Long-term treadmill exercise induces neuroprotective molecular changes in rat brain

2011 ◽  
Vol 111 (5) ◽  
pp. 1380-1390 ◽  
Author(s):  
S. Bayod ◽  
J. del Valle ◽  
A. M. Canudas ◽  
J. F. Lalanza ◽  
S. Sanchez-Roige ◽  
...  
Keyword(s):  
Treadmill Training ◽  
Sirtuin 1 ◽  
Male Rat ◽  
Cellular Mechanisms ◽  
Neuroprotective Effects ◽  
Positive Effects ◽  
Oxphos System ◽  
Adult Male Rat ◽  
Exercise Induced

Exercise enhances general health. However, its effects on neurodegeneration are controversial, and the molecular pathways in the brain involved in this enhancement are poorly understood. Here, we examined the effect of long-term moderate treadmill training on adult male rat cortex and hippocampus to identify the cellular mechanisms behind the effects of exercise. We compared three animal groups: exercised (30 min/day, 12 m/min, 5 days/wk, 36 wk), handled but nonexercised (treadmill handling procedure, 0 m/min), and sedentary (nonhandled and nonexercised). Moderate long-term exercise induced an increase in IGF-1 levels and also in energy parameters, such as PGC-1α and the OXPHOS system. Moreover, the sirtuin 1 pathway was activated in both the exercised and nonexercised groups but not in sedentary rats. This induction could be a consequence of exercise as well as the handling procedure. To determine whether the long-term moderate treadmill training had neuroprotective effects, we studied tau hyperphosphorylation and GSK3β activation. Our results showed reduced levels of phospho-tau and GSK3β activation mainly in the hippocampus of the exercised animals. In conclusion, in our rodent model, exercise improved several major brain parameters, especially in the hippocampus. These improvements induced the upregulation of sirtuin 1, a protein that extends life, the stimulation of mitochondrial biogenesis, the activation of AMPK, and the prevention of signs of neurodegeneration. These findings are consistent with other reports showing that physical exercise has positive effects on hormesis.

scholarly journals Molecular Mechanisms of Cardiac Remodeling and Regeneration in Physical Exercise

Cells ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 1128 ◽  
Author(s):  
Dominik Schüttler ◽  
Sebastian Clauss ◽  
Ludwig T. Weckbach ◽  
Stefan Brunner
Keyword(s):  
Cardiac Function ◽  
Intracellular Signaling ◽  
Molecular Mechanisms ◽  
Cardiac Tissue ◽  
Mammalian Target Of Rapamycin ◽  
Cellular Mechanisms ◽  
Innovative Strategies ◽  
Muscle Strengthening ◽  
Positive Effects ◽  
Exercise Induced

Regular physical activity with aerobic and muscle-strengthening training protects against the occurrence and progression of cardiovascular disease and can improve cardiac function in heart failure patients. In the past decade significant advances have been made in identifying mechanisms of cardiomyocyte re-programming and renewal including an enhanced exercise-induced proliferational capacity of cardiomyocytes and its progenitor cells. Various intracellular mechanisms mediating these positive effects on cardiac function have been found in animal models of exercise and will be highlighted in this review. 1) activation of extracellular and intracellular signaling pathways including phosphatidylinositol 3 phosphate kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR), EGFR/JNK/SP-1, nitric oxide (NO)-signaling, and extracellular vesicles; 2) gene expression modulation via microRNAs (miR), in particular via miR-17-3p and miR-222; and 3) modulation of cardiac cellular metabolism and mitochondrial adaption. Understanding the cellular mechanisms, which generate an exercise-induced cardioprotective cellular phenotype with physiological hypertrophy and enhanced proliferational capacity may give rise to novel therapeutic targets. These may open up innovative strategies to preserve cardiac function after myocardial injury as well as in aged cardiac tissue.

scholarly journals Long-Term Consequences of Neonatal Rearing on Central Corticotropin-Releasing Factor Systems in Adult Male Rat Offspring

2005 ◽  
Vol 30 (12) ◽  
pp. 2192-2204 ◽  
Author(s):  
Paul M Plotsky ◽  
K V Thrivikraman ◽  
Charles B Nemeroff ◽  
Christian Caldji ◽  
Shakti Sharma ◽  
...  
Keyword(s):  
Adult Male ◽  
Corticotropin Releasing Factor ◽  
Male Rat ◽  
Rat Offspring ◽  
Adult Male Rat ◽  
Long Term Consequences

Effect of Long-Term Ingestion of Chromium Compounds on Aggression, Sex Behavior and Fertility in Adult Male Rat

1997 ◽  
Vol 20 (3) ◽  
pp. 133-149 ◽  
Author(s):  
H. Bataineh ◽  
M. H. Al-Hamood ◽  
A. Elbetieha ◽  
I. Bani Hani
Keyword(s):  
Adult Male ◽  
Male Rat ◽  
Sex Behavior ◽  
Adult Male Rat ◽  
Chromium Compounds

scholarly journals Exercise and circulating BDNF: Mechanisms of release and implications for the design of exercise interventions

2018 ◽  
Vol 43 (11) ◽  
pp. 1095-1104 ◽  
Author(s):  
Jeremy J. Walsh ◽  
Michael E. Tschakovsky
Keyword(s):  
Acute Exercise ◽  
Brain Plasticity ◽  
Cognitive Stimulation ◽  
Brain Health ◽  
Research Directions ◽  
Exercise Interventions ◽  
Positive Effects ◽  
Exercise Induced ◽  
Circulating Levels

Engagement in regular bouts of exercise confers numerous positive effects on brain health across the lifespan. Acute bouts of exercise transiently improve cognitive function, while long-term exercise training stimulates brain plasticity, improves brain function, and helps to stave off neurological disease. The action of brain-derived neurotrophic factor (BDNF) is a candidate mechanism underlying these exercise-induced benefits and is the subject of considerable attention in the exercise–brain health literature. It is well established that acute exercise increases circulating levels of BDNF and numerous studies have sought to characterize this response for the purpose of improving brain health. Despite the interest in BDNF responses to exercise, little focus has been given to understanding the sources and mechanisms that underlie this response for the purpose of deliberately increasing circulating levels of BDNF. Here we review evidence to support that exploiting these mechanisms of BDNF release can help to optimize brain plasticity outcomes via exercise interventions, which could be especially relevant in the context of multimodal training (i.e., exercise and cognitive stimulation). Therefore, the purpose of this paper is to review the candidate sources of BDNF during exercise and the mechanisms of release. As well, we discuss strategies for maximizing BDNF responses to exercise, and propose novel research directions for advancing our understanding of these mechanisms.

Influence of pinealectomy on the suppression of gonadotrophin secretion induced by hyperprolactinaemia in the adult male rat

1983 ◽  
Vol 97 (3) ◽  
pp. 401-407 ◽  
Author(s):  
A. S. McNeilly ◽  
D. W. Lincoln
Keyword(s):  
Pineal Gland ◽  
Adult Male ◽  
Male Rats ◽  
Male Rat ◽  
Gonadotrophin Secretion ◽  
Adult Male Rat ◽  
Pituitary Glands ◽  
Hypothalamic Pituitary Axis

To investigate the role of the pineal gland in the long-term suppression of gonadotrophin secretion induced by prolactin, the effects of pinealectomy were studied in adult male rats with hyperprolactinaemia produced by the transplantation of two pituitary glands under the kidney capsule. Pinealectomy had no effect on basal levels of LH, FSH or prolactin. The presence of pituitary transplants induced a significant twofold increase in prolactin levels and a prolonged suppression in both LH and FSH. These changes were not affected by pinealectomy. Castration resulted in a similar rise in plasma levels of LH and FSH in rats with and without pituitary transplants. In control rats this rise in LH and FSH was reduced by testosterone-containing silicone elastomer implants (s.c) of 10 mm in length and delayed by implants of 30 mm. These rises in LH and FSH were significantly delayed (10-mm implant) or abolished (30-mm implant) in rats with pituitary transplants indicating an increase in sensitivity of the hypothalamic-pituitary axis to the negative feedback effects of testosterone in these animals compared to controls. These responses were not affected by pinealectomy. These results suggest that the pineal gland is not involved in the mechanism whereby pituitary grafts, possibly through their secretion of prolactin, cause long-term suppression of gonadotrophin secretion.

Studies on the control of gonadotrophin release in the gonadectomized male rat: evidence for a lack of involvement of the hypothalamic noradrenergic system in the long-term castrated rat

1984 ◽  
Vol 100 (2) ◽  
pp. 235-244 ◽  
Author(s):  
H. J. Herdon ◽  
D. M. Everard ◽  
C. A. Wilson
Keyword(s):  
Male Rat ◽  
Noradrenergic System ◽  
Short Term ◽  
Synthesis Inhibitor ◽  
Noradrenaline Concentration ◽  
Gonadotrophin Secretion ◽  
Adult Male Rat ◽  
6 Hydroxydopamine ◽  
Term Response

ABSTRACT The effects of castration with or without testosterone replacement in the adult male rat were studied to investigate possible hypothalamic mechanisms by which changes in gonadotrophin secretion occur at different times after castration, with particular reference to the continuing LH rise and its lack of suppression by testosterone in the long-term castrated rat. Castrated rats received either subcutaneous silicone elastomer implants containing testosterone or empty implants at the time of castration, and a sham-operated group served as controls. At 1, 10 and 40 days after castration, there were six-, 15- and 25-fold rises respectively in LH and 1·5-, two-and fivefold rises in FSH. However, there were no significant changes in hypothalamic noradrenaline concentration and turnover or in α-adrenoceptor density and affinity at any time after castration. Testosterone implants were effective in suppressing gonadotrophin release at 1 and 10 days, but not at 40 days after castration, and did not significantly affect hypothalamic noradrenaline turnover or α-adrenoceptors at any time. Neither acute inhibition of the noradrenergic system, using either the α-adrenoceptor blockers phenoxybenzamine and phentolamine or the synthesis inhibitor α-methyl-p-tyrosine, nor chronic depletion of hypothalamic noradrenaline by 6-hydroxydopamine had any significant effect on the normal rise in LH levels seen on days 10 and 40 after castration, and did not alter the ability of testosterone to suppress LH levels. This indicates that, in the long-term castrated rat, the noradrenergic system may not be involved in the control of gonadotrophin release. However, at 16 h after castration, α-adrenoceptor blockers and α-methyl-p-tyrosine did reduce LH levels, indicating that the noradrenergic system is likely to be involved in the short-term response to castration. J. Endocr. (1984) 100, 235–244

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