33 research outputs found

    Where Does Blood Flow Restriction Fit in the Toolbox of Athletic Development? A Narrative Review of the Proposed Mechanisms and Potential Applications

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    Blood flow-restricted exercise is currently used as a low-intensity time-efficient approach to reap many of the benefits of typical high-intensity training. Evidence continues to lend support to the notion that even highly trained individuals, such as athletes, still benefit from this mode of training. Both resistance and endurance exercise may be combined with blood flow restriction to provide a spectrum of adaptations in skeletal muscle, spanning from myofibrillar to mitochondrial adjustments. Such diverse adaptations would benefit both muscular strength and endurance qualities concurrently, which are demanded in athletic performance, most notably in team sports. Moreover, recent work indicates that when traditional high-load resistance training is supplemented with low-load, blood flow-restricted exercise, either in the same session or as a separate training block in a periodised programme, a synergistic and complementary effect on training adaptations may occur. Transient reductions in mechanical loading of tissues afforded by low-load, blood flow-restricted exercise may also serve a purpose during de-loading, tapering or rehabilitation of musculoskeletal injury. This narrative review aims to expand on the current scientific and practical understanding of how blood flow restriction methods may be applied by coaches and practitioners to enhance current athletic development models.publishedVersionPaid open acces

    Un "simposio di sapienza e affetto"

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    Muscle hypertrophy occurs following increased protein synthesis, which requires activation of the ribosomal complex. Additionally, increased translational capacity via elevated ribosomal RNA (rRNA) synthesis has also been implicated in resistance training-induced skeletal muscle hypertrophy. The time course of ribosome biogenesis following resistance exercise (RE) and the impact exerted by differing recovery strategies remains unknown. In the present study, the activation of transcriptional regulators, the expression levels of pre-rRNA, and mature rRNA components were measured through 48 h after a single-bout RE. In addition, the effects of either low-intensity cycling (active recovery, ACT) or a cold-water immersion (CWI) recovery strategy were compared. Nine male subjects performed two bouts of high-load RE randomized to be followed by 10 min of either ACT or CWI. Muscle biopsies were collected before RE and at 2, 24, and 48 h after RE. RE increased the phosphorylation of the p38-MNK1-eIF4E axis, an effect only evident with ACT recovery. Downstream, cyclin D1 protein, total eIF4E, upstream binding factor 1 (UBF1), and c-Myc proteins were all increased only after RE with ACT. This corresponded with elevated abundance of the pre-rRNAs (45S, ITS-28S, ITS-5.8S, and ETS-18S) from 24 h after RE with ACT. In conclusion, coordinated upstream signaling and activation of transcriptional factors stimulated pre-rRNA expression after RE. CWI, as a recovery strategy, markedly blunted these events, suggesting that suppressed ribosome biogenesis may be one factor contributing to the impaired hypertrophic response observed when CWI is used regularly after exercise

    Acute Resistance Exercise Induces Sestrin2 Phosphorylation and p62 Dephosphorylation in Human Skeletal Muscle

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    Sestrins (1, 2, 3) are a family of stress-inducible proteins capable of attenuating oxidative stress, regulating metabolism, and stimulating autophagy. Sequestosome1 (p62) is also a stress-inducible multifunctional protein acting as a signaling hub for oxidative stress and selective autophagy. It is unclear whether Sestrin and p62Ser403 are regulated acutely or chronically by resistance exercise (RE) or training (RT) in human skeletal muscle. Therefore, the acute and chronic effects of RE on Sestrin and p62 in human skeletal muscle were examined through two studies. In Study 1, nine active men (22.1 ± 2.2 years) performed a bout of single-leg strength exercises and muscle biopsies were collected before, 2, 24, and 48 h after exercise. In Study 2, 10 active men (21.3 ± 1.9 years) strength trained for 12 weeks (2 days per week) and biopsies were collected pre- and post-training. Acutely, 2 h postexercise, phosphorylation of p62Ser403 was downregulated, while there was a mobility shift of Sestrin2, indicative of increased phosphorylation. Forty-eight hours postexercise, the protein expression of both Sestrin1 and total p62 increased. Chronic exercise had no impact on the gene or protein expression of Sestrin2/3 or p62, but Sestrin1 protein was upregulated. These findings demonstrated an inverse relationship between Sestrin2 and p62 phosphorylation after a single bout of RE, indicating they are transiently regulated. Contrarily, 12 weeks of RT increased protein expression of Sestrin1, suggesting that despite the strong sequence homology of the Sestrin family, they are differentially regulated in response to acute RE and chronic RT

    Targeted mitochondrial therapy using MitoQ shows equivalent renoprotection to angiotensin converting enzyme inhibition but no combined synergy in diabetes.

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    Mitochondrial dysfunction is a pathological mediator of diabetic kidney disease (DKD). Our objective was to test the mitochondrially targeted agent, MitoQ, alone and in combination with first line therapy for DKD. Intervention therapies (i) vehicle (D); (ii) MitoQ (DMitoQ;0.6 mg/kg/day); (iii) Ramipril (DRam;3 mg/kg/day) or (iv) combination (DCoAd) were administered to male diabetic db/db mice for 12 weeks (n = 11-13/group). Non-diabetic (C) db/m mice were followed concurrently. No therapy altered glycaemic control or body weight. By the study end, both monotherapies improved renal function, decreasing glomerular hyperfiltration and albuminuria. All therapies prevented tubulointerstitial collagen deposition, but glomerular mesangial expansion was unaffected. Renal cortical concentrations of ATP, ADP, AMP, cAMP, creatinine phosphate and ATP:AMP ratio were increased by diabetes and mostly decreased with therapy. A higher creatine phosphate:ATP ratio in diabetic kidney cortices, suggested a decrease in ATP consumption. Diabetes elevated glucose 6-phosphate, fructose 6-phosphate and oxidised (NAD+ and NADP+) and reduced (NADH) nicotinamide dinucleotides, which therapy decreased generally. Diabetes increased mitochondrial oxygen consumption (OCR) at complex II-IV. MitoQ further increased OCR but decreased ATP, suggesting mitochondrial uncoupling as its mechanism of action. MitoQ showed renoprotection equivalent to ramipril but no synergistic benefits of combining these agents were shown

    Turning up the heat: an evaluation of the evidence for heating to promote exercise recovery, muscle rehabilitation and adaptation

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    Historically, heat has been used in various clinical and sports rehabilitation settings to treat soft tissue injuries. More recently, interest has emerged in using heat to pre-condition muscle against injury. The aim of this narrative review was to collate information on different types of heat therapy, explain the physiological rationale for heat therapy, and to summarise and evaluate the effects of heat therapy before, during and after muscle injury, immobilisation and strength training. Studies on skeletal muscle cells demonstrate that heat attenuates cellular damage and protein degradation (following in vitro challenges/insults to the cells). Heat also increases the expression of heat shock proteins (HSPs) and upregulates the expression of genes involved in muscle growth and differentiation. In rats, applying heat before and after muscle injury or immobilisation typically reduces cellular damage and muscle atrophy, and promotes more rapid muscle growth/regeneration. In humans, some research has demonstrated benefits of microwave diathermy (and, to a lesser extent, hot water immersion) before exercise for restricting muscle soreness and restoring muscle function after exercise. By contrast, the benefits of applying heat to muscle after exercise are more variable. Animal studies reveal that applying heat during limb immobilisation attenuates muscle atrophy and oxidative stress. Heating muscle may also enhance the benefits of strength training for improving muscle mass in humans. Further research is needed to identify the most effective forms of heat therapy and to investigate the benefits of heat therapy for restricting muscle wasting in the elderly and those individuals recovering from serious injury or illness

    A principled approach to skill acquisition in competitive surfing: Embracing representative learning design

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    The recent rise in professionalisation and institutionalisation of competitive surfing has resulted in a dramatic increase in the use of alternative training modalities. These are often employed in an attempt to increase exposure to surf-like activities when appropriate ocean conditions are not available. It is commonly accepted that practice sessions should be grounded in theory, with training content informed by a clear scientific rationale. Despite this, research is yet to offer surfing coaches and surfers effective strategies to assist in implementing appropriate ‘off water’ training modalities. It is widely accepted that integrating a representative learning design is crucial towards the transfer of performance to competition environments. Therefore, the aim of this paper is to promote representative learning design (RLD) as a contemporary, principled framework that can underpin the creation of surfing training design and performance. Examples of constraints relevant to surfing are considered, and the efficacy and rationale of popular training methods are challenged. Finally, practical implications and coaching tools to underpin the implementation of representative learning design in surf training are provided

    Improving in vitro Evaluation Capabilities of Cardiac Assist Devices through a Validated Exercise Simulation

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    Cardiac assist devices require thorough in vitro evaluation prior to in vivo animal trials, which is often undertaken in mock circulatory loops. To allow for best possible device development, mock circulatory loops need to be able to simulate a variety of patient scenarios. Transition from rest to exercise is one of the most commonly simulated patient scenarios, however, to validate in vitro exercise test beds, baseline data on how the healthy heart and circulatory system responds to exercise is required. Steady state and time response data for heart rate (HR), stroke volume (SV) and cardiac output (CO) was continuously recorded using impedance cardiography in 50 healthy subjects (27 male / 23 female) during exercise on a recumbent exercise ergometer. This data was then used to implement an exercise simulation in a mock circulatory loop and both the steady state and transient results were compared with the mean response of subjects transitioning from rest to 60 W exercise. When transitioning from rest to exercise the time constant (Ï„) and rise time (tr) for HR, SV and CO were between 10.6-19.3s and 24.7-44.3s respectively for both sexes. No significant differences between the genders were found for Ï„ and tr (p>0.05). Mock circulatory loop results of HR, SV and CO were in good accordance with human data. The present data was used to successfully validate in vitro exercise simulations and may be used to validate in silico numerical simulations of exercise, thus further improving the evaluation capabilities for existing and under development cardiac assist devices.</p
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