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Background: Rooms illuminated by "black light" (<400 nm wavelength) has become popular, but there is not enough scientific evidence to support its implementation. This study aims to assess the effects of violet light (392 nm) on the circadian rest–activity rhythm and the visual system through animal experimentation. Materials and results: Five groups of four mice were exposed to different white light, violet light, and dark periods, and their circadian rhythm was analyzed by measuring the circadian period using rest–activity cycles. Electroretinographic recordings and structural analysis of the retina were also performed on experimental animals. Results: Our study demonstrates that mice present normal circadian activity during exposure to violet light, taking rest not only under white light but under violet lighting periods. However, mice suffered a decrease in electrical retinal response after exposure to violet light as measured by electroretinography. Nevertheless, no structural changes were observed in the retinas of the animals under different lighting conditions. Conclusions: Violet light elicits circadian rest–activity rhythm in mice but alters their visual function, although no structural changes are observed after short periods of violet light exposure. [ABSTRACT FROM AUTHOR]

The aim of this study was to analyze the effects of high-frequency neuromuscular electrical stimulation training (NMES) on the structure, function and oxidative capacity of the skeletal muscle using a mice model (C57BL/6J strain, n=8). The left tibialis anterior muscle in mice was electro-stimulated (ST) whereas the right muscle was maintained as an internal control (CT). The ST limb was submitted to eight surface (100 Hz) NMES sessions in two weeks, with a minimum gap of 24 h between sessions. NMES training increased muscle mass (42.0±3.3 vs. 36.1±5.4 mg, p

Purpose: To determine if transcranial direct-current stimulation (tDCS) could be effective for the enhancement of swimming performance or mood state in elite athletes. Methods: Eight male elite triathletes (age = 20 [2] y, maximal oxygen uptake = 71 [4] mL·kg−1·min−1) participated in this crossover, counterbalanced, sham-controlled, double-blind study. Participants received either actual (20 min of anodal stimulation of the motor cortex at 2 mA) or sham tDCS and performed an 800-m swimming test in which rating of perceived exertion and blood lactate response were measured. Mood state (Brunel Mood Scale) was assessed before and after each tDCS session and after the swimming test. Heart-rate variability and central nervous system readiness were assessed before and after each tDCS session. The chances of finding differences between conditions were determined using magnitude-based inferences. Results: A significant and very likely higher Brunel Mood Scale–determined vigor self-perception was found with actual tDCS after the stimulation session (−0.1 [1.2] and 2.0 [2.3] for sham and actual tDCS, respectively; P =.018, effect size = 1.14) and after exercise (−4.1 [2.9] and −0.9 [3.6] for sham and actual tDCS, respectively; P =.022, effect size = 0.98). However, likely trivial and nonsignificant (P >.05) differences were found between conditions in performance (599 [38] s and 596 [39] s, respectively). Unclear and nonsignificant differences were observed between conditions for the rest of the study end points. Conclusions: tDCS elicited a marked increase in vigor self-perception that was maintained after exercise but failed to improve swimming performance in elite triathletes. [ABSTRACT FROM AUTHOR]

Macroautophagy/autophagy is a key process in the maintenance of cellular homeostasis. The age-dependent decline in retinal autophagy has been associated with photoreceptor degeneration. Retinal dysfunction can also result from damage to the retinal pigment epithelium (RPE), as the RPE-retina constitutes an important metabolic ecosystem that must be finely tuned to preserve visual function. While studies of mice lacking essential autophagy genes have revealed a predisposition to retinal degeneration, the consequences of a moderate reduction in autophagy, similar to that which occurs during physiological aging, remain unclear. Here, we described a retinal phenotype consistent with accelerated aging in mice carrying a haploinsufficiency for Ambra1, a pro-autophagic gene. These mice showed protein aggregation in the retina and RPE, metabolic underperformance, and premature vision loss. Moreover, Ambra1+/gt mice were more prone to retinal degeneration after RPE stress. These findings indicate that autophagy provides crucial support to RPE-retinal metabolism and protects the retina against stress and physiological aging. Abbreviations : 4-HNE: 4-hydroxynonenal; AMBRA1: autophagy and beclin 1 regulator 1, AMD: age-related macular degeneration;; GCL: ganglion cell layer; GFAP: glial fibrillary acidic protein; GLUL: glutamine synthetase/glutamate-ammonia ligase; HCL: hierarchical clustering; INL: inner nuclear layer; IPL: inner plexiform layer; LC/GC-MS: liquid chromatography/gas chromatography–mass spectrometry; MA: middle-aged; MTDR: MitoTracker Deep Red; MFI: mean fluorescence intensity; NL: NH4Cl and leupeptin; Nqo: NAD(P)H quinone dehydrogenase; ONL: outer nuclear layer; OPL: outer plexiform layer; OP: oscillatory potentials; OXPHOS: oxidative phosphorylation; PCR: polymerase chain reaction; PRKC/PKCα: protein kinase C; POS: photoreceptor outer segment; RGC: retinal ganglion cells; RPE: retinal pigment epithelium; SI: sodium iodate; TCA: tricarboxylic acid. [ABSTRACT FROM AUTHOR]