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.

Epinephrine is unessential for stimulation of liver glycogenolysis during exercise

1985 ◽  
Vol 58 (2) ◽  
pp. 544-548 ◽  
Author(s):  
K. I. Carlson ◽  
J. C. Marker ◽  
D. A. Arnall ◽  
M. L. Terry ◽  
H. T. Yang ◽  
...  
Keyword(s):  
Pancreatic Beta Cells ◽  
Liver Glycogen ◽  
Plasma Glucagon ◽  
Lateral Gastrocnemius ◽  
White Region ◽  
Exercise Induced ◽  
Fast Twitch ◽  
Liver Glycogenolysis ◽  
Stimulation Of

To determine the role of adrenal medullary hormones in controlling the rate of liver glycogenolysis during exercise, adrenodemedullated (ADM) and sham-operated (SO) rats were run on a rodent treadmill at 21 m/min up a 15% grade for 0, 30, or 60 min. Rats were anesthetized by intravenous injection of pentobarbital sodium, and liver, muscle, and blood were collected and frozen. Liver glycogen decreased at similar rates in ADM and SO rats. Hepatic adenosine 3′,5′-cyclic monophosphate (cAMP), plasma glucagon, and plasma free fatty acids increased to the same extent in both ADM and SO rats. The adrenodemedullation caused a reduction in glycogenolysis in the fast-twitch white region of the quadriceps, soleus, and lateral gastrocnemius during exercise. The normal exercise-induced increase in blood glucose and lactate and the decline in plasma insulin were not observed in the demedullated rats. During submaximal exercise the principal targets for epinephrine released from the adrenal medulla appear to be pancreatic beta-cells and skeletal muscle and not the liver.

Exercise, free radicals and oxidative stress

2002 ◽  
Vol 30 (2) ◽  
pp. 280-285 ◽  
Author(s):  
C. E. Cooper ◽  
N. B. J. Vollaard ◽  
T. Choueiri ◽  
M. T. Wilson
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
High Intensity ◽  
High Intensity Exercise ◽  
Minor Role ◽  
Exercise Induced ◽  
Haem Proteins ◽  
Sporting Performance

This article reviews the role of free radicals in causing oxidative stress during exercise. High intensity exercise induces oxidative stress and although there is no evidence that this affects sporting performance in the short term, it may have longer term health consequences. The mechanisms of exercise-induced oxidative stress are not well understood. Mitochondria are sometimes considered to be the main source of free radicals, but in vitro studies suggest they may play a more minor role than was first thought. There is a growing acceptance of the importance of haem proteins in inducing oxidative stress. The release of metmyoglobin from damaged muscle is known to cause renal failure in exercise rhabdomyolysis. Furthermore, levels of methaemoglobin increase during high intensity exercise, while levels of antioxidants, such as reduced glutathione, decrease. We suggest that the free-radical-mediated damage caused by the interaction of metmyoglobin and methaemoglobin with peroxides may be an important source of oxidative stress during exercise.

scholarly journals Acute high-intensity exercise and skeletal muscle mitochondrial respiratory function: role of metabolic perturbation

2021 ◽  
Vol 321 (5) ◽  
pp. R687-R698
Author(s):  
Matthew T. Lewis ◽  
Gregory M. Blain ◽  
Corey R. Hart ◽  
Gwenael Layec ◽  
Matthew J. Rossman ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
High Intensity ◽  
Respiratory Function ◽  
Complex I ◽  
High Intensity Exercise ◽  
Respiratory Capacity ◽  
Metabolic Perturbation ◽  
Exercise Induced ◽  
Mitochondrial Respiratory

Recently it was documented that fatiguing, high-intensity exercise resulted in a significant attenuation in maximal skeletal muscle mitochondrial respiratory capacity, potentially due to the intramuscular metabolic perturbation elicited by such intense exercise. With the utilization of intrathecal fentanyl to attenuate afferent feedback from group III/IV muscle afferents, permitting increased muscle activation and greater intramuscular metabolic disturbance, this study aimed to better elucidate the role of metabolic perturbation on mitochondrial respiratory function. Eight young, healthy males performed high-intensity cycle exercise in control (CTRL) and fentanyl-treated (FENT) conditions. Liquid chromatography-mass spectrometry and high-resolution respirometry were used to assess metabolites and mitochondrial respiratory function, respectively, pre- and postexercise in muscle biopsies from the vastus lateralis. Compared with CTRL, FENT yielded a significantly greater exercise-induced metabolic perturbation (PCr: −67% vs. −82%, Pi: 353% vs. 534%, pH: −0.22 vs. −0.31, lactate: 820% vs. 1,160%). Somewhat surprisingly, despite this greater metabolic perturbation in FENT compared with CTRL, with the only exception of respiratory control ratio (RCR) (−3% and −36%) for which the impact of FENT was significantly greater, the degree of attenuated mitochondrial respiratory capacity postexercise was not different between CTRL and FENT, respectively, as assessed by maximal respiratory flux through complex I (−15% and −33%), complex II (−36% and −23%), complex I + II (−31% and −20%), and state 3CI+CII control ratio (−24% and −39%). Although a basement effect cannot be ruled out, this failure of an augmented metabolic perturbation to extensively further attenuate mitochondrial function questions the direct role of high-intensity exercise-induced metabolite accumulation in this postexercise response.

Phenylephrine decreases frontal lobe oxygenation at rest but not during moderately intense exercise

2010 ◽  
Vol 108 (6) ◽  
pp. 1472-1478 ◽  
Author(s):  
Patrice Brassard ◽  
Thomas Seifert ◽  
Mads Wissenberg ◽  
Peter M. Jensen ◽  
Christian K. Hansen ◽  
...  
Keyword(s):  
Frontal Lobe ◽  
High Intensity ◽  
Sympathetic Activity ◽  
Near Infrared ◽  
Cerebral Metabolism ◽  
High Intensity Exercise ◽  
Mean Flow ◽  
Intense Exercise ◽  
Low Intensity ◽  
Low Intensity Exercise

Whether sympathetic activity influences cerebral blood flow (CBF) and oxygenation remains controversial. The influence of sympathetic activity on CBF and oxygenation was evaluated by the effect of phenylephrine on middle cerebral artery (MCA) mean flow velocity ( Vmean) and the near-infrared spectroscopy-derived frontal lobe oxygenation (ScO2) at rest and during exercise. At rest, nine healthy male subjects received bolus injections of phenylephrine (0.1, 0.25, and 0.4 mg), and changes in mean arterial pressure (MAP), MCA Vmean, internal jugular venous O2 saturation (SjvO2), ScO2, and arterial Pco2 (PaCO2) were measured and the cerebral metabolic rate for O2 (CMRO2) was calculated. In randomized order, a bolus of saline or 0.3 mg of phenylephrine was then injected during semisupine cycling, eliciting a low (∼110 beats/min) or a high (∼150 beats/min) heart rate. At rest, MAP and MCA Vmean increased ∼20% ( P < 0.001) and ∼10% ( P < 0.001 for 0.25 mg of phenylephrine and P < 0.05 for 0.4 mg of phenylephrine), respectively. ScO2 then decreased ∼7% ( P < 0.001). Phenylephrine had no effect on SjvO2, PaCO2, or CMRO2. MAP increased after the administration of phenylephrine during low-intensity exercise (∼15%), but this was attenuated (∼10%) during high-intensity exercise ( P < 0.001). The reduction in ScO2 after administration of phenylephrine was attenuated during low-intensity exercise (−5%, P < 0.001) and abolished during high-intensity exercise (−3%, P = not significant), where PaCO2 decreased 7% ( P < 0.05) and CMRO2 increased 17% ( P < 0.05). These results suggest that the administration of phenylephrine reduced ScO2 but that the increased cerebral metabolism needed for moderately intense exercise eliminated that effect.

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.

Sign in / Sign up

Export Citation Format

Share Document