A 10-day mild treadmill exercise performed before an epileptic seizure alleviates oxidative injury in the skeletal muscle and brain tissues of the rats

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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MyoD and Myogenin mRNA Levels after Single Session of Treadmill Exercise in Rat Skeletal Muscle

Journal of Physical Therapy Science ◽

10.1589/jpts.21.81 ◽

2009 ◽

Vol 21 (1) ◽

pp. 81-84 ◽

Cited By ~ 4

Author(s):

Takuya Miyata ◽

Shoji Tanaka ◽

Katsuhiko Tachino

Keyword(s):

Skeletal Muscle ◽

Treadmill Exercise ◽

Mrna Levels ◽

Single Session ◽

Rat Skeletal Muscle

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Effects of Treadmill Exercise on p-AMPK, p-ACC and Malonyl-CoA Expression of Skeletal Muscle and Cardiac Muscle in Diabetic Rats

Journal of The Korean Society of Living Environmental System ◽

10.21086/ksles.2016.04.23.2.276 ◽

2016 ◽

Vol 23 (2) ◽

pp. 276

Author(s):

Jin-Kyung Cho ◽

Yong-Suk Ji ◽

Kwang-Seok Hyun

Keyword(s):

Skeletal Muscle ◽

Cardiac Muscle ◽

Treadmill Exercise ◽

Diabetic Rats ◽

Malonyl Coa

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Ventricular volume overload alters cardiac output distribution in rats during exercise

Journal of Applied Physiology ◽

10.1152/jappl.1980.49.3.482 ◽

1980 ◽

Vol 49 (3) ◽

pp. 482-490 ◽

Cited By ~ 20

Author(s):

S. F. Flaim ◽

W. J. Minteer

Keyword(s):

Skeletal Muscle ◽

Cardiac Output ◽

Left Ventricular Volume ◽

Treadmill Exercise ◽

Volume Overload ◽

Ventricular Volume ◽

Major Effect ◽

Left Ventricular ◽

Radioactive Microsphere ◽

Radioactive Microsphere Technique

A rat model for chronic left ventricular volume overload (a-v fistula, 2 mo) was used to test the effects of acute exhaustive treadmill exercise (EX) (5 min, 70 ft/min, 0 degrees grade) on cardiocirculatory hemodynamics and cardiac output (CO) distribution during heart failure (HF). Control (C) and HF rats were studied at rest (R) and during the last minute of EX. Heart rate (HR), mean arterial pressure (MAP), and left ventricular end-diastolic (LVEDP) pressure were recorded and CO, blood flow (BF) to various regions, and total CO distribution were determined by the radioactive microsphere technique. In HF, biventricular hypertrophy and elevated LVEDP at R were correlated with an average shunt size equaling 37% of total CO. In both groups, CO and HR rose during EX with no change in MAP. Systemic CO in HF was reduced compared to C during both R and EX. BF to splanchnic, renal, cutaneous, and testicular circulations was compromised at R in HF, whereas only skeletal muscle BF was compromised in HF during EX. Data for CO distribution suggest that the major effect of HF during R was increased delivery to the coronary and the skeletal muscle beds at the expense of the cutaneous and renal beds, whereas %CO to the cerebral, hepatic, and gastrointestinal beds was spared. During EX, %CO to skeletal muscle beds in HF was attenuated compared to C, whereas that to the coronary bed was increased with no change in other regions.

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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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Expression of phospholemman and its association with Na+-K+-ATPase in skeletal muscle: effects of aging and exercise training

Journal of Applied Physiology ◽

10.1152/japplphysiol.00375.2005 ◽

2005 ◽

Vol 99 (4) ◽

pp. 1508-1515 ◽

Cited By ~ 29

Author(s):

Justin Reis ◽

Lianqin Zhang ◽

Steve Cala ◽

Korinne N. Jew ◽

Lisa C. Mace ◽

...

Keyword(s):

Skeletal Muscle ◽

Exercise Training ◽

Treadmill Exercise ◽

Accessory Protein ◽

Dependent Manner ◽

Muscle Type ◽

Effects Of Aging ◽

High Level ◽

Reduced Activity ◽

Α Subunits

Phospholemman (PLM) is a recently identified accessory protein of the Na+-K+-ATPase (NKA), with a high level of expression in skeletal muscle. The objectives of this study are to characterize the PLM in skeletal muscle and to test the hypothesis that, as an accessory protein of NKA, expression of PLM and its association with the α-subunits of NKA is regulated during aging and with exercise training. PLM was characterized in skeletal muscle of 6- and 16-mo-old sedentary middle-aged rats (Ms), and the effects of aging and exercise training were studied in Ms, 29-mo-old sedentary senescent, and 29-mo-old treadmill-exercised senescent rats. Expression of PLM was muscle-type dependent, and immunofluorescence study showed that PLM distributed predominantly on the sarcolemmal membrane of the muscle fibers. Anti-PLM antibody reduced activity of NKA, and thus PLM appears to be required for NKA to express its full activity in skeletal muscle. Expression of PLM was not altered with aging but increased after exercise training. Coimmunoprecipitation studies demonstrated that PLM associates with both the α1- and α2-subunit isoforms of NKA. Compared with Ms rats, levels of PLM-associated α1-subunit increased in 29-mo-old sedentary senescent rats, and treadmill exercise has a tendency to partially reverse it. There was no significant change in PLM-associated α2-subunit with age, and exercise training has a tendency to increase that level. It is concluded that, in skeletal muscle, PLM appears to be a protein integral to the NKA complex and that PLM has the potential to modulate NKA in an isoform-specific and muscle type-dependent manner in aging and after exercise training.

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Skeletal muscle vasodilation at the onset of exercise

Journal of Applied Physiology ◽

10.1152/jappl.1998.85.5.1649 ◽

1998 ◽

Vol 85 (5) ◽

pp. 1649-1654 ◽

Cited By ~ 32

Author(s):

John B. Buckwalter ◽

Stephen B. Ruble ◽

Patrick J. Mueller ◽

Philip S. Clifford

Keyword(s):

Blood Pressure ◽

Skeletal Muscle ◽

Blood Flow ◽

Muscarinic Receptors ◽

Treadmill Exercise ◽

Systemic Blood Pressure ◽

Systemic Blood ◽

Iliac Arteries ◽

Blood Flows ◽

Peak Blood

The purpose of this study was to determine whether β-adrenergic or muscarinic receptors are involved in skeletal muscle vasodilation at the onset of exercise. Mongrel dogs ( n = 7) were instrumented with flow probes on both external iliac arteries and a catheter in one femoral artery. Propranolol (1 mg), atropine (500 μg), both drugs, or saline was infused intra-arterially immediately before treadmill exercise at 3 miles/h, 0% grade. Immediate and rapid increases in iliac blood flow occurred with initiation of exercise under all conditions. Peak blood flows were not significantly different among conditions (682 ± 35, 646 ± 49, 637 ± 68, and 705 ± 50 ml/min, respectively). Although the doses of antagonists employed had no effect on heart rate or systemic blood pressure, they were adequate to abolish agonist-induced increases in iliac blood flow. Because neither propranolol nor atropine affected iliac blood flow, we conclude that activation of β-adrenergic and muscarinic receptors is not essential for the rapid vasodilation in active skeletal muscle at the onset of exercise in dogs.

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