Exercise-Induced Asthma in Children—A Comparative Study of Freeand Treadmill Running

PEDIATRICS ◽  
1999 ◽  
Vol 104 (Supplement_2) ◽  
pp. 380-380
Author(s):  
Christopher Randolph
Keyword(s):  
Comparative Study ◽  
Treadmill Running ◽  
Asthma In Children ◽  
Exercise Induced

Exercise-Induced Asthma in Children: a Comparative Study of Free and Treadmill Running

1998 ◽  
Vol 80 (3) ◽  
pp. 232-236 ◽  
Author(s):  
Servando Garcia de la Rubia ◽  
Manuel J Pajaron-Fernandez ◽  
Manuel Sanchez-Solis ◽  
Ignacio Martinez-Gonzalez Moro ◽  
Domingo Perez-Flores ◽  
...  
Keyword(s):  
Comparative Study ◽  
Treadmill Running ◽  
Asthma In Children ◽  
Exercise Induced

Suppression of Exercise-induced Asthma by Salbutamol, Theophylline, Atropine, Cromolyn, and Placebo in a Group of Asthmatic Children

PEDIATRICS ◽  
1975 ◽  
Vol 56 (5s) ◽  
pp. 930-934
Author(s):  
Simon Godfrey ◽  
Peter König
Keyword(s):  
Comparative Study ◽  
Exercise Test ◽  
Significant Degree ◽  
Cromolyn Sodium ◽  
The Other ◽  
Treadmill Running ◽  
Duration Of Action ◽  
Asthmatic Children ◽  
Site Of Action ◽  
Exercise Induced

A number of drugs are known to it exercise-induced asthma (EIA), but the results in some cases have been difficult to interpret due to the techniques employed. A comparative study was carried out in a group of children to investigate the effects of salbutamol, choline theophyllinate, cromolyn sodium, atropine, and placebo. The exercise test took the form of six minutes of standardized treadmill running. All the drugs, but not the placebo, were able to inhibit EIA to a significant degree, the effect being most marked with salbutamol. Cromolyn sodium caused no bronchodilatation at rest, while all the other drugs were bronchodilators, the effect being most marked with the aerosol atropine during exercise. It was impossible to distinguish the type of drug used for inhibition of EIA if it caused bronchodilatation at rest. The manner in which an exercise test can be used to investigate the duration of action or site of action of drugs is noted.

Exercise-induced bronchospasm in Ilesa, Nigeria: A Comparative study of rural and urban school children

2017 ◽  
Vol 17 (1) ◽  
pp. 25
Author(s):  
BP Kuti ◽  
KO Omole ◽  
DK Kuti ◽  
BI Oso ◽  
LO Mohammed ◽  
...  
Keyword(s):  
Comparative Study ◽  
School Children ◽  
Urban School ◽  
Rural And Urban ◽  
Exercise Induced

scholarly journals Sparassis crispa Intake Improves the Reduced Lipopolysaccharide-Induced TNF-α Production That Occurs upon Exhaustive Exercise in Mice

Nutrients ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 2049 ◽  
Author(s):  
Masataka Uchida ◽  
Naoki Horii ◽  
Natsuki Hasegawa ◽  
Eri Oyanagi ◽  
Hiromi Yano ◽  
...  
Keyword(s):  
Small Intestine ◽  
Edible Mushroom ◽  
Treadmill Running ◽  
Exhaustive Exercise ◽  
Tnf Α ◽  
Normal Chow ◽  
Sparassis Crispa ◽  
Exercise Induced ◽  
Α Level ◽  
Myd88 Protein

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.

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

1993 ◽  
Vol 75 (4) ◽  
pp. 1502-1506 ◽  
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.

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

2016 ◽  
Vol 310 (10) ◽  
pp. H1360-H1370 ◽  
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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