The purpose of this meta-analytic review was to examine the extent and quality of research on the post-activation potentiation acute effect of rest interval manipulation on jumping performance. This manuscript adopted the recommendations from the Preferred Reporting Items for Systematic Reviews and Meta-Analyses Statement. Criteria eligibility included crossover, randomised, non-randomised and counterbalanced studies that observed the voluntary muscle action-induced post-activation potentiation on jumping performance. Fourteen studies selected by two independent raters were included in the analysis. The rest intervals involved ranges including 0-3, 4-7, 8-12 and ≥16 min. The results demonstrated medium effect sizes for rest intervals 0-3 and 8-12 min (-0.25, confidence interval (CI): -0.51 to 0.01 for 0-3 min; 0.24, CI: -0.02 to 0.49 for 8-12 min) and a small effect for other ranges (0.15, CI: -0.08 to 0.38 for 4-7 min; 0.07, CI: -0.21 to 0.24 for ≥16 min). There was no evidence of heterogeneity for sub-groups (I2 = 0%; P < 0.001) and no indication of publication bias (Egger's test, P = 0.179). While a rest interval of 0-3 min induced a detrimental effect on jump performance, the range including 8-12 min had a beneficial impact on jump height. Findings suggest that the rest interval manipulation seems to affect post-activation potentiation magnitude and jump height.
Background: In the past, isometric exercises were proscribed for heart disease. However, recent evidence suggests that an isometric handgrip training (IHT) protocol -four sets of two minutes at 30% of maximum strength -produces favorable effects on the autonomic modulation and reduces resting systolic (SBP) and diastolic (DBP) blood pressure.
Introduction: Sepsis is defined as a multifactorial debilitating condition with high risks of death. The intense inflammatory response causes deleterious effects on the brain, a condition called sepsis-associated encephalopathy. Neuroinflammation or pathogen recognition are able to stress cells, resulting in ATP (Adenosine Triphosphate) release and P2X7 receptor activation, which is abundantly expressed in the brain. The P2X7 receptor contributes to chronic neurodegenerative and neuroinflammatory diseases; however, its function in long-term neurological impairment caused by sepsis remains unclear. Therefore, we sought to evaluate the effects of P2X7 receptor activation in neuroinflammatory and behavioral changes in sepsis-surviving mice.Methods: Sepsis was induced in wild-type (WT), P2X7−/−, and BBG (Brilliant Blue G)-treated mice by cecal ligation and perforation (CLP). On the thirteenth day after the surgery, the cognitive function of mice was assessed using the novel recognition object and Water T-maze tests. Acetylcholinesterase (AChE) activity, microglial and astrocytic activation markers, and cytokine production were also evaluated.Results: Initially, we observed that both WT and P2X7−/− sepsis-surviving mice showed memory impairment 13 days after surgery, once they did not differentiate between novel and familiar objects. Both groups of animals presented increased AChE activity in the hippocampus and cerebral cortex. However, the absence of P2X7 prevented partly this increase in the cerebral cortex. Likewise, P2X7 absence decreased ionized calcium-binding protein 1 (Iba−1) and glial fibrillary acidic protein (GFAP) upregulation in the cerebral cortex of sepsis-surviving animals. There was an increase in GFAP protein levels in the cerebral cortex but not in the hippocampus of both WT and P2X7−/− sepsis-surviving animals. Pharmacological inhibition or genetic deletion of P2X7 receptor attenuated the production of Interleukin-1β (IL-1β), Tumor necrosis factor-α (TNF-α), and Interleukin-10 (IL-10).Conclusion: The modulation of the P2X7 receptor in sepsis-surviving animals may reduce neuroinflammation and prevent cognitive impairment due to sepsis-associated encephalopathy, being considered an important therapeutic target.
Gouvêa, AL, Martinez, CG, and Kurtenbach, E. Determining maximal muscle strength in mice: validity and reliability of an adapted swimming incremental overload test. J Strength Cond Res XX(X): 000-000, 2018-At present, there are no reliable methods to determine maximal muscle strength in small rodents. Here, we established an adapted swimming incremental overload test (SIOT) as an instrument for this purpose. First, to validate the test, BALB/c mice received 20 mg·kg·d of dexamethasone (DEXA group) or water (control group). After 14 days, with a cumulative dose of 120 mg·kg of dexamethasone, the SIOT could detect a decrease of approximately 7% in muscle strength. In addition, this decrease was consistent with a significant reduction in body (above 13.5%) and muscle (approximately 15%) weight in DEXA atrophic animals. To establish the SIOT reliability, another group of animals was evaluated for 5 consecutive days. In this second protocol, the SIOT was executed with an initial load corresponding to 12% of the mouse body weight (BW) fixed to the tail. Increments between 1 and 5% of the BW were added during each attempt to obtain the highest load that was tolerated for a time interval of 5-7 seconds. On the last day, the SIOT reliability test was performed by 2 different raters to obtain the inter-rater reproducibility. The adapted SIOT was shown to be reliable when measured by the same rater (intraclass correlation coefficient [ICC] = 0.939) and by 2 different raters (ICC = 0.830). The Bland-Altman graphical representation did not demonstrate heteroscedastic errors. Therefore, the SIOT proved to be a sensitive and reliable method to measure muscle strength, and it can be applied to small animals in different models of muscle atrophy.
BackgroundThis study investigated the effects of methylmercury intoxication on mice skeletal muscle subjected or not to progressive resistance training (RT).MethodsFour experimental groups were formed. Control and Con + RT received water and methylmercury (MeHg) and MeHg + RT groups received methylmercury (5 mg/kg/day), via gavage for 14 days. The Con + RT and MeHg + RT animals performed weighted ladder climbing RT, three times a week for 4 weeks. Animal muscle strength and gastrocnemius and soleus cross‐section area, fibrosis, myosin heavy chains (MyHCs), E3‐ligases MAFbx and MuRF1, 20S proteasome (P20S) and LC3‐II content were analysed. In addition, P20S chymotrypsin‐like activity was evaluated.ResultsResistance training protected MeHg + RT mice against strength loss but not against muscle atrophy. The latter appeared to be associated with MyHCs significant content reductions observed in the MeHg and MeHg + RT groups. In soleus muscle, there was an increase in E3‐ligases and P20S levels and P20S activity in both methylmercury groups compared with control ones. This pattern was also observed for gastrocnemius muscle, except for P20S content and activity that decreased. The P‐AKT content decreased in the soleus and gastrocnemius of the MeHg animals while significant elevation of LC3‐II content levels occurred.ConclusionsThe accumulation of methylmercury caused an increase in skeletal muscle MyHCs degradation, resulting in muscle atrophy that was reinforced by the elevated fibrosis area. Although RT did not reverse this condition, maintenance of muscle strength levels in animals submitted to MeHg + RT was detected. We believe that RT somewhat protected MeHg from damage to neural muscle structures, to be further investigated.
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