scholarly journals Effect of Physical Exercise and Acute Escitalopram on the Excitability of Brain Monoamine Neurons: In Vivo Electrophysiological Study in Rats

2017 ◽  
Vol 20 (7) ◽  
pp. 585-592 ◽  
Author(s):  
Eliyahu Dremencov ◽  
Kristína Csatlósová ◽  
Barbora Ďurišová ◽  
Lucia Moravčíková ◽  
Ľubica Lacinová ◽  
...  
Author(s):  
Ni Made Ridla Parwata

Overtraining syndrome is a decrease in physical capacity, emotions and immunity due to training that is too often without adequate periods of rest. Overtraining is often experienced by athletes who daily undergo heavy training with short break periods. This research aims to look at the effect of overtraining aerobic physical exercise on memory in mice. The research method was experimental in vivo with the subject of adult male rat (Rattus Norvegicus) Winstar strain aged 8-10 weeks, body weight 200-250 gr. Divided into three groups, namely the control group, aerobic group and overtraining group. The results of memory tests with water E Maze showed an increase in the duration of travel time and the number of animal errors made by the overtraining group (p = 0.003). This study concludes that overtraining aerobic physical exercise can reduce memory in rat hippocampus.


2016 ◽  
Vol 38 (2) ◽  
pp. 487-501 ◽  
Author(s):  
Stella Petric ◽  
Sofia Klein ◽  
Lisa Dannenberg ◽  
Tillman Lahres ◽  
Lukas Clasen ◽  
...  

Background/Aims: Pannexin-1 (Panx1) is an ATP release channel that is ubiquitously expressed and coupled to several ligand-gated receptors. In isolated cardiac myocytes, Panx1 forms large conductance channels that can be activated by Ca2+ release from the sarcoplasmic reticulum. Here we characterized the electrophysiological function of these channels in the heart in vivo, taking recourse to mice with Panx1 ablation. Methods: Cardiac phenotyping of Panx1 knock-out mice (Panx1-/-) was performed by employing a molecular, cellular and functional approach, including echocardiography, surface and telemetric ECG recordings with QT analysis, physical stress testing and quantification of heart rate variability. In addition, an in vivo electrophysiological study entailed programmed electrical stimulation using an intracardiac octapolar catheter. Results: Panx1 deficiency results in a higher incidence of AV-block, delayed ventricular depolarisation, significant prolongation of QT- and rate corrected QT-interval and a higher incidence of atrial fibrillation after intraatrial burst stimulation. Conclusion: Panx1 seems to play an important role in murine cardiac electrophysiology and warrants further consideration in the context of hereditary forms of atrial fibrillation.


2015 ◽  
Vol 118 (8) ◽  
pp. 971-979 ◽  
Author(s):  
Andreas Buch Møller ◽  
Mikkel Holm Vendelbo ◽  
Britt Christensen ◽  
Berthil Forrest Clasen ◽  
Ann Mosegaard Bak ◽  
...  

Data from transgenic animal models suggest that exercise-induced autophagy is critical for adaptation to physical training, and that Unc-51 like kinase-1 (ULK1) serves as an important regulator of autophagy. Phosphorylation of ULK1 at Ser555 stimulates autophagy, whereas phosphorylation at Ser757 is inhibitory. To determine whether exercise regulates ULK1 phosphorylation in humans in vivo in a nutrient-dependent manner, we examined skeletal muscle biopsies from healthy humans after 1-h cycling exercise at 50% maximal O2 uptake on two occasions: 1) during a 36-h fast, and 2) during continuous glucose infusion at 0.2 kg/h. Physical exercise increased ULK1 phosphorylation at Ser555 and decreased lipidation of light chain 3B. ULK1 phosphorylation at Ser555 correlated positively with AMP-activated protein kinase-α Thr172 phosphorylation and negatively with light chain 3B lipidation. ULK1 phosphorylation at Ser757 was not affected by exercise. Fasting increased ULK1 and p62 protein expression, but did not affect exercise-induced ULK1 phosphorylation. These data demonstrate that autophagy signaling is activated in human skeletal muscle after 60 min of exercise, independently of nutritional status, and suggest that initiation of autophagy constitutes an important physiological response to exercise in humans.


2016 ◽  
Vol 4 (2) ◽  
pp. 216-220 ◽  
Author(s):  
Dario Moneghini ◽  
Alessandro Lipari ◽  
Guido Missale ◽  
Luigi Minelli ◽  
Gianpaolo Cengia ◽  
...  

2020 ◽  
Vol 2 (3) ◽  
pp. 226-235
Author(s):  
Yuzo Sato

Abstract In recent years, the Westernization of dietary habits and increasingly sedentary lifestyle have contributed to a marked increase in the number of type 2 diabetes patients. Sedentary behavior may play a significant role in the development and aggravation of type 2 diabetes. The results of various follow-up studies have demonstrated that proper diet combined with physical exercise is useful in the prevention and treatment of type 2 diabetes. A nationwide survey regarding exercise therapy for diabetes patients in Japan revealed that relatively few physicians provide patients with exercise guidance because of time constraints, that the physicians do not receive additional consultation fee, and that there is a lack of specialized physical exercise educators. Physical exercise promotes the utilization of glucose and free fatty acids in the muscles, and thus lowers blood glucose (BG) levels. Dietary restriction and physical exercise are effective in the prevention and treatment of type 2 diabetes by improving the in vivo sensitivity to insulin. Most adults with diabetes should engage in 150 min or more of moderate-to-vigorous intensity aerobic activity per week, spread out over at least 3 days/week, with no more than two consecutive days without activity. Mild-intensity resistance training such as half squat and calf raise is recommended for elderly individuals who have decreased muscle strength and mass (sarcopenia). Prolonged sitting should be interrupted every 30 min for BG benefits, particularly in adults with type 2 diabetes. Individuals with type 2 diabetes are also encouraged to increase their total daily unstructured physical activity (daily movement).


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