in atrophic muscle is regulated by DNA methylation of the nNOS promotor in soleus (Sol; slow-twitch fibre dominant) and extensor digitorum longus (EDL; fast-twitch fibre dominant) muscles. One week of cast immobilization induced significant muscle atrophy in Sol but not in EDL. We showed that 1 week of cast immobilization increased nNOS DNA methylation levels in Sol, although only a minor change was detected in EDL. Consistent with the increased DNA methylation levels in atrophic Sol, the gene expression levels of total nNOS and nNOSµ (i.e. the major splicing variant of nNOS in skeletal muscle) decreased. The abundance of the nNOS protein and cell membrane (especially type IIa fibre) immunoreactivity also decreased in atrophic Sol. These changes were not observed in EDL after 1 week of cast immobilization. Furthermore, despite the lack of significant atrophy, 12 h of cast immobilization decreased gene expression levels of total nNOS and nNOSµ in Sol. However, no association was detected between nNOS DNA methylation and gene expression. The expression of the nNOSβ gene, another splicing variant of nNOS, in EDL was unchanged by cast immobilization, whereas its expression was not detected in Sol. We concluded that chronic adaptation of nNOS gene expression in cast immobilized muscle may involve nNOS DNA methylation.

What is the central question of this study? What are the mechanisms responsible for the decline in cognitive performance following exposure to acute normobaric hypoxia? What are the main findings and their importance? We found that 1) performance of a complex central executive task (n-back) was reduced FiO 0.12; 2) there was a strong correlation between performance of the n-back task and reductions in SpO and cerebral oxygenation; and 3) plasma adrenaline, noradrenaline, cortisol, and copeptin were not correlated with cognitive performance. It is well established that hypoxia impairs cognitive function; however, the physiological mechanisms responsible for these effects have received relatively little attention. This study examined the effects of graded reductions in fraction of inspired oxygen (FiO ) on oxygen saturation (SpO ), cerebral oxygenation, cardiorespiratory variables, activity of the sympathoadrenal system (adrenaline, noradrenaline) and hypothalamic-pituitary-adrenal axis (cortisol, copeptin), and cognitive performance. Twelve healthy males (mean [SD], age: 22 [4] yrs, height: 178 [5] cm, mass: 75 [9] kg, FEV /FVC ratio: 85 [5] %) completed a 4-task battery of cognitive tests to examine inhibition, selective attention (Eriksen Flanker), executive function (n-back) and simple and choice reaction time (Deary-Liewald). Tests were completed before and following 60 minutes of exposure to FiO 0.2093, 0.17, 0.145, and 0.12. Following 60 minutes of exposure response accuracy in the n-back task was significantly reduced in FiO 0.12 compared to baseline (82 [9] vs. 93 [5] %; p

It has been suggested that breakfast omission, as opposed to breakfast consumption, has the detrimental effects on cognitive function. However, the effects of acute exercise following breakfast omission on cognitive function are poorly understood, particularly during exercise. The purpose of this study was to examine the interactive effects of breakfast and exercise on cognitive function. Ten participants completed cognitive tasks at rest and during exercise in the breakfast consumption or omission conditions. Blood glucose concentration was measured immediately after each cognitive task. We used cognitive tasks to assess working memory [Spatial Delayed Response (DR) task] and executive function [Go/No-Go (GNG) task]. The participants cycled ergometer for 30 min while keeping their heart rate at 140 beats·min(-1). Accuracy of the GNG task was lower at rest in the breakfast omission condition than that in the breakfast consumption condition (Go trial: P=0.012; No-Go trial: P=0.028). However, exercise improved accuracy of the Go trial in the breakfast omission condition (P=0.013). Reaction time in the Go trial decreased during exercise relative to rest in both conditions (P=0.002), and the degree of decreases in reaction time was not different between conditions (P=0.448). Exercise and breakfast did not affect the accuracy of the Spatial DR task. The present results indicate that breakfast omission impairs executive function, but acute exercise improved executive function even after breakfast omission. It appears that beneficial effects of acute exercise on cognitive function are intact following breakfast omission.

It has been suggested that acute exercise improves cognitive function. However, little is known about how exercise under hypoxia affects cognitive function. The purpose of this study was to determine if hypoxia alters working memory and executive function during prolonged exercise. Sixteen participants performed cognitive tasks at rest and during exercise under normoxia and hypoxia [fraction of inspired oxygen (FIO2) = 0.15, corresponding to an altitude of approximately 2600 m]. The level of hypoxia was moderate. We used a combination of Spatial Delayed Response (Spatial DR) task and Go/No-Go (GNG) task, where spatial working memory and executive function are required. Working memory was assessed by the accuracy of the Spatial DR task, and executive function was assessed by the accuracy and reaction time in the GNG task. The participants cycled an ergometer for 30 min under normoxia and moderate hypoxia while keeping their heart rate (HR) at 140 beats/min. They performed the cognitive tasks 5 min and 23 min after their HR reached 140 beats/min. Moderate hypoxia did not alter the accuracy of the Spatial DR (P = 0.38) and GNG tasks (P = 0.14). In contrast, reaction time in the GNG task significantly decreased during exercise relative to rest under normoxia and moderate hypoxia (P = 0.02). These results suggest that moderate hypoxia and resultant biological processes did not provide sufficient stress to impair working memory and executive function during prolonged exercise. The beneficial effects on speed of response appear to persist during prolonged exercise under moderate hypoxia.

Introduction We recently developed an animal model to investigate the effects of eccentric contraction (ECC) and blood flow restriction (BFR) on muscle tissue at the cellular level. This study clarified the effects of repeated BFR, ECC, and BFR combined with ECC (BFR+ECC) on muscle fiber hypertrophy. Methods Male Wistar rats were assigned to 3 groups: BFR, ECC, and BFR+ECC. The contralateral leg in the BFR group served as a control (CONT). Muscle fiber cross-sectional area (CSA) of the tibialis anterior was determined after the respective treatments for 6 weeks. Results CSA was greater in the BFR+ECC group than in the CONT (P Cnclusions These results suggest that repeated BFR alone as well as BFR+ECC induces muscle fiber hypertrophy at the cellular level. Muscle Nerve 55: 274-276, 2017.

The purpose of the present study was to examine whether the fixation distance in real three-dimensional space affects manual reaction time to peripheral visual stimuli. Light-emitting diodes were used for presenting a fixation point and four peripheral visual stimuli. The visual stimuli were located at a distance of 45cm and at 25° in the left, right, upper, and lower directions from the sagittal axis including the fixation point. Near (30cm), Middle (45cm), Far (90cm), and Very Far (300cm) fixation distance conditions were used. When one of the four visual stimuli was randomly illuminated, the participants released a button as quickly as possible. Results showed that overall peripheral reaction time decreased as the fixation distance increased. The significant interaction between fixation distance and stimulus location indicated that the effect of fixation distance on reaction time was observed at the left, right, and upper locations but not at the lower location. These results suggest that fixating at far distance would contribute to faster reaction and that the effect is specific to locations in the peripheral visual field. The present findings are discussed in terms of viewer-centered representation, the focus of attention in depth, and visual field asymmetry related to neurological and psychological aspects.

Mountains of the tropical Pacific are influenced by synoptic-scale air subsidence, which causes a temperature inversion and a distinct dry meteorological condition above the inversion. The inversion appears at a lower altitude in the eastern Pacific where descending air of the Walker circulation prevails. On the other hand, if or how the alpine ecosystem of the tropical mountains of the western Pacific is influenced by dry synoptic-scale air subsidence is not well documented. We studied the vegetation and climate of the summit zone of Mount Kinabalu (4095 m) of Borneo. The leaf-size spectrum and physiognomy of forest community changed abruptly along the slope approximately at 3200 m from microphyll to leptophyll, suggesting that dry climatological conditions influence the vegetation above that altitude. Mean daily vapor pressure deficits (VPDs), estimated daily potential evapotranspiration (ET0), and the ratio of 30-day total ET0 to 30-day total rainfall increased drastically during El Nino and t...

Introduction Carnitine palmitoyltransferase II (CPT II) deficiency is an inherited disorder involving β-oxidation of long-chain fatty acids (FAO), which leads to rhabdomyolysis and subsequent acute renal failure. The detailed mechanisms of disease pathogenesis remain unknown; however, the availability of relevant human cell types for investigation, such as skeletal muscle cells, is limited, and the development of novel disease models is required. Methods We generated human induced pluripotent stem cells (hiPSCs) from skin fibroblasts of a Japanese patient with CPT II deficiency. Mature myocytes were differentiated from the patient-derived hiPSCs by introducing myogenic differentiation 1 (MYOD1), the master transcriptional regulator of myocyte differentiation. Using an in vitro acylcarnitine profiling assay, we investigated the effects of a hypolipidemic drug, bezafibrate, and heat stress on mitochondrial FAO in CPT II-deficient myocytes and controls. Results CPT II-deficient myocytes accumulated more palmitoylcarnitine (C16) than did control myocytes. Heat stress, induced by incubation at 38 °C, leads to a robust increase of C16 in CPT II-deficient myocytes, but not in controls. Bezafibrate reduced the amount of C16 in control and CPT II-deficient myocytes. Discussion In this study, we induced differentiation of CPT II-deficient hiPSCs into mature myocytes in a highly efficient and reproducible manner and recapitulated some aspects of the disease phenotypes of CPT II deficiency in the myocyte disease models. This approach addresses the challenges of modeling the abnormality of FAO in CPT II deficiency using iPSC technology and has the potential to revolutionize translational research in this field.

Ageing is a risk factor involved in decline in cognitive function, particularly in executive function, processing speed and episodic memory [...]

Peripheral visual perception may be relevant to performance in sports. Peripheral visual perception seems to be impaired during strenuous exercise. The hypothesis proposed is that a decrease in cerebral oxygenation is associated with impairment in peripheral visual perception during strenuous exercise. Recent behavioral and physiological data are presented to support the hypothesis.

We recently developed an animal model to investigate the effects of eccentric contraction (ECC) and blood flow restriction (BFR) on muscle tissue at the cellular level. This study clarified the effects of repeated BFR, ECC, and BFR combined with ECC (BFR+ECC) on muscle fiber hypertrophy.Male Wistar rats were assigned to 3 groups: BFR, ECC, and BFR+ECC. The contralateral leg in the BFR group served as a control (CONT). Muscle fiber cross-sectional area (CSA) of the tibialis anterior was determined after the respective treatments for 6 weeks.CSA was greater in the BFR+ECC group than in the CONT (P 0.01) and ECC (P 0.05) groups. CSA was greater in the BFR group than that in the CONT group (P 0.05).These results suggest that repeated BFR alone as well as BFR+ECC induces muscle fiber hypertrophy at the cellular level. Muscle Nerve 55: 274-276, 2017.

Previous studies have shown that an enriched environment (EE) has an important effect on brain function via the neuronal nitric oxide synthase/nitric oxide (nNOS/NO) pathway in young and aged animals. However, whether EE induces its effect by altering nNOS expression levels and whether it lowers anxiety-like behaviors in aged mice remains unclear. Here, we show that nNOS expression levels increased with age in the hippocampus and cerebellum in aged mice, but not in the cortex. Moreover, EE reduced anxiety-like behaviors in aged mice and reduced nNOS expression levels in the cerebellum, but not in the cortex. The present study suggests that EE improves anxiety-like behaviors in aged mice by altering nNOS expression levels in the hippocampus or cerebellum.

Recently, we proposed that strenuous exercise impairs peripheral visual perception because visual responses to peripheral visual stimuli were slowed during strenuous exercise. However, this proposal was challenged because strenuous exercise is also likely to affect the brain network underlying motor responses. The purpose of the current study was to resolve this issue. Fourteen participants performed a visual reaction-time (RT) task at rest and while exercising at 50% (moderate) and 75% (strenuous) peak oxygen uptake. Visual stimuli were randomly presented at different distances from fixation in two task conditions: the Central condition (2° or 5° from fixation) and the Peripheral condition (30° or 50° from fixation). We defined premotor time as the time between stimulus onset and the motor response, as determined using electromyographic recordings. In the Central condition, premotor time did not change during moderate (167 ± 19 ms) and strenuous (168 ± 24 ms) exercise from that at rest (164 ± 17 ms). In the Peripheral condition, premotor time significantly increased during moderate (181 ± 18 ms, P < 0.05) and strenuous exercise (189 ± 23 ms, P < 0.001) from that at rest (173 ± 17 ms). These results suggest that increases in Premotor Time to the peripheral visual stimuli did not result from an impaired motor-response network, but rather from impaired peripheral visual perception. We conclude that slowed response to peripheral visual stimuli during strenuous exercise primarily results from impaired visual perception of the periphery.

It has been suggested that a single bout of exercise alters cognitive function. However, specific mechanisms by which exercise affects cognitive function are not fully understood. This chapter summarizes recent studies that examined the effects of cerebral oxygenation and cerebral blood flow on cognitive function during exercise. Despite the lack of definitive and conclusive evidence, improvements in cognitive function during exercise at moderate intensity were not directly associated with alterations in cerebral oxygenation and cerebral blood flow. Cognitive function appears not to be impaired even when cerebral oxygenation and cerebral blood flow were compromised to some extent during exercise. Further studies are needed to clarify how alterations in cerebral oxygenation and cerebral blood flow affect cognitive function during exercise in a variety of experimental conditions.

Strenuous exercise may have the detrimental effects on visual perception. However, it is unclear whether visual resolution is related to the detrimental effects on visual perception. The purpose of this study was to examine whether the effects of strenuous exercise on visual perception are dependent on visual resolution. Given that visual resolution decreases in the periphery of the visual field, we hypothesized that if visual resolution plays a role in the detrimental effects on visual perception, the detrimental effects may be exaggerated toward the periphery of the visual field. Simple visual reaction time was measured at rest and during cycling at 40% and 75% peak oxygen uptakes (VO(2)). Visual stimuli were randomly presented at 2°, 10°, 30°, and 50° to either the right or left of the midpoint between the eyes with equal probability. RT was fractionated into premotor and motor components (i.e. premotor time and motor time) based on electromyographic recording. The premotor time during exercise at 40% peak VO(2) was not different from that at rest. In contrast, the premotor time during exercise at 75% peak VO(2) was significantly longer than that at rest (p=0.018). The increase in the premotor time was observed irrespective of eccentricity, and the detrimental effects were not exaggerated toward the periphery of the visual field. The motor time was not affected by exercise. The current findings suggest that the detrimental effects of strenuous exercise on visual perception are independent of visual resolution.

This study tested whether cerebral oxygenation affects cognitive function during exercise. We measured reaction times (RT) of 12 participants while they performed a modified version of the Eriksen flanker task, at rest and while cycling. In the exercise condition, participants performed the cognitive task at rest and while cycling at three workloads [40, 60, and 80% of peak oxygen uptake (\( \dot{V}{\text{O}}_{ 2} \))]. In the control condition, the workload was fixed at 20 W. RT was divided into premotor and motor components based on surface electromyographic recordings. The premotor component of RT (premotor time) was used to evaluate the effects of acute exercise on cognitive function. Cerebral oxygenation was monitored during the cognitive task over the right frontal cortex using near-infrared spectroscopy. In the exercise condition, we found that premotor time significantly decreased during exercise at 60% peak \( \dot{V}{\text{O}}_{ 2} \) relative to rest. However, this improvement was not observed during exercise at 80% peak \( \dot{V}{\text{O}}_{ 2} \). In the control condition, premotor time did not change during exercise. Cerebral oxygenation during exercise at 60% peak \( \dot{V}{\text{O}}_{ 2} \) was not significantly different from that at rest, while cerebral oxygenation substantially decreased during exercise at 80% peak \( \dot{V}{\text{O}}_{ 2} \). The present results suggest that an improvement in cognitive function occurs during moderate exercise, independent of cerebral oxygenation.