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 Astrocytic glycogen-derived lactate fuels the brain during exhaustive exercise to maintain endurance capacity

2017 ◽  
Vol 114 (24) ◽  
pp. 6358-6363 ◽  
Author(s):  
Takashi Matsui ◽  
Hideki Omuro ◽  
Yu-Fan Liu ◽  
Mariko Soya ◽  
Takeru Shima ◽  
...  
Keyword(s):  
Muscle Glycogen ◽  
Defense Mechanism ◽  
Lactate Production ◽  
Exhaustive Exercise ◽  
Endurance Capacity ◽  
Similar Response ◽  
Lactate Transport ◽  
Brain Glycogen ◽  
The Brain

Brain glycogen stored in astrocytes provides lactate as an energy source to neurons through monocarboxylate transporters (MCTs) to maintain neuronal functions such as hippocampus-regulated memory formation. Although prolonged exhaustive exercise decreases brain glycogen, the role of this decrease and lactate transport in the exercising brain remains less clear. Because muscle glycogen fuels exercising muscles, we hypothesized that astrocytic glycogen plays an energetic role in the prolonged-exercising brain to maintain endurance capacity through lactate transport. To test this hypothesis, we used a rat model of exhaustive exercise and capillary electrophoresis-mass spectrometry–based metabolomics to observe comprehensive energetics of the brain (cortex and hippocampus) and muscle (plantaris). At exhaustion, muscle glycogen was depleted but brain glycogen was only decreased. The levels of MCT2, which takes up lactate in neurons, increased in the brain, as did muscle MCTs. Metabolomics revealed that brain, but not muscle, ATP was maintained with lactate and other glycogenolytic/glycolytic sources. Intracerebroventricular injection of the glycogen phosphorylase inhibitor 1,4-dideoxy-1,4-imino-d-arabinitol did not affect peripheral glycemic conditions but suppressed brain lactate production and decreased hippocampal ATP levels at exhaustion. An MCT2 inhibitor, α-cyano-4-hydroxy-cinnamate, triggered a similar response that resulted in lower endurance capacity. These findings provide direct evidence for the energetic role of astrocytic glycogen-derived lactate in the exhaustive-exercising brain, implicating the significance of brain glycogen level in endurance capacity. Glycogen-maintained ATP in the brain is a possible defense mechanism for neurons in the exhausted brain.

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.

Control of fructose 2,6-diphosphate in muscle of exercising fasted rats

1992 ◽  
Vol 262 (6) ◽  
pp. E919-E924 ◽  
Author(s):  
W. W. Winder ◽  
C. Duan
Keyword(s):  
Blood Glucose ◽  
Lactate Production ◽  
Quadriceps Muscle ◽  
Active Muscle ◽  
Lower Blood Glucose ◽  
Lower Blood ◽  
Exercise Induced ◽  
Grade One ◽  
Fasted Rats

This study examined the role of epinephrine in controlling intramuscular signals that may accelerate lactate production in less active muscles during exercise. Sham-operated (sham) or adrenodemedullated (ADM) rats were fasted 24 h and then were killed at rest or after running for 15 or 30 min on a treadmill (21 m/min, 15% grade). One-half of the ADM rats were infused with epinephrine (6 micrograms/h) intravenously (jugular catheter) during exercise. ADM rats exhibited lower blood glucose, blood lactate, white quadriceps muscle content of lactate, glucose 6-phosphate, fructose 6-phosphate, and adenosine 3',5'-cyclic monophosphate (cAMP) during exercise than did sham rats or epinephrine-infused ADM rats. The white quadriceps muscle contents of fructose 2,6-diphosphate (F-2,6-P2) and glucose 1,6-diphosphate (G-1,6-P2) (allosteric activators of glycolysis) were at least two times as high in sham rats and in epinephrine-infused rats as in ADM rats during exercise. We conclude that the exercise-induced rise in epinephrine is responsible for the acceleration of glycolysis in less active muscle during exercise. This effect is likely mediated by epinephrine-induced increases in cAMP, F-2,6-P2, and G-1,6-P2.

Protective role of l-carnitine supplementation against exhaustive exercise induced oxidative stress in rats

2011 ◽  
Vol 668 (3) ◽  
pp. 407-413 ◽  
Author(s):  
Elif Şıktar ◽  
Deniz Ekinci ◽  
Erdinç Şıktar ◽  
Şükrü Beydemir ◽  
İlhami Gülçin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protective Role ◽  
Exhaustive Exercise ◽  
Carnitine Supplementation ◽  
Exercise Induced

scholarly journals Nicotinamide Riboside supplementation does not alter whole-body or skeletal muscle metabolic responses to a single bout of endurance exercise

2020 ◽  
Author(s):  
Ben Stocks ◽  
Stephen P. Ashcroft ◽  
Sophie Joanisse ◽  
Yasir S. Elhassan ◽  
Gareth G. Lavery ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mrna Expression ◽  
Endurance Exercise ◽  
Vastus Lateralis ◽  
Whole Body ◽  
Endurance Capacity ◽  
Similar Response ◽  
Transcriptional Responses ◽  
Nicotinamide Riboside ◽  
Exercise Induced

AbstractOral supplementation of the NAD+ precursor Nicotinamide Riboside (NR) has been reported to increase Sirtuin (SIRT) signalling, mitochondrial biogenesis and endurance capacity in rodent skeletal muscle. However, whether NR supplementation can elicit a similar response in human skeletal muscle is unclear. This study aimed to assess the effect of 7-day NR supplementation on exercise-induced transduction and transcriptional responses in skeletal muscle of young, healthy, recreationally active human volunteers. In a double-blinded, randomised, counter-balanced, crossover design, eight male participants (age: 23 ± 4 years, VO2peak: 46.5 ± 4.4 mL·kg-1·min-1) received one week of NR or cellulose placebo (PLA) supplementation (1000 mg·d-1) before performing one hour of cycling at 60% Wmax. Muscle biopsies were collected prior to supplementation and pre-, immediately and three-hours post-exercise from the medial vastus lateralis, whilst venous blood samples were collected throughout the trial. Global acetylation, auto-PARylation of PARP1, acetylation of p53Lys382 and MnSODLys122 were unaffected by NR supplementation or exercise. Exercise led to an increase in AMPKThr172 (1.6-fold), and ACCSer79 (4-fold) phosphorylation, in addition to an increase in PGC-1α (∼5-fold) and PDK4 (∼10-fold) mRNA expression, however NR had no additional effect on this response. There was also no effect of NR supplementation on substrate utilisation at rest or during exercise or on skeletal muscle mitochondrial respiration. Finally, NR supplementation blunted the exercise induced activation of skeletal muscle NNMT mRNA expression, but had no effect on mRNA expression of NMRK1, NAMPT or NMNAT1, which were not significantly affected by NR supplementation or exercise. In summary, one week of NR supplementation does not augment skeletal muscle signal transduction pathways implicated in mitochondrial adaptation to endurance exercise.

scholarly journals Characterization and Modulation of Systemic Inflammatory Response to Exhaustive Exercise in Relation to Oxidative Stress

Antioxidants ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 401 ◽  
Author(s):  
Katsuhiko Suzuki ◽  
Takaki Tominaga ◽  
Ruheea Taskin Ruhee ◽  
Sihui Ma
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Mediator ◽  
Inflammatory Responses ◽  
Organ Damage ◽  
Exhaustive Exercise ◽  
Nuclear Factor ◽  
Internal Organs ◽  
Research Findings ◽  
Exercise Induced

Exhaustive exercise induces systemic inflammatory responses, which are associated with exercise-induced tissue/organ damage, but the sources and triggers are not fully understood. Herein, the basics of inflammatory mediator cytokines and research findings on the effects of exercise on systemic inflammation are introduced. Subsequently, the association between inflammatory responses and tissue damage is examined in exercised and overloaded skeletal muscle and other internal organs. Furthermore, an overview of the interactions between oxidative stress and inflammatory mediator cytokines is provided. Particularly, the transcriptional regulation of redox signaling and pro-inflammatory cytokines is described, as the activation of the master regulatory factor nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is involved directly or indirectly in controlling pro-inflammatory genes and antioxidant enzymes expression, whilst nuclear factor-kappa B (NF-κB) regulates the pro-inflammatory gene expression. Additionally, preventive countermeasures against the pathogenesis along with the possibility of interventions such as direct and indirect antioxidants and anti-inflammatory agents are described. The aim of this review is to give an overview of studies on the systematic inflammatory responses to exercise, including our own group as well as others. Moreover, the challenges and future directions in understanding the role of exercise and functional foods in relation to inflammation and oxidative stress are discussed.

Effects of exercise in normoxia and acute hypoxia on respiratory muscle metabolites

1986 ◽  
Vol 60 (4) ◽  
pp. 1274-1283 ◽  
Author(s):  
R. F. Fregosi ◽  
J. A. Dempsey
Keyword(s):  
Endurance Exercise ◽  
Muscle Glycogen ◽  
Respiratory Muscle ◽  
Acute Hypoxia ◽  
Lactate Concentration ◽  
Lactate Production ◽  
Exhaustive Exercise ◽  
Diaphragm Muscle ◽  
Arterial Blood ◽  
Glycogen Utilization

We determined changes in rat plantaris, diaphragm, and intercostal muscle metabolites following exercise of various intensities and durations, in normoxia and hypoxia (FIO2 = 0.12). Marked alveolar hyperventilation occurred during all exercise conditions, suggesting that respiratory muscle motor activity was high. [ATP] was maintained at rest levels in all muscles during all normoxic and hypoxic exercise bouts, but at the expense of creatine phosphate (CP) in plantaris muscle and diaphragm muscle following brief exercise at maximum O2 uptake (VO2max) in normoxia. In normoxic exercise plantaris [glycogen] fell as exercise exceeded 60% VO2max, and was reduced to less than 50% control during exhaustive endurance exercise (68% VO2max for 54 min and 84% for 38 min). Respiratory muscle [glycogen] was unchanged at VO2max as well as during either type of endurance exercise. Glucose 6-phosphate (G6P) rose consistently during heavy exercise in diaphragm but not in plantaris. With all types of exercise greater than 84% VO2max, lactate concentration ([LA]) in all three muscles rose to the same extent as arterial [LA], except at VO2max, where respiratory muscle [LA] rose to less than half that in arterial blood or plantaris. Exhaustive exercise in hypoxia caused marked hyperventilation and reduced arterial O2 content; glycogen fell in plantaris (20% of control) and in diaphragm (58%) and intercostals (44%). We conclude that respiratory muscle glycogen stores are spared during exhaustive exercise in the face of substantial glycogen utilization in plantaris, even under conditions of extreme hyperventilation and reduced O2 transport. This sparing effect is due primarily to G6P inhibition of glycogen phosphorylase in diaphragm muscle. The presence of elevated [LA] in the absence of glycogen utilization suggests that increased lactate uptake, rather than lactate production, occurred in the respiratory muscles during exhaustive exercise.

Exercise-induced oxidative stress: glutathione supplementation and deficiency

1994 ◽  
Vol 77 (5) ◽  
pp. 2177-2187 ◽  
Author(s):  
C. K. Sen ◽  
M. Atalay ◽  
O. Hanninen
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Critical Role ◽  
Lipid Peroxides ◽  
Thiobarbituric Acid ◽  
Repeated Administration ◽  
Exhaustive Exercise ◽  
Relative Role ◽  
Exercise Induced

Glutathione (GSH) plays a central role in coordinating the synergism between different lipid- and aqueous-phase antioxidants. We documented 1) how exogenous GSH and N-acetylcysteine (NAC) may affect exhaustive exercise-induced changes in tissue GSH status, lipid peroxides [thiobarbituric acid-reactive substances (TBARS)], and endurance and 2) the relative role of endogenous GSH in the circumvention of exercise-induced oxidative stress by using GSH-deficient [L-buthionine-(S,R)-sulfoximine (BSO)-treated] rats. Intraperitoneal injection of GSH remarkably increased plasma GSH; exogenous GSH per se was an ineffective delivery agent of GSH to tissues. Repeated administration of GSH (1 time/day for 3 days) increased blood and kidney total GSH [TGSH; GSH+oxidized GSH (GSSG)]. Neither GSH nor NAC influenced endurance to exhaustion. NAC decreased exercise-induced GSH oxidation in the lung and blood. BSO decreased TGSH pools in the liver, lung, blood, and plasma by approximately 50% and in skeletal muscle and heart by 80–90%. Compared with control, resting GSH-deficient rats had lower GSSG in the liver, red gastrocnemius muscle, heart, and blood; similar GSSG/TGSH ratios in the liver, heart, lung, blood, and plasma; higher GSSG/TGSH ratios in the skeletal muscle; and more TBARS in skeletal muscle, heart, and plasma. In contrast to control, exhaustive exercise of GSH-deficient rats did not decrease TGSH in the liver, muscle, or heart or increase TGSH of plasma; GSSG of muscle, blood, or plasma; or TBARS of plasma or muscle. GSH-deficient rats had approximately 50% reduced endurance, which suggests a critical role of endogenous GSH in the circumvention of exercise-induced oxidative stress and as a determinant of exercise performance.

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