Mind-muscle connection: effects of verbal instructions on muscle activity during bench press exercise

Different attentional foci may modify muscle activation during exercises. Our aim was to determine if it is possible to selectively activate the pectoralis major or triceps brachii muscles according to specific verbal instructions provided during the bench press exercise. 13 resistance-trained males (25.6\ub15.4 yrs, 182.7\ub19.1 cm, 86.4\ub19.7 kg) underwent an electromyographic signals acquisition of the sternocostal head, clavicular head of the pectoralis major, the anterior deltoid, and the long head of the triceps brachii (LT) during bench press exercise. Participants performed one non-instructed set (NIS) of 4 repetitions at 50% 1-repetition maximum (1-RM) and one NIS of 4 repetitions at 80% 1-RM. Four additional sets of 4 repetitions at 50% and 80% 1-RM were randomly performed with verbal instructions to isolate the chest muscles (chest instructed set, CIS) or to isolate the triceps muscles (triceps instructed set, TIS). Participants showed significantly higher LT activation during TIS compared to non-instructed set both at 50% (p=0.0199) and 80% 1-RM (p=0.0061) respectively. TIS elicited a significant (p=0.0250) higher activation of LT compared to CIS. Our results suggest that verbal instructions seem to be effective for increasing activity of the triceps brachii but not the pectoralis major during the bench press

Effects of eight weeks of time-restricted feeding (16/8) on basal metabolism, maximal strength, body composition, inflammation, and cardiovascular risk factors in resistance-trained males

Background: Intermittent fasting (IF) is an increasingly popular dietary approach used for weight loss and overall health. While there is an increasing body of evidence demonstrating beneficial effects of IF on blood lipids and other health outcomes in the overweight and obese, limited data are available about the effect of IF in athletes. Thus, the present study sought to investigate the effects of a modified IF protocol (i.e. time-restricted feeding) during resistance training in healthy resistance-trained males. Methods: Thirty-four resistance-trained males were randomly assigned to time-restricted feeding (TRF) or normal diet group (ND). TRF subjects consumed 100 % of their energy needs in an 8-h period of time each day, with their caloric intake divided into three meals consumed at 1 p.m., 4 p.m., and 8 p.m. The remaining 16 h per 24-h period made up the fasting period. Subjects in the ND group consumed 100 % of their energy needs divided into three meals consumed at 8 a.m., 1 p.m., and 8 p.m. Groups were matched for kilocalories consumed and macronutrient distribution (TRF 2826 \ub1 412.3 kcal/day, carbohydrates 53.2 \ub1 1.4 %, fat 24.7 \ub1 3.1 %, protein 22.1 \ub1 2.6 %, ND 3007 \ub1 444.7 kcal/day, carbohydrates 54.7 \ub1 2.2 %, fat 23.9 \ub1 3.5 %, protein 21.4 \ub1 1.8). Subjects were tested before and after 8 weeks of the assigned diet and standardized resistance training program. Fat mass and fat-free mass were assessed by dual-energy x-ray absorptiometry and muscle area of the thigh and arm were measured using an anthropometric system. Total and free testosterone, insulin-like growth factor 1, blood glucose, insulin, adiponectin, leptin, triiodothyronine, thyroid stimulating hormone, interleukin-6, interleukin-1\u3b2, tumor necrosis factor \u3b1, total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and triglycerides were measured. Bench press and leg press maximal strength, resting energy expenditure, and respiratory ratio were also tested. Results: After 8 weeks, the 2 Way ANOVA (Time * Diet interaction) showed a decrease in fat mass in TRF compared to ND (p = 0.0448), while fat-free mass, muscle area of the arm and thigh, and maximal strength were maintained in both groups. Testosterone and insulin-like growth factor 1 decreased significantly in TRF, with no changes in ND (p = 0.0476; p = 0.0397). Adiponectin increased (p = 0.0000) in TRF while total leptin decreased (p = 0.0001), although not when adjusted for fat mass. Triiodothyronine decreased in TRF, but no significant changes were detected in thyroid-stimulating hormone, total cholesterol, high-density lipoprotein, low-density lipoprotein, or triglycerides. Resting energy expenditure was unchanged, but a significant decrease in respiratory ratio was observed in the TRF group. Conclusions: Our results suggest that an intermittent fasting program in which all calories are consumed in an 8-h window each day, in conjunction with resistance training, could improve some health-related biomarkers, decrease fat mass, and maintain muscle mass in resistance-trained males

Mind-muscle connection: effects of verbal instructions on muscle activity during bench press exercise

Different attentional foci may modify muscle activation during exercises. Our aim was to determine if it is possible to selectively activate the pectoralis major or triceps brachii muscles according to specific verbal instructions provided during the bench press exercise. 13 resistance-trained males (25.6±5.4 yrs, 182.7±9.1 cm, 86.4±9.7 kg) underwent an electromyographic signals acquisition of the sternocostal head, clavicular head of the pectoralis major, the anterior deltoid, and the long head of the triceps brachii (LT) during bench press exercise. Participants performed one non-instructed set (NIS) of 4 repetitions at 50% 1-repetition maximum (1-RM) and one NIS of 4 repetitions at 80% 1-RM. Four additional sets of 4 repetitions at 50% and 80% 1-RM were randomly performed with verbal instructions to isolate the chest muscles (chest instructed set, CIS) or to isolate the triceps muscles (triceps instructed set, TIS). Participants showed significantly higher LT activation during TIS compared to non-instructed set both at 50% (p=0.0199) and 80% 1-RM (p=0.0061) respectively. TIS elicited a significant (p=0.0250) higher activation of LT compared to CIS. Our results suggest that verbal instructions seem to be effective for increasing activity of the triceps brachii but not the pectoralis major during the bench press

Phenomenological models of synaptic plasticity based on spike timing

Synaptic plasticity is considered to be the biological substrate of learning and memory. In this document we review phenomenological models of short-term and long-term synaptic plasticity, in particular spike-timing dependent plasticity (STDP). The aim of the document is to provide a framework for classifying and evaluating different models of plasticity. We focus on phenomenological synaptic models that are compatible with integrate-and-fire type neuron models where each neuron is described by a small number of variables. This implies that synaptic update rules for short-term or long-term plasticity can only depend on spike timing and, potentially, on membrane potential, as well as on the value of the synaptic weight, or on low-pass filtered (temporally averaged) versions of the above variables. We examine the ability of the models to account for experimental data and to fulfill expectations derived from theoretical considerations. We further discuss their relations to teacher-based rules (supervised learning) and reward-based rules (reinforcement learning). All models discussed in this paper are suitable for large-scale network simulations

Mycobacteria counteract a TLR-mediated nitrosative defense mechanism in a zebrafish infection model.

Pulmonary tuberculosis (TB), caused by the intracellular bacterial pathogen Mycobacterium tuberculosis (Mtb), is a major world health problem. The production of reactive nitrogen species (RNS) is a potent cytostatic and cytotoxic defense mechanism against intracellular pathogens. Nevertheless, the protective role of RNS during Mtb infection remains controversial. Here we use an anti-nitrotyrosine antibody as a readout to study nitration output by the zebrafish host during early mycobacterial pathogenesis. We found that recognition of Mycobacterium marinum, a close relative of Mtb, was sufficient to induce a nitrosative defense mechanism in a manner dependent on MyD88, the central adaptor protein in Toll like receptor (TLR) mediated pathogen recognition. However, this host response was attenuated by mycobacteria via a virulence mechanism independent of the well-characterized RD1 virulence locus. Our results indicate a mechanism of pathogenic mycobacteria to circumvent host defense in vivo. Shifting the balance of host-pathogen interactions in favor of the host by targeting this virulence mechanism may help to alleviate the problem of infection with Mtb strains that are resistant to multiple drug treatments

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure fl ux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defi ned as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (inmost higher eukaryotes and some protists such as Dictyostelium ) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the fi eld understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation it is imperative to delete or knock down more than one autophagy-related gene. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways so not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field

Muscle dysmorphia and its associated psychological and psychopathological features in three groups of Italian recreational athletes.

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