Glucocorticoid signaling and exercise-induced downregulation of the mineralocorticoid receptor in the induction of adult mouse dentate neurogenesis by treadmill running

Our previous study showed that lipopolysaccharide (LPS)-induced tumor necrosis factor (TNF)-α production is inhibited by acute exhaustive exercise in mice, leading to transient immunodepression after exercise. Sparassis crispa (SC), an edible mushroom, has immunopotentiative properties. This study aimed to clarify the effects of SC intake on reduced LPS-induced TNF-α production upon exhaustive exercise in mice. Male C3H/HeN mice were randomly divided into three groups: normal chow intake + resting sedentary, normal chow intake + acute exhaustive treadmill running exercise, and SC intake (chow containing 5% SC powder for 8 weeks) + the exhaustive exercise groups. Each group was injected with LPS immediately after the exhaustive exercise or rest. Plasma and tissue TNF-α levels were significantly decreased by exhaustive exercise. However, this reduction of the TNF-α level was partially attenuated in the plasma and small intestine by SC intake. Although levels of TLR4 and MyD88 protein expression were significantly decreased in tissues by exhaustive exercise, the reduction of TLR4 and MyD88 levels in the small intestine was partially attenuated by SC intake. These results suggest that SC intake attenuates exhaustive exercise-induced reduction of TNF-α production via the retention of TLR4 and MyD88 expression in the small intestine.

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Effect of estradiol on the temporal pattern of exercise-induced tissue glycogen depletion in male rats

Journal of Applied Physiology ◽

10.1152/jappl.1993.75.4.1502 ◽

1993 ◽

Vol 75 (4) ◽

pp. 1502-1506 ◽

Cited By ~ 34

Author(s):

T. P. Rooney ◽

Z. V. Kendrick ◽

J. Carlson ◽

G. S. Ellis ◽

B. Matakevich ◽

...

Keyword(s):

Temporal Pattern ◽

Vastus Lateralis ◽

Treadmill Running ◽

Male Rats ◽

Vastus Lateralis Muscle ◽

Glycogen Depletion ◽

Muscle Tissues ◽

Triacylglycerol Content ◽

Exercise Induced ◽

Glycogen Sparing

The effect of 17 beta-estradiol 3-benzoate (10 micrograms.01 ml of sunflower oil-1 x 100 g body wt-1) on the temporal pattern of exercise-induced tissue glycogen depletion and tissue lipid availability during submaximal treadmill running was determined in male rats. Animal were administered estradiol or oil for 5 days and were then time matched for motorized treadmill running for 30, 60, 90, or 120 min. Significant depletion of liver, soleus muscle, and red and white vastus lateralis muscle tissue glycogen occurred in oil-administered animals run between 30 and 120 min. The greatest extent of tissue glycogen depletion occurred during the first 30 min of exercise with the rate of glycogen depletion slowing between 30 and 120 min of exercise. Administration of estradiol attenuated the temporal pattern of glycogen depletion in both liver and muscle tissues. Significant depletion of red and white vastus glycogen of estradiol-administered animals did not occur until 90 and 120 min of exercise, respectively. Administration of estradiol significantly increased resting plasma free fatty acids and red and white vastus triacylglycerol content. These data indicate that estradiol administration for 5 days resulted in significant glycogen sparing of liver and muscle tissues during submaximal treadmill running for up to 120 min by altering the temporal pattern of glycogen depletion of male rats secondary to an estradiol-mediated increase in availability of lipid substrate during exercise.

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Exercise-induced protection against reperfusion arrhythmia involves stabilization of mitochondrial energetics

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00858.2015 ◽

2016 ◽

Vol 310 (10) ◽

pp. H1360-H1370 ◽

Cited By ~ 20

Author(s):

Rick J. Alleman ◽

Alvin M. Tsang ◽

Terence E. Ryan ◽

Daniel J. Patteson ◽

Joseph M. McClung ◽

...

Keyword(s):

Simultaneous Measurement ◽

Cardiac Electrophysiology ◽

Ischemia Reperfusion ◽

Antiarrhythmic Effect ◽

Treadmill Running ◽

Sprague Dawley ◽

Isolated Mitochondria ◽

Reperfusion Arrhythmia ◽

Exercise Induced

Mitochondria influence cardiac electrophysiology through energy- and redox-sensitive ion channels in the sarcolemma, with the collapse of energetics believed to be centrally involved in arrhythmogenesis. This study was conducted to determine if preservation of mitochondrial membrane potential (ΔΨm) contributes to the antiarrhythmic effect of exercise. We utilized perfused hearts, isolated myocytes, and isolated mitochondria exposed to metabolic challenge to determine the effects of exercise on cardiac mitochondria. Hearts from sedentary (Sed) and exercised (Ex; 10 days of treadmill running) Sprague-Dawley rats were perfused on a two-photon microscope stage for simultaneous measurement of ΔΨm and ECG. After ischemia-reperfusion, the collapse of ΔΨm was commensurate with the onset of arrhythmia. Exercise preserved ΔΨm and decreased the incidence of fibrillation/tachycardia ( P < 0.05). Our findings in intact hearts were corroborated in isolated myocytes exposed to in vitro hypoxia-reoxygenation, with Ex rats demonstrating enhanced redox control and sustained ΔΨm during reoxygenation. Finally, we induced anoxia-reoxygenation in isolated mitochondria using high-resolution respirometry with simultaneous measurement of respiration and H2O2. Mitochondria from Ex rats sustained respiration with lower rates of H2O2 emission than Sed rats. Exercise helps sustain postischemic mitochondrial bioenergetics and redox homeostasis, which is associated with preserved ΔΨm and protection against reperfusion arrhythmia. The reduction of fatal ventricular arrhythmias through exercise-induced mitochondrial adaptations indicates that mitochondrial therapeutics may be an effective target for the treatment of heart disease.

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Regular exercise improves cardiac contractile activation by modulating MHC isoforms and SERCA activity in orchidectomized rats

Journal of Applied Physiology ◽

10.1152/japplphysiol.00224.2015 ◽

2015 ◽

Vol 119 (7) ◽

pp. 831-839 ◽

Cited By ~ 4

Author(s):

Pavarana Vutthasathien ◽

Jonggonnee Wattanapermpool

Keyword(s):

Treadmill Running ◽

Moderate Intensity ◽

Sham Operation ◽

Regular Exercise ◽

Mobility Limitations ◽

Sham Surgery ◽

Myosin Light Chain 2 ◽

Cardiac Myofilament ◽

Contractile Activation ◽

Exercise Induced

Data from the trial known as Testosterone in Older Men with Mobility Limitations (TOM) has indicated an association between testosterone administration and a greater risk for adverse cardiovascular events. We therefore propose that regular exercise is a cardioprotective alternative that prevents detrimental changes in contractile activation when a deficiency in male sex hormones exists. Ten-week-old orchidectomized (ORX) rats were subjected to a 9-wk treadmill running program at moderate intensity starting 1 wk after surgery. Although exercise-induced cardiac hypertrophy was observed both in rats that underwent ORX and sham surgery, regular exercise enhanced cardiac myofilament Ca2+ sensitivity and myosin light-chain 2 phosphorylation only in rats that underwent a sham operation. Although the rats that had sham surgery and and given exercise exhibited no change in maximum developed tension, regular running prevented the suppression of maximum active tension in the hearts of ORX rats. Regular exercise also prevented a shift in myosin heavy chain (MHC) isoforms toward β-MHC, a reduction in sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) activity, and an increase in SERCA sensitivity in the hearts of ORX rats. Neither SERCA content nor its modulating component, phospholamban (PLB), was altered by exercise in either sham-operated or ORX rats. However, decreases in the phosphorylated Thr17 form of PLB and the phosphorylated Thr287 form of Ca2+/calmodulin-dependent kinase II in the hearts of ORX rats were abolished after regular exercise. These results thus support the use of regular running as a cardioprotective alternative to testosterone replacement in hypogonadal conditions.

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Exercise-induced satellite cell activation in growing and mature skeletal muscle

Journal of Applied Physiology ◽

10.1152/jappl.1987.63.5.1816 ◽

1987 ◽

Vol 63 (5) ◽

pp. 1816-1821 ◽

Cited By ~ 153

Author(s):

K. C. Darr ◽

E. Schultz

Keyword(s):

Satellite Cell ◽

Cross Sections ◽

Time Course ◽

Cell Activation ◽

Treadmill Running ◽

Rapid Decline ◽

Fiber Damage ◽

Single Bout ◽

Satellite Cell Activation ◽

Exercise Induced

The time course and extent of satellite cell activation were studied in the soleus (m-SOL) and extensor digitorum longus (m-EDL) muscles of untrained growing and mature rats after a single bout of prolonged eccentric treadmill running. At 24, 48, 72, and 120 h postexercise, satellite cell mitotic activity was quantitated in autoradiographs of whole-fiber segments after injection of [3H]thymidine. Fiber damage and localization of labeled cells were also examined in muscle cross sections. Labeling in growing muscles progressively increased to peak levels (approximately 250% of control) at 72 h postexercise, whereas mature muscles exhibited an earlier peak (approximately 250% of control) at 24 (m-SOL) and 48 (m-EDL) h, followed by a more rapid decline to control levels by 120 h postexercise. In all exercised muscles the calculated satellite cell activation was far greater than required to repair the small number (less than 3.0%) of necrotic fibers identified at the light-microscopic level. These results suggest that satellite cells were activated not only on fibers exhibiting overt necrosis but also on those with lesions not discernible with light microscopy.

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IL-6 is not essential for exercise-induced increases in glucose uptake

Journal of Applied Physiology ◽

10.1152/japplphysiol.00946.2012 ◽

2013 ◽

Vol 114 (9) ◽

pp. 1151-1157 ◽

Cited By ~ 12

Author(s):

Hayley M. O'Neill ◽

Rengasamy Palanivel ◽

David C. Wright ◽

Tara MacDonald ◽

James S. Lally ◽

...

Keyword(s):

Skeletal Muscle ◽

Steady State ◽

Glucose Uptake ◽

Substrate Utilization ◽

Treadmill Running ◽

Glucose Clearance ◽

Skeletal Muscle Glucose Uptake ◽

Exercise Induced ◽

Similar Body

Interleukin-6 (IL-6) increases glucose uptake in resting skeletal muscle. IL-6 is released from skeletal muscle during exercise; however; it is not known whether this IL-6 response is important for exercise-induced increases in skeletal muscle glucose uptake. We report that IL-6 knockout (KO) mice, 4 mo of age, have similar body weight to wild-type (WT), and, under resting conditions, oxygen consumption, food intake, substrate utilization, glucose tolerance, and insulin sensitivity are not different. Maximal exercise capacity is also similar to WT. We investigated substrate utilization and glucose clearance in vivo during steady-state treadmill running at 70% of maximal running speed and found that WT and IL-6 KO mice had similar rates of substrate utilization, muscle glucose clearance, and phosphorylation of AMP-activated protein kinase T172. These data provide evidence that IL-6 does not play a major role in regulating substrate utilization or skeletal muscle glucose uptake during steady-state endurance exercise.

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

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00400.2010 ◽

2011 ◽

Vol 300 (2) ◽

pp. E341-E349 ◽

Cited By ~ 76

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.

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Relationship between Plasma Cortisol and Peak Expiratory Flow Rate in Exercise-Induced Asthma and the Effect of Sodium Cromoglycate

Clinical Science ◽

10.1042/cs0450533 ◽

1973 ◽

Vol 45 (4) ◽

pp. 533-541

Author(s):

P. Jaffe ◽

P. König ◽

O. Ijaduola ◽

S. Walker ◽

S. Godfrey

Keyword(s):

Sodium Cromoglycate ◽

Peak Expiratory Flow ◽

Flow Rate ◽

Peak Expiratory Flow Rate ◽

Plasma Cortisol ◽

Treadmill Running ◽

Asthmatic Patients ◽

Control Subjects ◽

Expiratory Flow ◽

Exercise Induced

1. The changes in peak expiratory flow rate (PEF) and plasma cortisol were studied in relation to a 6 min period of treadmill running in six normal and eighteen asthmatic subjects. Of the asthmatics patients, five were not receiving treatment with steroids, six were receiving low doses of steroids (under 7·5 mg of prednisone daily) and seven were receiving high doses of steroids (over 7·5 mg of prednisone daily) at the time of study. 2. All subjects were studied twice within 1 week at similar times of day, once after premedication with sodium cromoglycate (SCG) and once after a placebo. 3. Resting PEF and plasma cortisol did not differ between placebo and SCG tests. 4. No change in PEF occurred as a result of exercise in the control subjects. The asthmatic patients developed post-exercise bronchoconstriction which was partly prevented by SCG but was not affected by steroids. 5. Plasma cortisol rose after exercise in the asthmatic subjects but not in the control subjects. The rise may have been related to the stress of exercise-induced asthma. SCG had no significant effect on plasma cortisol after exercise.

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