Acute effects of single dose transcranial direct current stimulation on muscle strength: A systematic review and meta-analysis.

Previous studies investigating the effects of transcranial direct current stimulation (tDCS) on muscle strength showed no consensus. Therefore, the purpose of this article was to systematically review the literature on the effects of single dose tDCS to improve muscle strength. A systematic literature search was conducted on PubMeb, ISI Web of Science, SciELO, and Scopus using search terms regarding tDCS and muscle strength. Studies were included in accordance with Population, Intervention, Comparison, Outcomes, and Setting (PICOS) including criteria. Healthy men and women, strength training practitioners or sedentary were selected. The acute effects of single dose anode stimulus of tDCS (a-tDCS) and the placebo stimulus of tDCS (sham) or no interventions were considered as an intervention and comparators, respectively. Measures related to muscle strength were analyzed. To conduct the analyses a weighted mean difference (WMD) and the standardized mean difference (SMD) were applied as appropriate. A total of 15 studies were included in this systematic review and 14 in meta-analysis. Regarding the maximal isometric voluntary contraction (MIVC), a small effect was seen between tDCS and Sham with significant difference between the conditions (SMD = 0.29; CI95% = 0.05 to 0.54; Z = 2.36; p = 0.02). The muscular endurance measured by the seconds sustaining a percentage of MIVC demonstrated a large effect between tDCS and Sham (WMD = 43.66; CI95% = 29.76 to 57.55; Z = 6.16; p < 0.001), showing an improvement in muscular endurance after exposure to tDCS. However, muscular endurance based on total work showed a trivial effect between tDCS and Sham with no significant difference (SMD = 0.22; CI95% = -0.11 to 0.54; Z = 1.32, p = 0.19). This study suggests that the use of tDCS may promote increase in maximal voluntary contraction and muscular endurance through isometric contractions

Correction: Acute effects of single dose transcranial direct current stimulation on muscle strength: A systematic review and meta-analysis.

[This corrects the article DOI: 10.1371/journal.pone.0209513.]

Effects of Incretin-Based Therapies on Neuro-Cardiovascular Dynamic Changes Induced by High Fat Diet in Rats.

BACKGROUND AND AIMS:Obesity promotes cardiac and cerebral microcirculatory dysfunction that could be improved by incretin-based therapies. However, the effects of this class of compounds on neuro-cardiovascular system damage induced by high fat diet remain unclear. The aim of this study was to investigate the effects of incretin-based therapies on neuro-cardiovascular dysfunction induced by high fat diet in Wistar rats. METHODS AND RESULTS:We have evaluated fasting glucose levels and insulin resistance, heart rate variability quantified on time and frequency domains, cerebral microcirculation by intravital microscopy, mean arterial blood pressure, ventricular function and mitochondrial swelling. High fat diet worsened biometric and metabolic parameters and promoted deleterious effects on autonomic, myocardial and haemodynamic parameters, decreased capillary diameters and increased functional capillary density in the brain. Biometric and metabolic parameters were better improved by glucagon like peptide-1 (GLP-1) compared with dipeptdyl peptidase-4 (DPP-4) inhibitor. On the other hand, both GLP-1 agonist and DPP-4 inhibitor reversed the deleterious effects of high fat diet on autonomic, myocardial, haemodynamic and cerebral microvascular parameters. GLP-1 agonist and DPP-4 inhibitor therapy also increased mitochondrial permeability transition pore resistance in brain and heart tissues of rats subjected to high fat diet. CONCLUSION:Incretin-based therapies improve deleterious cardiovascular effects induced by high fat diet and may have important contributions on the interplay between neuro-cardiovascular dynamic controls through mitochondrial dysfunction associated to metabolic disorders

Biometric, cumulative caloric intake, glucose and myocardial parameters after diets and incretin-based therapies.

<p>Biometric, cumulative caloric intake, glucose and myocardial parameters after diets and incretin-based therapies.</p

Experimental swelling protocol induced by Ca²⁺.

<p>Liraglutide and sitagliptin subgroups showed increased mitochondrial permeability transition pore resistance in brain (a) and heart (b) tissues. Analyses were made in rats having received liraglutide and sitagliptin for 4 weeks after high fat diet during 18 weeks. Data are shown as mean ± SEM; <i>n</i> = 5.</p

Composition of standard chow and high-fat diet.

<p>Composition of standard chow and high-fat diet.</p

Effects of high fat diet and incretin-based-therapies on autonomic nervous system.

<p><b>(a)</b> Effects of high fat diet alone or in combination with liraglitude or sitagliptin treatments on R-R intervals and time-domain parasympathetic indexes of heart rate variability (SDNN, pNN5% and RMSSD). (<b>b</b>) Effects of high fat diet alone or in combination with liraglitude or sitagliptin treatments on frequency-domain of heart rate variability (SDNN, pNN5% and RMSSD). High-frequency (HF), low- frequency (LF) power spectra and the ratio between low-frequency to high-frequency (LF HF^-1 ratio) power spectra are shown. The following groups (n = 5 each) were examined: Control (CTRL), high fat diet (HFD), high fat diet plus liraglutide (HFD Liraglutide) and high fat diet plus sitagliptin (HFD Sitagliptin). Data are shown as mean ± SEM; <i>n</i> = 5–8. *<i>p<</i>0.05 vs. CTRL; **<i>p<</i>0.01 vs. CTRL; ^†<i>p<</i>0.05 vs. HFD; ^†††<i>p<</i>0.001 vs. HFD; ^‡<i>p<</i> 0.05 vs. HFD Liraglutide; ^‡‡<i>p<</i>0.01 vs. HFD Liraglutide and ^‡‡‡<i>p<</i>0.001 vs. HFD Liraglutide.</p

3,5-Diiodothyronine protects against cardiac ischaemia-reperfusion injury in male rats

What is the central question of this study? 3,5-Diiodothyronine (3,5-T2) administration increases resting metabolic rate, prevents or treats liver steatosis in rodent models, and ameliorates insulin resistance: what are its effects on cardiac electrical and contractile properties and autonomic regulation? What is the main finding and its importance? Chronic 3,5-T2 administration has no adverse effects on cardiac function. Remarkably, 3,5-T2 improves the autonomous control of the rat heart and protects against ischaemia-reperfusion injury. The use of 3,5,3'-triiodothyronine (T3) and thyroxine (T4) to treat metabolic diseases has been hindered by potential adverse effects on liver, lipid metabolism and cardiac electrical properties. It is recognized that 3,5-diiodothyronine (3,5-T2) administration increases resting metabolic rate, prevents or treats liver steatosis in rodent models and ameliorates insulin resistance, suggesting 3,5-T2 as a potential therapeutic tool. However, a comprehensive assessment of cardiac electrical and contractile properties has not been made so far. Three-month-old Wistar rats were daily administered vehicle, 3,5-T2 or 3,5-T2+T4 and no signs of atrial or ventricular arrhythmia were detected in non-anaesthetized rats during 90 days. Cardiac function was preserved as heart rate, left ventricle diameter and shortening fraction in 3,5-T2-treated rats compared to vehicle and 3,5-T2+T4 groups. Power spectral analysis indicated an amelioration of the heart rate variability only in 3,5-T2-treated rats. An increased baroreflex sensitivity at rest was observed in both 3,5-T2-treated groups. Finally, 3,5-T2 Langendorff-perfused hearts presented a significant recovery of left ventricular function and remarkably smaller infarction area after ischaemia-reperfusion injury. In conclusion, chronic 3,5-T2 administration ameliorates tonic cardiac autonomic control and confers cardioprotection against ischaemia-reperfusion injury in healthy male rats