scholarly journals Is There a Progressive Withdrawal of Physiological Protections against High-Intensity Exercise-Induced Fatigue during Puberty?

Sports ◽  
2015 ◽  
Vol 3 (4) ◽  
pp. 346-357 ◽  
Author(s):  
Sébastien Ratel ◽  
Vincent Martin
Keyword(s):  
High Intensity ◽  
High Intensity Exercise ◽  
Exercise Induced

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.

HIGH INTENSITY EXERCISE INDUCED STEMI

2020 ◽  
Vol 75 (11) ◽  
pp. 2446
Author(s):  
Steve Noutong Njapo ◽  
Brittney Heard ◽  
Mohamed Morsy
Keyword(s):  
High Intensity ◽  
High Intensity Exercise ◽  
Exercise Induced

Effect of exercise intensity and AICAR on isoform-specific expressions of murine skeletal muscle PGC-1α mRNA: a role of β2-adrenergic receptor activation

2011 ◽  
Vol 300 (2) ◽  
pp. E341-E349 ◽  
Author(s):  
Miki Tadaishi ◽  
Shinji Miura ◽  
Yuko Kai ◽  
Emi Kawasaki ◽  
Keiichi Koshinaka ◽  
...  
Keyword(s):  
Exercise Intensity ◽  
High Intensity ◽  
Adrenergic Receptor ◽  
Skeletal Muscles ◽  
Receptor Activation ◽  
High Intensity Exercise ◽  
Treadmill Running ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Exercise Induced

There are three isoforms of peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α) mRNA, which promotes mitochondrial biogenesis in skeletal muscles. Compared with PGC-1α-a mRNA, PGC-1α-b or PGC-1α-c mRNA is transcribed by a different exon 1 of the PGC-1α gene. In this study, effects of exercise intensity and 5-aminoimidazole-4-carboxamide-1β-d-ribofuranoside (AICAR) on isoform-specific expressions of PGC-1α were investigated. All isoforms were increased in proportion to exercise intensity of treadmill running (10–30 m/min for 30 min). Preinjection of β2-adrenergic receptor (AR) antagonist (ICI 118551) inhibited the increase in PGC-1α-b and PGC-1α-c mRNAs, but not the increase in PGC-1α-a mRNA, in response to high-intensity exercise. Although high-intensity exercise activated α2-AMP-activated protein kinase (α2-AMPK) in skeletal muscles, inactivation of α2-AMPK activity did not affect high-intensity exercise-induced mRNA expression of all PGC-1α isoforms, suggesting that activation of α2-AMPK is not mandatory for an increase in PGC-1α mRNA by high-intensity exercise. A single injection in mice of AICAR, an AMPK activator, increased mRNAs of all PGC-1α isoforms. AICAR increased blood catecholamine concentrations, and preinjection of β2-AR antagonist inhibited the increase in PGC-1α-b and PGC-1α-c mRNAs but not the increase in PGC-1α-a mRNA. Direct exposure of epitrochlearis muscle to AICAR increased PGC-1α-a but not the -b isoform. These data indicate that exercise-induced PGC-1α expression was dependent on the intensity of exercise. Exercise or AICAR injection increased PGC-1α-b and PGC-1α-c mRNAs via β2-AR activation, whereas high-intensity exercise increased PGC-1α-a expression by a multiple mechanism in which α2-AMPK is one of the signaling pathways.

scholarly journals Circulating T-Regulatory Cells, Exercise and the Elite Adolescent Swimmer

2009 ◽  
Vol 21 (3) ◽  
pp. 305-317 ◽  
Author(s):  
Lori D. Wilson ◽  
Frank P. Zaldivar ◽  
Christina D. Schwindt ◽  
Jessica Wang-Rodriguez ◽  
Dan M. Cooper
Keyword(s):  
High Intensity ◽  
T Regulatory Cells ◽  
High Intensity Exercise ◽  
Regulatory Cells ◽  
Allergic Symptoms ◽  
Elite Swimmers ◽  
Exercise Induced

Brief high intensity exercise induces peripheral leukocytosis possibly leading to a higher incidence of allergic symptoms in athletes undergoing excessive training. We studied the exercise-induced alternation of circulating Tregs and FoxP3+ Tregs due to acute intense swim exercise in elite swimmers (n = 22, 12 males, age = 15.4 yrs). Twelve had prior or current rhinitis or asthma and 10 had no current or prior allergy or asthma. Circulating Tregs increased significantly (p < .001) following exercise (pre = 133 ± 11.2, post = 196 ± 17.6) as did FoxP3+ cells (pre = 44, post = 64 cells/μl). Increases in Tregs and FoxP3+ Tregs occurred to the same extent in both groups of adolescent swimmers.

scholarly journals Protection of Lotus Seedpod Proanthocyanidins on Organs and Tissues under High-intensity Excercise

2015 ◽  
Vol 9 (1) ◽  
pp. 296-300 ◽  
Author(s):  
Zhang Mengyan
Keyword(s):  
Blood Cell ◽  
High Intensity ◽  
Myocardial Damage ◽  
The Body ◽  
High Intensity Exercise ◽  
Protective Effects ◽  
Protective Function ◽  
Health Products ◽  
Exercise Induced ◽  
Lotus Seedpod

Lotus seedpod proanthocyanidins (LSPC) as a kind of polyphenols is widely used in medicines, cosmetics, health products. High-intensity exercise can cause damage to the body's organs and tissues. Different doses of LSPC is given to mice to check the function of protect effect to the body's organs and tissues under high-intensity exercise. The hemoglobin (HB) content, red blood cell (RBC) number and white blood cell (WBC) number were tested for mice after exercise. The activity of superoxide dismutase (SOD) and the contents of glutathione (GSH) and malondialdehyde (MDA) in muscle and viscera were evaluated. The result showed that LSPC can effectively reduce inflammation reaction in the body of mice with high intensity exercise, alleviate oxidative stress-induced injury of tissues and organs, and execute protective function on skeletal muscle and cardiac muscle. And the LSPC could enhance myocardial anti-oxygen and enzymatic activity which suggests the protective effects of resveratrol against exercise-induced myocardial damage in mice.

scholarly journals Cardiac perturbations after high-intensity exercise are attenuated in middle-aged compared with young endurance athletes: diminished stress or depleted stimuli?

2021 ◽  
Vol 320 (1) ◽  
pp. H159-H168
Author(s):  
Bryce N. Balmain ◽  
Surendran Sabapathy ◽  
Akira Yamada ◽  
Kenji Shiino ◽  
Jonathan Chan ◽  
...  
Keyword(s):  
Cardiac Remodeling ◽  
High Intensity ◽  
High Intensity Exercise ◽  
Endurance Athletes ◽  
Middle Aged ◽  
Stimulus Response ◽  
Induced Stress ◽  
Exercise Induced ◽  
Cycling Training ◽  
Important Stimulus

High-intensity endurance exercise elicits acute cardiac imbalances that may be an important stimulus for adaptive cardiac remodeling. This study highlights that following a bout of high-intensity exercise that is typical of routine day-to-day cycling training, exercise-induced autonomic, biochemical, and functional cardiac imbalances are attenuated in middle-aged relative to young well-trained cyclists. These findings suggest that aging may alter exercise-induced stress stimulus response that initiates cardiac remodeling in Athlete’s Heart.

scholarly journals Exercise-Induced Muscle Damage and Running Economy in Humans

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Cláudio de Oliveira Assumpção ◽  
Leonardo Coelho Rabello Lima ◽  
Felipe Bruno Dias Oliveira ◽  
Camila Coelho Greco ◽  
Benedito Sérgio Denadai
Keyword(s):  
Muscle Damage ◽  
High Intensity ◽  
Energy Demand ◽  
Negative Impact ◽  
High Intensity Exercise ◽  
Running Economy ◽  
Running Performance ◽  
Downhill Running ◽  
Short Period ◽  
Exercise Induced

Running economy (RE), defined as the energy demand for a given velocity of submaximal running, has been identified as a critical factor of overall distance running performance. Plyometric and resistance trainings, performed during a relatively short period of time (~15–30 days), have been successfully used to improve RE in trained athletes. However, these exercise types, particularly when they are unaccustomed activities for the individuals, may cause delayed onset muscle soreness, swelling, and reduced muscle strength. Some studies have demonstrated that exercise-induced muscle damage has a negative impact on endurance running performance. Specifically, the muscular damage induced by an acute bout of downhill running has been shown to reduce RE during subsequent moderate and high-intensity exercise (>65% VO2max). However, strength exercise (i.e., jumps, isoinertial and isokinetic eccentric exercises) seems to impair RE only for subsequent high-intensity exercise (~90% VO2max). Finally, a single session of resistance exercise or downhill running (i.e., repeated bout effect) attenuates changes in indirect markers of muscle damage and blunts changes in RE.

Effect of adrenodemedullation on metabolic responses to high-intensity exercise

1986 ◽  
Vol 251 (3) ◽  
pp. R552-R559
Author(s):  
J. C. Marker ◽  
D. A. Arnall ◽  
R. K. Conlee ◽  
W. W. Winder
Keyword(s):  
Soleus Muscle ◽  
High Intensity ◽  
Liver Glycogen ◽  
High Intensity Exercise ◽  
Metabolic Responses ◽  
Intense Exercise ◽  
Pentobarbital Sodium ◽  
Exercise Induced ◽  
Liver Glycogenolysis

To determine the role of epinephrine in glycogenolysis during high-intensity exercise, rats were adrenodemedullated (ADM) or sham operated (SHAM) and run for either 30 min at 38 m/min or for 5 min at 27, 38, or 48 m/min up a 15% grade. At the end of exercise the rats were anesthetized by intravenous injection of pentobarbital sodium. Liver, blood, and muscle samples were obtained. Plasma epinephrine values were 5.9 and 0.3 nM for SHAM and ADM animals, respectively, after 30 min of exercise. Liver glycogen decreased by 16 and 21 mg/g in the SHAM and ADM groups, respectively, and liver cAMP increased significantly in both groups. Glycogen in the soleus muscle decreased 80% in the SHAM but only 43% in the ADM animals after 30 min of exercise. The exercise-induced hyperglycemia observed in the SHAM animals was not present in the ADM animals. The responses of cyclic AMP, soleus glycogen, and blood glucose were similar in both the 5- and 30-min exercise groups. During intense exercise, epinephrine is unessential for stimulating liver glycogenolysis but does play an important role in stimulating glycogenolysis in the soleus muscle and in establishing exercise-induced hyperglycemia.

scholarly journals Sucrose But Not Nitrate Ingestion Reduces High-intensity Exercise-induced Gut Injury

2018 ◽  
Vol 50 (5S) ◽  
pp. 590-591
Author(s):  
Kristin L. Jonvik ◽  
Kaatje Lenaerts ◽  
Joey SJ Smeets ◽  
Jeroen Kolkman ◽  
Luc JC van Loon ◽  
...  
Keyword(s):  
High Intensity ◽  
High Intensity Exercise ◽  
Exercise Induced

scholarly journals Greater lactate accumulation following an acute bout of high-intensity exercise in males suppresses acylated ghrelin and appetite postexercise

2020 ◽  
Vol 128 (5) ◽  
pp. 1321-1328 ◽  
Author(s):  
Luke W. Vanderheyden ◽  
Greg L. McKie ◽  
Greg J. Howe ◽  
Tom J. Hazell
Keyword(s):  
Sodium Bicarbonate ◽  
High Intensity ◽  
High Intensity Exercise ◽  
Acylated Ghrelin ◽  
Acute Bout ◽  
Lactate Accumulation ◽  
Appetite Suppression ◽  
Exercise Induced ◽  
Dependent Mechanism ◽  
Caloric Deficit

We used sodium bicarbonate to increase lactate accumulation or sodium chloride as a placebo. Our findings further implicate lactate as a mediator of exercise-induced appetite suppression given exercise-induced increases in lactate during the sodium bicarbonate session altered peripheral concentrations of appetite-regulating hormones, culminating in a reduction of appetite. This supports a lactate-dependent mechanism of appetite suppression following high-intensity exercise and highlights the potential of using lactate as a means of inducing a caloric deficit.

Sign in / Sign up

Export Citation Format

Share Document