Endurance exercise training suppresses Parkinson disease-induced overexpression of apoptotic mediators in the heart

2021 ◽  
pp. 1-6
Author(s):  
Muhammed D. Al-Jarrah ◽  
Nour S. Erekat
Keyword(s):  
Exercise Training ◽  
Parkinson Disease ◽  
Endurance Exercise ◽  
Caspase 3 ◽  
P Value ◽  
Chronic Exercise ◽  
Sedentary Control ◽  
Animal Group ◽  
Endurance Exercise Training ◽  
Active Caspase

BACKGROUND We have shown elevated levels of p53 and active caspase-3 in the heart with Parkinson disease (PD). The main aim of this study is to examine the effect of treadmill training on the cardiac expression of p53 and active caspase-3 in the mouse with induced Parkinsonism. METHODS: Thirty randomly selected normal albino mice were equally divided into the following 3 groups: sedentary control (SC), sedentary Parkinson diseased (SPD), and exercised Parkinson diseased (EPD). 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and probenecid (MPTP/p) were used to induce chronic Parkinson disease in the SPD and EPD animals. The expression of p53 and active caspase-3 was investigated, using immunohistochemistry, in the heart in each animal group. RESULTS: Both p53 and active caspase-3 expression was significantly (p value <  0.05) reduced in the PD heart following endurance exercise training. CONCLUSION: Our present data suggest that chronic exercise training reduced PD-induced upregulation of p53 and active caspase-3 in the heart. Thus, our study suggests that inhibiting p53 and/or active caspase-3 may be considered as a therapeutic approach to ameliorate PD cardiomyopathy.

Endurance exercise training inhibits activity of plasma GOT and liver caspase-3 of rats exposed to stress by induction of heat shock protein 70

2004 ◽  
Vol 96 (5) ◽  
pp. 1776-1781 ◽  
Author(s):  
Toshio Mikami ◽  
Satoshi Sumida ◽  
Yoshitomo Ishibashi ◽  
Shigeo Ohta
Keyword(s):  
Heat Shock ◽  
Exercise Training ◽  
Heat Shock Protein ◽  
Endurance Exercise ◽  
Heat Shock Protein 70 ◽  
Caspase 3 ◽  
Treadmill Running ◽  
Exercise Stress ◽  
Endurance Exercise Training ◽  
Hepatic Protection

A single bout of exercise increases production of heat shock protein 70 (HSP70), which protects cells against various stresses. In this study, we investigated whether endurance exercise training enhances liver level of HSP70 and, if so, whether HSP70 contributes to hepatic protection against stress in vivo. Mice of an exercise-training group performed 60 min of treadmill running 5 days/wk for 4 wk. The resting level of liver HSP70 was 4.5 times higher in the trained than in sedentary mice. After 4 wk of exercise training, both groups of mice were exposed to the following stresses: 1) heat stress, 2) cold stress, 3) oxidative stress, 4) ethanol stress, and 5) exercise stress by compelling the mice to run on a treadmill until exhausted. After exposure to the stresses, the liver was immediately isolated. Elevation of liver HSP70 in the trained mice was evident, whereas no elevation was found in the sedentary mice. On exposure to heat, diethyldithiocarbamate and ethanol, activities of glutanic oxalacetic transaminase in plasma, and liver caspase-3, a key enzyme of apoptotic processing, were elevated in the sedentary mice but not in the trained mice. These results suggest that exercise training enhanced the resting level of liver HSP70 and hepatic protection against various stresses, at least partly attributing to the suppression of caspase-3 activity by the increase in HSP70.

Endurance exercise training decreases capillary basement membrane width in older nondiabetic and diabetic adults

1996 ◽  
Vol 80 (3) ◽  
pp. 747-753 ◽  
Author(s):  
J. R. Williamson ◽  
P. L. Hoffmann ◽  
W. M. Kohrt ◽  
R. J. Spina ◽  
A. R. Coggan ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Basement Membrane ◽  
Glucose Tolerance ◽  
Endurance Exercise ◽  
Older Men ◽  
Sedentary Control ◽  
Men And Women ◽  
Endurance Exercise Training ◽  
Older Men And Women

The objectives of these studies were to 1) evaluate the relationships among age, glucose intolerance, and skeletal muscle capillary basement membrane (CBM) width (CBMW) and 2) determine the effects of exercise training on CBMW by comparing values of young (28 +/- 4 yr) and older (63 +/- 7 yr) athletes with those of age-matched sedentary control subjects and by measuring CBMW in older men and women before and after a 9-mo endurance-exercise training program. CBMW was measured in tissue samples obtained from the gastrocnemius muscle. CBMW in sedentary 64 +/- 3-yr-old subjects was 25% thicker than in sedentary 24 +/- 3-yr-old subjects. CBMW was similar in young and older athletes and was thinner than the CBMW of age-matched sedentary control subjects. There were no differences in CBMW among older sedentary individuals with normal or impaired glucose tolerance or mild non-insulin-dependent diabetes mellitus. Nine months of endurance exercise training reduced CBMW in older men and women by 30-40%, to widths that were not different from those of the young subjects; this response was independent of glucose tolerance status. These findings suggest that habitual exercise prevents the thickening of the skeletal muscle CBM that is characteristic of advancing age. Moreover, the thickening of the CBM appears to be readily reversed as a result of exercise training, even in older individuals.

scholarly journals Endurance Exercise Training to Improve Economy of Movement of People With Parkinson Disease: Three Case Reports

2008 ◽  
Vol 88 (1) ◽  
pp. 63-76 ◽  
Author(s):  
Margaret Schenkman ◽  
Deborah Hall ◽  
Rajeev Kumar ◽  
Wendy M Kohrt
Keyword(s):  
Exercise Training ◽  
Parkinson Disease ◽  
Endurance Exercise ◽  
Rating Scale ◽  
Secondary Outcome ◽  
Home Exercise ◽  
Supervised Exercise ◽  
Endurance Exercise Training ◽  
Functional Reach Test ◽  
Economy Of Movement

Background and PurposeEven early in Parkinson disease (PD), individuals have reduced economy of movement. In this case report, the effects of endurance exercise training are examined on walking economy and other measures for 3 individuals in early and middle stages of PD.PatientsThe patients were 1 woman and 2 men with PD, aged 52 to 72 years, classified at Hoehn and Yahr stages 2 to 2.5.InterventionEach patient completed 4 months of supervised endurance exercise training and 12 months of home exercise, with monthly clinic follow-up sessions. Strategies were included to enhance adherence to exercise.OutcomesThe main outcome measure was economy of movement (rate of oxygen consumption during gait) measured at 4 treadmill speeds. Secondary outcome measures included the Unified Parkinson's Disease Rating Scale (UPDRS), Continuous-Scale Physical Functional Performance Test (CS-PFP), Functional Reach Test (FRT), and Functional Axial Rotation Test (FAR). Economy of movement improved for all 3 patients after 4 months of supervised exercise and remained above baseline at 16 months. Two patients also had scores that were above baseline for UPDRS total score, CS-PFP, FRT, and FAR, even at 16 months.Discussion and ConclusionsEvidence from these 3 individuals suggests that gains may occur with a treadmill training program that is coupled with specific strategies to enhance adherence to exercise.

scholarly journals The Effect of Endurance Exercise Training on the Expression of Brain Derived Neurotrophic Factor (BDNF) and Nerve Growth Factor (NGF) Genes of the Cerebellum in Diabetic Rat

2020 ◽  
Author(s):  
Asma Taheri ◽  
Hadi Rohani ◽  
Abdolhamid Habibi
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Exercise Training ◽  
Endurance Training ◽  
Endurance Exercise ◽  
Neurotrophic Factors ◽  
Diabetic Rat ◽  
P Value ◽  
Diabetic Patients ◽  
Endurance Exercise Training

Objective: Few studies have been conducted on variations of the central nervous system of diabetic patients and much fewer investigations done on the cerebellum of diabetes patients. The current research aims to investigate the effect of endurance training on neurotrophic factors affecting the cerebellum in the diabetic rat. Materials and Methods: This study is experimental.Twenty Wistar rat were randomly allocated in four groups including: (1) control (n=5), (2) diabetic exercise (n=5), (3) healthy-control (n=5), (4) and exercise-healthy (n=5). Diabetes were induced by intraperitoneal Streptozotocin injection. The endurance exercise training was performed at moderate intensity for six weeks. Expression of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) genes were measured using the Real-Time PCR method in the cerebellum of the rat. Two-way ANOVA test was used for comparing the means of expression of genes between groups. All statistical analyses were done using SPSS 22 software. Results: A significant increase was observed in the expression of NGF (from 1.03±0.11 to 1.61±0.24; P-value≤ 0.05) and BDNF (from 1.59±0.06 to 3.24±0.46; P-value≤ 0.05) genes in male rats with experimental diabetes and healthy subjects after six weeks endurance training. Conclusion: Endurance training may be helpful for diabetic patients by increasing the neurotrophic factors and thereby preventing diabetes-related neural complications.

Higher mitochondrial fatty acid oxidation following intermittent versus continuous endurance exercise training

1998 ◽  
Vol 76 (9) ◽  
pp. 891-894 ◽  
Author(s):  
P D Chilibeck ◽  
G J Bell ◽  
R P Farrar ◽  
T P Martin
Keyword(s):  
Fatty Acid ◽  
Exercise Training ◽  
Fatty Acid Oxidation ◽  
Endurance Exercise ◽  
High Intensity ◽  
Treadmill Running ◽  
Acid Oxidation ◽  
Interval Exercise ◽  
Endurance Exercise Training ◽  
Mitochondrial Fatty Acid

It has been well documented that skeletal muscle fatty acid oxidation can be elevated by continuous endurance exercise training. However, it remains questionable whether similar adaptations can be induced with intermittent interval exercise training. This study was undertaken to directly compare the rates of fatty acid oxidation in isolated subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondria following these different exercise training regimes. Mitochondria were isolated from the gastrocnemius-plantaris muscles of male Sprague-Dawley rats following exercise training 6 days per week for 12 weeks. Exercise training consisted of either continuous, submaximal, endurance treadmill running (n = 10) or intermittent, high intensity, interval running (n = 10). Both modes of training enhanced the oxidation of palmityl-carnitine-malate in both mitochondrial populations (p < 0.05). However, the increase associated with the intermittent, high intensity exercise training was significantly greater than that achieved with the continuous exercise training (p < 0.05). Also, the increases associated with the IMF mitochondria were greater than the SS mitochondria (p < 0.05). These data suggest that high intensity, intermittent interval exercise training is more effective for stimulation of fatty acid oxidation than continuous submaximal exercise training and that this adaptation occurs preferentially within IMF mitochondria.Key words: muscle, subsarcolemmal mitochondria, intermyofibrillar mitochondria.

Endurance exercise training increases insulin responsiveness in isolated adipocytes through IRS/PI3-kinase/Akt pathway

2005 ◽  
Vol 98 (3) ◽  
pp. 1037-1043 ◽  
Author(s):  
Sidney B. Peres ◽  
Solange M. Franzói de Moraes ◽  
Cecilia E. M. Costa ◽  
Luciana C. Brito ◽  
Julie Takada ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Exercise Training ◽  
Insulin Receptor ◽  
Endurance Exercise ◽  
Pi3 Kinase ◽  
Akt Pathway ◽  
Β Subunit ◽  
Endurance Exercise Training ◽  
Isolated Adipocytes

Endurance exercise training promotes important metabolic adaptations, and the adipose tissue is particularly affected. The aim of this study was to investigate how endurance exercise training modulates some aspects of insulin action in isolated adipocytes and in intact adipose tissue. Male Wistar rats were submitted to daily treadmill running (1 h/day) for 7 wk. Sedentary age-matched rats were used as controls. Final body weight, body weight gain, and epididymal fat pad weight did not show any statistical differences between groups. Adipocytes from trained rats were smaller than those from sedentary rats (205 ± 16.8 vs. 286 ± 26.4 pl; P < 0.05). Trained rats showed decreased plasma glucose (4.9 ± 0.13 vs. 5.3 ± 0.07 mM; P < 0.05) and insulin levels (0.24 ± 0.012 vs. 0.41 ± 0.049 mM; P < 0.05) and increased insulin-stimulated glucose uptake (23.1 ± 3.1 vs. 12.1 ± 2.9 pmol/cm2; P < 0.05) compared with sedentary rats. The number of insulin receptors and the insulin-induced tyrosine phosphorylation of insulin receptor-β subunit did not change between groups. Insulin-induced tyrosine phosphorylation insulin receptor substrates (IRS)-1 and -2 increased significantly (1.57- and 2.38-fold, respectively) in trained rats. Insulin-induced IRS-1/phosphatidylinositol 3 (PI3)-kinase (but not IRS-2/PI3-kinase) association and serine Akt phosphorylation also increased (2.06- and 3.15-fold, respectively) after training. The protein content of insulin receptor-β subunit, IRS-1 and -2, did not differ between groups. Taken together, these data support the hypothesis that the increased adipocyte responsiveness to insulin observed after endurance exercise training is modulated by IRS/PI3-kinase/Akt pathway.

scholarly journals Endurance exercise training normalizes repolarization and calcium-handling abnormalities, preventing ventricular fibrillation in a model of sudden cardiac death

2012 ◽  
Vol 113 (11) ◽  
pp. 1772-1783 ◽  
Author(s):  
Ingrid M. Bonilla ◽  
Andriy E. Belevych ◽  
Arun Sridhar ◽  
Yoshinori Nishijima ◽  
Hsiang-Ting Ho ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Cardiac Death ◽  
Outward Current ◽  
Calcium Handling ◽  
Transient Outward Current ◽  
Cellular Electrophysiology ◽  
Endurance Exercise Training

The risk of sudden cardiac death is increased following myocardial infarction. Exercise training reduces arrhythmia susceptibility, but the mechanism is unknown. We used a canine model of sudden cardiac death (healed infarction, with ventricular tachyarrhythmias induced by an exercise plus ischemia test, VF+); we previously reported that endurance exercise training was antiarrhythmic in this model (Billman GE. Am J Physiol Heart Circ Physiol 297: H1171–H1193, 2009). A total of 41 VF+ animals were studied, after random assignment to 10 wk of endurance exercise training (EET; n = 21) or a matched sedentary period ( n = 20). Following (>1 wk) the final attempted arrhythmia induction, isolated myocytes were used to test the hypotheses that the endurance exercise-induced antiarrhythmic effects resulted from normalization of cellular electrophysiology and/or normalization of calcium handling. EET prevented VF and shortened in vivo repolarization ( P < 0.05). EET normalized action potential duration and variability compared with the sedentary group. EET resulted in a further decrement in transient outward current compared with the sedentary VF+ group ( P < 0.05). Sedentary VF+ dogs had a significant reduction in repolarizing K+ current, which was restored by exercise training ( P < 0.05). Compared with controls, myocytes from the sedentary VF+ group displayed calcium alternans, increased calcium spark frequency, and increased phosphorylation of S2814 on ryanodine receptor 2. These abnormalities in intracellular calcium handling were attenuated by exercise training ( P < 0.05). Exercise training prevented ischemically induced VF, in association with a combination of beneficial effects on cellular electrophysiology and calcium handling.

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