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This study attempted to clarify the relationships between marathon time and monthly training volume, training frequency and the longest (LRD) or average running distance per workout (ARD), as well as their interactions.Male recreational runners (n = 587) participating in the Hokkaido Marathon 2017 completed a questionnaire before the race; of these, 494 finished the race. We assessed age, running career, body height, body weight, body mass index (BMI), monthly training volume, training frequency, the LRD and the ARD. These indicators were each divided into 4 or 5 homogeneous subgroups to determine whether the other indicators in each subgroup predicted marathon time.In the training frequency subgroups, there were significant correlations between monthly training volume, the LRD or the ARD and marathon time, except for the subgroup that trained 2 times per week or less; in this subgroup, the relationship between the ARD and marathon time was not significant. In all monthly training volume subgroups, there were no significant relationships between training frequency, the LRD or the ARD and marathon time. In the ≥ 21 km LRD and ≥ 10 km ARD subgroups, there were significant correlations between monthly training volume and marathon time (all P 0.01); these correlations were not significant in the 1-20 km LRD and 10 km ARD subgroups.These results indicate that monthly training volume is the most important factor in predicting marathon time and that the influence of monthly training volume is only significant if the running distance per workout exceeded a certain level.

This study aimed to reveal the key lifestyle elements that improve physical and mental health in university students by focusing on physical activity, nutrition, and sleep. This cross-sectional study was conducted between October 2021 and December 2021. The participants were 290 first-year students (mean age, 18.63 ± .63 years; age range, 18 to 23; 198 female). The outcomes were daily step counts measured using accelerometers, dietary intake by nutrient category, sleep duration, subjective sleep quality, exercise frequency and duration by exercise type, screen time, depression level, and subjective fatigue by body part. Depression and subjective eye fatigue represent mental and physical health outcomes. Subjective sleep quality predicted depression (β = −1.22, P < .001) and eye fatigue (β = −.23, P < .01) in the path analysis. Participants with higher subjective sleep quality performed more frequent aerobic exercise ( P < .01), longer session times of physical relaxation exercise ( P < .05), and shorter screen time ( P < .05). Subjective sleep quality could be a key factor for high mental and physical health. Furthermore, performing aerobic and relaxation exercises and reducing screen time are important for improving the subjective sleep quality.

High-intensity intermittent (or interval) training (HIIT) has started to gain popularity as a time-effective approach to providing beneficial effects to the brain and to peripheral organs. However, it still remains uncertain whether HIIT enhances hippocampal functions in terms of neurogenesis and spatial memory due to unconsidered HIIT protocol for rodents. Here, we established the HIIT regimen for rats with reference to human study. Adult male Wistar rats were assigned randomly to Control, moderate-intensity continuous training (MICT; 20 m/min, 30 min/day, 5 times/week), and HIIT (60 m/min, 10 30-s bouts of exercise, interspaced with 2.5 min of recovery, 5 times/week) groups. The ratios of exercise time and volume between MICT and HIIT were set as 6:1 and 2:1–4:1, respectively. After 4 weeks of training, all-out time in the incremental exercise test was prolonged for exercise training. In skeletal muscle, the plantaris citrate synthase activity significantly increased only in the HIIT group. Simultaneously, both HIIT and MICT led to enhanced spatial memory and adult hippocampal neurogenesis (AHN) as well as enhanced protein levels of hippocampal brain-derived neurotrophic factor (BDNF) signaling. Collectively, we suggest that HIIT could be a time-efficient exercise protocol that enhances hippocampal memory and neurogenesis in rats and is associated with hippocampal BDNF signaling.

A colorimetric naked-eye chemosensor for histidine (His) was established by mixing a thiazolylazo dye and Ni2+ in a 1:1 M ratio (TAMSMB-Ni2+). Due to the interaction of Ni2+ with His, TAMSMB was regenerated upon the addition of His to TAMSMB-Ni2+ to lead a significant hypsochromic shift in absorption spectra accompanied by a visual color change from red to yellow which can be directly observed by the naked eye. On the other hands, other amino acids did not trigger any significant changes in absorption properties and solution color. Moreover, it exhibited the selective recognition of His without obvious interference from other amino acids. Thus, TAMSMB-Ni2+ can act as a simple and efficient colorimetric chemosensor for His with sensitivity and selectivity in aqueous solution.

The pyrogallol red-based Zn2+ complex (PR-Zn2+) between commercially available anionic dye, pyrogallol red (PR), and Zn2+ in the presence of cationic poly(diallyldimethylammonium chloride) (PDADMAC) was applied to the colorimetric recognition of pyrophosphate (PPi) in a pure aqueous solution under physiological pH. Upon the gradual addition of PPi to PR-Zn2+, the distinct color change from blue to pink could be recognized with the naked eye accompanied by a hypsochromic shift from 600 to 550 nm in the absorption spectra, indicating that PR was released from PR-Zn2+ through the interaction of PPi with Zn2+. No significant absorption spectral and color changes were observed in the presence of other anions including ATP and ADP with the structure similar to PPi. Moreover, other coexisting anions cause little or no interference to the detection of PPi. The results showed that PR-Zn2+ in the presence of PDADMAC could be a good naked-eye and colorimetric chemosensor for selective detection of PPi in aqueous solution. This study demonstrates that the combination of an organic dye, an oppositely charged polyelectrolyte, and a metal ion is a potential candidate for the easy construction of a new chemosensor system.

A new colorimetric chemosensor based on a simple ternary mixture of an anionic dye, pyrogallol red (PR), a cationic polyelectrolyte, poly(diallyldimethylammonium chloride) (PDADMAC), and a metal chelator, N-(2-hydroxyethyl) ethylenediaminetriacetic acid (HEDTA) for the colorimetric detection of Fe2+ and Fe3+ has been developed in an aqueous solution buffered at pH 5. Upon addition of Fe2+ or Fe3+ to the mixture, the absorption spectra showed a bathochromic shift; correspondingly, the solution color changed from red to blue, whereas other metal ions basically resulted in insignificant spectral and color changes. From the competitive experiments, no obvious interferences for the colorimetric detection of Fe2+ and Fe3+ were observed in the presence other metal ions. The results indicated that the mixture could be used as a potential Fe2+ and Fe3+ colorimetric and naked eye chemosensor in aqueous media. This research demonstrates that the ternary ensemble consisted of an organic dye, an oppositely charged polyelectrolyte, and a metal chelator is a versatile and convenient tool for the facile preparation of a novel chemosensor system.

We have developed a colorimetric chemosensor for the selective and sensitive detection of Cys based on the complex (CA-2Pb2+) between a commercially available natural organic dye, carminic acid (CA) and Pb2+ in pure aqueous solution at physiological pH. The addition of Cys to the CA-2Pb2+ solution resulted in a distinct color change from purple to red together with a remarkable absorption spectral change by the restoration of CA through a displacement mechanism with formation of the Cys-Pb2+ complex, whereas other amino acids and glutathione induce no or minimal spectral and color changes. Moreover, the other amino acids and GSH do not affect the detection ability of CA-2Pb2+ for Cys. The reversibility even through several cycles was established for practical applications. The results indicate that CA-2Pb2+ may be useful as a potential colorimetric and naked-eye chemosensor for Cys over Hcy and GSH in aqueous solution.

The pyrogallol red (PR)-based Cu2+ complex was proven to be an effective and selective colorimetric chemosensing ensemble for recognition of oxalate over other anions in a perfect aqueous solution. The addition of oxalate to the PR-Cu2+ complex resulted in a colour change from purple to orange colour due to the regeneration of PR by the chelation of oxalate with Cu2+ , while other anions did not induce any significant colour change. Moreover, it was revealed that no obvious interference was observed during the titrations with oxalate into each other anion. Therefore, the PR-Cu2+ complex can be used as a simple and practical colorimetric chemosensor for detecting oxalate.

The pyrogallol red (PR)-based Cu

[Aims/hypothesis]: Type 2 diabetes is likely to be an independent risk factor for hippocampal-based memory dysfunction, although this complication has yet to be investigated in detail. As dysregulated glycometabolism in peripheral tissues is a key symptom of type 2 diabetes, it is hypothesised that diabetes-mediated memory dysfunction is also caused by hippocampal glycometabolic dysfunction. If so, such dysfunction should also be ameliorated with moderate exercise by normalising hippocampal glycometabolism, since 4 weeks of moderate exercise enhances memory function and local hippocampal glycogen levels in normal animals., [Methods]: The hippocampal glycometabolism in OLETF rats (model of human type 2 diabetes) was assessed and, subsequently, the effects of exercise on memory function and hippocampal glycometabolism were investigated., [Results]: OLETF rats, which have memory dysfunction, exhibited higher levels of glycogen in the hippocampus than did control rats, and breakdown of hippocampal glycogen with a single bout of exercise remained unimpaired. However, OLETF rats expressed lower levels of hippocampal monocarboxylate transporter 2 (MCT2, a transporter for lactate to neurons). Four weeks of moderate exercise improved spatial memory accompanied by further increase in hippocampal glycogen levels and restoration of MCT2 expression independent of neurotrophic factor and clinical symptoms in OLETF rats., [Conclusions/interpretation]: Our findings are the first to describe detailed profiles of glycometabolism in the type 2 diabetic hippocampus and to show that 4 weeks of moderate exercise improves memory dysfunction in type 2 diabetes via amelioration of dysregulated hippocampal glycometabolism. Dysregulated hippocampal lactate-transport-related glycometabolism is a possible aetiology of type-2-diabetes-mediated memory dysfunction., This research was supported in part by the ‘Global Initiative for Sports Neuroscience (GISN): For Development of Exercise Prescription Enhancing Cognitive Functions’, by special funds for Education and Research of the Ministry of Education, Culture, Sports, Science and Technology (MEXT) granted to the ‘Body and Mind Integrated Sports Sciences (BAMIS) Project’ and to the ‘Human High Performance (HHP) Research Project’ and by the Japan Society for the Promotion of Science (Grants-in-aid for Scientific Research A, No. 15H01828; Challenging Exploratory Research, No. 23650384).

Although voluntary running has beneficial effects on hippocampal cognitive functions if done abundantly, it is still uncertain whether resistance running would be the same. For this purpose, voluntary resistance wheel running (RWR) with a load is a suitable model, since it allows increased work levels and resultant muscular adaptation in fast-twitch muscle. Here, we examined whether RWR would have potential effects on hippocampal cognitive functions with enhanced hippocampal brain-derived neurotrophic factor (BDNF), as does wheel running without a load (WR). Ten-week-old male Wistar rats were assigned randomly to sedentary (Sed), WR, and RWR (to a maximum load of 30% of body weight) groups for 4 wk. We found that in RWR, work levels increased with load, but running distance decreased by about half, which elicited muscular adaptation for fast-twitch plantaris muscle without causing any negative stress effects. Both RWR and WR led to improved spatial learning and memory as well as gene expressions of hippocampal BDNF signaling-related molecules. RWR increased hippocampal BDNF, tyrosine-related kinase B (TrkB), and cAMP response element-binding (CREB) protein levels, whereas WR increased only BDNF. With both exercise groups, there were correlations between spatial memory and BDNF protein ( r = 0.41), p-CREB protein ( r = 0.44), and work levels ( r = 0.77). These results suggest that RWR plays a beneficial role in hippocampus-related cognitive functions associated with hippocampal BDNF signaling, even with short distances, and that work levels rather than running distance are more determinant of exercise-induced beneficial effects in wheel running with and without a load.

Mild exercise activates hippocampal neurons through the glutamatergic pathway and also promotes adult hippocampal neurogenesis (AHN). We hypothesized that such exercise could enhance local androgen synthesis and cause AHN because hippocampal steroid synthesis is facilitated by activated neurons via N -methyl- D -aspartate receptors. Here we addressed this question using a mild-intense treadmill running model that has been shown to be a potent AHN stimulator. A mass-spectrometric analysis demonstrated that hippocampal dihydrotestosterone increased significantly, whereas testosterone levels did not increase significantly after 2 wk of treadmill running in both orchidectomized (ORX) and sham castrated (Sham) male rats. Furthermore, analysis of mRNA expression for the two isoforms of 5α-reductases ( srd5a1 , srd5a2 ) and for androgen receptor (AR) revealed that both increased in the hippocampus after exercise, even in ORX rats. All rats were injected twice with 5′-bromo-2′deoxyuridine (50 mg/kg body weight, i.p.) on the day before training. Mild exercise significantly increased AHN in both ORX and Sham rats. Moreover, the increase of doublecortin or 5′-bromo-2′deoxyuridine/NeuN-positive cells in ORX rats was blocked by s.c. flutamide, an AR antagonist. It was also found that application of an estrogen receptor antagonist, tamoxifen, did not suppress exercise-induced AHN. These results support the hypothesis that, in male animals, mild exercise enhances hippocampal synthesis of dihydrotestosterone and increases AHN via androgenenic mediation.

Non-technical summary Exercise training elicits an increase in the basal level of muscular glycogen. This happens when glycogen recovers to above its basal level (supercompensation) after it decreases with acute exercise. Although untested, it is hypothesized that, similar to that of skeletal muscle, brain glycogen supercompensation occurs after acute exhaustive exercise. We provide evidence that exhaustive exercise induces glycogen supercompensation not only in skeletal muscles, but also in the brain. Furthermore, we observed exercise training-induced increases in basal glycogen levels in the cortex and hippocampus, which are involved in motor control and cognitive function. This suggests that, like skeletal muscles, the brain adapts metabolically, probably to meet the increased energy demands of exercise training.

The brain is considered to be an organ which can be affected by conditioning or exercise, just like muscles. Exercise activates the brain and enhances several neuronal functions and may lead to several neuronal plastic changes. Neuronal c-Fos accumulation in any hypothalamic nuclei increased only with supra-LT exercise, revealing a LT-like activation pattern. In the brain stem, both supra-LT and below-LT exercise activated the VLM and NTS. In case of hippocampus, its activation was induced by under-LT exercise, which increased regional blood flow through neurovascular coupling. Thus, we found that regions of brain activation were determined differently based on exercise intensity. In the further, more research on exercise intensive is indispensable. In this paper, we reviewed: (1) Hippocampal plasticity through exercise (2) Brain region-specific differential activation patterns with exercise below and above the lactate threshold (3) Hippocampal neuronal activity induced by mild exercise below the lactate threshold: regional blood flow monitoring in the hippocampus (4) Acute mild exercise induces BDNF and short-term training causes AHN (5) Why below-LT exercise is sufficient for hippocampal plasticity (6) Hippocampal activation mechanism during exercise. In particular, based on our recent findings, our focus was directed upon exercise-induced brain activation and neurogenesis.

Although exercise training improves hippocampus-related cognition, the optimum exercise intensity is still disputed. Based on the lactate threshold (LT, approximately 20 m/min on treadmill) of rats, we have shown that 2 weeks of training with stress-free mild exercise (ME,LT), but not intense exercise (IE,LT), comprising exercise stress, promotes adult hippocampal neurogenesis (Okamoto et al., PNAS, 2012), a potential substrate for memory improvement. These results led us to postulate that long-term ME, but not IE, training leads to improved hippocampal function as assessed with a Morris water maze (MWM) task. To test this hypothesis, we investigated the changes in physiological stress levels and MWM task performance in rats assigned to 6 weeks of sedentary control (CONT), ME-training or IE-training conditions. Results showed that, compared to the other conditions, only IE causes general adaptive syndrome (GAS), including adrenal hypertrophy, thymic atrophy and hypercorticosteronemia. In the MWM, ME led to enhanced memory, but not learning, compared with CONT, while IE produced no change in either capacity, probably due to GAS. These findings support the hypothesis that 6 weeks of continuous ME training leads to enhanced hippocampus-related memory, which may have implications for both healthy adults and subjects with low physical capacity.

In two separate experiments, voluntary resistance wheel running with 30% of body weight (RWR), rather than wheel running (WR), led to greater enhancements, including adult hippocampal neurogenesis and cognitive functions, in conjunction with hippocampal brain‐derived neurotrophic factor (BDNF) signaling (Lee et al., J Appl Physiol, 2012; Neurosci Lett., 2013). Here we aimed to unravel novel molecular factors and gain insight into underlying molecular mechanisms for RWR‐enhanced hippocampal functions; a high‐throughput whole‐genome DNA microarray approach was applied to rats performing voluntary running for 4 weeks. RWR rats showed a significant decrease in average running distances although average work levels increased immensely, by about 11‐fold compared to WR, resulting in muscular adaptation for the fast‐twitch plantaris muscle. Global transcriptome profiling analysis identified 128 (sedentary × WR) and 169 (sedentary × RWR) up‐regulated (>1.5‐fold change), and 97 (sedentary × WR) and 468 (sedentary × RWR) down‐regulated (, New information on the voluntary RWR influenced transcriptome in rat hippocampus. Selected gene candidates may be a critical role in the development of hippocampal adaptations in RWR.

While increasing evidence demonstrates that physical exercise promotes brain health, little is known on how the reduction of physical activity affects brain function. We investigated whether the cessation of wheel running alters anxiety-like and depression-like behaviors and its impact on adult hippocampal neurogenesis in mice. Male C57BL/6 mice (4 weeks old) were assigned to one of the following groups, and housed until 21 weeks old; (1) no exercise control (noEx), housed in a standard cage; (2) exercise (Ex), housed in a running wheel cage; and (3) exercise-no exercise (Ex-noEx), housed in a running wheel cage for 8 weeks and subsequently in a standard cage. Behavioral evaluations suggested that Ex-noEx mice were more anxious compared to noEx control mice, but no differences were found in depression-like behavior. The number of BrdU-labeled surviving cells in the dentate gyrus was significantly higher in Ex but not in Ex-noEx compared with noEx, indicating that the facilitative effects of exercise on cell survival are reversible. Surprisingly, the ratio of differentiation of BrdU-positive cells to doublecortin-positive immature neurons was significantly lower in Ex-noEx compared to the other groups, suggesting that the cessation of wheel running impairs an important component of hippocampal neurogenesis in mice. These results indicate that hippocampal adaptation to physical inactivity is not simply a return to the conditions present in sedentary mice. As the impaired neurogenesis is predicted to increase a vulnerability to stress-induced mood disorders, the reduction of physical activity may contribute to a greater risk of these disorders. © 2013 Elsevier B.V.

Recently, we reported that voluntary resistance wheel running with a resistance of 30% of body weight (RWR), which produces shorter distances but higher work levels, enhances spatial memory associated with hippocampal brain-derived neurotrophic factor (BDNF) signaling compared to wheel running without a load (WR) [17]. We thus hypothesized that RWR promotes adult hippocampal neurogenesis (AHN) as a neuronal substrate underlying this memory improvement. Here we used 10-week-old male Wistar rats divided randomly into sedentary (Sed), WR, and RWR groups. All rats were injected intraperitoneally with the thymidine analogue 5-Bromo-2'-deoxuridine (BrdU) for 3 consecutive days before wheel running. We found that even when the average running distance decreased by about half, the average work levels significantly increased in the RWR group, which caused muscular adaptation (oxidative capacity) for fast-twitch plantaris muscle without causing any negative stress effects. Additionally, immunohistochemistry revealed that the total BrdU-positive cells and newborn mature cells (BrdU/NeuN double-positive) in the dentate gyrus increased in both the WR and RWR groups. These results provide new evidence that RWR has beneficial effects on AHN comparable to WR, even with short running distances.

Our six-week treadmill running training (forced exercise) model has revealed that mild exercise (ME) with an intensity below the lactate threshold (LT) is sufficient to enhance spatial memory, while intense exercise (IE) above the LT negates such benefits. To help understand the unrevealed neuronal and signaling/molecular mechanisms of the intensity-dependent cognitive change, in this rat model, we here investigated plasma corticosterone concentration as a marker of stress, adult hippocampal neurogenesis (AHN) as a potential contributor to this ME-induced spatial memory, and comprehensively delineated the hippocampal transcriptomic profile using a whole-genome DNA microarray analysis approach through comparison with IE. Results showed that only IE had the higher corticosterone concentration than control, and that the less intense exercise (ME) is better suited to improve AHN, especially in regards to the survival and maturation of newborn neurons. DNA microarray analysis using a 4 × 44 K Agilent chip revealed that ME regulated more genes than did IE (ME: 604 genes, IE: 415 genes), and only 41 genes were modified with both exercise intensities. The identified molecular components did not comprise well-known factors related to exercise-induced AHN, such as brain-derived neurotrophic factor. Rather, network analysis of the data using Ingenuity Pathway Analysis algorithms revealed that the ME-influenced genes were principally related to lipid metabolism, protein synthesis and inflammatory response, which are recognized as associated with AHN. In contrast, IE-influenced genes linked to excessive inflammatory immune response, which is a negative regulator of hippocampal neuroadaptation, were identified. Collectively, these results in a treadmill running model demonstrate that long-term ME, but not of IE, with minimizing running stress, has beneficial effects on increasing AHN, and provides an ME-specific gene inventory containing some potential regulators of this positive regulation. This evidence might serve in further elucidating the mechanism behind ME-induced cognitive gain.