Effects of photobiomodulation on the fatigue level in elderly women: an isokinetic dynamometry evaluation.

Aging is responsible by a series of morphological and functional modifications that lead to a decline of muscle function, particularly in females. Muscle tissue in elderly people is more susceptible to fatigue and, consequently, to an increased inability to maintain strength and motor control. In this context, therapeutic approaches able of attenuating muscle fatigue have been investigated. Among these, the photobiomodulation demonstrate positive results to interacts with biological tissues, promoting the increase in cell energy production. Thus, the aim of this study was to investigate the effects of photobiomodulation (808 nm, 250 J/cm(2), 100 mW, 7 J each point) in the fatigue level and muscle performance in elderly women. Thirty subjects entered a crossover randomized double-blinded placebo-controlled trial. Photobiomodulation was delivered on the rectus femoris muscle of the dominant limb immediately before the fatigue protocol. In both sessions, peripheral muscle fatigue was analyzed by surface electromyography (EMG) and blood lactate analysis. Muscle performance was evaluated using an isokinetic dynamometer. The results showed that photobiomodulation was able of reducing muscle fatigue by a significant increase of electromyographic fatigue index (EFI) (p = 0.047) and decreasing significantly lactate concentration 6 min after the performance of the fatigue protocol (p = 0. 0006) compared the placebo laser session. However, the photobiomodulation was not able of increasing muscle performance measured by the isokinetic dynamometer. Thus, it can be conclude that the photobiomodulation was effective in reducing fatigue levels. However, no effects of photobiomodulation on muscle performance was observed.

Resistance exercise: a non-pharmacological strategy to minimize or reverse sleep deprivation-induced muscle atrophy.

Sleep is important for maintenance of skeletal muscle health. Sleep debt can induce muscle atrophy by increasing glucocorticoids and decreasing testosterone, growth hormone and insulin-like growth factor-I. These hormonal alterations result in a highly proteolytic environment characterized by decreased protein synthesis and increased degradation. Given that sleep deprivation is increasingly prevalent in modern society, strategies to minimize or reverse its adverse effects need to be investigated. Resistance exercise has been suggested as an intervention that would benefit the muscle health. The practice of this type of exercise can increase the concentration of testosterone, growth hormone and insulin-like growth factor I and stimulate the protein synthesis through a key signaling molecule, mammalian target of rapamycin. Thus, we hypothesized that resistance exercise is an important non-pharmacological strategy to counteract deleterious effects of sleep debt on skeletal muscle.

Sleep and muscle recovery: endocrinological and molecular basis for a new and promising hypothesis.

Sleep is essential for the cellular, organic and systemic functions of an organism, with its absence being potentially harmful to health and changing feeding behavior, glucose regulation, blood pressure, cognitive processes and some hormonal axes. Among the hormonal changes, there is an increase in cortisol (humans) and corticosterone (rats) secretion, and a reduction in testosterone and Insulin-like Growth Factor 1, favoring the establishment of a highly proteolytic environment. Consequently, we hypothesized that sleep debt decreases the activity of protein synthesis pathways and increases the activity of degradation pathways, favoring the loss of muscle mass and thus hindering muscle recovery after damage induced by exercise, injuries and certain conditions associated with muscle atrophy, such as sarcopenia and cachexia.