The influence of age on the treadmill exercise-induced c-Fos expression in the hippocampus of rats

SummaryIschemia/reperfusion damage evokes systemic inflammation and endothelial dysfunction in patients with intermittent claudication. We compared the effects of aspirin with those of a nitric oxide-donating aspirin in preventing the acute, systemic endothelial dysfunction provoked by exercise-induced ischemia of the lower limbs in patients with intermittent claudication. In a prospective, randomized, single-blind, parallel-groups trial among 44 patients with intermittent claudication we compared four weeks of aspirin (100 mg o.d.) with NCX 4016 (800 mg b.i.d.). Primary end point was the exercise-induced changes in brachial flow-mediated vasodilation (FMD) at day 28; secondary end points were effort-induced changes of markers of neutrophil (plasma elastase) and endothelial (soluble VCAM-1) activation. Baseline FMD was comparable in the two groups, both on day I (pre-treatment: aspirin = 3.1 ± 0.5%, nitroaspirin = 3.9 ± 0.7%, p=NS), and on day 28 (aspirin = 3.4 ± 0.7%, NCX 4016 = 3.2 ± 0.6%, p=NS). Maximal treadmill exercise induced an acute worsening of FMD in both groups at baseline (aspirin = –1.15%, nitroaspirin = –1.76%); after four weeks treatment, the impairment of FMD induced by exercise was still present in the aspirin-treated group (- 1.46%) while it was abolished in the NCX 4016-treated group (+ 0.79%, p= 0.038 vs. aspirin). Similarly, exercise induced an increase of plasma elastase and of sVCAM-l which were not affected by aspirin while they were suppressed by NCX 4016. Maximal treadmill exercise induces a systemic arterial endothelial dysfunction in patients with intermittent claudication. A nitric oxide-donating aspirin, but not aspirin, prevents effort-induced endothelial dysfunction.

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The B2 Receptor of Bradykinin Is Not Essential for the Post-Exercise Increase in Glucose Uptake by Insulin-Stimulated Mouse Skeletal Muscle

Physiological Research ◽

10.33549/physiolres.932085 ◽

2011 ◽

pp. 511-519 ◽

Cited By ~ 7

Author(s):

G. G. SCHWEITZER ◽

C. M. CASTORENA ◽

T. HAMADA ◽

K. FUNAI ◽

E. B. ARIAS ◽

...

Keyword(s):

Skeletal Muscle ◽

Blood Glucose ◽

Glucose Uptake ◽

Insulin Action ◽

Plasma Insulin ◽

Treadmill Exercise ◽

Post Exercise ◽

Skeletal Muscle Glucose Uptake ◽

Glucose Plasma ◽

Exercise Induced

Bradykinin can enhance skeletal muscle glucose uptake (GU), and exercise increases both bradykinin production and muscle insulin sensitivity, but bradykinin’s relationship with post-exercise insulin action is uncertain. Our primary aim was to determine if the B2 receptor of bradykinin (B2R) is essential for the post-exercise increase in GU by insulin-stimulated mouse soleus muscles. Wildtype (WT) and B2R knockout (B2RKO) mice were sedentary or performed 60 minutes of treadmill exercise. Isolated soleus muscles were incubated with [3H]-2-deoxyglucose ±insulin (60 or 100 μU/ml). GU tended to be greater for WT vs. B2RKO soleus with 60 μU/ml insulin (P=0.166) and was significantly greater for muscles with 100 μU/ml insulin (P<0.05). Both genotypes had significant exercise-induced reductions (P<0.05) in glycemia and insulinemia, and the decrements for glucose (~14 %) and insulin (~55 %) were similar between genotypes. GU tended to be greater for exercised vs. sedentary soleus with 60 μU/ml insulin (P=0.063) and was significantly greater for muscles with 100 μU/ml insulin (P<0.05). There were no significant interactions between genotype and exercise for blood glucose, plasma insulin or GU. These results indicate that the B2R is not essential for the exercise-induced decrements in blood glucose or plasma insulin or for the post-exercise increase in GU by insulin-stimulated mouse soleus muscle.

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Free dopamine in dog plasma: lack of relationship with sympathoadrenal activity

Journal of Applied Physiology ◽

10.1152/jappl.1985.58.3.763 ◽

1985 ◽

Vol 58 (3) ◽

pp. 763-769 ◽

Cited By ~ 3

Author(s):

J. M. Pequignot ◽

R. Favier ◽

D. Desplanches ◽

L. Peyrin ◽

R. Flandrois

Keyword(s):

Treadmill Exercise ◽

Activity Levels ◽

O2 Uptake ◽

Arterial Partial Pressure ◽

Combined Exercise ◽

Dog Plasma ◽

Sympathoadrenal Activity ◽

Submaximal Work ◽

Exercise Induced ◽

The Relationship

To investigate the relationship between dopamine (DA) released into the bloodstream and sympathoadrenal activity, levels of free DA, norepinephrine (NE), and epinephrine (E) in plasma were recorded in four dogs subjected to three tests: treadmill exercise at two work levels [55 and 75% maximal O2 uptake; 15 min], normobaric hypoxia (12% O2; 1 h), combined exercise and hypoxia. Normoxic exercise induced slight nonsignificant decreases in the arterial partial pressure of O2 (PaO2), increases in NE [median values and ranges during submaximal work vs. rest: 1086 (457–1,637) vs. 360 (221–646) pg/ml; P less than 0.01] and E [277 (151–461) vs. 166 (95–257) pg/ml; P less than 0.05], but it failed to alter the DA level. Hypoxia elicited large decreases in PaO2 [hypoxia vs. normoxia: 42.8 (40.3–50.0) vs. 97.6 (83.2–117.6) Torr; P less than 0.01], increases in DA [230 (105–352) vs. 150 (85–229) pg/ml; P less than 0.01] and NE [383 (219–1,165) vs. 358 (210–784) pg/ml; P less than 0.05], but it failed to alter the E level. Combined exercise and hypoxia further increased NE levels but did not alter the DA response to hypoxia alone. The data indicate that free DA in plasma may vary independently of the sympathoadrenal activity.

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The Effect of Sulfinpyrazone on Treadmill Exercise-Induced Angina Pectoris

Cardiology ◽

10.1159/000175974 ◽

1993 ◽

Vol 83 (4) ◽

pp. 228-233

Author(s):

Daniel Lewis, Jr. ◽

James W. Davis ◽

Khatab M. Hassanein

Keyword(s):

Angina Pectoris ◽

Treadmill Exercise ◽

Exercise Induced

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Hypoxia preconditioning promotes endurance exercise capacity of mice by activating skeletal muscle Nrf2

Journal of Applied Physiology ◽

10.1152/japplphysiol.00347.2019 ◽

2019 ◽

Vol 127 (5) ◽

pp. 1267-1277

Author(s):

Linjia Wang ◽

Simin Yang ◽

Lu Yan ◽

Hao Wei ◽

Jianxiong Wang ◽

...

Keyword(s):

Skeletal Muscle ◽

Exercise Capacity ◽

Treadmill Exercise ◽

Related Factor ◽

Nuclear Factor ◽

Wild Type ◽

Hypoxia Preconditioning ◽

Nrf2 Knockout ◽

Exercise Induced ◽

Induced Changes

Elite endurance athletes are used to train under hypoxic/high-altitude conditions, which can elicit certain stress responses in skeletal muscle and helps to improve their physical performance. Nuclear factor erythroid 2-related factor 2 (Nrf2) regulates cellular redox homeostasis and metabolism in skeletal muscle, playing important roles in adaptation to various stresses. In this study, Nrf2 knockout (KO) and wild-type (WT) mice were preconditioned to 48 h of hypoxia exposure (11.2% oxygen), and the effects of hypoxia preconditioning (HP) on exercise capacity and exercise-induced changes of antioxidant status, energetic metabolism, and mitochondrial adaptation in skeletal muscle were evaluated. Nrf2 knockout (KO) and wild-type (WT) mice were exposed to normoxia or hypoxia for 48 h before taking incremental treadmill exercise to exhaustion under hypoxia. The skeletal muscles were collected immediately after the incremental treadmill exercise to evaluate the impacts of HP and Nrf2 on the exercise-induced changes. The results indicate the absence of Nrf2 did not affect exercise capacity, although the mRNA expression of certain muscular genes involved in antioxidant, glycogen and fatty acid catabolism was decreased in Nrf2 KO mice. However, 48-h HP enhanced exercise capacity in WT mice but not in Nrf2 KO mice, and the exercise capacity of WT mice was significantly higher than that of Nrf2 KO mice. These findings suggest HP promotes exercise capacity of mice with the participation of the Nrf2 signal in skeletal muscle. NEW & NOTEWORTHY Hypoxia preconditioning (HP) activated the nuclear factor erythroid 2-related factor 2 (Nrf2) signal, which was involved in HP-elicited adaptation responses to hypoxia, oxidative, and metabolic stresses in skeletal muscle. On the other hand, Nrf2 deficiency abolished the enhanced exercise capacity after the 48-h HP. Our results indicate that Nrf2 plays an essential role in the exercise capacity-enhancing effect of HP, possibly by modulating muscular antioxidative responses, the mRNA expression of muscular genes involved in glycogen and fatty acid metabolism, as well as mitochondrial biogenesis, and through the cross talk with AMPK and hypoxia-inducible factor-1α signaling.

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Exercise-induced ST-segment elevation during treadmill exercise testing

International Journal of Cardiology ◽

10.1016/j.ijcard.2008.12.046 ◽

2010 ◽

Vol 143 (3) ◽

pp. e54-e56

Author(s):

Salvatore Patanè ◽

Filippo Marte

Keyword(s):

Exercise Testing ◽

Treadmill Exercise ◽

St Segment Elevation ◽

St Segment ◽

Exercise Induced ◽

Treadmill Exercise Testing

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Muscle injury, impaired muscle function and insulin resistance in Chromogranin A-knockout mice

Journal of Endocrinology ◽

10.1530/joe-16-0370 ◽

2017 ◽

Vol 232 (2) ◽

pp. 137-153 ◽

Cited By ~ 4

Author(s):

Kechun Tang ◽

Teresa Pasqua ◽

Angshuman Biswas ◽

Sumana Mahata ◽

Jennifer Tang ◽

...

Keyword(s):

Tissue Damage ◽

Muscle Function ◽

Chromogranin A ◽

Secretory Pathway ◽

Treadmill Exercise ◽

Tubular Aggregates ◽

Skeletal Muscle Function ◽

Regulated Secretory Pathway ◽

Exercise Induced ◽

Stimulation Of

Chromogranin A (CgA) is widely expressed in endocrine and neuroendocrine tissues as well as in the central nervous system. We observed CgA expression (mRNA and protein) in the gastrocnemius (GAS) muscle and found that performance of CgA-deficient Chga-KO mice in treadmill exercise was impaired. Supplementation with CgA in Chga-KO mice restored exercise ability suggesting a novel role for endogenous CgA in skeletal muscle function. Chga-KO mice display (i) lack of exercise-induced stimulation of pAKT, pTBC1D1 and phospho-p38 kinase signaling, (ii) loss of GAS muscle mass, (iii) extensive formation of tubular aggregates (TA), (iv) disorganized cristae architecture in mitochondria, (v) increased expression of the inflammatory cytokines Tnfα, Il6 and Ifnγ, and fibrosis. The impaired maximum running speed and endurance in the treadmill exercise in Chga-KO mice correlated with decreased glucose uptake and glycolysis, defects in glucose oxidation and decreased mitochondrial cytochrome C oxidase activity. The lack of adaptation to endurance training correlated with the lack of stimulation of p38MAPK that is known to mediate the response to tissue damage. As CgA sorts proteins to the regulated secretory pathway, we speculate that lack of CgA could cause misfolding of membrane proteins inducing aggregation of sarcoplasmic reticulum (SR) membranes and formation of tubular aggregates that is observed in Chga-KO mice. In conclusion, CgA deficiency renders the muscle energy deficient, impairs performance in treadmill exercise and prevents regeneration after exercise-induced tissue damage.

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Percent change in B-type natriuretic peptide levels during treadmill exercise as a screening test for exercise-induced myocardial ischemia

American Heart Journal ◽

10.1016/j.ahj.2004.12.003 ◽

2005 ◽

Vol 150 (4) ◽

pp. 695-700 ◽

Cited By ~ 25

Author(s):

Htut Kyaw Win ◽

Su-Min Chang ◽

Michael Raizner ◽

Gopi Shah ◽

Faiz Al Basky ◽

...

Keyword(s):

Myocardial Ischemia ◽

Natriuretic Peptide ◽

Screening Test ◽

Treadmill Exercise ◽

Percent Change ◽

Exercise Induced

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Treadmill Exercise’s Reduction of Agouti-Related Protein Expression in Rat Liver

International Journal of Sport Nutrition and Exercise Metabolism ◽

10.1123/ijsnem.19.5.473 ◽

2009 ◽

Vol 19 (5) ◽

pp. 473-484 ◽

Cited By ~ 3

Author(s):

Abbass Ghanbari-Niaki ◽

Rozita Fathi ◽

Sayed Alireza Hossaini Kakhak ◽

Zhara Farshidi ◽

Sara Barmaki ◽

...

Keyword(s):

Mrna Expression ◽

Rat Liver ◽

Treadmill Exercise ◽

Training Group ◽

Liver Glycogen ◽

Related Protein ◽

Orexigenic Peptide ◽

Male Wistar Rats ◽

Exercise Induced ◽

Agouti Related Protein

Agouti-related protein (AGRP) is an orexigenic peptide secreted from the arcuate nucleus (ARC) of the hypothalamus. AGRP increases food intake and plays a role in energy balance, adiposity, weight gain, and growth-hormone release. The objective of the current study was to examine the effects of running exercise on resting hepatic, fundus, and pancreas AGRP mRNA expression, as well as liver glycogen and ATP contents, using a rat model. Twenty adult male Wistar rats (12–14 wk old, 200–220 g) were randomly assigned to control (n = 10) and training (n = 10) groups. The training group was exercised for 8 wk on a motor-driven treadmill (26 m/min, 0% grade, 60 min, 5 d/wk). Twenty-four hours before sacrifice the rats were further divided into fed control (FEC), fed trained (FET), fasted control (FAC), and fasted trained (FAT) groups. The liver, fundus, and pancreas were excised and frozen in liquid nitrogen for later analysis. Results demonstrated that 8 wk of treadmill exercise reduced hepatic but not fundus and pancreatic AGRP expression and enhanced glycogen and ATP concentrations (p < .001) in trained-rat liver, whereas fasting lowered liver glycogen and ATP levels and increased hepatic AGRP mRNA expression in nonexercising controls. Data indicate that both treadmill-exercise-induced decrease and fast-induced increase in rat liver AGRP expression might depend on liver glycogen content as an important source for energy provision.

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EXERCISE-INDUCED BENEFITS ON GLUCOSE HANDLING IN A MODEL OF DIET-INDUCED OBESITY ARE REDUCED BY CONCURRENT NICOTINAMIDE MONONUCLEOTIDE

10.1101/2020.06.22.164459 ◽

2020 ◽

Author(s):

Josephine Yu ◽

D. Ross Laybutt ◽

Lynn-Jee Kim ◽

Lake-Ee Quek ◽

Lindsay E. Wu ◽

...

Keyword(s):

Treadmill Exercise ◽

Control Diet ◽

Redox Status ◽

Metabolic Effects ◽

Mitochondrial Activity ◽

List Type ◽

Diet Induced Obesity ◽

Triglyceride Accumulation ◽

Nicotinamide Mononucleotide ◽

Exercise Induced

ABSTRACTObjectiveAlmost 40% of adults worldwide are classified as overweight or obese. Exercise is a beneficial intervention in obesity, partly due to increases in mitochondrial activity, with a potential role for the concomitant increase in nicotinamide adenine dinucleotide (NAD+). Recent studies have shown that increasing NAD+ levels through pharmacological supplementation with precursors such as nicotinamide mononucleotide (NMN) improved metabolic health in high fat diet (HFD) fed mice. We examined the combined effects of NMN and treadmill exercise on the metabolic dysregulation in HFD-induced obesity.MethodsFive-week old female C57BL/6J mice were exposed to control diet or HFD. Mice fed HFD were treated with NMN in drinking water (400mg/kg; HNMN), treadmill exercise (HEx) or combined NMN and exercise (HNEx).ResultsUnexpectedly, NMN administration impaired several aspects of exercise-induced benefits in HFD mice, including glucose tolerance, glucose stimulated insulin secretion from islets and reduced hepatic triglyceride accumulation. Mechanistically, HNEx mice displayed increased antioxidant and reduced prooxidant gene expression in both islets and muscle, suggesting that altered redox status is associated with the loss of exercise-induced health benefits with NMN co-treatment.ConclusionOur data show that NMN treatment blocks the beneficial metabolic effects of exercise in a mouse model of diet-induced obesity in association with disturbances in redox metabolism.HighlightsNMN dampened exercise-induced benefits on glucose handling in diet-induced obesity.NMN administration in exercise enhanced ratio of antioxidants to prooxidants.We suggest NMN administration may not be beneficial when NAD+ levels are replete.

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