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.

No abstract

Peak workload during immersed incremental cycle exercise is lower in cold water (18 °C) due to the higher [Formula: see text] during submaximal exercise, while the greater [Formula: see text] in cold water was due to a larger V T.

Hyperthermia increases ventilation in resting and exercising humans (White, J Appl Physiol 101: 655–663, 2006; Fujii et al. J Appl Physiol 104:998–1005, 2008), though what mechanisms mediate this response remains unclear. Carotid chemoreceptors can contribute to ventilatory regulation. Since hyperthermia can augment carotid chemoreceptor activity as demonstrated under in vitro conditions (Eyzaguirre and Zapata, J Appl Physiol 57: 931–957, 1984), this increased activity may in part mediate hyperthermia induced hyperventilation in humans. Regarding this, we previously reported that carotid chemoreceptor is not a main factor mediating hyperthermia induced hyperventilation at rest (Fujii et al. Exp Physiol 93: 994–1001, 2008). However, given hyperthermia induced hyperventilation differs between rest and exercise (Fujii et al. J Appl Physiol 104:998–1005, 2008), the results obtained at rest may not be representative of the response in exercise. Therefore, the purpose of this study was to evaluate whether carotid chemoreceptors contribute to hyperthermia‐induced hyperventilation in exercising humans. Eleven healthy young males (21 ± 3 years) performed cycling in the heat (37 °C) (35–55 min) at a fixed submaximal workload equal to ~55% of the individual's pre‐determined peak oxygen uptake. In order to suppress carotid chemoreceptor activity, 30‐s hyperoxic breathing (100% O2) was performed at rest (before exercise), 5 min into exercise, as well as at increasing levels of hyperthermia as defined by an increase in esophageal temperature (an index of body core temperature) of 0.5, 1.0, and 1.5 °C above levels measured at 5‐min into exercise. Ventilation during exercise gradually increased as esophageal temperature increased (all P < 0.05), indicating that hyperthermia induced hyperventilation occurred. Carotid chemoreceptor inhibition with hyperoxic breathing suppressed ventilation at rest as well as during exercise regardless of the level of hyperthermia (all P < 0.05). Hyperoxia induced changes in ventilation (as assessed by % change from pre‐hyperoxic level) were −15 ± 7 % at rest and −15 ± 6 % at 5 min into exercise. The hyperoxia induced changes in ventilation during exercise for an esophageal temperature increase of 0.5, 1.0, and 1.5 °C were −18 ± 7 %, −17 ± 7 %, and −19 ± 8 %, all of which were not different from the 5‐min exercise level (all P > 0.05). These results demonstrate that carotid chemoreceptor contribution to ventilation during exercise is not modulated by the level of hyperthermia. Thus, we show that carotid chemoreceptors are not largely involved in the regulation of hyperthermia induced hyperventilation in exercising humans irrespective of state of hyperthermia. Support or Funding Information This study was supported by the grants from Ministry of Education, Culture, Sports, Science and Technology in Japan and Japan Society for the Promotion of Science. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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.

Although contractile interstitial cells (CIC) in the alveolar septum have been suggested to be involved in hypoxic pulmonary vasoconstriction (HPV), direct demonstration of cellular contraction under hypoxia has been lacking. To achieve this, we purified CIC from collagenase-dissociated bovine lung cells and examined the response of these cells to hypoxia. Prostaglandin (PG) F synthase served as a marker of CIC, and the isolated PGF synthase-positive cells were shown to preserve the ultrastructural features characteristic of CIC, most notably bundles of microfilaments. Isolated CIC seeded onto collagen gel disks became embedded and formed a lattice network with collagen fibrils. Exposure of these CIC-bearing gels to hypoxia (PO2 = 20-40 Torr) evoked a reversible reduction in gel volume, as assessed by measuring the surface area of the gel disks photographically. Thus CIC were shown to contract under hypoxia, providing the supportive evidence for the involvement of CIC in HPV.

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 aims to investigate the effects of 10 minutes of VR exergaming on mood and executive function. Methods A total of 12 participants played the exergame “FitXR” under 3 conditions: (1) a VR exergame condition (ie, exercise with a head-mounted display condition [VR-EX]) in which they played using a head-mounted display, (2) playing the exergame in front of a flat display (2D-EX), and (3) a resting condition in which they sat in a chair. 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 (rest and VR-EX: t11=3.69, P=.003) as well as the TDMS arousal (rest vs 2D-EX: t11=5.34, P<.001; rest vs VR-EX: t11=5.99, P<.001; 2D-EX vs VR-EX: t11=3.02, P=.01) and vitality scores (rest vs 2D-EX: t11=3.74, P=.007; rest vs VR-EX: t11=4.84, P=.002; 2D-EX vs VR-EX: t11=3.53, P=.006), 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 (r=0.58, P=.046). This suggests that the effect of exergaming 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 as an individual approaches the limits of available attentional capacity. Future research must examine the combination of exercise and VR that enhances both brain function and mood.

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.