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When one is exposed to a stressful situation in their daily life, a common response is hyperventilation. Although the physiological significance of stress-induced hyperventilation remains uncertain, this response may blunt perception of the stress-inducing stimulus. This study examined the effects of voluntary hyperventilation and resultant hypocapnia on the local skin thermal detection threshold in normothermic resting humans. Local skin thermal detection thresholds were measured in 15 young adults (three females) under three breathing conditions: 1) spontaneous breathing (Control trial), 2) voluntary hypocapnic hyperventilation (HH trial), and 3) voluntary normocapnic hyperventilation (NH trial). Local skin thermal detection thresholds were measured using thermostimulators containing a Peltier element that were attached to the forearm and forehead. The temperature of the probe was initially equilibrated to the skin temperature, then gradually increased or decreased at a constant rate (±0.1 °C/s) until the participants felt warmth or coolness. The difference between the initial skin temperature and the local skin temperature at which the participant noticed warmth/coolness was assessed as an index of the local skin warm/cool detection threshold. Local detection of warm and cool stimuli did not differ between the Control and NH trials, but it was blunted in the HH trial as compared with the Control and NH trials, except for detection of warm stimuli on the forearm. These findings suggest that hyperventilation-induced hypocapnia, not hyperventilation per se, attenuates local skin thermal perception, though changes in responses to warm stimuli may not be clearly perceived at some skin areas (e.g., forearm).

L-menthol is known to activate transient receptor potential melastatin 8 (TRPM8) and induce analgesia to thermal stimuli. However, since thermal stimulation leads to the interaction among the other TRP channels, it was unclear whether L-menthol causes analgesia to stimuli other than thermal stimuli. Therefore, we aimed to investigate whether activating TRPM8 via topical application of 10% menthol solution attenuates pain-related somatosensory-evoked potentials (pSEPs) and affects numerical rating scale (NRS) score using intra-epidermal electrical stimulation (IES). We applied 10% L-menthol or control solution on the dorsum of the right hand of 25 healthy participants. The pSEP and NRS, elicited by IES, and sensory threshold were measured before and after each solution was applied. The results showed that the topical application of 10% L-menthol solution significantly reduced N2–P2 amplitude in pSEPs compared with the control solution. Moreover, the N2 latency was significantly prolonged upon the topical application of L-menthol solution. NRS scores were similar under both conditions. These results suggest that topical application of L-menthol does not alter subjective sensation induced using IES, although it may attenuate afferent signals at free nerve endings even with stimuli that do not directly activate TRP channels.

Cao, Yinhang, Naoto Fujii, Tomomi Fujimoto, Yin-Feng Lai, Takeshi Ogawa, Tsutomu Hiroyama, Yasushi Enomoto, and Takeshi Nishiyasu. CO

BACKGROUND Virtual reality (VR) exergaming is a new intervention strategy to help humans engage in physical activity to enhance mood. VR exergaming may improve both mood and executive function by acting on the prefrontal cortex, expanding the potential benefits. However, the impact of VR exergaming on executive function has not been fully investigated, and associated intervention strategies have not yet been established. OBJECTIVE This study investigated the effects on mood and executive function of 10 minutes of VR exergaming. METHODS A total of 12 participants played an exergame, “FitXR” under three conditions: a virtual reality exergame (VR-EX) condition in which they played using a head-mounted display (HMD); playing the exergame in front of a flat display (2D-EX), and a resting condition in which they sat in a chair (RS). The color-word Stroop task (CWST), which assesses executive function, the short form of the Profile of Mood States second edition (POMS2) and the short form of the Two-Dimensional Mood Scale (TDMS), which assess mood, were administered before and after the exercise or rest conditions. RESULTS The VR-EX condition increased the POMS2 vigor-activity score, and the TDMS arousal and vitality scores, suggesting that VR exergaming enhanced mood. Conversely, there was no effect on CWST performance in either the 2D-EX or VR-EX conditions. Interestingly, the VR-EX condition showed a significant positive correlation between changes in CWST arousal and reaction time. This suggests that the exergaming effect on improving executive function may disappear under an excessively increased arousal level in VR exergaming. CONCLUSIONS Our findings showed that 10 minutes of VR exergaming enhanced mood, but did not affect executive function. This suggests that some VR content may increase cognitive demands, leading to psychological fatigue and cognitive decline (cognitive fatigue) as an individual approaches the limits of available attentional capacity. Although VR exergaming has the potential to induce physical activity by enhancing mood, there is insufficient evidence on executive function effects. To further increase the value of VR exergaming, it is essential to further examine the combination of exercise and VR that enhances both brain function and mood.

Injuries are inevitable for athletes, and when injuries end up causing chronic pain, they usually force athletes to withdraw from training. Chronic pain is known to be caused by plastic changes in the brain; thus, the purpose of this study was to assess the somatosensory evoked potential (SEP) and the paired-pulse inhibition (PPI) in athletes suffering from chronic pain as compared to pain-free athletes. Twenty track and field (T&F) athletes, that were also undergraduate students, were recruited for this study. These athletes (12 men; 8 women) were divided into two groups of 10 based on their self-reporting of actively experiencing chronic pain (defined as pain that persisted for more than 3 months) or not. Both SEP and PPI in the primary somatosensory cortex (SI) were elicited by constant current square-wave pulses (of 0.2 ms duration) that were delivered to the right median nerve by an electrical stimulator through a surface bar electrode with a cathode proximal. Paired-pulse stimulation was set at interstimulus intervals of 30 and 100 ms. Subjects were randomly presented with 1,500 single- and paired-pulse stimuli at 2 Hz. Our measurements demonstrated a trend toward a lower N20 and P25 amplitude as well as a disinhibition of the PPI_30 ms in the athletes suffering from chronic pain. These findings suggest that chronic pain may modulate excitatory and inhibitory function of the SI in athletes as well as in patients suffering from complex regional pain syndrome or fibromyalgia.

The aim of this study was to investigate individual interoception by comparing the responses of swimmers and baseball players when exposed to specific water environments, depending on training content and environment. Forty-eight healthy male university students were evaluated for their interoceptive response (accuracy, sensibility, and awareness) and heart rate following 25 min of water immersion (WI) at 35 °C. We assessed three conditions: pre-WI, during WI, and post-WI. The results indicated that interoceptive accuracy (IAcc) did not differ between groups because both swimming and baseball do not require emotional expression, as opposed to an activity such as dance. The heart rate was significantly decreased at post-WI compared to that at pre-WI. The IAcc of post-WI presented as higher than that of pre-WI. In addition, there was a significant negative correlation between the ratio of IAcc and that of HR among subjects. Moreover, the attention regulation subscale of the MAIA changed in the WI environment and the ratio of IAcc was negatively correlated with that of the not-distracting subscale of the MAIA. These results suggested that interoception did not differ among the athletes who had long-term training, which enabled them to acquire multi-modal sensorimotor integration, compared to that of non-athlete control participants. We conclude that interoception did not differ among athletes who had long-term training compared to that of non-athlete control participants.

Hypothermia can occur during aquatic exercise despite production of significant amounts of heat by the active muscles. Because the characteristics of human thermoregulatory responses to cold during exercise have not been fully elucidated, we investigated the effect of low-intensity exercise on the shivering response to core cooling in cool water. Eight healthy young men (24 ± 3 yr) were cooled through cool water immersion while resting (rest trial) and during loadless pedaling on a water cycle ergometer (exercise trial). Before the cooling, body temperature was elevated by hot water immersion to clearly detect a core temperature at which shivering initiates. Throughout the cooling period, mean skin temperature remained around the water temperature (25°C) in both trials, whereas esophageal temperature (Tes) did not differ between the trials ( P > 0.05). The Tes at which oxygen uptake (V̇o2) rapidly increased, an index of the core temperature threshold for shivering, was lower during exercise than rest (36.2 ± 0.4°C vs. 36.5 ± 0.4°C, P < 0.05). The sensitivity of the shivering response, as indicated by the slope of the Tes-V̇o2 relation, did not differ between the trials (−441.3 ±177.4 ml·min−1·°C−1 vs. −411.8 ± 268.1 ml·min−1·°C−1, P > 0.05). The thermal sensation response to core cooling, assessed from the slope and intercept of the regression line relating Tes and thermal sensation, did not differ between the trials ( P > 0.05). These results suggest that the core temperature threshold for shivering is delayed during low-intensity exercise in cool water compared with rest although shivering sensitivity is unaffected.

Hyperthermia causes hyperventilation at rest and during exercise. We previously reported that carotid chemoreceptors partly contribute to the hyperthermia-induced hyperventilation at rest. However, given that a hyperthermia-induced hyperventilation markedly differs between rest and exercise, the results obtained at rest may not be representative of the response in exercise. Therefore, we evaluated whether carotid chemoreceptors contribute to hyperthermia-induced hyperventilation in exercising humans. Eleven healthy young men (23 ± 2 yr) cycled in the heat (37°C) at a fixed submaximal workload equal to ~55% of the individual’s predetermined peak oxygen uptake (moderate intensity). To suppress carotid chemoreceptor activity, 30-s hyperoxia breathing (100% O2) was performed at rest (before exercise) and during exercise at increasing levels of hyperthermia as defined by an increase in esophageal temperature of 0.5°C (low), 1.0°C (moderate), 1.5°C (high), and 2.0°C (severe) above resting levels. Ventilation during exercise gradually increased as esophageal temperature increased (all P ≤ 0.05), indicating that hyperthermia-induced hyperventilation occurred. Hyperoxia breathing suppressed ventilation in a greater manner during exercise (−9 to −13 l/min) than at rest (−2 ± 1 l/min); however, the magnitude of reduction during exercise did not differ at low (0.5°C) to severe (2.0°C) increases in esophageal temperature (all P > 0.05). Similarly, hyperoxia-induced changes in ventilation during exercise as assessed by percent change from prehyperoxic levels were not different at all levels of hyperthermia (~15–20%, all P > 0.05). We show that in young men carotid chemoreceptor contribution to hyperthermia-induced hyperventilation is relatively small at low-to-severe increases in body core temperature induced by moderate-intensity exercise in the heat. NEW & NOTEWORTHY Exercise-induced increases in hyperthermia cause a progressive increase in ventilation in humans. However, the mechanisms underpinning this response remain unresolved. We showed that in young men hyperventilation associated with exercise-induced hyperthermia is not predominantly mediated by carotid chemoreceptors. This study provides important new insights into the mechanism(s) underpinning the regulation of hyperthermia-induced hyperventilation in humans and suggests that factor(s) other than carotid chemoreceptors play a more important role in mediating this response.

This study aimed to determine whether heat exposure attenuates motor control performance and learning, and blunts cardiovascular and thermoregulatory responses to visuomotor accuracy tracking (VAT) tasks. Twenty-nine healthy young adults (22 males) were divided into two groups performing VAT tasks (5 trials × 10 blocks) in thermoneutral (NEUT: 25 °C, 45% RH, n = 14) and hot (HOT: 35 °C, 45% RH, n = 15) environments (acquisition phase). One block of the VAT task was repeated at 1, 2, and 4 h after the acquisition phase (retention phase). Heat exposure elevated skin temperature to ~3 °C with a marginally increased core body temperature. VAT performance (error distance of curve tracking) was more attenuated overall in HOT than in NEUT in the acquisition phase without improvement in magnitude alteration. Heat exposure did not affect VAT performance in the retention phase. The mean arterial blood pressure and heart rate, but not for sweating and cutaneous vascular responses to VAT acquisition trials, were more attenuated in HOT than in NEUT without any retention phase alternations. We conclude that skin temperature elevation exacerbates motor control performance and blunts cardiovascular response during the motor skill acquisition period. However, these alternations are not sustainable thereafter.

Response inhibition plays an essential role in preventing anticipated and unpredictable events in our daily lives. It is divided into proactive inhibition, where subjects postpone responses to an upcoming signal, and reactive inhibition, where subjects stop an impending movement based on the presentation of a signal. Different types of sensory input are involved in both inhibitions; however, differences in proactive and reactive inhibition with differences in sensory modalities remain unclear. This study compared proactive and reactive inhibitions induced by visual, auditory, and somatosensory signals using the choice reaction task (CRT) and stop-signal task (SST). The experiments showed that proactive inhibitions were significantly higher in the auditory and somatosensory modalities than in the visual modality, whereas reactive inhibitions were not. Examining the proactive inhibition-associated neural processing, the auditory and somatosensory modalities showed significant decreases in P3 amplitudes in Go signal-locked event-related potentials (ERPs) in SST relative to those in CRT; this might reflect a decreasing attentional resource on response execution in SST in both modalities. In contrast, we did not find significant differences in the reactive inhibition-associated ERPs. These results suggest that proactive inhibition varies with different sensory modalities, whereas reactive inhibition does not.

INTRODUCTION Caffeine is an exercise performance enhancer widely used by individuals engaged in training or competition under heat-stressed conditions. Caffeine ingestion during exercise in the heat is believed to be safe because it does not greatly affect body temperature responses, heart rate, or body fluid status. However, it remains unknown whether caffeine affects hyperthermia-induced hyperventilation or reductions in the cerebral blood flow index. We tested the hypothesis that under conditions inducing severe hyperthermia, caffeine exacerbates hyperthermia-induced hyperventilation and reduces the cerebral blood flow index during exercise. METHODS Using a randomized, single-blind, crossover design, 12 physically active healthy young men (23 ± 2 yr) consumed a moderate dose of caffeine (5 mg·kg-1) or placebo in the heat (37°C). Approximately 60 min after the ingestion, they cycled for ~45 min at a workload equal to ~55% of their predetermined peak oxygen uptake (moderate intensity) until their core temperature increased to 2.0°C above its preexercise baseline level. RESULTS In both trials, ventilation increased and the cerebral blood flow index assessed by middle cerebral artery mean blood velocity decreased as core temperature rose during exercise (P < 0.05), indicating that hyperthermia-induced hyperventilation and lowering of the cerebral blood flow occurred. When core temperature was elevated by 1.5°C or more (P < 0.05), ventilation was higher and the cerebral blood flow was lower throughout the caffeine trial than the placebo trial (P < 0.05). CONCLUSIONS A moderate dose of caffeine exacerbates hyperthermia-induced hyperventilation and reductions in the cerebral blood flow index during exercise in the heat with severe hyperthermia.

Hypoxic modulation of nitric oxide (NO) production pathways in the cutaneous microvasculature and its interaction with cold-induced reflex vasoconstriction, independent of local cooling, have yet to be identified. This study assessed the contribution of NO to nonglabrous microvasculature perfusion during hypoxia and whole body cooling with concomitant inhibition of NO synthase [NOS; via N G-nitro-L-arginine methyl ester (L-NAME)] and the nitrite reductase, xanthine oxidase (via allopurinol), two primary sources of NO production. Thirteen volunteers were exposed to independent and combined cooling via water-perfused suit (5°C) and normobaric hypoxia (FI O2, 0.109 + 0.002). Cutaneous vascular conductance (CVC) was assessed across four sites with intradermal microdialysis perfusion of 1) lactated Ringers solution (control), 2) 20 mmol L-NAME, 3) 10 mol allopurinol, or 4) combined L-NAME/allopurinol. Effects and interactions were assessed via four-way repeated measures ANOVA. Independently, L-NAME reduced CVC (43%, P < 0.001), whereas allopurinol did not alter CVC (P = 0.5). Cooling decreased CVC (P = 0.001), and the reduction in CVC was consistent across perfusates (~30%, P = 0.9). Hypoxia increased CVC (16%, P = 0.01), with this effect abolished by L-NAME infusion (P = 0.04). Cold-induced vasoconstriction was blunted by hypoxia, but importantly, hypoxia increased CVC to a similar extent (39% at the Ringer site) irrespective of environmental temperature; thus, no interaction was observed between cold and hypoxia (P = 0.1). L-NAME restored vasoconstriction during combined cold-hypoxia (P = 0.01). This investigation suggests that reflex cold-induced cutaneous vasoconstriction acts independently of NO suppression, whereas hypoxia-induced cutaneous vasodilatation is dependent on NOS-derived NO production.

Twenty minutes of voluntary hypocapnic hyperventilation prior to exercise reduces the aerobic metabolic rate with a compensatory increase in the anaerobic metabolic rate without affecting exercise ...

Background The physical and mental impacts of breast cancer diagnosis on women are substantial. Several studies have investigated the negative mental health effects of breast cancer. However, in recent years, there has also been growing interest in post-traumatic growth, a positive response to stressful events. Considering positive psychology focuses on such virtues, proactive coping theory was chosen as a theoretical guide. This study investigates how breast cancer patients’ post-traumatic growth is associated with proactive coping and mental well-being. Methods A self-administered questionnaire survey was conducted with 80 breast cancer patients aged 20–70 years attending an outpatient clinic. The survey was conducted using the Posttraumatic Growth Inventory-Japanese version (PTGI-J), Proactive Coping Inventory-Japanese version and the Japanese version of the General Health Questionnaire. Single regression and multiple regression analyses with PTGI-J as the dependent variable were performed. Results The multiple regression analysis extracted proactive coping (P = 0.006), emotional support seeking (P = 0.004) and avoidance coping (P = 0.001) as factors associated with post-traumatic growth in breast cancer patients. Conclusions These results suggest that using proactive coping for conflicts caused by a breast cancer diagnosis and temporary avoidant coping for daily stresses during the treatment process may enhance post-traumatic growth while preventing deterioration in mental well-being. Additionally, seeking emotional support is important for post-traumatic growth.

To investigate the effect of voluntary hypocapnic hyperventilation or moderate hypoxia on metabolic and heart rate responses during high-intensity intermittent exercise. Ten males performed three 30-s bouts of high-intensity cycling [Ex1 and Ex2: constant-workload at 80% of the power output in the Wingate anaerobic test (WAnT), Ex3: WAnT] interspaced with 4-min recovery periods under normoxic (Control), hypocapnic or hypoxic (2500 m) conditions. Hypocapnia was developed through voluntary hyperventilation for 20 min prior to Ex1 and during each recovery period. End-tidal CO2 pressure was lower before each exercise in the hypocapnia than control trials. Oxygen uptake ( $$\dot{V}{\text{O}}_{ 2}$$ ) was lower in the hypocapnia than control trials (822 ± 235 vs. 1645 ± 245 mL min−1; mean ± SD) during Ex1, but not Ex2 or Ex3, without a between-trial difference in the power output during the exercises. Heart rates (HRs) during Ex1 (127 ± 8 vs. 142 ± 10 beats min−1) and subsequent post-exercise recovery periods were lower in the hypocapnia than control trials, without differences during or after Ex2, except at 4 min into the second recovery period. $$\dot{V}{\text{O}}_{ 2}$$ did not differ between the control and hypoxia trials throughout. These results suggest that during three 30-s bouts of high-intensity intermittent cycling, (1) hypocapnia reduces the aerobic metabolic rate with a compensatory increase in the anaerobic metabolic rate during the first but not subsequent exercises; (2) HRs during the exercise and post-exercise recovery periods are lowered by hypocapnia, but this effect is diminished with repeated exercise bouts, and (3) moderate hypoxia (2500 m) does not affect the metabolic response during exercise.

This study investigated the effects of water temperature on cardiorespiratory responses and exercise performance during immersed incremental cycle exercise until exhaustion. Ten healthy young men performed incremental cycle exercise on a water cycle ergometer at water temperatures (T w) of 18, 26 and 34 °C. Workload was initially set at 60 W and was increased by 20 W every 2 min for the first four levels and then by 10 W every minute until the subject could no longer continue. During submaximal exercise (60–120 W), $$\dot{V}{\text{O}}_{2}$$ was greater at T w = 18 °C than at 26 or 34 °C. Maximal workload was lower at T w = 18 °C than at 26 or 34 °C [T w = 18 °C: 138 ± 16 (SD) W, T w = 26 °C: 157 ± 16 W, T w = 34 °C: 156 ± 18 W], whereas $$\dot{V}$$ O2peak did not differ among the three temperatures [T w = 18 °C: 3156 ± 364 (SD) ml min−1, T w = 26 °C: 3270 ± 344 ml min−1, T w = 34 °C: 3281 ± 268 ml min−1]. Minute ventilation ( $$\dot{V}_{\text{E}}$$ ) and tidal volume (V T) during submaximal exercise were higher at T w = 18 °C than at 26 or 34 °C, while respiratory frequency (f R) did not differ with respect to T w. Peak workload during immersed incremental cycle exercise is lower in cold water (18 °C) due to the higher $$\dot{V}{\text{O}}_{2}$$ during submaximal exercise, while the greater $$\dot{V}_{\text{E}}$$ in cold water was due to a larger V T.

The ether coordination of the oxygen atom to the copper(II) center supported by dipicolylamine (DPA)-derived ligands,N-[2-(2-pyridylmethyloxy)ethyl]-N,N-bis(2-pyridylmethyl)amine (LPy), N-[2-(2-quinolylmethyloxy)ethyl]-N,N-bis(2-pyridylmethyl)amine (LQ), N-[3-(2-pyridylmethyloxy)-1-propyl]-N,N-bis(2-pyridylmethyl)amine (L′Py), N-{2-[1-(2-pyridyl)ethyloxy]ethyl}-N,N-bis(2-pyridylmethyl)amine (LPy*1), N-[2-(2-pyridylmethyloxy)-1-propyl]-N,N-bis(2-pyridylmethyl)amine (LPy*2), and N-[2-(carboxymethyloxy)ethyl]-N,N-bis(2-pyridylmethyl)amine (HLCOO), have been examined. The factors that facilitate the coordination of the ether oxygen atom of these ligands to the copper center and the control of chirality around the copper-coordinated oxygen atom are discussed. The copper center exhibits a pentacoordinate geometry with these ligands, as evidenced by X-ray crystallography. The steric effect of the quinoline ring in the LQ complex prevents the coordination of a perchlorate anion to the copper center, which affords the pentacoordinate divalent complex with a shorter copper–oxygen bond than that for the corresponding pyridine ligand (LPy). The six-membered chelate in the L′Py complex also exhibits a shorter Cu–O distance. The conformation of the oxygen atom of the LPy complex is unstable because of fast lone pair inversion, but this inversion is prevented for the complexes with chiral ligands, LPy*1 and LPy*2. Upon chelation to the metal center, the HLCOO ligand forms a pentacoodinate monomer complex that further affords a 1-D polymer structure. With respect to the oxygen chirality, the water content of the solvent governs the formation of either a homochiral polymer (R-R-R-R- or S-S-S-S-) or an alternative chirality polymer (R-S-R-S-). In this case, the isomers with respect to the oxygen chirality were separated and characterized.

The ether oxygen coordination to the zinc center in the complexes with dipicolylamine (DPA)-derived ligands, N-(2-methoxyethyl)-N,N-bis(2-pyridylmethyl)amine (L), N-(3-methoxypropyl)-N,N-bis(2-pyridylmethyl)amine (L′), and N-{3-(2-pyridylmethyloxy)propyl}-N,N-bis(2-pyridylmethyl)amine (LPy) has been discussed. Upon chelation of the oxygen atom, L forms a five-membered chelate ring with respect to the 2-aminoethyl ether moiety whereas L′ forms a six-membered chelate in 3-aminopropyl ether unit. This difference was highlighted by the crystal structures of ZnCl2 complexes, in which [Zn(L)Cl2] (1) exhibited ether oxygen coordination but [Zn(L′)Cl2] (2) had the ether oxygen non-coordinated. The terminal pyridyl group of LPy facilitates the ether oxygen atom coordination via a metal binding from the basal plane trans to the aliphatic nitrogen.

This article is dedicated to late Dr. Ito for his distinguished invention, fantastic technology, and warmhearted humanityRefractive index lithography was performed on polymer films consist of a photo-acid generator (PAG), t-BOC-protected naphthazarine as an acid chromic dye. The key reaction is the chemically amplified de-protection of the t-BOC group, by which color of the material change followed by refractive index change. Naphthazarine-containing polymer was also prepared. The induced refractive index was as large as 4X10-3, which is enough large to apply to optical waveguide fabrication.

Aquatic exercise such as swimming is performed in the water of 18 to 34 °C because of the differences in ambient environmental conditions. Heat conductivity of water is greater than that of air, therefore water temperature would have a considerable impact on physiological responses and exercise performance. A previous study has shown that, oxygen consumption (V(·)O2) during immersed cycle exercise at submaximal workload is greater in cold water (18 °C) compared to moderately cool and warm water (25 and 34 °C) [1]. Furthermore, previous studies have reported decreased V(·)O2 at maximal work (V(·)O2peak) in the cold water [2], while others have reported no change [3]. Therefore, consensus views on whether difference in water temperature affects V(·)O2peak and exercise performance hasn't been obtained. The purpose of this study was to investigate the effects of water temperature on physiological responses and exercise performance using immersed incremental cycle exercise until exhaustion.

Although some polymethoxyflavones possess several important biological properties, including neuroprotective, anticancer, and anti-inflammatory ones, sudachitin, a polymethoxyflavone from Citrus sudachi, has been little studied. In this study, we found that sudachitin inhibited nitric oxide production by suppressing the expression of inducible nitric oxide synthase in lipopolysaccharide-stimulated macrophages, indicating that sudachitin has an anti-inflammatory effect.