Endurance exercise‐induced and mental fatigue and the brain

2020 ◽  
Author(s):  
Romain Meeusen ◽  
Jeroen Van Cutsem ◽  
Bart Roelands
Keyword(s):  
Endurance Exercise ◽  
Mental Fatigue ◽  
Exercise Induced ◽  
The Brain

scholarly journals From Exercise to Cognitive Performance: Role of Irisin

2021 ◽  
Vol 11 (15) ◽  
pp. 7120
Author(s):  
Mirko Pesce ◽  
Irene La Fratta ◽  
Teresa Paolucci ◽  
Alfredo Grilli ◽  
Antonia Patruno ◽  
...  
Keyword(s):  
The Elderly ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Beneficial Effects ◽  
General Exercise ◽  
Fibronectin Type Iii ◽  
Exercise Induced ◽  
Fibronectin Type Iii Domain ◽  
The Brain

The beneficial effects of exercise on the brain are well known. In general, exercise offers an effective way to improve cognitive function in all ages, particularly in the elderly, who are considered the most vulnerable to neurodegenerative disorders. In this regard, myokines, hormones secreted by muscle in response to exercise, have recently gained attention as beneficial mediators. Irisin is a novel exercise-induced myokine, that modulates several bodily processes, such as glucose homeostasis, and reduces systemic inflammation. Irisin is cleaved from fibronectin type III domain containing 5 (FNDC5), a transmembrane precursor protein expressed in muscle under the control of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α). The FNDC5/irisin system is also expressed in the hippocampus, where it stimulates the expression of the neurotrophin brain-derived neurotrophic factor in this area that is associated with learning and memory. In this review, we aimed to discuss the role of irisin as a key mediator of the beneficial effects of exercise on synaptic plasticity and memory in the elderly, suggesting its roles within the main promoters of the beneficial effects of exercise on the brain.

scholarly journals Exercise-Induced Lactate Release Mediates Mitochondrial Biogenesis in the Hippocampus of Mice via Monocarboxylate Transporters

2021 ◽  
Vol 12 ◽  
Author(s):  
Jonghyuk Park ◽  
Jimmy Kim ◽  
Toshio Mikami
Keyword(s):  
Blood Lactate ◽  
Mitochondrial Biogenesis ◽  
High Intensity ◽  
Lactate Concentration ◽  
High Intensity Exercise ◽  
Mtdna Copy Number ◽  
Single Bout ◽  
Extracellular Lactate ◽  
Exercise Induced ◽  
The Brain

Regular exercise training induces mitochondrial biogenesis in the brain via activation of peroxisome proliferator-activated receptor gamma-coactivator 1α (PGC-1α). However, it remains unclear whether a single bout of exercise would increase mitochondrial biogenesis in the brain. Therefore, we first investigated whether mitochondrial biogenesis in the hippocampus is affected by a single bout of exercise in mice. A single bout of high-intensity exercise, but not low- or moderate-intensity, increased hippocampal PGC-1α mRNA and mitochondrial DNA (mtDNA) copy number at 12 and 48h. These results depended on exercise intensity, and blood lactate levels observed immediately after exercise. As lactate induces mitochondrial biogenesis in the brain, we examined the effects of acute lactate administration on blood and hippocampal extracellular lactate concentration by in vivo microdialysis. Intraperitoneal (I.P.) lactate injection increased hippocampal extracellular lactate concentration to the same as blood lactate level, promoting PGC-1α mRNA expression in the hippocampus. However, this was suppressed by administering UK5099, a lactate transporter inhibitor, before lactate injection. I.P. UK5099 administration did not affect running performance and blood lactate concentration immediately after exercise but attenuated exercise-induced hippocampal PGC-1α mRNA and mtDNA copy number. In addition, hippocampal monocarboxylate transporters (MCT)1, MCT2, and brain-derived neurotrophic factor (BDNF) mRNA expression, except MCT4, also increased after high-intensity exercise, which was abolished by UK5099 administration. Further, injection of 1,4-dideoxy-1,4-imino-D-arabinitol (glycogen phosphorylase inhibitor) into the hippocampus before high-intensity exercise suppressed glycogen consumption during exercise, but hippocampal lactate, PGC-1α, MCT1, and MCT2 mRNA concentrations were not altered after exercise. These results indicate that the increased blood lactate released from skeletal muscle may induce hippocampal mitochondrial biogenesis and BDNF expression by inducing MCT expression in mice, especially during short-term high-intensity exercise. Thus, a single bout of exercise above the lactate threshold could provide an effective strategy for increasing mitochondrial biogenesis in the hippocampus.

scholarly journals Exercise: Teaching myocytes new tricks

2017 ◽  
Vol 123 (2) ◽  
pp. 460-472 ◽  
Author(s):  
Scott K. Powers
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Cardiac Myocytes ◽  
Endurance Exercise ◽  
Ischemia Reperfusion ◽  
Muscle Fibers ◽  
Cardiac Phenotype ◽  
Endurance Exercise Training ◽  
Skeletal Muscle Fibers ◽  
Exercise Induced

Endurance exercise training promotes numerous cellular adaptations in both cardiac myocytes and skeletal muscle fibers. For example, exercise training fosters changes in mitochondrial function due to increased mitochondrial protein expression and accelerated mitochondrial turnover. Additionally, endurance exercise training alters the abundance of numerous cytosolic and mitochondrial proteins in both cardiac and skeletal muscle myocytes, resulting in a protective phenotype in the active fibers; this exercise-induced protection of cardiac and skeletal muscle fibers is often referred to as “exercise preconditioning.” As few as 3–5 consecutive days of endurance exercise training result in a preconditioned cardiac phenotype that is sheltered against ischemia-reperfusion-induced injury. Similarly, endurance exercise training results in preconditioned skeletal muscle fibers that are resistant to a variety of stresses (e.g., heat stress, exercise-induced oxidative stress, and inactivity-induced atrophy). Many studies have probed the mechanisms responsible for exercise-induced preconditioning of cardiac and skeletal muscle fibers; these studies are important, because they provide an improved understanding of the biochemical mechanisms responsible for exercise-induced preconditioning, which has the potential to lead to innovative pharmacological therapies aimed at minimizing stress-induced injury to cardiac and skeletal muscle. This review summarizes the development of exercise-induced protection of cardiac myocytes and skeletal muscle fibers and highlights the putative mechanisms responsible for exercise-induced protection in the heart and skeletal muscles.

Exhaustive endurance exercise activates brain glycogen breakdown and lactate production more than insulin-induced hypoglycemia

2021 ◽  
Author(s):  
Takashi Matsui
Keyword(s):  
Endurance Exercise ◽  
Lactate Production ◽  
Severe Hypoglycemia ◽  
Exercise Group ◽  
Exhaustive Exercise ◽  
Endurance Capacity ◽  
Brain Glycogen ◽  
Insulin Group ◽  
Exercise Induced

Brain glycogen localized in astrocytes produces lactate via cAMP signaling, which regulates memory functions and endurance capacity. Exhaustive endurance exercise with hypoglycemia decreases brain glycogen, although the mechanism underlying this phenomenon remains unclear. Since insulin-induced hypoglycemia decreases brain glycogen, this study tested the hypothesis that hypoglycemia mediates exercise-induced brain glycogen decrease. To test the hypothesis, the effects of insulin- and exhaustive exercise-induced hypoglycemia on brain glycogen levels were compared using the microwave irradiation method in adult Wistar rats. The insulin challenge and exhaustive exercise induced similar levels of severe hypoglycemia. Glycogen in the hypothalamus and cerebellum decreased similarly with the insulin challenge and exhaustive exercise; however, glycogen in the cortex, hippocampus, and brainstem of the exercise group were lower compared to the insulin group. Blood glucose correlated positively with brain glycogen, but the slope of regression lines was greater in the exercise group compared to the insulin group in the cortex, hippocampus, and brainstem, but not the hypothalamus and cerebellum. Brain lactate and cAMP levels in the hypothalamus and cerebellum increased similarly with the insulin challenge and exhaustive exercise, but those in the cortex, hippocampus, and brainstem of the exercise group were higher compared to the insulin group. These findings support the hypothesis that hypoglycemia mediates the exercise-induced reduction in brain glycogen, at least in the hypothalamus and cerebellum. However, glycogen reduction during exhaustive endurance exercise in the cortex, hippocampus, and brainstem is not due to hypoglycemia alone, implicating the role of exercise-specific neuronal activity in brain glycogen decrease.

scholarly journals Potential signaling pathways of acute endurance exercise-induced cardiac autophagy and mitophagy and its possible role in cardioprotection

2017 ◽  
Vol 67 (6) ◽  
pp. 639-654 ◽  
Author(s):  
Youngil Lee ◽  
Insu Kwon ◽  
Yongchul Jang ◽  
Wankeun Song ◽  
Ludmila M. Cosio-Lima ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Endurance Exercise ◽  
Exercise Induced

scholarly journals Identification of human exercise-induced myokines using secretome analysis

2014 ◽  
Vol 46 (7) ◽  
pp. 256-267 ◽  
Author(s):  
Milène Catoire ◽  
Marco Mensink ◽  
Eric Kalkhoven ◽  
Patrick Schrauwen ◽  
Sander Kersten
Keyword(s):  
Plasma Level ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Acute Exercise ◽  
Exercise Intervention ◽  
Training Intervention ◽  
Secretome Analysis ◽  
Exercise Training Intervention ◽  
Exercise Induced ◽  
Male Subjects

Endurance exercise is associated with significant improvements in cardio-metabolic risk parameters. A role for myokines has been hypothesized, yet limited information is available about myokines induced by acute endurance exercise in humans. Therefore, the aim of the study was to identify novel exercise-induced myokines in humans. To this end, we carried out a 1 h one-legged acute endurance exercise intervention in 12 male subjects and a 12 wk exercise training intervention in 18 male subjects. Muscle biopsies were taken before and after acute exercise or exercise training and were subjected to microarray-based analysis of secreted proteins (secretome). For acute exercise, secretome analysis resulted in a list of 86 putative myokines, which was reduced to 29 by applying a fold-change cut-off of 1.5. Based on that shortlist, a selection of putative myokines was measured in the plasma by ELISA or multiplex assay. From that selection, CX3CL1 (fractalkine) and CCL2 (MCP-1) increased at both mRNA and plasma levels. From the known myokines, only IL-6 and FGF 21 changed at the mRNA level, whereas none of the known myokines changed at the plasma level. Secretome analysis of exercise training intervention resulted in a list of 69 putative myokines. Comparing putative myokines altered by acute exercise and exercise training revealed a limited overlap of only 13 genes. In conclusion, this study identified CX3CL1 and CCL2 as myokines that were induced by acute exercise at the gene expression and plasma level and that may be involved in communication between skeletal muscle and other organs.

Baroreflex control of heart rate by oxytocin in the solitary-vagal complex

2002 ◽  
Vol 282 (2) ◽  
pp. R537-R545 ◽  
Author(s):  
Keila T. Higa ◽  
Eliana Mori ◽  
Fabiano F. Viana ◽  
Mariana Morris ◽  
Lisete C. Michelini
Keyword(s):  
Heart Rate ◽  
Male Rats ◽  
Motor Nucleus ◽  
Baroreflex Control ◽  
Dorsal Motor Nucleus ◽  
Loading And Unloading ◽  
Reflex Control ◽  
Exercise Induced ◽  
Baroreceptor Reflex Control ◽  
The Brain

Previous work demonstrated that oxytocinergic projections to the solitary vagal complex are involved in the restraint of exercise-induced tachycardia (2). In the present study, we tested the idea that oxytocin (OT) terminals in the solitary vagal complex [nucleus of the solitary tract (NTS)/dorsal motor nucleus of the vagus (DMV)] are involved in baroreceptor reflex control of heart rate (HR). Studies were conducted in male rats instrumented for chronic cardiovascular monitoring with a cannula in the NTS/DMV for brain injections. Basal mean arterial pressure and HR and reflex HR responses during loading and unloading of the baroreceptors (phenylephrine/sodium nitroprusside intravenously) were recorded after administration of a selective OT antagonist (OTant) or OT into the NTS/DMV. The NTS/DMV was selected for study because this region contains such a specific and dense concentration of OT-immunoreactive terminals. Vehicle injections served as a control. OT and OTant changed baroreflex control of HR in opposite directions. OT (20 pmol) increased the maximal bradycardic response (from −56 ± 9 to −75 ± 11 beats/min), whereas receptor blockade decreased the bradycardia (from −61 ± 13 to −35 ± 2 beats/min). OTant also reduced the operating range of the reflex, thus decreasing baroreflex gain (from −5.68 ± 1.62 to −2.83 ± 1.05 beats · min−1 · mmHg−1). OT injected into the NTS/DMV of atenolol-treated rats still potentiated the bradycardic responses to pressor challenges, whereas OT injections had no effect in atropine-treated rats. The brain stem effect was specific because neither vehicle administration nor injection of OT or OTant into the fourth cerebral ventricle had any effect. Our data suggest that OT terminals in the solitary vagal complex modulate reflex control of the heart, acting to facilitate vagal outflow and the slowdown of the heart.

Exogenous L-lactate promotes astrocyte plasticity but is not sufficient for enhancing striatal synaptogenesis or motor behavior in mice

2020 ◽  
Author(s):  
Adam J. Lundquist ◽  
Tyler J. Gallagher ◽  
Giselle M. Petzinger ◽  
Michael W. Jakowec
Keyword(s):  
Motor Behavior ◽  
Early Gene ◽  
Specific Gene ◽  
Motor Circuits ◽  
Specific Manner ◽  
Primary Astrocytes ◽  
Exercise Induced ◽  
The Brain

AbstractL-lactate is an energetic and signaling molecule that is key to the metabolic and neuroplastic connection between astrocytes and neurons and may be involved in exercise-induced neuroplasticity. This study sought to explore the role of L-lactate in astrocyte reactivity and neuroplasticity. Using in vitro cultures of primary astrocytes, we show L-lactate increased expression of plasticity-related genes, including neurotrophic factors, Bdnf, Gdnf, Cntf and the immediate early gene cFos. L-lactate’s promotion of neurotrophic factor expression may be mediated in part by the lactate receptor HCAR1 since application of the HCAR1 agonist 3,5-DHBA also increased expression of Bdnf in primary astrocytes. In vivo L-lactate administration to healthy mice caused a similar increase in the expression of plasticity-related genes as well as increased astrocyte morphological complexity in a region-specific manner, with increased astrocytic response found in the striatum but not the ectorhinal cortex, regions of the brain where increases in regional cerebral blood flow are increased or unaltered, respectively, with motor behavior. Additionally, L-lactate administration did not cause synaptogenesis or improve motor behavior based on the latency to fall on the accelerating rotarod, suggesting that L-lactate administration can initiate astrocyte-specific gene expression, but the activation of motor circuits is necessary to initiate striatal neuroplasticity. These results suggest that peripheral L-lactate is likely an important molecular component of exercise-induced neuroplasticity by acting in an astrocyte-specific manner to prime the brain for neuroplasticity.

scholarly journals Keto-Adaptation and Endurance Exercise Capacity, Fatigue Recovery, and Exercise-Induced Muscle and Organ Damage Prevention: A Narrative Review

Sports ◽  
2019 ◽  
Vol 7 (2) ◽  
pp. 40 ◽  
Author(s):  
Sihui Ma ◽  
Katsuhiko Suzuki
Keyword(s):  
Exercise Capacity ◽  
Endurance Exercise ◽  
Ketone Bodies ◽  
Organ Damage ◽  
The Body ◽  
Narrative Review ◽  
Endurance Capacity ◽  
Muscle Health ◽  
Improve Exercise Capacity ◽  
Exercise Induced

A ketogenic diet (KD) could induce nutritional ketosis. Over time, the body will acclimate to use ketone bodies as a primary fuel to achieve keto-adaptation. Keto-adaptation may provide a consistent and fast energy supply, thus improving exercise performance and capacity. With its anti-inflammatory and anti-oxidative properties, a KD may contribute to muscle health, thus preventing exercise-induced fatigue and damage. Given the solid basis of its potential to improve exercise capacity, numerous investigations into KD and exercise have been carried out in recent years. This narrative review aims to summarize recent research about the potential of a KD as a nutritional approach during endurance exercise, focusing on endurance capacity, recovery from fatigue, and the prevention of exhaustive exercise-induced muscle and organ damage.

scholarly journals Exercise-induced enhancement of lipid peroxide metabolism in tissues and their transference into the brain in rat.

1983 ◽  
Vol 29 (2) ◽  
pp. 141-151 ◽  
Author(s):  
Masashige SUZUKI ◽  
Shinichiro KATAMINE ◽  
Sachie TATSUMI
Keyword(s):  
Lipid Peroxide ◽  
Exercise Induced ◽  
The Brain
Sign in / Sign up

Export Citation Format

Share Document