2 edition of Effects of exhaustive exercise on heart mitochondria from trained and sedentary rats. found in the catalog.
Effects of exhaustive exercise on heart mitochondria from trained and sedentary rats.
Walter Louis Sembrowich
Written in English
|The Physical Object|
|Pagination||viii, 52 l.|
|Number of Pages||52|
Gul M, Demircan B, Taysi S, et al. Effects of endurance training and acute exhaustive exercise on antioxidant defense mechanisms in rat heart. Comp Biochem Physiol A Mol Integr Physiol. Feb;(2); Gul M, Atalay M, Hanninen O. Endurance training and glutathione-dependent antioxidant defense mechanism in heart of the diabetic rats. Increased subsarcolemmal lipids in type 2 diabetes: effect of training on localization of lipids, mitochondria, and glycogen in sedentary human skeletal muscle. Joachim Nielsen, Martin Mogensen, Birgitte F. Vind, Kent Sahlin, Kurt Højlund, Henrik D. Schrøder, and ; Niels Ørtenblad.
Mitochondrial dysfunction and reduced oxidative capacity in skeletal muscle have been linked to the pathogenesis of sarcopenia, aging disabilities, and frailty ().Sedentary lifestyle, an escalating epidemic in Western societies, is associated with loss of mitochondrial content and function (2, 3).Increased mitochondrial content in response to exercise training was first reported by Holloszy in. [Purpose] The purpose of this study was to investigate the effects of 8 weeks of endurance exercise on the cardiac mitochondrial function of mice. [Subjects] Ten SvJ/C57BL6 Male mice were used. The mice were randomly divided into an exercise group (n=5; mean ± SD weight, ± g) and a control (n=5; mean ± SD weight, ± g).
Oxidant stress is one of the factors proposed to be responsible for damaged erythrocytes observed during and after exercise. The impact of exertional oxidant stress after acute exhaustive treadmill running on erythrocyte damage was investigated in sedentary (Sed) and exercise-trained (ET) rats treated with or without antioxidant vitamins C and E. Exhaustive exercise led to statistically. Objective. To test the hypothesis that salidroside (SAL) can protect heart from exhaustive exercise-induced injury by enhancing mitochondrial respiratory function and mitochondrial biogenesis key signaling pathway PGC-1 α –NRF1/NRF2 in rats. Methods. Male Sprague-Dawley rats were divided into 4 groups: sedentary (C), exhaustive exercise (EE), low-dose SAL (LS), and high-dose SAL (HS).
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The present study investigated the effect of training and exhaustive exercise on the mitochondria of gas- trocnemius muscle of rats. MATERIALS AND METHODS.
Sixteen male rats of the Sprague-Dawley strain, with initial body weights between and g, were used in this investigation. Several investigators [1, 12, 13, 14, 20, 26] have observed ultrastructure changes in rats’ hearts following prolonged, exhaustive exercise.
King and Gollnick  and Banister et al.  reported changes in mitochondria ultrastructure similar to changes observed with ischemia [5, 6].Author: R. Barnard, A. Thorstensson. The aim of the present study was to ascertain the effects of training and exhaustive exercise on mitochondrial capacities to oxidize pyruvate, 2-oxoglutarate, palmitoylcarnitine, succinate and ferrocytochrome c in various tissues of the by: Malondialdehyde level in heart tissue was not affected by acute exhaustive exercise in untrained and trained rats.
The activities of glutathione peroxidase and glutathione reductase enzymes. The bradycardia of exercise training can result from adaptations at the effector organ, such as changes in acetylcholine, choline acetyltransferase, or acetylcholinesterase; from an increase in vagal efferent nerve activity; or from a reduction in sympathetic efferent nerve activity.
Previous chapter. in Cited by: 4. Exercise Training Alleviates Hypoxia-induced Mitochondrial Dysfunction in the Lymphocytes of Sedentary Males. Sci. Rep.
6, ; doi: /srep (). Exercise training counteracts urothelial carcinoma-induced alterations in skeletal muscle mitochondria phospholipidome in an animal model Javier-Fernando Montero-Bullon 1 Tânia Melo 1, 4.
The effects of exercise training on mitochondrial proteome in hypertensive hearts at 2 moments, before and after hypertension development, were here evaluated. In this context, the decrease in abundance of complex I in exercise groups when compared with control groups (Figure 3, B) is strongly associated with an increase in reactive oxygen species.
We examined the effects of exercise training on markers of both brain and muscle mitochondrial biogenesis in relation to endurance capacity assessed by a treadmill run to fatigue (RTF) in mice. Male ICR mice were assigned to exercise (EX) or sedentary (SED) conditions (n = 16–19/group).
EX mice performed 8 wk of treadmill running for 1 h/day. After 3 weeks of being sedentary or with exercise training, MI operations were per-formed. The following eight weeks of exercise initiated for rats to adapt to training for ﬁve days. Exercise intensity was 15 m/min and 20 (pexercise had a signiﬁcant effect on heart weight and heart weight/body weight in S-MI-E.
All of these findings indicate that SAL can protect the heart from exhaustive exercise-induced injury by improving mitochondrial respiratory function and mitochondrial biogenesis.
In conclusion, exhaustive exercise can induce heart injury, including structural injury, enzyme abnormalities, reduced respiratory function, and the downregulation of mitochondrial biogenesis. Simply put, more exercise produced more mitochondria/cell “furnaces” for more energy to make the exercise easier.
The effects of endurance training on the mitochondria of muscle cells were clearly beneficial. Animals to Humans. The early studies laid the groundwork for.
Purpose. Exercise training increases aerobic capacity and is beneficial for health, whereas low aerobic exercise capacity is a strong independent predictor of cardiovascular disease and premature death.
The purpose of the present study was to determine the metabolic profiles in a rat model of inborn low versus high capacity runners (LCR/HCR) and to determine the effect of inborn aerobic capacity.
Effects of aging and exercise training on apoptosis in the heart. (A) Cleaved capase-3 protein levels and (B) DNA fragmentation through quantification of mono. Extremely heavy or exhaustive exercise fosters mitochondrial disturbances that could permanently damage its function in health and disease.
Exercise-induced mitochondrial dysfunction might be a key proxy for heart abnormalities, chronic fatigue and overtraining syndrome, or muscle degeneration in athletic environment. Surprisingly, the protective effect is similar after short-term (3 to 5 days) and long-term (weeks to months) exercise training.
40,46,61 In a trial specifically designed to assess the loss of cardioprotective effects after training cessation, Lennon et al 62 were able to show a persistence of protection against myocardial stunning for up to 9.
Kraus H. () Influence of Exercise on Electron Transport Capacity of Heart Mitochondria. In: Pernow B., Saltin B. (eds) Muscle Metabolism During Exercise. Advances in Experimental Medicine and. The Protective Effects of Salidroside from Exhaustive Exercise-Induced Heart Injury by Enhancing the PGC-1 α–NRF1/NRF2 Pathway and Mitochondrial Respiratory Function in Rats Zheng Ping, 1 Long-fei Zhang, 1 Yu-juan Cui, 1 Yu-mei Chang, 1 Cai-wu Jiang, 2 Zhen-zhi Meng, 3 Peng Xu, 1 Hai-yan Liu, 1 Dong-ying Wang, 1 and Xue-bin Cao 1, *.
If exercise was to be accepted as a stress inducer and had a similar resistance generating effect on proximal tubule cells, the kidneys of exercisers would be more resistant to subsequent attacks and the renal functional capacity of trained athletes would be greater than those having a sedentary lifestyle.
Exercise-induced heart mitochondrial cholesterol depletion inﬂuences the inhibition of mitochondrial swelling The signiﬁcance of the reduction of the cholesterol pool in heart mitochondria after exercise The rats were randomly divided into sedentary control (C) and long-lasting endurance exercise (E) groups.
Two years of exercise training during middle age may reduce or reverse the cardiac consequences of a sedentary lifestyle. Two years of exercise training may be an effective lifestyle modification for rejuvenating aging hearts and reducing the risk of heart failure.Exhaustive endurance exercise was performed by rats on a treadmill.
Wistar rats at 4 weeks of age (Shanghai SLAC Experimental Animal Center, Shanghai, China) were divided into 3 groups, 12 animals per group: control (sedentary), endurance exercise (EE), and EE+nutrient-dosed. Nutrients and doses (mg/kg/day) were as.Aging is a natural, multifactorial and multiorganic phenomenon wherein there are gradual physiological and pathological changes over time.
Aging has been associated with a decrease of autophagy capacity and mitochondrial functions, such as biogenesis, dynamics, and mitophagy. These processes are essential for the maintenance of mitochondrial structural integrity and, therefore, for cell life.