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Light microscope images taken from the thoracic aorta of sedentary and trained normotensive (WKY) and hypertensive (SHR) rats showing elastic lamellas (thick open arrows) and fibrils (thin arrows) stained in purple and smooth muscle cells in rose with the nucleus stained in pale blue (asterisks). Observe that SHRS versus WKYS exhibited an increased content of elastic fibres but paler staining – changes that are absent in the SHRT group. Scale bar = 100 µm. The colours refer to the online version.
Source publication
Pharmacological antihypertensive therapies decrease both wall hypertrophy and collagen, but are unable to diminish the elastic content in the thoracic aorta. We investigated the effects of exercise training on aortic structure and function.
Spontaneously hypertensive rats (SHR) and normotensive rats (WKY), submitted to low-intensity training (T) or...
Contexts in source publication
Context 1
... mRNA expres- sions of -actin, elastin and collagen I and III were com- pletely normalized by training in the SHR group, with no significant changes in the WKY controls ( fig. 2 ). Figure 3 illustrates and compares the aortic wall ap- pearance in sedentary and trained WKY and SHR. In all groups, the aortic wall exhibited 7-8 elastic lamellas and many elastic fibrils that extended from the lamellas and permeated the smooth muscle cell layer. ...
Context 2
... the internal elastic lamina. It is important to note that training in both groups caused a marked reor- ganization of the smooth muscle cells: they presented a more elongated shape and are disposed preferentially along the circumferential axis of the vessel, an anatom- ical organization that reminds us of the contractile phe- notype of the cell ( fig. 5 b, d; table 3 ). In the SHR group, training also decreased the number of elastic fibrils, prevented both rupture and duplication of the internal elastic lamina and reduced the collagen contend both in the tunica media and around the endothelium ( fig. 5 c, d; table 3 ). With the exception of the reorganization of smooth muscle cells, training caused ...
Context 3
... an anatom- ical organization that reminds us of the contractile phe- notype of the cell ( fig. 5 b, d; table 3 ). In the SHR group, training also decreased the number of elastic fibrils, prevented both rupture and duplication of the internal elastic lamina and reduced the collagen contend both in the tunica media and around the endothelium ( fig. 5 c, d; table 3 ). With the exception of the reorganization of smooth muscle cells, training caused minor changes in the extracellular matrix components of the aorta in the WKY ...
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Citations
... Except for cells, the homograft is composed of extracellular matrix where elastin and collagen are the main components of the aorta and the pulmonary artery, providing strength and elasticity to the tissue (Burkert et al. 2021). Healthy vessels express lower content of collagen compared to vessels from older individuals and vessels exposed to hypertension, with intact elastic fibers (without fragmentation) and surrounding fibrillin to anchor mature elastin fibers to surrounding tissue (Kielty et al. 2002;Jordão et al. 2011;Halushka et al. 2016). Typical elastin degeneration signs are increased complexity, splitting, fragmentation and thinning of the fiber (Dingemans et al. 2006;Halushka et al. 2016). ...
According to guidelines, total ischemic time for homografts at processing must be kept short to avoid degeneration. Many homografts are discarded due to practical inability to finish all steps from procurement to cryopreservation within the time limit. Although, several studies have shown that homografts with prolonged ischemic time show adequate quality and performance. Twenty aortic and 12 pulmonary homografts were collected and biopsies were retrieved at preparation (day 0) and after 1, 2, 3, 4, 7, 14, 21, 28, and 60 days in antibiotic decontamination at 4 °C. Biopsies were prepared for light microscopy (LM) and transmission electron microscopy (TEM). Assessment generated scores for cells, elastin, and collagen. Relative differences between times were compared with Wilcoxon signed rank test. Bonferroni corrected p value of 0.0056 was considered significant. LM could only reveal decrease in cell count at 60 days in aortic homografts, no other differences was detected. TEM showed affected cell appearance in day 3 and day 4 and beyond for aortic and pulmonary homografts respectively. Elastin appearance was affected at day 60 for aortic and day 21 for pulmonary homografts. Collagen appearance was affected at day 28 for aortic homografts, with no significant differences in pulmonary homografts. Cell degeneration starts early after homograft procurement, but elastic and collagen fibers are more resistant to degeneration. Overall structure integrity as seen in LM was not affected at all, while TEM could reveal small degeneration signs in individual elastic fibers and collagen bundles at 21 and 28 days respectively.
... From human studies, most of the mechanisms shown to be involved with PWV reduction are systemic, such as increases in plasma nitrite concentration and plasma NOx [48][49][50] and decreases in plasma levels of endothelin-1 and noradrenaline [48,49]. On the other hand, animal studies have shown important alterations both in the aortic extracellular matrix proteins and in the hypertrophy of vascular smooth muscle cells (VSMC), which contribute to altering vessel remodeling, but not all animal studies evaluate PWV [51]. Therefore, the present study used a non-invasive technique, previously validated by our group [8], which allows measuring PWV and performing histological and molecular analyses in the vessel of the same animal for a better understanding of the possible mechanisms. ...
... In addition, less aortic collagen level has been demonstrated after aerobic training [19,60] which contributes to decreased arterial stiffening. The mechanism induced by aerobic training to reduce the level of aortic COL1 protein may involve a lower sympathetic drive to the vessel [17,51] since the synthesis of collagen is mediated by increased sympathetic nerve activity through the beta receptor [61]. ...
(1) Background: Arterial stiffness is an important predictor of cardiovascular events. Perindopril and physical exercise are important in controlling hypertension and arterial stiffness, but the mechanisms are unclear. (2) Methods: Thirty-two spontaneously hypertensive rats (SHR) were evaluated for eight weeks: SHRC (sedentary); SHRP (sedentary treated with perindopril—3 mg/kg) and SHRT (trained). Pulse wave velocity (PWV) analysis was performed, and the aorta was collected for proteomic analysis. (3) Results: Both treatments determined a similar reduction in PWV (−33% for SHRP and −23% for SHRT) vs. SHRC, as well as in BP. Among the altered proteins, the proteomic analysis identified an upregulation of the EH domain-containing 2 (EHD2) protein in the SHRP group, required for nitric oxide-dependent vessel relaxation. The SHRT group showed downregulation of collagen-1 (COL1). Accordingly, SHRP showed an increase (+69%) in the e-NOS protein level and SHRT showed a lower COL1 protein level (−46%) compared with SHRC. (4) Conclusions: Both perindopril and aerobic training reduced arterial stiffness in SHR; however, the results suggest that the mechanisms can be distinct. While treatment with perindopril increased EHD2, a protein involved in vessel relaxation, aerobic training decreased COL1 protein level, an important protein of the extracellular matrix (ECM) that normally enhances vessel rigidity.
... To the best of our knowledge, there is no study in the literature analyzing the effects of exercise training on the structure and function of brain arteries in hypertensive rats. Since we showed previously that exercise training corrects the deleterious remodeling of peripheral vasculature (Melo et al., 2003;Jordão et al., 2011;Silva et al., 2015), we sought now to evaluate training-induced changes on main brain arteries and their effects on blood pressure and cerebral blood flow both at rest and during exercise. ...
... Rats were submitted to a moderate-intensity training protocol (T = 50-60% of maximal exercise capacity, 0% grade, five days/week, 1 h/day) or kept sedentary (S) for three months (Ceroni et al., 2009;Jordão et al., 2011). Maximal exercise tests (Ceroni et al., 2009;Jordão et al., 2011) performed at weeks 0, 6, and 12, were used to determine (week 0), adjust the training intensity (week 6), and compare the efficacy of T and S protocols (week 12). ...
... Rats were submitted to a moderate-intensity training protocol (T = 50-60% of maximal exercise capacity, 0% grade, five days/week, 1 h/day) or kept sedentary (S) for three months (Ceroni et al., 2009;Jordão et al., 2011). Maximal exercise tests (Ceroni et al., 2009;Jordão et al., 2011) performed at weeks 0, 6, and 12, were used to determine (week 0), adjust the training intensity (week 6), and compare the efficacy of T and S protocols (week 12). Rats assigned to S protocol were handled every day. ...
Remodeling of capillary rarefaction and deleterious arteries are characteristic hallmarks of hypertension that are partially corrected by exercise training. In addition, experimental evidence showed capillary rarefaction within the brain cortex and reduced cerebral blood flow. There is no information on hypertension- and exercise-induced effects on capillary profile and function within preautonomic nuclei. We sought now to evaluate the effects of hypertension and exercise training (T) on the capillary network within hypothalamic paraventricular (PVN) and solitary tract (NTS) nuclei, and on the remodeling of brain arteries. Age-matched spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY), submitted to moderate T or kept sedentary (S) for three months, were chronically cannulated for hemodynamic recordings at rest. Rats were anesthetized for i.v. administration of fluorescein isothiocyanate (FITC)-dextran (capillary volume/density measurements) or 4% paraformaldehyde perfusion (basilar, middle, and posterior arteries' morphometry) followed by brain harvesting and processing. Other groups of conscious rats had carotid blood flow (CBF, ultrasound flowmeter) acquired simultaneously with hemodynamic recordings at rest and exercise. SHR-S exhibited elevated pressure and heart rate, reduced CBF, increased wall/lumen ratio of arteries, but no capillary rarefaction within the PVN and NTS. T improved performance gain and caused resting bradycardia in both groups; reduction of pressure and sympathetic vasomotor activity and normalization of the wall/lumen ratio were only observed in SHR-T. T groups responded with marked PVN and NTS capillary angiogenesis and augmented CBF during exercise; to avoid overperfusion at rest, reduced basal CBF was observed only in WKY-T. Data indicated that the absence of SHR-S capillary rarefaction and the intense SHR-T angiogenesis within autonomic areas associated with correction of deleterious arteries' remodeling are essential adjustments to hypertension and exercise training, respectively. These adaptive responses maintain adequate baseline perfusion in SHR-S and SHR-T preautonomic nuclei, augmenting it in exercised rats when a well-coordinated autonomic control is required.
... 92,93 No tecido vascular, a HAS caracteriza-se por desorganização das células musculares lisas, aumento dos depósitos de colágeno e diminuição da razão elastina/colágeno, além da formação de fibra elástica anormal e lâmina elástica interna com menor área fenestrada. 94 Todas essas alterações estruturais da parede do vaso, que ocorrem tanto em território arterial como arteriolar, elevam a rigidez do sistema vascular, com consequente aumento da velocidade da onda O exercício físico, por meio do aumento do estresse tangencial derivado da fricção do fluxo sanguíneo na superfície endotelial da parede do vaso (definido como força de cisalhamento e comumente descrito pelo termo "shear stress"), estimula positivamente o tecido endotelial, com aumento da produção de enzimas antioxidantes e agentes vasodilatadores, além de diminuição da ação dos radicais livres, das citocinas pró-inflamatórias, das moléculas de adesão e dos agentes vasoconstritores, restaurando, assim, o equilíbrio do funcionamento endotelial. 97,98 Estudos experimentais 94 em ratos espontaneamente hipertensos demonstram a reorganização de todas as estruturas vasculares da artéria aorta após a implementação de um período de exercício aeróbico. ...
... Immediately after respiratory arrest, a ventral incision was made in the midline of the thoracic region to expose the heart. Rats were submitted to transcardiac perfusion with ~100 ml of sterile saline followed by ~200 ml of 4% paraformaldehyde in buffered PBS, using a peristaltic Milan pump, at 20-30ml/min rate [15]. Segments (~5 mm) of descending thoracic aorta, femoral artery and common carotid artery were collected for smooth muscle, elastic and collagen tissue analyses (5 rats of each group). ...
... For morphological, smooth muscle and elastic tissue analyses, vessel samples were cleaned and fixed for 24 h in 4% buffered paraformaldehyde solution in 0.1 mol/l phosphate buffer, pH 7.2. Samples were then dehydrated in graded ethanol concentrations (70, 80, 90 and 100%) and embedded in histological paraplast, as previously described [15]. Serial transverse slices (microtome, 10 µm thick sections) were obtained from each artery; 10 to 15 sections were mounted on glass slide and stained with hematoxylin and eosin (smooth muscle constituents) or Weigert-hematoxylin (elastic lamellas/ fibrils). ...
Pulse wave velocity (PWV) has become a gold standard index to quantify the stiffness of the aorta and is a predictor of cardiovascular events. A recent paper compared the pOpmètre®, a device for measuring the finger-toe PWV, with other techniques and demonstrated its accuracy and validity. However, human devices do not allow the advancement of our knowledge on conditioning mechanisms. Based on its human validation, a new device, pOpmètre® 1.0 was designed for estimation of PWV in small animals and this present study aimed to standardize the pOpmètre® for estimation of arterial stiffness in rats, and to confirm its liability and stability as well as the reproducibility of assessments. Therefore several precautions were taken into consideration like as the correct position of the animal and photodiodes according to manufacturers’ suggestions. Results indicated that estimation of PWV through the new pOpmètre® 1.0 device exhibits good internal consistency, stability and objectivity in all tests performed between days and evaluators. Importantly, data suggest for the first time that this new device is able to detect changes in arterial stiffness that are conditioned by age and pressure-related arterial remodeling.
• This new pOpmètre® device is able to detect changes in vessel structure.
• This new pOpmètre® device exhibits good internal consistency, stability and objectivity in all tests performed
• Correct position of the animal and photodiodes are crucial to obtain a very stable signal.
... I t is well known that physical inactivity is an independent risk factor for cardiovascular diseases, obesity, and diabetes and an important cause of deaths occurring worldwide (1,2). In contrast, physical activity is a healthy lifestyle that has been used as a nonpharmacological tool for the treatment of cardiometabolic diseases (2)(3)(4)(5)(6)(7). Remarkable evidence has shown that exercise training changes vascular function and structure in healthy animal models and humans (for a review, see GREEN et al., 2017 [2]). ...
... After that, artery sections (1 μm) were mounted on glass slides and stained with toluidine blue. Thin sections (60 nm) contrasted with 4% uranyl acetate and 0.4% lead citrate were examined with an electron microscope (LEO906E) as described by Jordão et al. (2011) (5). ...
... After that, artery sections (1 μm) were mounted on glass slides and stained with toluidine blue. Thin sections (60 nm) contrasted with 4% uranyl acetate and 0.4% lead citrate were examined with an electron microscope (LEO906E) as described by Jordão et al. (2011) (5). ...
Purpose:
The beneficial effects of exercise training (ET) on the cardiovascular system are well known. Since our knowledge of exercise-induced vascular function is still limited, we aimed to uncover the molecular mechanisms conditioning the improved vascular relaxation in muscular arteries.
Methods:
Male Wistar-Kyoto rats with the same ability to run on a treadmill after maximal exercise tests were allocated to the following two groups: trained (Tr, treadmill, 50-60% of maximal capacity, 5 days/week) and untrained (UnTr). After 13 weeks, the femoral arteries were harvested and used for functional, structural and molecular analyses.
Results:
Acetylcholine (ACh)-induced relaxation and nitric oxide (NO) production were enhanced in arteries from Tr compared to UnTr rats. Tr arteries exhibited reduced miRNA-124a expression (whose target is caveolin-1), increased the density of caveolae aligned along the sarcolemma and reduced ACh-induced relaxation in the presence of Methyl-β-cyclodextrin, which disrupts caveolae. Higher endothelial NO synthase (eNOS) expression with lower miRNA-155 expression and the posttranslational modification of eNOS (phosphorylation of stimulatory Ser1177 and dephosphorylation of inhibitory Thr495) by the PI3-kinase/Akt1/2/3 pathway also contributed to the higher NO production induced by ET. Furthermore, increased Cu/Zn- and EC-superoxide dismutase (SOD) expression and enhanced effects of their pharmacological scavenger activity on the ACh-induced response were observed in Tr arteries.
Conclusions:
The results of the present study provide a molecular basis for exercise-induced NO bioavailability in healthy femoral arteries. Increased caveolae domain and eNOS expression/activity in Tr arteries are associated with downregulation of miRNA-124a and-155, as well as are involved with higher antioxidant defense, subsequently inducing a favorable endothelium-dependent milieu in Tr arteries.
... Dentre os mecanismos induzidos pelo treinamento físico aeróbio, que contribuem para melhorar a rigidez dos vasos, podemos citar a melhora do estresse oxidativo, 42 a menor deposição de colágeno e aumento de elastina na túnica média das artérias, principalmente em situações de envelhecimento 19,32 e hipertensão. 45 No entanto, somente alguns trabalhos mostraram os efeitos do treinamento aeróbio na VOP e na densidade de colágeno na artéria do mesmo indivíduo. 19,31 Dados recentes de nosso laboratório têm sugerido que o sistema renina angiotensina tem papel importante na regulação da VOP, uma vez que tanto o treinamento aeróbio como o tratamento com inibidor da enzima de conversão da angiotensina (perindopril) determina redução de VOP em animais hipertensos. ...
The purpose of the cardiovascular system is to maintain complete perfusion and, to this end, it has an efficient pump (the heart) and an appropriate conduction system, represented by arterial and venous vessels. This article addresses the different functional and structural adjustments resulting from physical training in the vascular system, which contribute mainly to improve the physical capacity of individuals. Therefore, the system has several mechanisms, including neural, hormonal and local mechanisms, which may be evaluated by different techniques, both in vivo and in vitro. After a period of physical training, a better interrelationship between neural and local systems has been evidenced, promoting less sympathetic nervous activity accompanied by more pronounced sympatholysis. In addition, physical training improves vascular reactivity of arteries by improving nitric oxide bioavailability. In the vascular wall, training improves balance between extracellular matrix components, favoring reduced of stiffness of the large arteries and reduced wall-to-lumen ratio in locomotor and non-locomotor muscle arterioles, which contributes to improving vessel distensibility and total peripheral resistance, especially in pathological cases. Finally, physical training favors microcirculatory angiogenesis, which contributes significantly to tissue nutrition.
... 17 In an animal model, Jordao et al. demonstrated that low-intensity training could reduce blood pressure, heart rate, and pulse pressure. 18 Interestingly, this experiment showed restoration of aorta elastic tissue in spontaneous hypertensive rats. 18 However, Gardner et al. 19 showed that PAD patients who engaged in physical activity that goes beyond light intensity at baseline regularly had a lower mortality rate than the sedentary group who performed either no physical activity or only light-intensity activities. ...
... 18 Interestingly, this experiment showed restoration of aorta elastic tissue in spontaneous hypertensive rats. 18 However, Gardner et al. 19 showed that PAD patients who engaged in physical activity that goes beyond light intensity at baseline regularly had a lower mortality rate than the sedentary group who performed either no physical activity or only light-intensity activities. Although the mechanisms of the beneficial effects of light intensity exercise are unclear, one possible mechanism concerns the anti-oxidation state. ...
Objective: The purpose of this study was to determine the effect of the arm-swing exercise on cardio-ankle vascular
index (CAVI), ankle-brachial index (ABI), heart rate and blood pressure (BP) in older adults with abnormal CAVI values.
Material and Method: Seventeen participants aged 50 or over were asked to do the arm-swing exercise at least 30
minutes a day, at least 3 times per week for 8 weeks. The vascular function parameters, CAVI and ABI, resting heart rate
and blood pressure were measured before and after exercising. The comparison of these parameters was performed
using statistical analysis.
Results: It was shown that the arm-swing exercise could lower both left and right CAVI significantly (left CAVI, pre: 10.0±
0.2 vs. post: 9.7±0.2, p-value=0.017 and right CAVI, pre: 10.0±0.2 vs. post: 9.7±0.2, p-value=0.034). Furthermore,
the arm-swing exercise also reduced arterial blood pressure and pulse pressure significantly (systolic BP, pre:
141.9±4.3 mmHg vs. post: 130.5±4.8 mmHg, p-value=0.004, diastolic BP, pre: 82.1±1.6 mmHg vs. post: 76.5±1.7
mmHg, p-value=0.003, and pulse pressure, pre: 59.7±3.7 vs. post: 54.0±4.0 mmHg, p-value=0.031). However, the
study demonstrated that ABI, resting heart rate and body mass index were not affected by the exercise.
Conclusion: This study demonstrated that 8 weeks of the arm-swing exercise could lower systolic and diastolic
blood pressure. This simple physical activity could also reduce CAVI values in older adults.
... Nevertheless, experiments in the thoracic aorta of aSHR identified elevated mRNA expression of α-actin (+9-fold), elastin (+6-fold) and collagen I and III (+11-fold) in comparison with normotensives27. Moreover, as observed in ySHR, the content of connective tissue, elastic fibers, and fibrils, as well as the CSA, were higher in the aorta of aSHR in comparison with age-matched control 27 . ...
... Morphological and functional alterations on organs associated with BP control (e.g., heart, kidney) and on blood vessels are one of the most evident alterations triggered by PE in aSHR. In the aorta, for example, low to moderate aerobic physical training performed 5 days per week, one hour per day, over three months caused decrease on smooth cells volume, elastic components and connective tissue in the aorta 27 . These effects are followed by significant decrease in the mRNA expression of α-actin, elastin, and collagen I and III 27 . ...
... In the aorta, for example, low to moderate aerobic physical training performed 5 days per week, one hour per day, over three months caused decrease on smooth cells volume, elastic components and connective tissue in the aorta 27 . These effects are followed by significant decrease in the mRNA expression of α-actin, elastin, and collagen I and III 27 . Results were not different in the heart since collagen content and cardiac load were decreased, and myocardial performance index (MPI) and left ventricular chamber diameter were increased in aSHR submitted to moderate aerobic exercise during 10 weeks 68 . ...
In 2016, cardiovascular disease remains the first cause of mortality worldwide [1]. Coronary artery disease, which is the most important precursor of myocardial infarction (MI), is the main component of total cardiovascular mortality, being responsible for approximately seven million of deaths [1]. In approximately 20% of infarcted patients, MI is recurrent in the first year after the event [2]. Moreover, among cardiovascular disease, coronary artery disease accounts for the most increased index of life years lost due to morbidity and/or mortality [1]. Sedentarism highly contributes to cardiovascular disease burden, especially for coronary artery disease, and is also one of the MI risk factors [3]. For many years, it was recommended to avoid physical activity after a cardiovascular event; nowadays, it is a consensus that exercise training (ET) should be part of cardiac rehabilitation programs. There is increasing evidence confirming that, when adequately prescribed and supervised, ET after MI can prevent future complications and increase the quality of life and longevity of infarcted patients [4, 5]. ET after MI follows international specialized guidelines; however, there are different protocols adopted by several societies worldwide in cardiac rehabilitation [6], and there is still lack of information on which type and regimen of exercise may be the ideal after MI, as well as how these exercises act to promote beneficial effects to cardiovascular and other organic systems. Thus, experimental studies are important contributors to elicit mechanisms behind clinical results, and to test and compare different ET protocols. Therefore, exercise prescription can be optimized, individualized, and safely practiced by patients. In this chapter, we present a brief review of MI pathophysiology followed by an updated discussion of the most relevant discoveries regarding ET and MI in basic science.
... Also, the physical capacity was decreased in sedentary groups around 40-50% compared with initial condition. It was expected that older rats present lower performance at the maximal capacity test, at the end of the protocol rats were 10 weeks older (they were 10 months old), thus it could be the reason for the decline in strength, since studies in young rats already showed that physical inactivity reduces the performance (25-35%) after 13 weeks (Ceroni et al., 2009;Jordao, Ladd, Coppi, Chopard, & Michelini, 2011), while in old rats the exercise capacity decreased significantly with age and sedentarism. ...
Moderate physical exercise acts at molecular and behavioural levels, such as interfering in neuroplasticity, cell death, neurogenesis, cognition and motor functions. Therefore, the aim of this study is to analyse the cellular effects of moderate treadmill running upon substantia nigra during early neurodegeneration. Aged male Lewis rats (9-month-old) were exposed to rotenone 1mg/kg/day (8 weeks) and 6 weeks of moderate treadmill running, beginning 4 weeks after rotenone exposure. Substantia nigra was extracted and submitted to proteasome and antioxidant enzymes activities, hydrogen peroxide levels and Western blot to evaluate tyrosine hydroxylase (TH), alpha-synuclein, Tom-20, PINK1, TrkB, SLP1, CRMP-2, Rab-27b, LC3II and Beclin-1 level. It was demonstrated that moderate treadmill running, practiced during early neurodegeneration, prevented the increase of alpha-synuclein and maintained the levels of TH unaltered in substantia nigra of aged rats. Physical exercise also stimulated autophagy and prevented impairment of mitophagy, but decreased proteasome activity in rotenone-exposed aged rats. Physical activity also prevented H2O2 increase during early neurodegeneration, although the involved mechanism remains to be elucidated. TrkB levels and its anterograde trafficking seem not to be influenced by moderate treadmill running. In conclusion, moderate physical training could prevent early neurodegeneration in substantia nigra through the improvement of autophagy and mitophagy.
KEYWORDS: Mitophagy, proteasome activity, oxidative stress, rotenone, treadmill running
