Dynamic Contractility and Efficiency Impairments in Stretch-Shortening Cycle Are Stretch-Load-Dependent After Training-Induced Muscle Damage

<p>Vaczi, M, Racz, L, Hortobagyi, T, and Tihanyi, J. Dynamic contractility and efficiency impairments in stretch-shortening cycle are stretch-load-dependent after training-induced muscle damage. J Strength Cond Res 27(8): 2171-2179, 2013To determine the acute task and stretch-load dependency of neuromuscular impairments after muscle-damaging exercises, we examined the magnitude of strength deficits in isometric and stretch-shortening cycle (SSC) contractions after a single bout of exercise. Ten trained men performed 90 unilateral isokinetic eccentric-concentric knee extensions on a dynamometer. Plasma creatine kinase activity, muscle soreness, maximal isometric torque, short-range stiffness, and peak torque in the eccentric phase of the SSC contraction at 3 stretch-loads (120, 150, and 180 J) were determined in the quadriceps before and 24 hours after exercise. During SSC, positive mechanical work and efficiency were also calculated. Creatine kinase and soreness increased at 24 hours (p <0.05). In each of the 3 stretch-load conditions, muscle damage affected short-range stiffness less than isometric and peak SSC torque (p <0.05), providing evidence for a selective impairment in contractile function after muscle damage. With greater SSC stretch-load peak, SSC torque deficit increased linearly, whereas short-range stiffness deficit was unaffected. Efficiency declined only at the 180-J condition (p <0.05) as a result of decreased positive work (p <0.05). It was concluded that intense exercise produced microtrauma in the muscle, and a selective loss of force generating capacity, which suggests greater damage to the contractile machinery. Practitioners may expect greater acute impairment of force generation in movements that use large loads in their daily training drills. However, altered knee flexion strategy during SSC may compensate for the force deficit, preserving mechanical efficiency at smaller stretch-loads.</p>

Strategies for Improving Bioavailability, Bioactivity, and Physical-Chemical Behavior of Curcumin

Curcumin (CCM) is one of the most frequently explored plant compounds with various biological actions such as antibacterial, antiviral, antifungal, antineoplastic, and antioxidant/anti-inflammatory properties. The laboratory data and clinical trials have demonstrated that the bioavailability and bioactivity of curcumin are influenced by the feature of the curcumin molecular complex types. Curcumin has a high capacity to form molecular complexes with proteins (such as whey proteins, bovine serum albumin, &beta;-lactoglobulin), carbohydrates, lipids, and natural compounds (e.g., resveratrol, piperine, quercetin). These complexes increase the bioactivity and bioavailability of curcumin. The current review provides these derivatization strategies for curcumin in terms of biological and physico-chemical aspects with a strong focus on different type of proteins, characterization methods, and thermodynamic features of protein&ndash;curcumin complexes, and with the aim of evaluating the best performances. The current literature review offers, taking into consideration various biological effects of the CCM, a whole approach for CCM-biomolecules interactions such as CCM-proteins, CCM-nanomaterials, and CCM-natural compounds regarding molecular strategies to improve the bioactivity as well as the bioavailability of curcumin in biological systems

Genetic covariance between central corneal thickness and anterior chamber volume: a hungarian twin study.

BACKGROUND: Few, and inconsistent, studies have showed high heritability of some parameters of the anterior segment of the eye; however, no heritability of anterior chamber volume (ACV) has been reported, and no study has been performed to investigate the correlation between the ACV and central corneal thickness (CCT). METHODS: Anterior segment measurements (Pentacam, Oculus) were obtained from 220 eyes of 110 adult Hungarian twins (41 monozygotic and 14 same-sex dizygotic pairs; 80% women; age 48.6 +/- 15.5 years) obtained from the Hungarian Twin Registry. RESULTS: Age- and sex-adjusted heritability of ACV was 85% (bootstrapped 95% confidence interval; CI: 69% to 93%), and 88% for CCT (CI: 79% to 95%). Common environmental effects had no influence, and unshared environmental factors were responsible for 12% and 15% of the variance, respectively. The correlation between ACV and CCT was negative and significant (r ph = -0.35, p < .05), and genetic factors accounted for the covariance significantly (0.934; CI: 0.418, 1.061) based on the bivariate Cholesky decomposition model. CONCLUSION: These findings support the high heritability of ACV and central corneal thickness, and a strong genetic covariance between them, which underscores the importance of identification of the specific genetic factors and the family risk-based screening of disorders related to these variables, such as open-angle and also angle closure glaucoma and corneal endothelial alterations

The inheritance of corneal endothelial cell density

BACKGROUND: Although it is known that some corneal diseases and degenerations have a significant heritable background, heritability on corneal endothelial cell density (ECD) has never been clearly determined. Our aim was to determine the heritability of corneal ECD. MATERIAL AND METHODS: Corneal ECD of 114 eyes (66 eyes of 33 monozygotic and 48 eyes of 24 dizygotic pairs; mean age 49.0 +/- 15.5 years) was investigated by Konan Noncon Robo NSP-9900 specular microscopy. Structural equation modeling (ACE model) was applied. RESULTS: Endothelial corneal cell density was highly heritable (82.0%, 95%CI, 70.0-92.0%), whereas the unique environmental contribution was 18.0% (95%CI, 8.0-29.0%). Shared environmental factors had no influence on the endothelial corneal cell density. DISCUSSION: In this twin study, we established first that the density of the corneal endothelial cells is strongly heritable, which should stimulate future genetic studies to identify genes and pathways that are involved in determining ECD which might in turn lead to future treatments to prevent EC loss