Running, compared to pedaling is a whole-body locomotive movement that may confer more mental health via strongly stimulating brains, although running impacts on mental health but their underlying brain mechanisms have yet to be determined; since almost the mechanistic studies have been done with pedaling. We thus aimed at determining the acute effect of a single bout of running at moderate-intensity, the most popular condition, on mood and executive function as well as their neural substrates in the prefrontal cortex (PFC). Twenty-six healthy participants completed both a 10-min running session on a treadmill at 50%$${\dot{\text{V}}\text{O}}_{{{\text{2peak}}}}$$ V ˙ O 2peak and a resting control session in randomized order. Executive function was assessed using the Stroop interference time from the color-word matching Stroop task (CWST) and mood was assessed using the Two-Dimensional Mood Scale, before and after both sessions. Prefrontal hemodynamic changes while performing the CWST were investigated using functional near-infrared spectroscopy. Running resulted in significant enhanced arousal and pleasure level compared to control. Running also caused significant greater reduction of Stroop interference time and increase in Oxy-Hb signals in bilateral PFCs. Besides, we found a significant association among pleasure level, Stroop interference reaction time, and the left dorsolateral PFCs: important brain loci for inhibitory control and mood regulation. To our knowledge, an acute moderate-intensity running has the beneficial of inducing a positive mood and enhancing executive function coinciding with cortical activation in the prefrontal subregions involved in inhibitory control and mood regulation. These results together with previous findings with pedaling imply the specificity of moderate running benefits promoting both cognition and pleasant mood.
Recent studies have reported that acute aerobic exercise modulates intracortical excitability in the primary motor cortex (M1). However, whether acute low-intensity aerobic exercise can also modulate M1 intracortical excitability, particularly intracortical excitatory circuits, remains unclear. In addition, no previous studies have investigated the effect of acute aerobic exercise on short-latency afferent inhibition (SAI). The aim of this study was to investigate whether acute low-intensity aerobic exercise modulates intracortical circuits in the M1 hand and leg areas. Intracortical excitability of M1 (Experiments 1, 2) and spinal excitability (Experiment 3) were measured before and after acute low-intensity aerobic exercise. In Experiment 3, skin temperature was also measured throughout the experiment. Transcranial magnetic stimulation was applied over the M1 non-exercised hand and exercised leg areas in Experiments 1, 2, respectively. Participants performed 30 min of low-intensity pedaling exercise or rested while sitting on the ergometer. Short- and long-interval intracortical inhibition (SICI and LICI), and SAI were measured to assess M1 inhibitory circuits. Intracortical facilitation (ICF) and short-interval intracortical facilitation (SICF) were measured to assess M1 excitatory circuits. We found that acute low-intensity aerobic exercise decreased SICI and SAI in the M1 hand and leg areas. After exercise, ICF in the M1 hand area was lower than in the control experiment, but was not significantly different to baseline. The single motor-evoked potential, resting motor threshold, LICI, SICF, and spinal excitability did not change following exercise. In conclusion, acute low-intensity pedaling modulates M1 intracortical circuits of both exercised and non-exercised areas, without affecting corticospinal and spinal excitability.
Long-term skills training is known to induce neuroplastic alterations, but it is still debated whether these changes are always modality-specific or can be supramodal components. To address this issue, we compared finger-targeted somatosensory-evoked and auditory-evoked potentials under both Go (response) and Nogo (response inhibition) conditions between 10 baseball players, who require fine hand/digit skills and response inhibition, to 12 matched track and field (T&F) athletes. Electroencephalograms were obtained at nine cortical electrode positions. Go potentials, Nogo potentials, and Go/Nogo reaction time (Go/Nogo RT) were measured during equiprobable somatosensory and auditory Go/Nogo paradigms. Nogo potentials were obtained by subtracting Go trial from Nogo trial responses. Somatosensory Go P100 latency and Go/Nogo RT were significantly shorter in the baseball group than the T&F group, while auditory Go N100 latency and Go/Nogo RT did not differ between groups. Additionally, somatosensory subtracted Nogo N2 latency was significantly shorter in the baseball group than the T&F group. Furthermore, there were significant positive correlations between somatosensory Go/Nogo RT and both Go P100 latency and subtracted Nogo N2 latency, but no significant correlations among auditory responses. We speculate that long-term skills training induce predominantly modality-specific neuroplastic changes that can improve both execution and response inhibition.
Acute aerobic exercise at a mild intensity improves cognitive function. However, the response to exercise exhibits inter-individual differences, and the mechanisms underlying these differences remain unclear. The objective of this study was to determine potential factors in the brain that underlie differential responses to exercise in terms of cognitive improvement using functional near-infrared spectroscopy. Fourteen healthy subjects participated in these experiments. Participants performed a low intensity cycling exercise at 30% maximal oxygen uptake (VO) for 10 min and performed a spatial memory task before and after exercising (5 and 30 min). The spatial memory task comprised two levels of difficulty (low: 1-dot EXERCISE, high: 3-dot EXERCISE). Cortical oxy-hemoglobin (OHb) levels were recorded using near-infrared spectroscopy during both the exercise and the spatial memory task phases. Regions of interests included the dorsolateral prefrontal cortex (DLPFC), ventrolateral prefrontal cortex (VLPFC), and frontopolar area (FPA). The participants were divided into two groups depending on whether they were responders (improved task reaction time) or non-responders (no improvement). Subsequently, we analyzed the group characteristics and differences in the change in OHb levels during exercise and spatial working memory tasks. Acute mild exercise significantly improved mean reaction times in the 1-dot memory task but not in the 3-dot task across the participants. In the 1-dot EXERCISE, 10 subjects were responders and four subjects were non-responders, whereas in the 3-dot EXERCISE, seven subjects were non-responders. In responders, during exercise, we found higher OHb levels in the right VLPFC response for the 1-dot memory task. Acute mild exercise caused inter-individual differences in spatial memory improvement, which were associated with changes in OHb activity in the prefrontal area during the exercise phase but not during the actual spatial memory task. Therefore, individuals who respond with higher reactivity to mild intensity exercise in the VLPFC might obtain larger spatial working memory improvements following exercise than non-responders.
Background para-Tyramine (p-TA) is a biogenic amine which is involved in multiple neuronal signal transductions. Since the concentration of p-TA in dog cerebrospinal fluid (CSF) has been reported to be greater than that in plasma, it is proposed that clearance of cerebral p-TA is important for normal function. The purpose of this study was to examine the role of the blood–brain barrier and blood-cerebrospinal fluid barrier (BCSFB) in p-TA clearance from the brain.MethodsIn vivo [3H]p-TA elimination from rat cerebral cortex and from CSF was examined after intracerebral and intracerebroventricular administration, respectively. To evaluate BCSFB-mediated p-TA transport, [3H]p-TA uptake by isolated rat choroid plexus and conditionally immortalized rat choroid plexus epithelial cells, TR-CSFB3 cells, was performed.ResultsThe half-life of [3H]p-TA elimination from rat CSF was found to be 2.9 min, which is 62-fold faster than that from rat cerebral cortex. In addition, this [3H]p-TA elimination from the CSF was significantly inhibited by co-injection of excess unlabeled p-TA. Thus, carrier-mediated p-TA transport process(es) are assumed to take part in p-TA elimination from the CSF. Since it is known that transporters at the BCSFB participate in compound elimination from the CSF, [3H]p-TA transport in ex vivo and in vitro models of rat BCSFB was examined. The [3H]p-TA uptake by isolated rat choroid plexus and TR-CSFB3 cells was time-dependent and was inhibited by unlabeled p-TA, indicating carrier-mediated p-TA transport at the BCSFB. The p-TA uptake by isolated choroid plexus and TR-CSFB3 cells was not reduced in the absence of extracellular Na+ and Cl−, and in the presence of substrates of typical organic cation transporters. However, this p-TA uptake was significantly inhibited by cationic drugs such as propranolol, imipramine, amantadine, verapamil, and pyrilamine. Moreover, p-TA uptake by TR-CSFB3 cells took place in an oppositely-directed H+ gradient manner. Therefore, this suggested that p-TA transport at the BCSFB involves cationic drug-sensitive transport systems which are distinct from typical plasma membrane organic cation transporters.ConclusionOur study indicates that p-TA elimination from the CSF is greater than that from the cerebral cortex. Moreover, it is suggested that cationic drug-sensitive transport systems in the BCSFB participate in this p-TA elimination from the CSF.
Although it has been hypothesized that moderate to vigorous exercise immediately modulates cognition via ascending arousal system activation, such activation during very-light to light exercise has remained uncertain. Here, we aimed to uncover the exact exercise intensity necessary for ascending arousal system activation using pupillometry. The pupil diameter, psychological arousal, and ventilation during graded exercise of 26 young males were analyzed based on %$${\dot{V}}_{{\text{O}}_{\text{2peak}}}$$ V ˙ O 2peak . Pupils dilated with very-light exercise compared to rest, stabilized, and then drastically increased again with moderate exercise and above. Pupil dilation with very-light exercise was positively correlated with increases in psychological arousal. Thus, we have shown that there are two phases of pupil dilation during graded exercise: one with very-light exercise coinciding with psychological arousal response, and the other with moderate exercise or above similar to the ventilation increase pattern. This unique pupil dilation pattern provides physiological evidence of ascending arousal system activation with very-light exercise.
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