No full-text available
To read the full-text of this research,
you can request a copy directly from the authors.
Exercise-induced skeletal muscle signaling pathways and human athletic performance
Abstract
Skeletal muscle is a highly malleable tissue capable of altering its phenotype in response to external stimuli including exercise. This response is determined by the mode, (endurance- versus resistance-based), volume, intensity and frequency of exercise performed with the magnitude of this response-adaptation the basis for enhanced physical work capacity. However, training-induced adaptations in skeletal muscle are variable and unpredictable between individuals. With the recent application of molecular techniques to exercise biology, there has been a greater understanding of the multiplicity and complexity of cellular networks involved in exercise responses. This review summarizes the molecular and cellular events mediating adaptation processes in skeletal muscle in response to exercise. We discuss established and novel cell signaling proteins mediating key physiological responses associated with enhanced exercise performance and the capacity for reactive oxygen and nitrogen species to modulate training adaptation responses. We also examine the molecular bases underpinning heterogeneous responses to resistance and endurance exercise and the dissociation between molecular 'markers' of training adaptation and subsequent exercise performance.
... L'exercice chronique correspond à une situation où l'exercice est pratiqué de façon régulière permettant ainsi des adaptations bénéfiques au niveau cardio-vasculaire et musculaire (Camera et al., 2016;Nystoriak & Bhatnagar, 2018) qui sont associées à des bénéfices importants pour la santé (Arem et al., 2015;Wahid et al., 2016). Au niveau cardio-vasculaire, ces adaptations vont résulter en une augmentation du débit cardiaque ainsi qu'un contrôle vasomoteur beaucoup plus fin permettant ainsi d'augmenter l'oxygénation des organes au cours de l'exercice (Green et al., 2011;Nystoriak & Bhatnagar, 2018). ...
... Les adaptations bénéfiques de l'exercice chronique au niveau systémique sont souvent associées à l'exercice aérobie cependant, concernant le muscle squelettique, l'exercice chronique en résistance et aérobie permettent tous deux d'améliorer la fonction musculaire. Ces deux modalités d'entraînement induisent des stimuli différents activant des voies cellulaires distinctes qui se traduisent par des adaptations spécifiques (Camera et al., 2016). En effet, l'entraînement en résistance induit des effets sur la masse musculaire et la capacité de production de force (Lixandrão et al., 2018;Schoenfeld et al., 2016) alors que l'entraînement aérobie augmente la capacité musculaire à utiliser l'O 2 pour produire de l'énergie (Hawley et al., 2018). ...
... En effet, l'exercice chronique aérobie est associé à une augmentation de la densité et de la tortuosité capillaire qui serait induite par un facteur de croissance, le vascular endothelial growth factor (VEGF) produit majoritairement par le muscle et l'endothélium (Olver et al., 2015). L'ensemble de ces adaptations semblent être initiées par un facteur de transcription précis : le PGC1-α (Arany et al., 2008;Camera et al., 2016;Kang et al., 2013) dont l'activation se fait par la déplétion importante en énergie (Cantó & Auwerx, 2009) et l'augmentation de la concentration en EORs p. 98 (Ferraro et al., 2014) au cours de ce type d'exercice. De plus, il est intéressant de noter que l'augmentation de la concentration en EORs au cours de l'exercice aérobie permet de stimuler la production d'enzymes antioxydantes (Merry & Ristow, 2016) provoquant ainsi l'augmentation de leur activité au sein du muscle squelettique (Laughlin et al., 1990;Plant et al., 2003;Powers et al., 1994). ...
Sickle cell disease (SCD) is a group of hemoglobin disorders sharing a nucleotide mutation in the β-globin gene, such as homozygous sickle cell anaemia (SS) and sickle cell-hemoglobin C disease (SC), with various clinical severities. SCD patients are characterized by a limited exercise capacity caused by cardio-
vascular abnormalities but skeletal muscle implication remains unclear. Recently, few studies characterized skeletal muscle in SS patients and showed an amyotrophy, a profound microvasculature remodeling and a decreased maximal strength however an exercise-induced skeletal muscle dysfunction are yet to described in SCD patients. It was also hypothesized that oxidative stress may be increased and participate in the skeletal muscle abnormalities observed in SCD patients. Chronic aerobic exercise is known to increase the antioxidant capacity in the skeletal muscle, but the effects of this type exercise have not been described in the skeletal muscle of SCD patients. Hence, the aim of this thesis work is 1) to characterize skeletal muscle function
during exercise in S/S et S/C patients and 2) to study the effects of chronic exercise on pro/antioxidant balance in the skeletal muscle of transgenic sickle cell mice. In a first study it was shown that S/S and S/C patients exhibit a profound skeletal muscle dysfunction characterized by an increased fatigability of the quadriceps. Also, the skeletal muscle dysfunction seems to be explained by intramuscular alterations specific to sickle cell disease rather than the clinical severity. In a second study, Townes sickle cell mice performed 8 weeks of moderate aerobic exercise and we observed an altered response of pro/antioxidant balance in the skeletal muscle of S/S mice. To conclude, the results of this work strengthen the idea that skeletal muscle is key
therapeutic target in the exercise rehabilitation of sickle cell disease patients.
... Remarkably, endurance training (a kind of training that recruits the aerobic system, improving resistance to prolonged effort) leads to accumulation of PGC-1a in mitochondria, where it forms a transcriptional complex with TFAM in the hypervariable mitochondrial DNA (mtDNA) region named D-loop. 69 As a consequence, endurance training apparently increases mitochondrial density, promotes FFA oxidation in muscle fibers through induction of b-oxidation enzymes, and provides better oxygen distribution to muscles. Recent evidence also suggests that endurance training increases gene expression and protein content of several FFA transporters that may facilitate the uptake and delivery of FFA to mitochondria. ...
... Intracellular alterations triggered by muscle activity induce a number of signaling pathways that eventually regulate short-term (glycolytic/aerobic) and long-term cell metabolism (protein turnover and gene expression synthesis). 69,82,83 Several muscle cell regulation points are potential targets of training to induce muscle protein synthesis. Most regard messenger RNA (mRNA) induction and stabilization and inhibition of degradation. ...
It is widely accepted that metabolic changes associated with training are influenced by a person's genetic background. In this review, we explore the polymorphisms underlying interindividual variability in response to training of weight loss and muscle mass increase in obese individuals, with or without lymphedema, and in normal-weight subjects. We searched PubMed for articles in English published up to May 2019 using the following keywords: (((physical training[Title/Abstract] OR sport activity[Title/Abstract]) AND predisposition[Title/Abstract]) AND polymorphism [Title/Abstract]). We identified 38 single-nucleotide polymorphisms that may modulate the genetic adaptive response to training. The identification of genetic marker(s) that improve the beneficial effects of training may in perspective make it possible to assess training programs, which in combination with dietary intervention can optimize body weight reduction in obese subjects, with or without lymphedema. This is particularly important for patients with lymphedema because obesity can worsen the clinical status, and therefore, a personalized approach that could reduce obesity would be fundamental in the clinical management of lymphedema.
... As bone and muscle are reported to work together as a functional unit [28], and it is well known from studies on Earth that muscles atrophy quickly when they are not used, as reviewed in [11,13,29], it is not surprising that muscle atrophy occurs quickly on exposure to microgravity. As muscles function via neural input at neuromuscular junctions, the loss of muscle integrity in microgravity could be due to the direct effects of loading on muscles and/or the loss of the integrity of the neural component for muscle stimulation. ...
Homo sapiens and their predecessors evolved in the context of the boundary conditions of Earth, including a 1 g gravity and a geomagnetic field (GMF). These variables, plus others, led to complex organisms that evolved under a defined set of conditions and define how humans will respond to space flight, a circumstance that could not have been anticipated by evolution. Over the past ~60 years, space flight and living in low Earth orbit (LEO) have revealed that astronauts are impacted to varying degrees by such new environments. In addition, it has been noted that astronauts are quite heterogeneous in their response patterns, indicating that such variation is either silent if one remained on Earth, or the heterogeneity unknowingly contributes to disease development during aging or in response to insults. With the planned mission to deep space, humans will now be exposed to further risks from radiation when traveling beyond the influence of the GMF, as well as other potential risks that are associated with the actual loss of the GMF on the astronauts, their microbiomes, and growing food sources. Experimental studies with model systems have revealed that hypogravity conditions can influence a variety biological and physiological systems, and thus the loss of the GMF may have unanticipated consequences to astronauts’ systems, such as those that are electrical in nature (i.e., the cardiovascular system and central neural systems). As astronauts have been shown to be heterogeneous in their responses to LEO, they may require personalized countermeasures, while others may not be good candidates for deep-space missions if effective countermeasures cannot be developed for long-duration missions. This review will discuss several of the physiological and neural systems that are affected and how the emerging variables may influence astronaut health and functioning.
... A különféle fizikális edzésformák különböző hatást fognak eredményezni a betegeknél. Az állóképességi edzés az oxidatív metabolizmusra lesz jótékony hatással, viszont az izomtömeg megtartására vagy növelésére nem alkalmas, ezzel szemben az ellenállásos edzés bizonyos terjedelmi és intenzitási zónákban képes izom-hipertrófiát előidézni [9,10]. Ezek a terjedelmi és intenzitási zónák azonban megkövetelnek bizonyos fokú erőnlétet, ami daganatos betegek esetében korlátozó tényező lehet, ugyanis a betegeknél kialakulhat krónikus fáradtság, kardiológiai problémák, sok esetben a motiváció radikális csökkenése, amely hatások korlátozni fogják mozgásképességüket, így a javallott terápiát is. ...
Introduction:
In patients with cancer, loss of muscle mass is observed in many cases and tumour types. This can lead to a drastic deterioration in the patient's quality of life, with the inability to support themselves. Nowadays, in addition to primary treatment of the tumour, physical training of patients has become a priority in order to maintain their quality of life. One key to this is resistance training to prevent sudden muscle loss, which the patient can do alongside primary treatment, and isometric training may be one option.
Objective:
Our aim was to measure the activation frequency characteristics of the biceps brachii muscle in our subjects during a fatigue protocol while creating a constant controlled isometric tension in the muscle.
Method:
19 healthy university students participated in our study. After determining the dominant side, the subjects' single repetition maximum was assessed using the GymAware RS tool and then 65% and 85% of this was calculated. We placed electrodes on the biceps brachii muscle and had them hold the weight at 65% and 85% until full fatigue. Immediately afterwards, subjects performed an isometric maximal contraction (Imax). The measured electromyography recordings were divided into 3 equal parts, then the first, middle and last 3 s (W1, W2, W3) were analyzed.
Results:
Our results show that, consistent with fatigue, at both 1RM 65% and 1RM 85% load, the activity of the low-frequency motor units increases, while the activation of the high-frequency motor units decreases.
Discussion:
The present study is consistent with our previous study.
Conclusion:
Our test protocol is not suitable for prolonged activation of high-frequency motor units because the activity of high-frequency motor units decreases over time. Orv Hetil. 2023; 164(10): 376-382.
... Exercise training also alters DNA methylation of specific genes and pathways within the skeletal muscle in people with varying degrees of insulin sensitivity (Garcia et al., 2022). The skeletal muscle adapts to exercise through a variety of pathways, including muscle contraction/ATP biosynthesis coupling, and energy utilization upon activation of mechano-and other metabolic sensors Camera et al., 2016;Fan and Evans, 2017). Although considerable effort has been made to reveal the comprehensive changes stimulated by exercise (Pilegaard et al., 2000;Mahoney et al., 2005;Catoire et al., 2012), many regulators of the skeletal muscle remain undiscovered. ...
Exercise intervention at the early stage of type 2 diabetes mellitus (T2DM) can aid in the maintenance of blood glucose homeostasis and prevent the development of macrovascular and microvascular complications. However, the exercise-regulated pathways that prevent the development of T2DM remain largely unclear. In this study, two forms of exercise intervention, treadmill training and voluntary wheel running, were conducted for high-fat diet (HFD)-induced obese mice. We observed that both forms of exercise intervention alleviated HFD-induced insulin resistance and glucose intolerance. Skeletal muscle is recognized as the primary site for postprandial glucose uptake and for responsive alteration beyond exercise training. Metabolomic profiling of the plasma and skeletal muscle in chow, HFD, and HFD-exercise groups revealed robust alterations in metabolic pathways by exercise intervention in both cases. Overlapping analysis identified 9 metabolites, including beta-alanine, leucine, valine, and tryptophan, which were reversed by exercise treatment in both the plasma and skeletal muscle. Transcriptomic analysis of gene expression profiles in the skeletal muscle revealed several key pathways involved in the beneficial effects of exercise on metabolic homeostasis. In addition, integrative transcriptomic and metabolomic analyses uncovered strong correlations between the concentrations of bioactive metabolites and the expression levels of genes involved in energy metabolism, insulin sensitivity, and immune response in the skeletal muscle. This work established two models of exercise intervention in obese mice and provided mechanistic insights into the beneficial effects of exercise intervention on systemic energy homeostasis.
... thought to promote muscle hypertrophy in resistance training (33,34). Resistance training promotes muscle growth and improves body composition (35). ...
Background:
The demand for safe and efficacious botanical formulations to increase muscle mass, strength, and stamina is increasing among athletes and the general population. The nutraceutical supplements of medicinal plant origin exert minimal health concern.
Objective:
This randomized, double-blind, placebo-controlled study was aimed to evaluate the ergogenic potential of a proprietary, standardized formulation (LI12542F6) of Sphaeranthus indicus flower head and Mangifera indica stem bark extracts.
Methods:
Forty male participants 18-40 years of age were assigned to receive either a placebo (n = 20) or 650 mg/day LI12542F6 (n = 20) for 56 days. All participants performed a fixed set of resistance exercises during the intervention. The primary endpoint was the change from baseline muscle strength, assessed by one-repetition maximum (1-RM) bench and leg presses, and handgrip strength. The secondary endpoints included cable pull-down repetitions, time to exhaustion on a treadmill, mid-upper arm circumference (MUAC), body composition using dual-energy x-ray absorptiometry (DEXA), and free testosterone and cortisol levels in serum.
Results:
Fifty-six days supplementation of LI12542F6 significantly improved baseline bench press (P < 0.0001), leg press (P < 0.0001), handgrip strength (P < 0.0006), number of repetitions (P < 0.0001), and time to exhaustion (P < 0.0008), compared to placebo. Post-trial, the LI12542F6 group also showed significantly increased MUAC and improved body composition and serum hormone levels. The participants' hematology, clinical chemistry, and vital signs were within the normal range. No adverse events were observed.
Conclusion:
This study demonstrates that LI12542F6 supplementation significantly increases muscle strength and size and improves endurance in healthy men. Also, LI12542F6 is well-tolerated by the participants.
... It has been suggested that there is a mechanosensitive signaling pathway likely involving integrins and acting through phosphatidic acid (PA) and focal adhesion kinase (FAK) that can activate mTORC1 after RE (Brook et al., 2016). The main downstream targets of activated mTORC1 are ribosomal protein s6p70 kinase (S6K1) and eukaryotic initiation factor 4E-binding protein (4E-BP1), which further regulate protein synthesis and ribosomal biogenesis (Koopman et al., 2006;Camera et al., 2016;Chaillou, 2017). Some studies demonstrated that within 1 h, 4 h (Kumar et al., 2009), or even 24 h after an acute RE training older adults do not exhibit any changes in mTORC1, S6K1 and 4E-BP1 phosphorylation, whereas their younger counterparts display an increase in mTOR activation already 3 h after RE, and an increase in phosphorylation of S6K1 and 4E-BP1 6 h after an acute RE bout . ...
It is well established that resistance training increases muscle mass. Indeed, there is evidence to suggest that a single session of resistance training is associated with an increase in muscle protein synthesis in young adults. However, the fundamental mechanisms that are involved in regulating muscle protein turnover rates after an acute bout of physical exercise are unclear. Therefore, this review will briefly focus on summarizing the potential mechanisms behind the growth of skeletal muscle after physical exercise. We also present mechanistic differences that may exist between young and older individuals during muscle protein synthesis and breakdown after physical exercise. Pathways leading to the activation of AKT/mTOR signals after resistance exercise and the activation of AMPK signaling pathway following a HIIT (High intensity interval training) are discussed.
... The quest to increase skeletal muscle performance is widely pursued by athletes. Exercise is widely used to increase skeletal muscle performance, especially for athletes (Camera et al., 2016;Schoenfeld et al., 2016;McKendry et al., 2021). Resistance exercise could significantly induce muscle hypertrophy. ...
Exercise is reported to play a crucial role in skeletal muscle performance. However, the underlying mechanism is still unknown. Thus, we investigated the effect of high-intensity aerobic exercise on skeletal muscle performance. In this study, the male C57BL/6J mice were accepted by high-intensity aerobic exercise for 8 weeks to establish an exercise model. It was observed that high-intensity aerobic exercise markedly affected the expression of genes in skeletal muscle. Moreover, high-intensity aerobic exercise significantly improved skeletal muscle grip strength and serum testosterone levels. HE staining showed that the cross-sectional area (CSA) of the skeletal muscle was successfully increased after 8 weeks of high-intensity aerobic exercise. Additionally, we found that high-intensity aerobic exercise changed gut microbiota structure by altering the abundance of Akkermansia , Allobaculum , and Lactobacillus , which might be related to testosterone production. However, the beneficial effects disappeared after the elimination of the gut microbiota and recovered after fecal microbiota transplantation (FMT) experiments for 1 week. These results indicated that the beneficial effects of high-intensity aerobic exercise on skeletal muscle were partly dependent on the gut microbiota. Our results suggested that long-term high loading intensity of aerobic exercise could improve skeletal muscle performance, which was probably due to the gut microbiota-testosterone axis.
... an adaptation to physical exercise that is carried out occurs by involving many molecular pathways that play a role in regulating muscle contraction and the biosynthetic pathway for ATP formation, such as mitogen activated protein kinases (MAPKs), AMP activated protein kinase (AMPK), Sirtuins (SIRTs), and oxygen sensors prolyl hydroxylases (PHDs) (Camera et. al., 2016;Fan and Evan, 2017;Kjøbsted et. al., 2018). All these changes require a good balance so that the work of the organs and the condition of the body is not disturbed, that is what is called homeostasis. Thus, in athletes, if the homeostatic response fails, it will reduce their physical performance and performance (Giriwijoyo and Sidik, 2012 ...
... Integrins are involved in several processes regarding the communication and signalling between the extracellular matrix, cell membrane, and cytoskeleton. It has been shown that FAK is mechanically sensitive and activates mTORC1 complex through a TSC2-dependent mechanism (Camera et al. 2016). Another molecule involved in the mechano-activation of mTORC1 is phosphatidic acid (PA), a lipid signalling molecule that binds to the FKBP-rapamycin-bindingdomain of mTORC1, leading to its activation (Yoon et al. 2011). ...
Skeletal muscle is essential in locomotion and plays a role in whole-body metabolism, particularly during exercise. Skeletal muscle is the largest ‘reservoir’ of amino acids, which can be released for fuel and as a precursor for gluconeogenesis. During exercise, whole-body, and more specifically skeletal muscle, protein catabolism is increased, but protein synthesis is suppressed. Metabolism of skeletal muscle proteins can support energy demands during exercise, and persistent exercise (i.e. training) results in skeletal muscle protein remodelling. Exercise is generally classified as being either ‘strength’ or ‘aerobic/endurance’ in nature, and the type of exercise will reflect the phenotypic and metabolic adaptations of the muscle. In this chapter, we describe the impact of various exercise modes on protein metabolism during and following exercise.
... Swimming exercise, for example, has shown neuroprotection in animal models of Alzheimer [35], spinal muscular atrophy [36], depression [37], and amyotrophic lateral sclerosis, thorough increasing the production and release of growth factors [38]. However, the beneficial effect of exercise performance depends on factors like intensity and frequency to trigger efficient cellular adaptation mechanisms to oxidative stress and increase the antioxidative response stimulated by mitochondrial biogenesis [39,40]. ...
Exercise performance and zinc administration individually yield a protective effect on various neurodegenerative models, including ischemic brain injury. Therefore, this work was aimed at evaluating the combined effect of subacute prophylactic zinc administration and swimming exercise in a transient cerebral ischemia model. The prophylactic zinc administration (2.5 mg/kg of body weight) was provided every 24 h for four days before a 30 min common carotid artery occlusion (CCAO), and 24 h after reperfusion, the rats were subjected to swimming exercise in the Morris Water Maze (MWM). Learning was evaluated daily for five days, and memory on day 12 postreperfusion; anxiety or depression-like behavior was measured by the elevated plus maze and the motor activity by open-field test. Nitrites, lipid peroxidation, and the activity of superoxide dismutase (SOD) and catalase (CAT) were assessed in the temporoparietal cortex and hippocampus. The three nitric oxide (NO) synthase isoforms, chemokines, and their receptor levels were measured by ELISA. Nissl staining evaluated hippocampus cytoarchitecture and Iba-1 immunohistochemistry activated the microglia. Swimming exercise alone could not prevent ischemic damage but, combined with prophylactic zinc administration, reversed the cognitive deficit, decreased NOS and chemokine levels, prevented tissue damage, and increased Iba-1 (+) cell number. These results suggest that the subacute prophylactic zinc administration combined with swimming exercise, but not the individual treatment, prevents the ischemic damage on day 12 postreperfusion in the transient ischemia model.
... The beneficial effects of exercise training on the skeletal muscle are well-established [20,21]. Regular exercise promotes skeletal muscle functional adaptations including mitochondrial biogenesis, followed by increased antioxidant capacity [22,23]. The alterations in muscle phenotype induced by exercise are responsible for muscle protection against stress and more specifically, against doxorubicin-induced atrophy [23,24]. ...
Doxorubicin is an anti-neoplasmic drug that prevents DNA replication but induces senescence and cellular toxicity. Intensive research has focused on strategies to alleviate the doxorubicin-induced skeletal myotoxicity. The aim of the present review is to critically discuss the relevant scientific evidence about the role of exercise and growth factor administration and offer novel insights about newly developed-tools to combat the adverse drug reactions of doxorubicin treatment on skeletal muscle. In the first part, we discuss current data and mechanistic details on the impact of doxorubicin on skeletal myotoxicity. We next, review key aspects about the role of regular exercise and the impact of growth factors either administered pharmacologically or via genetic interventions. Future strategies such as combination of exercise and growth factor administration remain to be established to combat the pharmacologically-induced myotoxicity.
... This may be related to the larger stroke force and power produced by short-distance competitors compared to long-distance competitors, as shown in the study by Petrovic et al. [17]. Skeletal muscle is a highly malleable tissue capable of adapting in response to exercise, which may vary between endurance and resistance exercises, and the volume, intensity and frequency of exercise [32]. Therefore, training-induced adaptations in skeletal muscles are different between athletes from different sports or different specializations within their sport [26,[33][34][35][36]. Methentis et al. [33] conducted a fiber-level analysis of the difference in muscle morphology of differently trained individuals and whether muscle morphology is associated with the rate of force development. ...
This study determined to what degree anthropometrics and body composition are associated with force and power outputs of a single-stroke kayak test (SSKT). Body height (BH), sitting height, biacromial distance, arm span, stroke length, body mass index (BMI), percent of skeletal muscle mass (PSMM), skeletal muscle mass index (SMMI), percent body fat (PBF) and maximal and relative force (SSKTFmax and SSKTFrel) and power (SSKTPmax and SSKTPrel) of the SSKT were assessed in 21 male kayak competitors, including sprint specialists and long-distance specialists. Correlation analysis established the association (p < 0.05) between SSKTFmax and BM (r = 0.511), BMI (r = 0.495) and SMMI (r = 0.530). A significant correlation (p < 0.05) also occurred between SSKTPmax and BMI (r = 0.471) and SMMI (r = 0.489). Regression analysis determined a significant association of the anthropometrics-body composition model of kayakers with SSKTFmax (R 2 = 0.790), SSKTFRel (R 2 = 0.748), SSKTPmax (R 2 = 0.676) and SSKTPrel (R 2 = 0.625). A longer and wider upper body supported by higher amounts of skeletal muscle mass per square of body size provides higher force outcomes in a complex single-handed SSKT, while the PSMM provides higher outcomes in SSKTPmax.
... Physical exercise directly benefits skeletal muscle metabolism and systemic energy homeostasis [5]. The adaptation of skeletal muscles to exercise involves muscle contraction via molecular pathways coupled to adenosine 5 -triphosphate (ATP) biosynthesis along with energy expenditure, which is achieved by the activation of various sensors such as mitogen-activated protein kinases (MAPKs), sirtuins (SIRTs), and adenosine monophosphate (AMP)-activated protein kinase (AMPK) [6][7][8]. The exercise-induced stimulus is then transduced to downstream transcription factors of the target genes associated with glucose and lipid metabolism, as well as mitochondrial biogenesis. ...
The microbiome has emerged as a key player contributing significantly to the human physiology over the past decades. The potential microbial niche is largely unexplored in the context of exercise enhancing capacity and the related mitochondrial functions. Physical exercise can influence the gut microbiota composition and diversity, whereas a sedentary lifestyle in association with dysbiosis can lead to reduced well-being and diseases. Here, we have elucidated the importance of diverse microbiota, which is associated with an individual’s fitness, and moreover, its connection with the organelle, the mitochondria, which is the hub of energy production, signaling, and cellular homeostasis. Microbial by-products, such as short-chain fatty acids, are produced during regular exercise that can enhance the mitochondrial capacity. Therefore, exercise can be employed as a therapeutic intervention to circumvent or subside various metabolic and mitochondria-related diseases. Alternatively, the microbiome–mitochondria axis can be targeted to enhance exercise performance. This review furthers our understanding about the influence of microbiome on the functional capacity of the mitochondria and exercise performance, and the interplay between them.
... Achievement is a concrete skill or result that can be achieved at a certain time or period. Muray in Beck (1990) and Camera (2016) defines achievement as follows: "to overcome obstacles, to exercise power, to strive to do something difficult as well and as quickly as possible" It means, "the need for achievement is overcoming obstacles, exercising strength, trying to do something difficult as well and as quickly as possible." based on this opinion, the achievements in this study are the results that students in the learning process have achieved. ...
The level of physical fitness during the coronavirus pandemic has become a basic need because exercise can increase immunity and improve physical fitness. Lack of physical activity during a pandemic can increase the risk of disease and obesity. So that the nutritional status increases while it is not accompanied by physical activity in sports students. This study aims to determine the level of physical fitness in terms of its relationship with nutritional status and learning achievement of students of the Sports Science Study Program at the State University of Medan. This research is a correlational study to find the relationship between two or more variables. This study has two independent variables, namely physical fitness and nutritional status, and one dependent variable, namely learning achievement in practical courses. The participants in this study were students following the Physical Fitness training course, amounting to 42 students. The results in this study indicate that there is no significant relationship between nutritional status and student achievement. There is a significant relationship between physical fitness and student achievement. There is a significant relationship between nutritional status and physical fitness with student achievement. Physical fitness contributed to student learning achievement by providing an effective contribution of 39%, while nutritional status was 72.53%.
... Upon initiation of resistance exercise, there is an immediate increase in 'anabolic' kinase activity, including activation of the Akt/S6K pathway. Following energy consumption, redox potentials activate 'metabolic' kinases, such as AMPK, which ultimately enhance muscle function through the regulation of mitochondrial protein synthesis and oxidative capacity [43]. Consistent with our results, miR-193b deficiency enhanced the expression of PDK1 in db/db mice, followed by activation of the Akt/mTOR/S6K pathway, as well as the AMPK signalling pathway, and decreased the expression of MuRF1 and Atrogin-1 (Fig. 5l, m and ESM Fig. 3b). ...
Aims/hypothesis
Type 2 diabetes is associated with a reduction in skeletal muscle mass; however, how the progression of sarcopenia is induced and regulated remains largely unknown. We aimed to find out whether a specific microRNA (miR) may contribute to skeletal muscle atrophy in type 2 diabetes.
Methods
Adeno-associated virus (AAV)-mediated skeletal muscle miR-193b overexpression in C57BLKS/J mice, and skeletal muscle miR-193b deficiency in db/db mice were used to explore the function of miR-193b in muscle loss. In C57BL/6 J mice, tibialis anterior-specific deletion of 3-phosphoinositide-dependent protein kinase-1 (PDK1), mediated by in situ AAV injection, was used to confirm whether miR-193b regulates muscle growth through PDK1. Serum miR-193b levels were also analysed in healthy individuals ( n = 20) and those with type 2 diabetes ( n = 20), and correlations of miR-193b levels with HbA 1c , fasting blood glucose (FBG), body composition, triacylglycerols and C-peptide were assessed.
Results
In this study, we found that serum miR-193b levels increased in individuals with type 2 diabetes and negatively correlated with muscle mass in these participants. Functional studies further showed that AAV-mediated overexpression of miR-193b induced muscle loss and dysfunction in healthy mice. In contrast, suppression of miR-193b attenuated muscle loss and dysfunction in db/db mice. Mechanistic analysis revealed that miR-193b could target Pdk1 expression to inactivate the Akt/mammalian target of rapamycin (mTOR)/p70S6 kinase (S6K) pathway, thereby inhibiting protein synthesis. Therefore, knockdown of PDK1 in healthy mice blocked miR-193b-induced inactivation of the Akt/mTOR/S6K pathway and impairment of muscle growth.
Conclusions/interpretation
Our results identified a previously unrecognised role of miR-193b in muscle function and mass that could be a potential therapeutic target for treating sarcopenia.
Graphical abstract
... Studies involving trained individuals, which link performance with physiological data, are lacking and should be addressed in future studies. Moreover, the individual training status has a significant influence on shortterm and long-term response to a specific training stimulus [89]. Especially in the context of CT, it is a challenge to describe individual performance capabilities [39]. ...
Background
Concurrent training can be an effective and time-efficient method to improve both muscle strength and aerobic capacity. A major challenge with concurrent training is how to adequately combine and sequence strength exercise and aerobic exercise to avoid interference effects. This is particularly relevant for athletes.
Objective
We aimed to examine the acute effects of aerobic exercise on subsequent measures of muscle strength and power in trained male individuals.
Design
We performed a systematic review with meta-analysis.
Data Sources
Systematic literature searches in the electronic databases PubMed, Web of Science, and Google Scholar were conducted up to July 2021.
Eligibility Criteria for Selecting Studies
Studies were included that applied a within-group repeated-measures design and examined the acute effects of aerobic exercise (i.e., running, cycling exercise) on subsequent measures of lower limb muscle strength (e.g., maximal isometric force of the knee extensors) and/or proxies of lower limb muscle power (e.g., countermovement jump height) in trained individuals.
Results
Fifteen studies met the inclusion criteria. Aerobic exercise resulted in moderate declines in muscle strength (standardized mean difference [SMD] = 0.79; p = 0.003). Low-intensity aerobic exercise did not moderate effects on muscle strength (SMD = 0.65; p = 0.157) while moderate-to-high intensity aerobic exercise resulted in moderate declines in muscle strength (SMD = 0.65; p = 0.020). However, the difference between subgroups was not statistically significant ( p = 0.979). Regarding aerobic exercise duration, large declines in muscle strength were found after > 30 min (SMD = 1.02; p = 0.049) while ≤ 30 min of aerobic exercise induced moderate declines in muscle strength (SMD = 0.59; p = 0.013). The subgroup difference was not statistically significant ( p = 0.204). Cycling exercise resulted in significantly larger decrements in muscle strength (SMD = 0.79; p = 0.002) compared with running (SMD = 0.28; p = 0.035). The difference between subgroups was statistically significant ( p < 0.0001). For muscle power, aerobic exercise did not result in any statistically significant changes (SMD = 0.04; p = 0.846).
Conclusions
Aerobic exercise induced moderate declines in measures of muscle strength with no statistically significant effects on proxies of muscle power in trained male individuals. It appears that higher compared with lower intensity as well as longer compared with shorter aerobic exercise duration exacerbate acute declines in muscle strength. Our results provide evidence for acute interference effects when aerobic exercies is performed before strength exercises. These findings may help practitioners to better prescribe single training sessions, particularly if environmental and/or infrastructural reasons (e.g., availability of training facilities) do not allow the application of strength training before aerobic exercise.
... Undertaking regular exercise is an established mediator of numerous physiological and psychological health benefits [1]. The specificity of training dictates that physiological and metabolic bodily adaptations after exercise training are dependent on the specific mode, volume and intensity of exercise training practiced [2,3]. Exercise has been traditionally categorized into resistance or endurance/aerobic modalities that typically produce different, and at times, contrasting phenotypic responses from each other [4]. ...
Concurrent training incorporates dual exercise modalities, typically resistance and aerobic-based exercise, either in a single session or as part of a periodized training program, that can promote muscle strength, mass, power/force and aerobic capacity adaptations for the purposes of sports performance or general health/wellbeing. Despite multiple health and exercise performance-related benefits, diminished muscle hypertrophy, strength and power have been reported with concurrent training compared to resistance training in isolation. Dietary protein is well-established to facilitate skeletal muscle growth, repair and regeneration during recovery from exercise. The degree to which increased protein intake can amplify adaptation responses with resistance exercise, and to a lesser extent aerobic exercise, has been highly studied. In contrast, much less focus has been directed toward the capacity for protein to enhance anabolic and metabolic responses with divergent contractile stimuli inherent to concurrent training and potentially negate interference in muscle strength, power and hypertrophy. This review consolidates available literature investigating increased protein intake on rates of muscle protein synthesis, hypertrophy, strength and force/power adaptations following acute and chronic concurrent training. Acute concurrent exercise studies provide evidence for the significant stimulation of myofibrillar protein synthesis with protein compared to placebo ingestion. High protein intake can also augment increases in lean mass with chronic concurrent training, although these increases do not appear to translate into further improvements in strength adaptations. Similarly, the available evidence indicates protein intake twice the recommended intake and beyond does not rescue decrements in selective aspects of muscle force and power production with concurrent training.
... There is broad scientific consensus that long term endurance training causes adaptations of the cardiovascular system (Blomqvist and Saltin, 1983;Hellsten and Nyberg, 2015) and within the exercised skeletal muscles (Egan and Zierath, 2013;Camera et al., 2016). More recently, it has been shown that other organ systems are as well subject to change as a result of chronic endurance exercise. ...
The impact of endurance training on spinal neural circuitries remains largely unknown. Some studies have reported higher H-reflexes in endurance trained athletes and therefore, adaptations within the Ia afferent pathways after long term endurance training have been suggested. In the present study we tested the hypothesis that cyclists ( n = 12) demonstrate higher Hoffmann reflexes (H-reflexes) compared to recreationally active controls ( n = 10). Notwithstanding, highly significant differences in endurance performance (VO 2peak : 60.6 for cyclists vs. 46.3 ml/min/kg for controls ( p < 0.001) there was no difference in the size of the SOL H-reflex between cyclists and controls (H max /M max ratio 61.3 vs. 60.0%, respectively ( p = 0.840). Further analyses of the H and M recruitment curves for SOL revealed a significant steeper slope of the M recruitment curve in the group of cyclists (76.2 ± 3.8° vs. 72.0 ± 4.4°, p = 0.046) without a difference in the H-recruitment curve (84.6 ± 3.0° vs. 85.0 ± 2.8°, p = 0.784) compared to the control group. Cycling is classified as an endurance sport and thus the findings of the present study do not further support the assumption that long-term aerobic training leads to a general increase of the H-reflex. Amongst methodological differences in assessing the H-reflex, the training-specific sensorimotor control of the endurance sport itself might differently affect the responsiveness of spinal motoneurons on Ia-afferent inputs.
... Exercise-induced muscle damage (EIMD) is recognized as the outcome of intense to moderate physical activity (Camera et al., 2016;Chazaud, 2016). This damage manifests itself as a temporary decrease in muscle function, increases in serum creatine kinase (CK) and lactate dehydrogenase (LDH) concentrations, increases in myoglobin and delayed onset muscle soreness (DOMS) . ...
Exercise-induced muscle damage (EIMD) causes increased soreness, impaired function of muscles, and reductions in muscle force. Accumulating evidence suggests the beneficial effects of creatine on EIMD. Nevertheless, outcomes differ substantially across various articles. The main aim of this meta-analysis was to evaluate the effect of creatine on recovery following EIMD. Medline, Embase, Cochrane Library, Scopus, and Google Scholar were systematically searched up to March 2021. The Cochrane Collaboration tool for examining the risk of bias was applied for assessing the quality of studies. Weighted mean difference (WMD), 95% confidence interval (CI), and random-effects model, were applied for estimating the overall effect. Between studies, heterogeneity was examined using the chi-squared and I² statistics. Nine studies met the inclusion criteria. Pooled data showed that creatine significantly reduced creatine kinase (CK) concentration overall (WMD = −30.94; 95% CI: −53.19, −8.69; p = .006) and at three follow-up times (48, 72, and 96 hr) in comparison with placebo. In contrast, effects were not significant in lactate dehydrogenase (LDH) concentration overall (WMD = −5.99; 95% CI: −14.49, 2.50; p = .167), but creatine supplementation leaded to a significant reduction in LDH concentrations in trials with 48 hr measurement of LDH. The current data indicate that creatine consumption is better than rest after diverse forms of damaging and exhaustive exercise or passive recovery. The benefits relate to a decrease in muscle damage indices and improved muscle function because of muscle power loss after exercise.
Practical applications
Creatine supplementation would be effective in reducing the immediate muscle damage that happens <24, 24, 48, 72, and 96 hr post-exercise. In the current meta-analysis, the positive effects of creatine could cause a decrease in CK concentration overall. But, due to high heterogeneity and the medium risk of bias for articles, we suggest that these results are taken into account and the facts are interpreted with caution by the readers.
... One of the defining characteristics of exercise is its ability to initiate a complex assortment of highly coordinated molecular and cellular signaling events, as well as transcriptional regulators, which in turn have profound positive effects on muscle tissue (Bamman et al., 2014). Upon exposure to physical activity demands, muscle responds in a coordinated fashion by initiating various signaling events that drive changes in gene expression of intracellular processes, such as metabolism, alterations in hormone signaling, defense mechanisms against oxidative stress, DNA damage and repair, protein turnover, and muscle remodeling (Phillips et al., 2013;Camera et al., 2016). Thus, customary stimuli by appropriate activity or exercise prompt changes in gene expression, which ultimately results in an integrated physiological and functional adaptation in skeletal muscle and the surrounding soft tissue. ...
Muscle quality (MQ), defined as the amount of strength and/or power per unit of muscle mass, is a novel index of functional capacity that is increasingly relied upon as a critical biomarker of muscle health in low functioning aging and pathophysiological adult populations. Understanding the phenotypical attributes of MQ and how to use it as an assessment tool to explore the efficacy of resistance exercise training interventions that prioritize functional enhancement over increases in muscle size may have implications for populations beyond compromised adults, including healthy young adults who routinely perform physically demanding tasks for competitive or occupational purposes. However, MQ has received far less attention in healthy young populations than it has in compromised adults. Researchers and practitioners continue to rely upon static measures of lean mass or isolated measures of strength and power, rather than using MQ, to assess integrated functional responses to resistance exercise training and physical stress. Therefore, this review will critically examine MQ and the evidence base to establish this metric as a practical and important biomarker for functional capacity and performance in healthy, young populations. Interventions that enhance MQ, such as high-intensity stretch shortening contraction resistance exercise training, will be highlighted. Finally, we will explore the potential to leverage MQ as a practical assessment tool to evaluate function and enhance performance in young populations in non-traditional research settings.
... Most studies examining factors that determine individual responsivity to RET have primarily focused on variability in the anabolic muscle growth response (for review see (Lavin et al., 2019;Camera et al., 2016;Camera, 2018;Sparks, 2017)). Relatively few studies examined physiological mechanisms contributing to the variability in the muscle strength response in older adults (Kostek et al., 2005;Ahtiainen et al., 2016;Marcus et al., 2013;Ivey et al., 2000). ...
Background
Older adults display wide individual variability (heterogeneity) in the effects of resistance exercise training on muscle strength. The mechanisms driving this heterogeneity are poorly understood. Understanding of these mechanisms could permit development of more targeted interventions and/or improved identification of individuals likely to respond to resistance training interventions. Thus, this study assessed potential physiological factors that may contribute to strength response heterogeneity in older adults: neural activation, muscle hypertrophy, and muscle contractility.
Methods
In 24 older adults (72.3 ± 6.8 years), we measured the following parameters before and after 12 weeks of progressive resistance exercise training: i) isometric leg extensor strength; ii) isokinetic (60°/sec) leg extensor strength; iii) voluntary (neural) activation by comparing voluntary and electrically-stimulated muscle forces (i.e., superimposed doublet technique); iv) muscle hypertrophy via dual-energy x-ray absorptiometry (DXA) estimates of regional lean tissue mass; and v) intrinsic contractility by electrically-elicited twitch and doublet torques. We examined associations between physiological factors (baseline values and relative change) and the relative change in isometric and isokinetic muscle strength.
Results
Notably, changes in quadriceps contractility were positively associated with the relative improvement in isokinetic (r = 0.37–0.46, p ≤ 0.05), but not isometric strength (r = 0.09–0.21). Change in voluntary activation did not exhibit a significant association with the relative improvements in either isometric or isokinetic strength (r = 0.35 and 0.33, respectively; p > 0.05). Additionally, change in thigh lean mass was not significantly associated with relative improvement in isometric or isokinetic strength (r = 0.09 and −0.02, respectively; p > 0.05). Somewhat surprising was the lack of association between exercise-induced changes in isometric and isokinetic strength (r = 0.07).
Conclusions
The strength response to resistance exercise in older adults appears to be contraction-type dependent. Therefore, future investigations should consider obtaining multiple measures of muscle strength to ensure that strength adaptations are comprehensively assessed. Changes in lean mass did not explain the heterogeneity in strength response for either contraction type, and the data regarding the influence of voluntary activation was inconclusive. For isokinetic contraction, the strength response was moderately explained by between-subject variance in the resistance-exercise induced changes in muscle contractility.
... Confirmation of adequate statistical power was determined a priori from the applied statistical test, mean, SD, and effect size on primary variable markers, which included: (1) gastrointestinal integrity (ie, plasma I-FABP), function (ie, breath hydrogen), and GIS 10,15-17 ; (2) circulating leukocyte, endotoxin, and cytokine profiles 6,8,14,15 ; (3) total body water, plasma osmolality, plasma volume change 6,15 ; (4) rate of skeletal muscle glycogen resynthesis 25,26 ; (5) phosphorylation of intramuscular signaling proteins 27,28 ; and 6) performance. 29,30 Using a standard alpha (.05) and beta value (0.80), the current participant sample size, within a repeated-measures crossover design, is estimated to provide adequate statistical power (power* = 0.80-0.99) ...
Purpose:
This study aimed to determine the effects of an acute "train-low" nutritional protocol on markers of recovery optimization compared to standard recovery nutrition protocol.
Methods:
After completing a 2-hour high-intensity interval running protocol, 8 male endurance athletes consumed a standard dairy milk recovery beverage (CHO; 1.2 g/kg body mass [BM] of carbohydrate and 0.4 g/kg BM of protein) and a low-carbohydrate (L-CHO; isovolumetric with 0.35 g/kg BM of carbohydrate and 0.5 g/kg BM of protein) dairy milk beverage in a double-blind randomized crossover design. Venous blood and breath samples, nude BM, body water, and gastrointestinal symptom measurements were collected preexercise and during recovery. Muscle biopsy was performed at 0 hour and 2 hours of recovery. Participants returned to the laboratory the following morning to measure energy substrate oxidation and perform a 1-hour distance test.
Results:
The exercise protocol resulted in depletion of muscle glycogen stores (250 mmol/kg dry weight) and mild body-water losses (BM loss = 1.8%). Neither recovery beverage replenished muscle glycogen stores (279 mmol/kg dry weight) or prevented a decrease in bacterially stimulated neutrophil function (-21%). Both recovery beverages increased phosphorylation of mTORSer2448 (main effect of time = P < .001) and returned hydration status to baseline. A greater fold increase in p-GSK-3βSer9/total-GSK-3β occurred on CHO (P = .012). Blood glucose (P = .005) and insulin (P = .012) responses were significantly greater on CHO (618 mmol/L per 2 h and 3507 μIU/mL per 2 h, respectively) compared to L-CHO (559 mmol/L per 2 h and 1147 μIU/mL per 2 h, respectively). Rates of total fat oxidation were greater on CHO, but performance was not affected.
Conclusion:
A lower-carbohydrate recovery beverage consumed after exercise in a "train-low" nutritional protocol does not negatively impact recovery optimization outcomes.
... 44 ST stimulates signaling pathways leading to muscle hypertrophy and, consequently, increases muscle strength and power, while in AT, the signaling pathways stimulate an improvement in the aerobic capacity of muscles. 45 The present study demonstrated that CT causes more significant improvements in MS in different muscle groups of patients with T1DM compared with those resulting from AT. In fact, CT may improve many metabolic, neuroendocrine, osteopathic, and neuromuscular processes. ...
Background:
The present study aimed to systematically review the literature on the effects of physical training on neuromuscular parameters in patients with type 1 diabetes mellitus (T1DM).
Methods:
The PubMed, Scopus, EMBASE, and COCHRANE databases were accessed in September 2020. Clinical trials that evaluated the effects of physical training on neuromuscular parameters (maximum strength, resistance strength, muscle power, muscle quality, and muscle thickness) of patients with T1DM compared with a control group were considered eligible. The results were presented as the standardized mean difference with 95% confidence intervals. Effect size (ES) calculations were performed using the fixed effect method, with α = .05.
Results:
Combined training increased the maximum strength levels in individuals with T1DM to a lesser extent than in healthy individuals (ES: 0.363; P = .038). Strength training increased the maximum strength (ES: 1.067; P < .001), as well as combined training (ES: 0.943; P < .001); both compared with aerobic training in patients with T1DM. Strength training increased the maximum strength in a similar magnitude to combined training in patients with T1DM (ES: -0.114; P = .624).
Conclusion:
Both combined training and strength training represent effective strategies for improving the maximum strength in individuals with T1DM.
... Undoubtedly, the constant physical exercise in high performance athletes generates adaptations and changes in their physiological functions [8], that result in metabolic adjustments, which impact the cardiac and pulmonary systems, among others. At a molecular level, this is evident in the phenotypic changes of soft tissues [9], accompanied by the activation or repression of specific signaling in gene expression pathways [10], a relevant aspect when identifying the high rate of sports injuries. Sports injuries depend largely on external and internal factors [11], related to vulnerability to these kind of injuries. ...
Objective To characterize the incidence of sports injuries in weightlifters in the league.
Materials and method. We performed a descriptive correlational study of a sample of 46 athletes with an average age of 18.60 ± 1.96 years, where anthropometric parameters and history of sports injuries were evaluated through a technical sheet. Additionally, the Sit and Reach and Schöberg tests were used, applying descriptive statistics as a comparison of means with Pearson Chi-square (p <0.05). Results Normality was found in the anthropometric parameters, where the predominant lesions were sprains and inflammatory processes in lower and upper limbs. In the same way, high and moderate correlations were observed between the type, the location of the injury, and the relationship between muscle flexibility and muscle stretching time. Conclusions. Injuries in weightlifters indicate a higher prevalence towards sprains and inflammatory processes in the lower limbs, which denotes a greater study in terms of the incidence and association with the heating and stretching processes.
... Confirmation of adequate statistical power was determined a priori from the applied statistical test, mean, standard deviation, and effect size on markers of (1) gastrointestinal integrity (i.e., plasma I-FABP), function (i.e., breath hydrogen), and GIS (Costa et al., 2017aSnipe et al., 2018a,b); (2) circulating leukocyte, endotoxin and cytokine profiles (Costa et al., , 2011; (3) total body water, plasma osmolality, plasma volume change ; (4) rate of skeletal muscle glycogen resynthesis (Betts et al., 2007;Alghannam et al., 2016); (5) phosphorylation of intramuscular signaling proteins (Camera et al., 2015(Camera et al., , 2016; and (6) performance (Oliver et al., 2007). Using a standard alpha (0.05) and beta value (0.80), the current participant sample size, within a repeated measures cross-over design, is estimated to provide adequate statistical power (power * 0.80-0.99) ...
We compared the impact of two different, but commonly consumed, beverages on integrative markers of exercise recovery following a 2 h high intensity interval exercise (i.e., running 70–80% V̇ O 2 max intervals and interspersed with plyometric jumps). Participants ( n = 11 males, n = 6 females) consumed a chocolate flavored dairy milk beverage (CM: 1.2 g carbohydrate/kg BM and 0.4 g protein/kg BM) or a carbohydrate-electrolyte beverage (CEB: isovolumetric with 0.76 g carbohydrate/kg BM) after exercise, in a randomized-crossover design. The recovery beverages were provided in three equal boluses over a 30 min period commencing 1 h post-exercise. Muscle biopsies were performed at 0 h and 2 h in recovery. Venous blood samples, nude BM and total body water were collected before and at 0, 2, and 4 h recovery. Gastrointestinal symptoms and breath hydrogen (H 2 ) were collected before exercise and every 30 min during recovery. The following morning, participants returned for performance assessment. In recovery, breath H 2 reached clinical relevance of >10 ppm following consumption of both beverages, in adjunct with high incidence of gastrointestinal symptoms (70%), but modest severity. Blood glucose response was greater on CEB vs. CM ( P < 0.01). Insulin response was greater on CM compared with CEB ( P < 0.01). Escherichia coli lipopolysaccharide stimulated neutrophil function reduced on both beverages (49%). p-GSK-3β/total-GSK-3β was greater on CM compared with CEB ( P = 0.037); however, neither beverage achieved net muscle glycogen re-storage. Phosphorylation of mTOR was greater on CM than CEB ( P < 0.001). Fluid retention was lower ( P = 0.038) on CEB (74.3%) compared with CM (82.1%). Physiological and performance outcomes on the following day did not differ between trials. Interconnected recovery optimization markers appear to respond differently to the nutrient composition of recovery nutrition, albeit subtly and with individual variation. The present findings expand on recovery nutrition strategies to target functionality and patency of the gastrointestinal tract as a prerequisite to assimilation of recovery nutrition, as well as restoration of immunocompetency.
... In response to skeletal muscle contraction, a multitude of cellular events are initiated that modulate the expression of specific gene sets that encode proteins that ultimately form the basis of adaptation responses [63]. The majority of studies investigating molecular responses to HIIT have focused on pathways regulating mitochondrial biogenesis and insulin sensitivity in skeletal muscle [27]. ...
Exercise training in combination with optimal nutritional support is an effective strategy to maintain or increase skeletal muscle mass. A single bout of resistance exercise undertaken with adequate protein availability increases rates of muscle protein synthesis and, when repeated over weeks and months, leads to increased muscle fiber size. While resistance-based training is considered the ‘gold standard’ for promoting muscle hypertrophy, other modes of exercise may be able to promote gains in muscle mass. High-intensity interval training (HIIT) comprises short bouts of exercise at or above the power output/speed that elicits individual maximal aerobic capacity, placing high tensile stress on skeletal muscle, and somewhat resembling the demands of resistance exercise. While HIIT induces rapid increases in skeletal muscle oxidative capacity, the anabolic potential of HIIT for promoting concurrent gains in muscle mass and cardiorespiratory fitness has received less scientific inquiry. In this review, we discuss studies that have determined muscle growth responses after HIIT, with a focus on molecular responses, that provide a rationale for HIIT to be implemented among populations who are susceptible to muscle loss (e.g. middle-aged or older adults) and/or in clinical settings (e.g. pre- or post-surgery).
... Confirmation of adequate statistical power was determined a priori from the applied statistical test, mean, standard deviation, and effect size on markers of [1] gastrointestinal integrity (i.e., plasma I-FABP), function (i.e., breath hydrogen), and GIS (6,14,22,34); [2] circulating leukocyte, endotoxin and cytokine profiles (5)(6)(7)9); [3] total body water, plasma osmolality, plasma volume change (6, 7); [4] rate of skeletal muscle glycogen resynthesis (35,36); [5] phosphorylation of intramuscular signaling proteins (37)(38)(39); and [6] performance (27,29). Using a standard alpha (0.05) and beta value (0.80), the current participant sample size, within a repeated measures cross-over design, is estimated to provide adequate statistical power (power * 0.80-0.99) ...
This study aimed to determine the effects of flavored dairy milk based recovery beverages of different nutrition compositions on markers of gastrointestinal and immune status, and subsequent recovery optimisation markers. After completing 2 h high intensity interval running, participants ( n = 9) consumed a whole food dairy milk recovery beverage (CM, 1.2 g/kg body mass (BM) carbohydrate and 0.4 g/kg BM protein) or a dairy milk based supplement beverage (MBSB, 2.2 g/kg BM carbohydrate and 0.8 g/kg BM protein) in a randomized crossover design. Venous blood samples, body mass, body water, and breath samples were collected, and gastrointestinal symptoms (GIS) were measured, pre- and post-exercise, and during recovery. Muscle biopsies were performed at 0 and 2 h of recovery. The following morning, participants returned to the laboratory to assess performance outcomes. In the recovery period, carbohydrate malabsorption (breath H 2 peak: 49 vs . 24 ppm) occurred on MBSB compared to CM, with a trend toward greater gut discomfort. No difference in gastrointestinal integrity (i.e., I-FABP and sCD14) or immune response (i.e., circulating leukocyte trafficking, bacterially-stimulated neutrophil degranulation, and systemic inflammatory profile) markers were observed between CM and MBSB. Neither trial achieved a positive rate of muscle glycogen resynthesis [−25.8 (35.5) mmol/kg dw/h]. Both trials increased phosphorylation of intramuscular signaling proteins. Greater fluid retention (total body water: 86.9 vs . 81.9%) occurred on MBSB compared to CM. Performance outcomes did not differ between trials. The greater nutrient composition of MBSB induced greater gastrointestinal functional disturbance, did not prevent the post-exercise reduction in neutrophil function, and did not support greater overall acute recovery.
... In this case the activation of ubiquitin induces acceleration of proteolysis leading to muscle break down, atrophy, and necrosis [278]. Again, drug-and non-drug-induced rhabdomyolysis, have the same mechanisms and responses as those founded during an EIMD situation, specifically of those that are observed during the first 24-48 h post-exercise [14,15,18,21,55,63,65,66,71,72,[74][75][76][77][78][79][80]87,90,93,103,116,117,[120][121][122][123][136][137][138][140][141][142][143][144]146,148,[196][197][198]200,[279][280][281][282][283][284][285]. Therefore, EIMD can be applied in studies investigating the phenotypes that are more prone to rhabdomyolysis or in studies investigating the protective effects of dietary compounds to it. ...
Subclinical, low-grade, inflammation is one of the main pathophysiological mechanisms underlying the majority of chronic and non-communicable diseases. Several methodological approaches have been applied for the assessment of the anti-inflammatory properties of nutrition, however, their impact in human body remains uncertain, because of the fact that the majority of the studies reporting anti-inflammatory effect of dietary patterns, have been performed under laboratory settings and/or in animal models. Thus, the extrapolation of these results to humans is risky. It is therefore obvious that the development of an inflammatory model in humans, by which we could induce inflammatory responses to humans in a regulated, specific, and non-harmful way, could greatly facilitate the estimation of the anti-inflammatory properties of diet in a more physiological way and mechanistically relevant way. We believe that exercise-induced muscle damage (EIMD) could serve as such a model, either in studies investigating the homeostatic responses of individuals under inflammatory stimuli or for the estimation of the anti-inflammatory or pro-inflammatory potential of dietary patterns, foods, supplements, nutrients, or phytochemicals. Thus, in this review we discuss the possibility of exercise-induced muscle damage being an inflammation model suitable for the assessment of the anti-inflammatory properties of diet in humans.
... Дослідження із застосуванням ліпосомальних мембран показали, що, з одного боку, біологічно активні субстанції, що мають прооксидатнтну дію, але захищені саме таким чином, здатні інгібувати індуковане іонами заліза перекисне окиснення ліпідів [32]. Але слід зауважити, що, з іншого боку, окислювальний стрес не надто високої вираженості, властивий фізичним навантаженням помірної інтенсивності, сприяє синтезу оксиду азоту й деякою мірою є позитивним для спорту вищих досягнень [31]. ...
Today, sports anemia occurs in elite sports quite often, although it is not a disease (does not apply to ICD-10), but only a pathological condition. Sports anemia is characterized by changes in the red link of the blood, and it is associated with a decrease in the content of erythrocytes and / or hemoglobin. However, this condition leads to a significant decrease in physical performance, and, consequently, the effectiveness of the competitive activity of representatives, first of all, of cyclic sports. Athletes are more sensitive to the effects of anemia and iron deficiency than people who are not constantly exposed to intense physical activity, since performance depends on the maximum oxygen consumption and utilization of active muscles. Sports anemia is often iron deficient, as well as B12 and folate deficient. Therefore, the assessment of various factors accompanying the development of anemia and the development of technologies for the correction of this pathological condition is an important task of sports laboratory diagnostics, as well as pharmacology and nutritional science of sports. Material and methods. We conducted a randomized, double-blind, placebo-controlled study to assess the safety and effectiveness of the effect of a course use of the Santeferra dietary supplement containing liposomal ferric iron in the form of pyrophosphate, vitamins B9, B12 and ascorbic acid on the results of training activities of representatives of cyclic sports with predominantly an aerobic energy supply mechanism. In the course of a dynamic study, which lasted 60 days, the parameters of hematological homeostasis and accumulation, metabolism and transport of iron (content of serum iron, transferrin, ferritin, folic acid, iron binding capacity of serum, saturation of transferrin with iron), as well as the level of serum erythropoietin and the severity of oxidative stress were assessed directly in the membranes of erythrocytes. In parallel, we determined the indicators of aerobic endurance: the absolute and relative values of the maximum oxygen consumption and the PWC170 value. Results and discussion. We found out that in the study sample of 67 athletes who specialized in sports with aerobic energy supply (running disciplines of athletics, rowing and canoeing, triathlon, cross-country skiing), 19 (28.35%) had manifestations of sports anemia, and 23 (34.32%) had latent iron deficiency, which also negatively effect on their physical performance. The course application of Santefrerra, 1 capsule per day for 60 days, helped to normalize the accumulation, transport and metabolism of iron, as well as to significantly reduce the manifestations of oxidative stress that occurs under the influence of prolonged physical exertion. In athletes with anemia and latent iron deficiency, practically no changes in the content of erythropoietin in the blood serum were found. At the end of the course of taking a dietary supplement, the indicators of the relative maximum oxygen consumption in the athletes of the main group increased by 11.5% (P <0.05) and the results of the PWC170 test by 11.4% (P <0.05) which displays predominantly aerobic endurance. In the placebo-control groups, we noted no positive dynamics in indicators of the red link of hematological homeostasis and the accumulation, metabolism and transport of iron, as well as the parameters of the prooxidant-antioxidant balance directly in the erythrocyte membranes during the 60-day observation period. Indicators of aerobic endurance also remained unchanged. Conclusion. Thus, the course using Santeferra is not accompanied by the development of side effects and is effective for the treatment of iron deficiencies in athletes
... Training is mainly classified as resistance or endurance training, with differing effects depending on exercise type, duration, intensity and frequency. Consequently, athletes need to carefully match the training with their respective objectives [1,2]. Resistance training mainly changes the morphology of skeletal muscle, improves Abbreviations 4E-BP1, 4E-binding protein 1; 4HNE, 4-hydroxynonenal; Akt, protein kinase B; AMPK, AMP-activated protein kinase; EE, endurance exercise; ERK1/2, extracellular signal-regulated kinases 1/2; FoxO1, Forkhead box-containing protein O1; GSK3b, glycogen synthase kinase 3b; LC-3, microtubule-associated protein 1 light chain 3; MAFbx, Muscle Atrophy F-box; MAPK, mitogen-activated protein kinase; mTOR, mechanistic target of rapamycin; MuRF1, Muscle RING-Finger Protein; OL, overload; OL+EE30, OL and EE for 30 min; OL+EE90, OL and EE for 90 min; p70S6K, p70 S6 kinase; PGC-1a, peroxisome proliferator-activated receptor c coactivator-1a; PI3K, phosphoinositide 3-kinase; S6, S6 ribosomal protein S6; VEGF, vascular endothelial growth factor. ...
For many ball games, both resistance and endurance training are necessary to improve muscle strength and endurance capacity. Endurance training has been reported to inhibit muscle strength and hypertrophy, but some studies have reported that endurance exercise (EE) does not inhibit the effects of resistance exercise. Here, we examined the effect of short- or long-duration EE on mouse skeletal muscle hypertrophy induced by functional overload (OL) at the molecular level. Plantaris muscle hypertrophy was induced by OL with synergist ablation in mice. Body mass was reduced with endurance training, but EE duration (30 or 90 min) had no effect. The ratio of plantaris muscle weight to body weight was higher in the OL and EE for 30 min (OL+EE30) and OL and EE for 90 min (OL+EE90) groups compared with the OL group. Expression of mechanistic target of rapamycin signaling proteins, which is related to protein synthesis and hypertrophy, was increased in the OL+EE30 group. Expression of Forkhead box-containing protein O1, which is related to protein breakdown and atrophy, remained unchanged. However, microtubule-associated protein 1 light chain 3, a known marker of autophagy, and MAFbx, which is related to protein breakdown, were significantly increased in the OL+EE90 group. Furthermore, markers of oxidative stress, ubiquitin and 4-hydroxynonenal were also significantly increased in the OL+EE90 group compared with other groups. In conclusion, EE duration did not affect body mass and plantaris mass and did not interfere with mechanistic target of rapamycin signaling, but it did increase ubiquitinated proteins and oxidative stress. It is therefore necessary to consider training durations for EE when combining endurance and resistance training.
... Moreover, research is needed to integrate acute responses to sprint interval exercise with beneficial outcomes (Gibala & Hawley, 2017). One step in this direction would be to monitor acute responses to sprint interval exercise with the use of blood biomarkers, since the cumulative effects of acute exercise sessions are considered to result in chronic responses to training (Camera et al., 2016), a notion that highlights the importance of properly designing single training units. Training sessions should induce sufficient stress (metabolic, cellular, etc.) to provoke adaptations, and exercise intensity is considered an important factor. ...
Purpose: Sprint interval exercise is a time-efficient way of inducing beneficial adaptations. However, little is known about its minimal effective volume, especially in swimming. The aim of the present study was to evaluate and compare the effects of two sprint interval swimming sets of different low volumes on blood biomarkers. Method: Twenty-one master swimmers [11 females aged 38.5 (8.5) years, 10 males aged 42.7 (5.7) years] completed two freestyle swimming sets of 4 × 50 m and 4 × 25 m at maximal intensity and a work-to-rest ratio of 1:1, on different days, in random and counterbalanced order. Blood samples were taken before, immediately after and one hour after exercise for determination of a number of biochemical parameters. Results: Swimming speed was higher in the 4 × 25-m set. Lactate, glucose, insulin, glucagon, cortisol, and reduced glutathione increased immediately post-exercise, while uric acid increased 1 h post-exercise (p < .05). All aforementioned biomarkers, excluding glucagon, increased more with the 4 × 50-m set, compared to the 4 × 25-m set (p < .05). Session rating of perceived exertion was higher after the 4 × 50-m set (p = .011). Conclusion: Both sprint interval swimming sets elicited increases in blood biomarkers in master swimmers. The set of higher volume elicited greater increases in most of the biochemical markers studied but also in subjective load. Thus, although the set of higher volume was more efficient in perturbing blood biomarkers, even the very low-volume set induced metabolic stress that may trigger adaptive mechanisms. ARTICLE HISTORY
... In the present study, a large proportion of participants showed an unfavorable body composition, despite sport participation. In this regard, it is well known that physical exercise and training are potent stimuli that elicit positive adaptation [51][52][53][54][55][56][57][58][59][60]. However, a previous study indicated that youth soccer players might fail to reach the recommended physical activity levels during days without sports practice. ...
The anthropometric profile assessment is an important aspect to consider during the growth stages of youth sport practitioners due to its usefulness in controlling maturity status and overall health. We performed an anthropometric profile evaluation in a sample of youth goalkeepers (n = 42) during a training camp, dividing them into three categories based on their years from peak height velocity (YPHV). We also checked if the selection of goalkeepers was associated with the birth quartile. The results showed that most of the participants’ anthropometric parameters followed the normal trend according to the maturation stages. However, several subjects showed an overweight/obese condition and/or high waist circumference. Non-optimal values were found, mostly in the group of goalkeepers around the PHV. In addition, no selection based on birth quartile was seen. Therefore, the anthropometric profile and body composition of youth goalkeepers are physiologically affected by maturity status. However, several subjects were found to be overweight/obese and at cardiometabolic risk, suggesting that children and adolescents, although practicing sport, should pay attention to potentially contributing factors such as the attainment of the recommended levels of physical activity, lowering sedentary time, and adopt a healthy lifestyle.
... Whilst single gene models might give some insight into how humans respond to exercise Kikuchi & Nakazato, 2015;He et al., 2018), adaptation to exercise is not determined by a single gene. Instead, groups of genes influence the various different cellular pathways (Camera et al., 2016) that control adaptation. By looking at just one gene, such as ACTN3, there is a risk of ignoring the effects of these other genes. ...
Variation between individuals in response to a stimulus is a well-established phenomenon. This thesis discusses the drivers of this inter-individual response, identifying three major determinants; genetic, environmental, and epigenetic variation between individuals. Focusing on genetic variation, the thesis explores how this information may be useful in elite sport, aiming to answer the question “Is there utility to genetic information in elite sport?” The current literature was critically analysed, with a finding that the majority of exercise genomics research explains what has happened previously, as opposed to assisting practitioners in modifying athlete preparation and enhancing performance. An exploration of the potential ways in which genetic information may be useful in elite sport then follows, including that of inter- individual variation in response to caffeine supplementation, the use of genetic information to assist in reducing hamstring injuries, and whether genetic information may help identify future elite athletes. These themes are then explored via empirical work. In the first study, an internet-based questionnaire assessed the frequency of genetic testing in elite athletes, finding that around 10% had undertaken such a test. The second study determined that a panel of five genetic variants could predict the magnitude of improvements in Yo-Yo test improvements following a standardised training programme in youth soccer players. The third study demonstrated the effectiveness of a panel of seven genetic variants in predicting the magnitude of neuromuscular fatigue in youth soccer players. The fourth and final study recruited five current or former elite athletes, including an Olympic Champion, and created the most comprehensive Total Genotype Score in the published literature to date, to determine whether their scores deviated significantly from a control population of over 500 non-athletes. The genetic panels were unable to adequately discriminate the elite performers from non-athletes, suggesting that, at this time, genetic testing holds no utility in the identification of future elite performers. The wider utilisation of genetic information as a public health tool is discussed, and a framework for the implementation of genetic information in sport is also proposed. In summary, this thesis suggests that there is great potential for the use of genetic information to assist practitioners in the athlete management process in elite sport, and demonstrates the efficacy of some commercially available panels, whilst cautioning against the use of such information as a talent identification tool. The major limitation of the current thesis is the low sample sizes of many of the experimental chapters, a common issue in exercise genetics research. Future work should aim to further explore the implementation of genetic information in elite sporting environments.
... [14][15][16] Chronic responses to training are likely the result of cumulative acute effects of individual exercise bouts. 17 Thus, changes in typical acute responses might be reflective of chronic adaptations. Small but meaningful changes in biochemical markers can imply the activation of adaptation-inducing mechanisms, in accordance with the concepts of adaptive homeostasis 18 and hormesis. ...
Purpose:
To evaluate and compare the effects of 2 sprint interval training (SIT) sets of different distances on biochemical markers indicative of metabolism, stress, and antioxidant capacity in competitive swimmers and, to investigate the potential influence of gender on these markers.
Methods:
Twenty-four adolescent, well-trained swimmers (12 men and 12 women) participated in the study. In a random and counterbalanced order, the swimmers completed 2 SIT sets (8 × 50 m and 8 × 25 m) in freestyle with maximal intensity on different days. Work-to-rest ratio was 1:1 in both sets. Blood samples were drawn preexercise, immediately postexercise, and 1 hour postexercise to evaluate the effects of the SIT sets on a number of biochemical parameters.
Results:
Swimming speed was higher at 8 × 25 m. The 2 SIT sets induced significant increases in lactate, glucose, insulin, glucagon, cortisol, and uric acid (P ≤ .001). No differences in these parameters were found between sets, except for irisin (higher in 8 × 50 m; P = .02). Male swimmers were faster and had higher lactate and uric acid concentrations, as well as lower reduced glutathione concentration, than female swimmers (P < .01).
Conclusions:
The 2 swimming SIT sets induced increases in most of the biochemical markers studied. The 2-fold difference between sets in distance did not differentiate the effects of sprint interval exercise on most biochemical parameters. Thus, low-volume SIT sets seem to be effective stimuli for competitive swimmers.
... Endurance-based signals activate stress-sensing pathways such as CAMKII (Ca 2+ /calmodulin-dependent protein kinase II), p38 MAPK (p38 mitogen-activated kinase), AMPK (AMP-dependent kinase), as well as SIRT1. The SIRT1 protein post-translationally modifies PGC-1α, which leads to an oxidative phenotype via the co-activation of nuclear-and mitochondrial-encoded genes (154,155). ...
There are many situations of excessive production of reactive oxygen species (ROS) such as radiation, ischemia/reperfusion (I/R), and inflammation. ROS contribute to and arises from numerous cellular pathologies, diseases, and aging. ROS can cause direct deleterious effects by damaging proteins, lipids, and nucleic acids as well as exert detrimental effects on several cell signaling pathways. However, ROS are important in many cellular functions. The injurious effect of excessive ROS can hypothetically be mitigated by exogenous antioxidants, but clinically this intervention is often not favorable. In contrast, molecular hydrogen provides a variety of advantages for mitigating oxidative stress due to its unique physical and chemical properties. H2 may be superior to conventional antioxidants, since it can selectively reduce ●OH radicals while preserving important ROS that are otherwise used for normal cellular signaling. Additionally, H2 exerts many biological effects, including anti-oxidation, anti-inflammation, anti-apoptosis, and anti-shock. H2 accomplishes these effects by indirectly regulating signal transduction and gene expression, each of which involve multiple signaling pathways and crosstalk. The Keap1-Nrf2-ARE signaling pathway, which can be activated by H2 , plays a critical role in regulating cellular redox balance, metabolism, and inducing adaptive responses against cellular stress. H2 also influences the crosstalk among the regulatory mechanisms of autophagy and apoptosis, which involve MAPKs, p53, Nrf2, NF-κB, p38 MAPK, mTOR, etc. The pleiotropic effects of molecular hydrogen on various proteins, molecules and signaling pathways can at least partly explain its almost universal pluripotent therapeutic potential.
... An alternative explanation could involve the increase in locomotor activity in P3 fasting rats [74,75]. Because exercise is known to result in changes in gene transcription that ultimately improve muscle performance through notably regulation of protein synthesis [76], it is tempting to propose that the increased drive for refeeding in late fasting (P3) triggers an increase in locomotor activity, which in turn induces transcriptional regulations in favor of protein synthesis. ...
Food deprivation resulting in muscle atrophy may be detrimental to health. To better understand how muscle mass is regulated during such a nutritional challenge, the current study deciphered muscle responses during phase 2 (P2, protein sparing) and phase 3 (P3, protein mobilization) of prolonged fasting in rats. This was done using transcriptomics analysis and a series of biochemistry measurements. The main findings highlight changes for plasma catabolic and anabolic stimuli, as well as for muscle transcriptome, energy metabolism, and oxidative stress. Changes were generally consistent with the intense use of lipids as fuels during P2. They also reflected increased muscle protein degradation and repressed synthesis, in a more marked manner during P3 than P2 compared to the fed state. Nevertheless, several unexpected changes appeared to be in favor of muscle protein synthesis during fasting, notably at the level of the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway, transcription and translation processes, and the response to oxidative stress. Such mechanisms might promote protein sparing during P2 and prepare the restoration of the protein compartment during P3 in anticipation of food intake for optimizing the effects of an upcoming refeeding, thereby promoting body maintenance and survival. Future studies should examine relevance of such targets for improving nitrogen balance during catabolic diseases.
... In many sports, athletes aim to output their maximum performance during competitions or games. To consistently achieve this, improving their strength and endurance by as much as possible is crucial (Camera, Smiles, & Hawley, 2016). Skeletal muscle is one of the major tissues wherein the training effects appear most remarkably. ...
Concurrent training involves a combination of two different modes of training. In this study, we conducted an experiment by combining resistance and endurance training. The purpose of this study was to investigate the influence of the order of concurrent training on signal molecules in skeletal muscle. The phosphorylation levels of p70 S6 kinase, S6 ribosomal protein, and 4E-binding protein 1, which are related to hypertrophy signaling, increased significantly in the resistance-endurance order group as compared with in control group not the endurance-resistance order group. The gene expressions related to metabolism were not changed by the order of concurrent training. The mitochondrial respiratory chain complex was evaluated by western blot. Although both groups of concurrent training showed a significant increase in MTCO1, UQCRC2, and ATP5A protein levels, we could not detect a difference based on the order of concurrent training. In conclusion, a concurrent training approach involving resistance training before endurance training on the same day is an effective way to activate both mTOR signaling and mitochondria biogenesis.
It has been proposed for years that physical exercise ameliorates metabolic diseases. Optimal exercise timing in humans and mammals has indicated that circadian clocks play a vital role in exercise and body metabolism. Skeletal muscle metabolism exhibits a robust circadian rhythm under the control of the suprachiasmatic nucleus of the hypothalamus. Clock genes also control the development, differentiation, and function of skeletal muscles. In this review, we aimed to clarify the relationship between exercise, skeletal muscles, and the circadian clock. Health benefits can be attained by the scheduling of exercise at the best circadian time. Exercise therapy for metabolic diseases and cardiovascular health is a key adjuvant method. This review highlights the importance of exercise timing in maintaining healthy metabolism and circadian clocks.
La alta incidencia de lesiones deportivas en atletas de élite es una preocupación en medicina deportiva. Se puede lograr una visión amplia sobre las lesiones deportivas en Colombia y sobre su fisiopatología desde el ámbito de la genómica, la cual podría responder a numerosas lesiones deportivas a partir de la Identificación de polimorfismos de nucleótido único que conducen a discapacidades que afectan la salud de los deportistas y frecuentemente los distancian del campo de juego.
Objetivo:
Determinar la asociación entre polimorfismos de nucleótido único en varios genes con lesiones deportivas en el fútbol.
Materiales y métodos:
Se realizó búsqueda en las bases de datos PubMed, ScienceDirect y EBSCO de estudios publicados en los últimos 6 años hasta enero de 2020, incluyendo estudios en inglés y portugués, correspondientes a estudios clínicos de casos y controles, donde el grupo experimental fueran practicantes de fútbol y los controles fueran personas presumiblemente saludables. Se evaluó la calidad y el sesgo de los artículos finales mediante la escala de puntuación de Jadad o el sistema de puntuación de calidad de Oxford. A partir de los datos obtenidos se identificó la heterogeneidad con la prueba de I2 y el estadístico Q, para la estimación del efecto en los estudios de cohorte se utilizaron odds ratio y valor p< 0.05, obteniendo los forest plot de cada gen. Resultados. 10 de los 1928 estudios fueron seleccionados, se encontró un grado de heterogeneidad en todos los estudios, como el riesgo de lesión de los polimorfismos de nucleótido único para ACNT3 (OR= 0, 98; IC del 95%: 0.64-1.50), MMP (OR …
Recently, evidence derived from different studies has shown that metabolic routes determine the fate of immune cells and impact the immune response, giving rise to an enormous potentially opportunity to treat autoimmunity, cancer, infections or inflammatory diseases. This chapter explores the general metabolic signatures and metabolic drivers of T and B cells from ontogeny, following to activation, functional differentiation, effector functions and finally exhaustion to depicts how the metabolic switching is related with development and functionality of the adaptive immune cells.
In this chapter, we discuss the effects of acute and chronic exercise in metabolic reprograming. The exercise causes considerable systemic disturbance in the homeostasis. However, exercise increases the blood flow and nutrient delivery to the skeletal muscle to supply the energy substrate and oxygen via sustained muscle contraction. The disruption in homeostasis is proportional to the skeletal muscle mass involved in exercise as well as the intensity and duration of exercise. Thus, different types of cells undergo metabolic reprograming for adaptation to exercise. This adaptation starts after one bout of exercise, with increased mRNA expression to supply the new challenges to cells; however, the effects of adaptive reprograming are slow, and it is achieved with continuous exercise training. We focused on the skeletal muscle, adipose tissue, and immune cells adaptations induced by acute and chronic exercises. Exercise training induces an anti-inflammatory milieu and improves cellular metabolism; thus, as we discuss in the following sections, training is an excellent non-pharmacological tool in the treatment of chronic inflammatory diseases.
Skeletal muscle phenotype may influence the response sensitivity of myocellular regulatory mechanisms to contractile activity. To examine this, we employed an ex vivo endurance-type dynamic contraction model to evaluate skeletal muscle phenotype-specific protein signaling responses in rat skeletal muscle. Preparations of slow-twitch soleus and fast-twitch extensor digitorum longus skeletal muscle from 4-wk old female Wistar rats were exposed to an identical ex vivo dynamic endurance-type contraction paradigm consisting of 40 minutes of stretch-shortening contractions under simultaneous low-frequency electrostimulation delivered in an intermittent pattern. Phosphorylation of proteins involved in metabolic signaling and signaling for translation initiation was evaluated at 0, 1, and 4 hours after stimulation by immunoblotting. For both muscle phenotypes, signaling related to metabolic events was upregulated immediately after stimulation, with concomitant absence of signaling for translation-initiation. Signaling for translation-initiation was then activated in both muscle phenotypes at 1-4 hours after stimulation, coinciding with attenuated metabolic signaling. The recognizable pattern of signaling responses support how our ex vivo dynamic muscle contraction model can be utilized to infer a stretch-shortening contraction pattern resembling stretch-shortening contraction of in vivo endurance exercise. Moreover, using this model, we observed that some specific signaling proteins adhering to metabolic events or to translation initation exhibited phosphorylation changes in a phenotype-dependent manner, whereas other signaling proteins exhibited phenotype-independent changes. These findings may aid the interpretation of myocellular signaling outcomes adhering to mixed muscle samples collected during human experimental trials.
In volumetric muscle loss (VML), the severity of trauma ex-ceeds a muscle’s regenerative capacity. VML causes perma-nent functional impairments for which there are norehabilitative, pharmacological, or regenerative medicine in-terventions. Driving failed regeneration in VML is a hostilemicroenvironment characterized by heightened inflammation,fibrosis, and denervation, which may reduce the remainingmuscle tissue’s quality, and stimulate intramuscular adiposetissue (IMAT) expansion. IMAT is increased in various muscledisease states, and has known lipotoxic effects on regenera-tion and contractile function. The contribution of ectopic fatdeposition to the hostile VML microenvironment at the injurysite and in the remaining tissue warrants further investigation.Targeting IMAT may lead to novel therapeutic strategies forimproving functional outcomes in VML.
Abstrak Pandemi Covid-19 beresiko menyebabkan pola sedentary lifestyle dalam kehidupan manusia, namun tidak cukup banyak penelitian terkait perubahan pola aktivitas olahraga yang dilakukan mahasiswa selama pandemi Covid-19. Penelitian ini bertujuan untuk mengetahui perbandingan pola aktivitas olahraga pada mahasiswa fakultas olahraga dan mahasiswa fakultas non-olahraga sebelum dan selama masa pandemi Covid-19. Penelitian menggunakan metode kuantitatif dan disajikan secara deskriptif. Data didapatkan melalui survey online questionnaire dengan menggunakan Google Form yang diisi oleh 573 mahasiswa. Data hasil penelitian dianalisis dengan menggunakan perhitungan persentase dan Wilcoxon test. Simpulan penelitian menunjukkan bahwa terdapat perubahan yang signifikan pola aktivitas olahraga yang meliputi kebiasaan olahraga, frekuensi latihan, dan jenis aktivitas olahraga pada mahasiswa fakultas olahraga dan mahasiswa fakultas non-olahraga pada sebelum dan selama masa pandemi Covid-19 (p < 0,05).
Purpose
Lifelong exercise is known to attenuate sarcopenia (age-associated reduction in muscle mass and function); however, the underlying molecular mechanisms remain unclear. As microRNAs are widely involved in the regulation of skeletal muscle growth and development, we aimed to evaluate the effects of lifelong regular exercise on age-related alterations in muscle microRNA expression profiles as well as on skeletal muscle atrophy, apoptosis, and mitochondria and autophagy dysfunction.
Methods
Female 8-month-old Sprague-Dawley rats were divided into four groups; 1) 18 months of moderate-intensity continuous training (MICT) initiated at 8 months (adult-MICT, n = 12), 2) 8 months of MICT initiated at 18 months (presarcopenia-MICT, n = 12), 3) 8-month-old adult sedentary controls (adult-SED), and 4) 26-month-old aging sedentary controls (old-SED). Age skeletal muscles were then subjected to quantitative reverse transcription–polymerase chain reaction, Kyoto Encyclopedia of Genes and Genomes, immunoblotting, and miR-486 3′ untranslated region luciferase reporter gene analyses.
Results
Age-related loss of miR-486 expression was improved, skeletal muscle atrophy and apoptosis were downregulated, and mitochondrial activity and autophagy were upregulated in the adult-MICT group. Kyoto Encyclopedia of Genes and Genomes analysis revealed that the PI3K/Akt pathway was upregulated in adult-MICT rats compared with that in old-SED. In vitro analyses in rat skeletal muscle L6 cells further confirmed that miR-486 targets PTEN, not SAV1, thereby activating the PI3K/Akt pathway and indirectly inhibiting HIPPO signaling.
Conclusions
Compared with presarcopenia-MICT rats, adult-MICT rats experienced greater beneficial effects regarding ameliorated age-related alterations in muscle miRNA expression profile, skeletal muscle atrophy, apoptosis, and mitochondria and autophagy dysfunction, which is potentially associated with the increased miR-486 expression and concomitant targeting of the PTEN/Akt signaling pathway.
Critical biological processes are under control of the circadian clock. Disruption of this clock, e.g. during aging, results in increased risk for development of chronic disease. Exercise is a protective intervention that elicits changes in both age and circadian pathologies, yet its role in regulating circadian gene expression in peripheral tissues is unknown. We hypothesized that voluntary wheel running would restore disrupted circadian rhythm in aged mice. We analyzed wheel running patterns and expression of circadian regulators in male and female C57Bl/6J mice in adult (~4 months) and old (~18 months) ages. As expected, young female mice ran further than male mice, and old mice ran significantly less than young mice. Older mice of both sexes had a delayed start time in activity which likely points to a disrupted diurnal running pattern and circadian disruption. Voluntary wheel running rescued some circadian dysfunction in older females. This effect was not present in older males, and whether this was due to low wheel running distance or circadian output is not clear and warrants a future study. Overall, we show that voluntary wheel running can rescue some circadian dysfunction in older female but not male mice; and these changes are tissue dependent. While voluntary running was not sufficient to fully rescue age-related changes in circadian rhythm, ongoing studies will determine if forced exercise (e.g. treadmill) and/or chrono-timed exercise can improve age-related cardiovascular, skeletal muscle, and circadian dysfunction.
Elevated plasma homocysteine concentration is a risk factor for cardiovascular disease, which seems to be the main cause of increased mortality in patients with type 2 diabetes. Previous studies have demonstrated the effect of exercise on homocysteine levels and the magnitude of these benefits seems to depend on the type, mode and frequency of training. The present study aimed to compare the effects of aerobic and resistance training on plasma homocysteine in individuals with type 2 diabetes. The study included 15 individuals undergoing aerobic training, 14 subjects undergoing resistance training, and 18 individuals in the control group. Homocysteine, total cholesterol and fractions, glucose, and anthropometric measurements were conducted. The training program lasted 16 weeks. Aerobic training was performed twice a week and lasted 75 min, and resistance training was performed twice a week and lasted 75 min. Homocysteine levels were not significantly different between before and after training. High-density lipoprotein levels increased in both training groups and decreased in the control group. Glucose levels decreased after aerobic and resistance training. Body fat mass (percentage and total) decreased in both training group, but with more expression in the aerobic group. We conclude that 16-week aerobic and resistance training programs did not significantly affect plasma homocysteine levels in patients with type 2 diabetes. Nevertheless, these training programs yielded positive results in HDL control, plasma glucose, and body composition.
Several experimental and human studies documented the preventive and therapeutic effects of exercise on the normal physiological function of different body systems during aging as well as various diseases. Recent studies using cellular and molecular (biochemical, proteomics, and genomics) techniques indicated that exercise modifies intracellular and extracellular signaling and pathways. In addition, in vivo or in vitro experiments, particularly, using knockout and transgenic animals, helped to mimic physiological conditions during and after exercise. According to the findings of these studies, some important signaling pathways modulated by exercise are Ca²⁺-dependent calcineurin/activated nuclear factor of activated T-cells, mammalian target of rapamycin, myostatin/Smad, and AMP-activated protein kinase regulation of peroxisome proliferator-activated receptor-gamma coactivator 1-alpha. Such modulations contribute to cell adaptation and remodeling of muscle fiber type in response to exercise. Despite great improvement in this field, there are still several unanswered questions as well as unfixed issues concerning clinical trials’ biases and limitations. Nevertheless, designing multicenter standard clinical trials while considering individual variability and the exercise modality and duration will improve the perspective we have on the mechanisms mediating adaptation to exercise and final outcomes.
A popular belief is that reactive oxygen species (ROS) and reactive nitrogen species (RNS) produced during exercise by the mitochondria and other subcellular compartments ubiquitously cause skeletal muscle damage, fatigue and impair recovery. However, the importance of ROS/RNS as signals in the cellular adaptation process to stress is now evident. In an effort to combat the perceived deleterious effects of ROS/RNS it has become common practice for active individuals to ingest supplements with antioxidant properties, but interfering with ROS/RNS signalling in skeletal muscle signalling during acute exercise may blunt favorable adaptation. There is building evidence that antioxidant supplementation can attenuate endurance training-induced and ROS/RNS-mediated enhancements in antioxidant capacity, mitochondrial biogenesis, cellular defense mechanisms and insulin sensitivity. However, this is not a universal finding, potentially indicating that there is redundancy in the mechanisms controlling skeletal muscle adaptation to exercise, meaning that in some circumstances the negative impact of antioxidants on acute exercise response can be overcome by training. Antioxidant supplementation has been more consistently reported to have deleterious effects on the response to overload stress and high intensity training suggesting that remodelling of skeletal muscle following resistance and high intensity exercise is more dependent on ROS/RNS signalling. Importantly there is no convincing evidence to suggest that antioxidant supplementation enhances exercise-training adaptions. Overall, ROS/RNS are likely to exhibit a non-linear (hermetic) pattern on exercise adaptations, where physiological doses are beneficial and high exposure (which would seldom be achieved during normal exercise training) may be detrimental. This article is protected by copyright. All rights reserved.
Skeletal muscle is a critical organ serving as the primary site for postprandial glucose disposal and the generation of contractile force. The size of human skeletal muscle mass is dependent upon the temporal relationship between changes in muscle protein synthesis (MPS) and muscle protein breakdown. The aim of this chapter is to review our current understanding of how resistance exercise influences protein turnover with a specific emphasis on the molecular factors regulating MPS. We also will discuss recent data relating to the prescription of resistance exercise to maximize skeletal muscle hypertrophy. Finally, we evaluate the impact of age and periods of disuse on the loss of muscle mass and the controversy surround the etiology of muscle disuse atrophy.
Myogenesis is a crucial process governing skeletal muscle development and homeostasis. Differentiation of primitive myoblasts into mature myotubes requires a metabolic switch to support the increased energetic demand of contractile muscle. Skeletal myoblasts specifically shift from a highly glycolytic state to relying predominantly on oxidative phosphorylation (OXPHOS) upon differentiation. We have found that this phenomenon requires dramatic remodeling of the mitochondrial network involving both mitochondrial clearance and biogenesis. During early myogenic differentiation, autophagy is robustly upregulated and this coincides with DNM1L/DRP1 (dynamin 1-like)-mediated fragmentation and subsequent removal of mitochondria via SQSTM1 (sequestosome 1)-mediated mitophagy. Mitochondria are then repopulated via PPARGC1A/PGC-1α (peroxisome proliferator-activated receptor gamma, coactivator 1 alpha)-mediated biogenesis. Mitochondrial fusion protein OPA1 (optic atrophy 1 [autosomal dominant]) is then briskly upregulated, resulting in the reformation of mitochondrial networks. The final product is a myotube replete with new mitochondria. Respirometry reveals that the constituents of these newly established mitochondrial networks are better primed for OXPHOS and are more tightly coupled than those in myoblasts. Additionally, we have found that suppressing autophagy with various inhibitors during differentiation interferes with myogenic differentiation. Together these data highlight the integral role of autophagy and mitophagy in myogenic differentiation.
Exercise is essential in regulating energy metabolism and whole-body insulin sensitivity. To explore the exercise signaling network, we undertook a global analysis of protein phosphorylation in human skeletal muscle biopsies from untrained healthy males before and after a single high-intensity exercise bout, revealing 1,004 unique exercise-regulated phosphosites on 562 proteins. These included substrates of known exercise-regulated kinases (AMPK, PKA, CaMK, MAPK, mTOR), yet the majority of kinases and substrate phosphosites have not previously been implicated in exercise signaling. Given the importance of AMPK in exercise-regulated metabolism, we performed a targeted in vitro AMPK screen and employed machine learning to predict exercise-regulated AMPK substrates. We validated eight predicted AMPK substrates, including AKAP1, using targeted phosphoproteomics. Functional characterization revealed an undescribed role for AMPK-dependent phosphorylation of AKAP1 in mitochondrial respiration. These data expose the unexplored complexity of acute exercise signaling and provide insights into the role of AMPK in mitochondrial biochemistry.
Autophagy contributes to remodeling of skeletal muscle and is sensitive to contractile activity and prevailing energy availability. We investigated changes in targeted genes and proteins with roles in autophagy following 5 days of energy balance (EB), energy deficit (ED) and resistance exercise (REX) after ED. Muscle biopsies from 15 subjects (8 males, 7 females) were taken at rest following 5 days of EB [45 kcal∙kg fat free mass (FFM)(-1)∙day(-1)] and 5 days of ED (30 kcal∙kg FFM(-1)∙day(-1)). After ED, subjects completed a bout of REX and consumed either placebo (PLA) or 30 g whey protein (PRO) immediately post-exercise. Muscle biopsies were obtained at 1 and 4 h into recovery in each trial. Resting protein levels of autophagy-related gene protein 5 (Atg5) decreased after ED compared to EB (~23%, P<0.001) and remained below EB from 1-4 h post-exercise in PLA (~17%) and at 1 h in PRO (~18%, P<0.05). In addition, conjugated Atg5 (cAtg12) decreased below EB in PLA at 4 h (~20, P<0.05); however its values were increased above this time point in PRO at 4 h alongside increases in FOXO1 above EB (~22-26%, P<0.05). Notably, these changes were subsequent to increases in unc-51 like kinase 1Ser757 phosphorylation (~60%) 1 h post-exercise in PRO. No significant changes in gene expression of selected autophagy markers were found, but EGR-1 increased above ED and EB in PLA (~417-864%) and PRO (~1417-2731%) trials 1 h post-exercise (P<0.001). Post-exercise protein availability, compared to placebo, can selectively promote autophagic responses to REX in ED.
Copyright © 2014, American Journal of Physiology - Regulatory, Integrative and Comparative Physiology.
We determined the effects of 'periodized nutrition' on skeletal muscle and whole-body responses to a bout of prolonged exercise the following morning. Seven cyclists completed two trials receiving isoenergetic diets differing in the timing of ingestion: They consumed either 8 g•kg(-1) BM of CHO before undertaking an evening session of high-intensity training (HIT) and slept without eating (FASTED), or 4 g•kg(-1) BM of CHO before HIT then 4 g•kg(-1) BM of CHO before sleeping (FED). The next morning subjects completed 2 h cycling (120SS) while overnight fasted. Muscle biopsies were taken on day 1 (D1) before and 2 h after HIT and on Day 2 (D2) pre-, post-, and 4 h after 120SS. Muscle [glycogen] was higher in FED at all times post-HIT (P< 0.001). HIT increased PGC1α mRNA (P< 0.01) while PDK4 mRNA was elevated to a greater extent in FASTED (P< 0.05). Resting phosphorylation of AMPK(Thr172), p38MAPK(Thr180/Tyr182) and p-ACC(Ser79) (D2) was greater in FASTED (P< 0.05). Fat oxidation during 120SS was higher in FASTED (P< 0.01) coinciding with increases in ACC(Ser79) and CPT1, as well as mRNA expression of CD36 and FABP3 (P< 0.05). Methylation on the gene promoter for COX4I1 and FABP3 increased 4 h after 120SS in both trials, while methylation of the PPARδ promoter increased only in FASTED. We provide evidence for shifts in DNA methylation that correspond with inverse changes in transcription for metabolically adaptive genes, although delaying post-exercise feeding failed to augment markers of mitochondrial biogenesis.
Copyright © 2014, Journal of Applied Physiology.
To test the hypothesis that antioxidants can attenuate high-intensity interval training-induced improvements in exercise performance.
Two groups of recreationally active males performed a high-intensity interval running protocol, four times per week for 4 wk. Group 1 (n = 8) consumed 1 g of vitamin C daily throughout the training period, whereas Group 2 (n = 7) consumed a visually identical placebo. Pre- and posttraining, subjects were assessed for VO2max, 10 km time trial, running economy at 12 km/h and distance run on the YoYo intermittent recovery tests level 1 and 2 (YoYoIRT1/2). Subjects also performed a 60 min run before and after training at a running velocity of 65% of pretraining VO2max so as to assess training-induced changes in substrate oxidation rates.
Training improved (P < .0005) VO2max, 10 km time trial, running economy, YoYoIRT1 and YoYoIRT2 in both groups, although there was no difference (P = .31, 0.29, 0.24, 0.76 and 0.59) between groups in the magnitude of training-induced improvements in any of the aforementioned parameters. Similarly, training also decreased (P < .0005) mean carbohydrate and increased mean fat oxidation rates during submaximal exercise in both groups, although no differences (P = .98 and 0.94) existed between training conditions.
Daily oral consumption of 1 g of vitamin C during a 4 wk high-intensity interval training period does not impair training-induced improvements in the exercise performance of recreationally active males.
Macroautophagy (autophagy) is a critical cellular stress response; however, the signal transduction pathways controlling autophagy induction in response to stress are poorly understood. Here we reveal a new mechanism of autophagy control whose deregulation disrupts mitochondrial integrity and energy homeostasis in vivo. Stress conditions including hypoxia and exercise induce reactive oxygen species (ROS) through upregulation of a protein complex involving REDD1, an mTORC1 inhibitor and the pro-oxidant protein TXNIP. Decreased ROS in cells and tissues lacking either REDD1 or TXNIP increases catalytic activity of the redox-sensitive ATG4B cysteine endopeptidase, leading to enhanced LC3B delipidation and failed autophagy. Conversely, REDD1/TXNIP complex expression is sufficient to induce ROS, suppress ATG4B activity and activate autophagy. In Redd1-/- mice, deregulated ATG4B activity and disabled autophagic flux cause accumulation of defective mitochondria, leading to impaired oxidative phosphorylation, muscle ATP depletion and poor exercise capacity. Thus, ROS regulation through REDD1/TXNIP is physiological rheostat controlling stress-induced autophagy.
In humans, nutrient deprivation and extreme endurance exercise both activate autophagy. We hypothesized that cumulating fasting and cycling exercise would potentiate activation of autophagy in skeletal muscle. Well-trained athletes were divided into control (n = 8), low-intensity (LI, n = 8), and high-intensity (HI, n = 7) exercise groups and submitted to fed and fasted sessions. Muscle biopsy samples were obtained from the vastus lateralis before, at the end, and 1 h after a 2 h LI or HI bout of exercise. Phosphorylation of ULK1(Ser317) was higher after exercise (P < 0.001). In both the fed and the fasted states, LC3bII protein level and LC3bII/I were decreased after LI and HI (P < 0.05), while p62/SQSTM1 was decreased only 1 h after HI (P < 0.05), indicating an increased autophagic flux after HI. The autophagic transcriptional program was also activated, as evidenced by the increased level of LC3b, p62/SQSTM1, GabarapL1, and Cathepsin L mRNAs observed after HI but not after LI. The increased autophagic flux after HI exercise could be due to increased AMP-activated protein kinase α (AMPKα) activity, as both AMPKα(Thr172) and ACC(Ser79) had a higher phosphorylation state after HI (P < 0.001). In summary, the most effective strategy to activate autophagy in human skeletal muscle seems to rely on exercise intensity more than diet.-Schwalm, C., Jamart, C., Benoit, N., Naslain, D., Prémont, C., Prévet, J., Van Thienen, R., Deldicque, L., Francaux, M. Activation of autophagy in human skeletal muscle is dependent on exercise intensity and AMPK activation.
© FASEB.
Alterations in skeletal muscle contractile activity necessitate an efficient remodeling mechanism. In particular, mitochondrial turnover is essential for tissue homeostasis during muscle adaptations to chronic use and disuse. While mitochondrial biogenesis appears to be largely governed by the transcriptional co-activator peroxisome proliferator co-activator 1 alpha (PGC-1α), selective mitochondrial autophagy (mitophagy) is thought to mediate organelle degradation. However, whether PGC-1α plays a direct role in autophagy is currently unclear.
To investigate the role of the co-activator in autophagy and mitophagy during skeletal muscle remodeling, PGC-1α knockout (KO) and overexpressing (Tg) animals were unilaterally denervated, a common model of chronic muscle disuse.
Animals lacking PGC-1α exhibited diminished mitochondrial density alongside myopathic characteristics reminiscent of autophagy-deficient muscle. Denervation promoted an induction in autophagy and lysosomal protein expression in wild-type (WT) animals, which was partially attenuated in KO animals, resulting in reduced autophagy and mitophagy flux. PGC-1α overexpression led to an increase in lysosomal capacity as well as indicators of autophagy flux but exhibited reduced localization of LC3II and p62 to mitochondria, compared to WT animals. A correlation was observed between the levels of the autophagy-lysosome master regulator transcription factor EB (TFEB) and PGC-1α in muscle, supporting their coordinated regulation.
Our investigation has uncovered a regulatory role for PGC-1α in mitochondrial turnover, not only through biogenesis but also via degradation using the autophagy-lysosome machinery. This implies a PGC-1α-mediated cross-talk between these two opposing processes, working to ensure mitochondrial homeostasis during muscle adaptation to chronic disuse.
Chaperone-assisted selective autophagy (CASA) is a tension-induced degradation pathway essential for muscle maintenance. Impairment of CASA causes childhood muscle dystrophy and cardiomyopathy. However, the importance of CASA for muscle function in healthy individuals has remained elusive so far. Here we describe the impact of strength training on CASA in a group of healthy and moderately trained men. We show that strenuous resistance exercise causes an acute induction of CASA in affected muscles to degrade mechanically damaged cytoskeleton proteins. Moreover, repeated resistance exercise during 4 wk of training led to an increased expression of CASA components. In human skeletal muscle, CASA apparently acts as a central adaptation mechanism that responds to acute physical exercise and to repeated mechanical stimulation.
The view of the lysosome as the terminal end of cellular catabolic pathways has been challenged by recent studies showing a central role of this organelle in the control of cell function. Here we show that a lysosomal Ca(2+) signalling mechanism controls the activities of the phosphatase calcineurin and of its substrate TFEB, a master transcriptional regulator of lysosomal biogenesis and autophagy. Lysosomal Ca(2+) release through mucolipin 1 (MCOLN1) activates calcineurin, which binds and dephosphorylates TFEB, thus promoting its nuclear translocation. Genetic and pharmacological inhibition of calcineurin suppressed TFEB activity during starvation and physical exercise, while calcineurin overexpression and constitutive activation had the opposite effect. Induction of autophagy and lysosomal biogenesis through TFEB required MCOLN1-mediated calcineurin activation. These data link lysosomal calcium signalling to both calcineurin regulation and autophagy induction and identify the lysosome as a hub for the signalling pathways that regulate cellular homeostasis.
Physical exercise is a stress that can substantially modulate cellular signaling mechanisms to promote morphological and metabolic adaptations. Skeletal muscle protein and organelle turnover is dependent on two major cellular pathways: FOXO transcription factors that regulate two main proteolytic systems, the ubiquitin-proteasome and the autophagy-lysosome systems, including mitochondrial autophagy, and the MTORC1 signaling associated with protein translation and autophagy inhibition. In recent years, it has been well documented that both acute and chronic endurance exercise can affect the autophagy pathway. Importantly, substantial efforts have been made to better understand discrepancies in the literature on its modulation during exercise. A single bout of endurance exercise increases autophagic flux when the duration is long enough and this response is dependent on nutritional status since autophagic flux markers and mRNA coding for actors involved in mitophagy are more abundant in the fasted state. In contrast, strength and resistance exercises preferentially raise ubiquitin-proteasome system activity and involve several protein synthesis factors, such as the recently characterized DAGK for MTOR activation. In this review, we discuss recent progress on the impact of acute and chronic exercise on cell component turnover systems, with particular focus on autophagy, which until now has been relatively overlooked in skeletal muscle. We especially highlight the most recent studies on the factors that can impact its modulation, including the mode of exercise and the nutritional status, and also discuss the current limitations in the literature in order to encourage further works on this topic.
The goal of this study was to determine whether the mechanical activation of mechanistic target of rapamycin (mTOR) signalling is associated with changes in phosphorylation of tuberous sclerosis complex-2 (TSC2) and targeting of mTOR and TSC2 to the lysosome. As a source of mechanical stimulation, mouse skeletal muscles were subjected to eccentric contractions (ECs). The results demonstrated that ECs induced hyper-phosphorylation of TSC2 and at least part of this increase occurred on residue(s) that fall within RxRxxS/T consensus motif(s). Furthermore, in control muscles, we found that both mTOR and TSC2 are highly enriched at the lysosome. Intriguingly, ECs enhanced the lysosomal association of mTOR and almost completely abolished the lysosomal association of TSC2. Based on these results, we developed a new model that could potentially explain how mechanical stimuli activate mTOR signalling. Furthermore, this is the first study to reveal that the activation of mTOR is associated with the translocation of TSC2 away from the lysosome. Since a large number of signalling pathways rely on TSC2 to control mTOR signalling, our results have potentially revealed a fundamental mechanism via which not only mechanical, but also various other types of stimuli, control mTOR signalling. © 2013 The Authors. The Journal of Physiology
Autophagy is a catabolic pathway that has a fundamental role in the adaptation to fasting and primarily relies on the activity of the endolysosomal system, to which the autophagosome targets substrates for degradation. Recent studies have revealed that the lysosomal–autophagic pathway plays an important part in the early steps of lipid degradation. In this review, we discuss the transcriptional mechanisms underlying co-regulation between lysosome, autophagy, and other steps of lipid catabolism, including the activity of nutrient-sensitive transcription factors (TFs) and of members of the nuclear receptor family. In addition, we discuss how the lysosome acts as a metabolic sensor and orchestrates the transcriptional response to fasting.
AMPK and mTOR play principal roles in governing metabolic programs; however, mechanisms underlying the coordination of the two inversely regulated kinases remain unclear. In this study we found, most surprisingly, that the late endosomal/lysosomal protein complex v-ATPase-Ragulator, essential for activation of mTORC1, is also required for AMPK activation. We also uncovered that AMPK is a residential protein of late endosome/lysosome. Under glucose starvation, the v-ATPase-Ragulator complex is accessible to AXIN/LKB1 for AMPK activation. Concurrently, the guanine nucleotide exchange factor (GEF) activity of Ragulator toward RAG is inhibited by AXIN, causing dissociation from endosome and inactivation of mTORC1. We have thus revealed that the v-ATPase-Ragulator complex is also an initiating sensor for energy stress and meanwhile serves as an endosomal docking site for LKB1-mediated AMPK activation by forming the v-ATPase-Ragulator-AXIN/LKB1-AMPK complex, thereby providing a switch between catabolism and anabolism. Our current study also emphasizes a general role of late endosome/lysosome in controlling metabolic programs.
Purpose:
We determined the effect of protein supplementation on anabolic signaling and rates of myofibrillar and mitochondrial protein synthesis after a single bout of concurrent training.
Methods:
Using a randomized crossover design, eight healthy males were assigned to experimental trials consisting of resistance exercise (8 × 5 leg extension, 80% 1RM) followed by cycling (30 min at approximately 70% V˙O2peak) with either postexercise protein (PRO, 25-g whey protein) or placebo (PLA) ingestion. Muscle biopsies were obtained at rest and at 1 and 4 h after exercise.
Results:
Akt and mTOR phosphorylation increased 1 h after exercise with PRO (175%-400%, P < 0.01) and was different from PLA (150%-300%, P < 0.001). Muscle RING finger 1 and atrogin-1 messenger RNA (mRNA) were elevated after exercise but were higher with PLA compared with those in PRO at 1 h (50%-315%, P < 0.05), whereas peroxisome proliferator-activated receptor gamma coactivator 1-alpha mRNA increased 4 h after exercise (620%-730%, P < 0.001), with no difference between treatments. Postexercise rates of myofibrillar protein synthesis increased above rest in both trials (75%-145%, P < 0.05) but were higher with PRO (67%, P < 0.05), whereas mitochondrial protein synthesis did not change from baseline.
Conclusions:
Our results show that a concurrent training session promotes anabolic adaptive responses and increases metabolic/oxidative mRNA expression in the skeletal muscle. PRO ingestion after combined resistance and endurance exercise enhances myofibrillar protein synthesis and attenuates markers of muscle catabolism and thus is likely an important nutritional strategy to enhance adaptation responses with concurrent training.
Following damage, cells reseal their plasma membrane (PM) and repair the underlying cortical cytoskeleton. While many different proteins have been implicated in cell repair, the potential role of specific lipids has not been explored. Here we report that cell damage elicits rapid formation of spatially organized lipid domains around the damage site, with different lipids concentrated in different domains as a result of both de novo synthesis and transport. One of these lipids-diacylglycerol (DAG)-rapidly accumulates in a broad domain that overlaps the zones of active Rho and Cdc42, GTPases which regulate repair of the cortical cytoskeleton. Formation of the DAG domain is required for Cdc42 and Rho activation and healing. Two DAG targets, protein kinase C (PKC) beta and eta are recruited to cell wounds and play mutually antagonistic roles in the healing process: PKC beta participates in Rho and Cdc42 activation while PKC eta inhibits Rho and Cdc42 activation. The results reveal an unexpected diversity in subcellular lipid domains and the importance of such domains for a basic cellular process.
The myofibrillar protein synthesis (MPS) response to resistance exercise (REX) and protein ingestion during energy deficit (ED) is unknown. We determined, in young men (n=8) and women (n=7), protein signaling, resting post-absorptive MPS during energy balance [EB: 45 kcal•(kg FFM•d)(-1)] and after 5d of ED [30 kcal•(kg FFM•d)(-1)] as well as MPS while in ED after acute REX in the fasted state and with the ingestion of whey protein (15 and 30 g). Post-absorptive rates of MPS were 27% lower in ED than EB (P<0.001), but REX stimulated MPS to rates equal to EB. Ingestion of 15 and 30 g of protein after REX in ED increased MPS ~16 and ~34% above resting EB, (P<0.02). p70 S6K(thr389) phosphorylation increased above EB only with combined exercise and protein intake (~2-7 fold; P<0.05). In conclusion, short-term ED reduces post-absorptive MPS, however, a bout of REX in ED restores MPS to values observed at rest in EB. The ingestion of protein after REX further increases MPS above resting EB in a dose-dependent manner. We conclude that combining REX with increased protein availability after exercise enhances rates of skeletal muscle protein synthesis during short term ED and could, in the long term, preserve muscle mass.
Muscle hypertrophy following resistance training (RT) involves activation of myofibrillar protein synthesis (MPS) to expand the myofibrillar protein pool. The degree of hypertrophy following RT is, however, highly variable and thus we sought to determine the relationship between the acute activation of MPS and RT-induced hypertrophy. We measured MPS and signalling protein activation after the first session of resistance exercise (RE) in untrained men (n = 23) and then examined the relation between MPS with magnetic resonance image determined hypertrophy. To measure MPS, young men (24±1 yr; body mass index = 26.4±0.9 kg•m(2)) underwent a primed constant infusion of L-[ring-(13)C6] phenylalanine to measure MPS at rest, and acutely following their first bout of RE prior to 16 wk of RT. Rates of MPS were increased 235±38% (P<0.001) above rest 60-180 min post-exercise and 184±28% (P = 0.037) 180-360 min post exercise. Quadriceps volume increased 7.9±1.6% (-1.9-24.7%) (P<0.001) after training. There was no correlation between changes in quadriceps muscle volume and acute rates of MPS measured over 1-3 h (r = 0.02), 3-6 h (r = 0.16) or the aggregate 1-6 h post-exercise period (r = 0.10). Hypertrophy after chronic RT was correlated (r = 0.42, P = 0.05) with phosphorylation of 4E-BP1(Thr37/46) at 1 hour post RE. We conclude that acute measures of MPS following an initial exposure to RE in novices are not correlated with muscle hypertrophy following chronic RT.
The aim of the current review is to discuss applications and mechanism of eccentric exercise in training regimes of competitive sports. Eccentric muscle work is important in most sports. Eccentric muscle contractions enhance the performance during the concentric phase of stretch shortening cycles, which is important in disciplines like sprinting, jumping, throwing and running. Muscles activated during lengthening movements can also function as shock absorbers, to decelerate during landings tasks or to precisely deal with high external loading in sports like alpine skiing. Of the few studies available on trained subjects reveal that eccentric training can further enhance maximal muscle strength and power. It can further optimize muscle length for maximal tension development at a greater degree of extension, and has potential to improve muscle coordination during eccentric tasks. In skeletal muscles, these functional adaptations are based on increases in muscle mass, fascicles length, number of sarcomeres and cross sectional area of type II fibers. Identified modalities for eccentric loading in athletic populations involve classical isotonic exercises, accentuated jumping exercises, eccentric overloading exercises and eccentric cycle ergometry. We conclude that eccentric exercise offers a promising training modality to enhance performance and to prevent injuries in athletes. However, further research is necessary to better understand how the neuromuscular system adapts to eccentric loading in athletes.
In this double-blind, randomized, controlled trial we investigated the effects of vitamin C and E supplementation on endurance training adaptations in humans.
Fifty-four young men and women were randomly allocated to receive either 1000 mg vitamin C and 235 mg vitamin E daily or a placebo for 11 weeks. During supplementation, the participants completed an endurance training programme consisting of 3-4 sessions per week (primarily running), divided into high intensity interval sessions (4-6x4-6 minutes; >90% of maximal heart rate (HRmax)) and steady state continuous sessions (30-60 minutes; 70-90% of HRmax). Maximal oxygen uptake (VO2max), submaximal running, and a 20 m shuttle run test were assessed and blood samples and muscle biopsies were collected, before and after the intervention.
The vitamin C and E group increased their VO2max (8±5%) and performance in the 20 m shuttle test (10±11%) to the same degree as the placebo group (8±5% and 14±17%, respectively). However, the mitochondrial marker cytochrome c oxidase subunit IV (COX4; +59±97%) and cytosolic peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1alpha; +19±51%) increased in m. vastus lateralis in the placebo group, but not in the vitamin C and E group (COX4: -13±54%, PGC-1alpha: -13±29%; p≤0.03, between groups). Furthermore, mRNA levels of CDC42 and mitogen-activated protein kinase 1 (MAPK1) in the trained muscle were lower in the vitamin C and E group (p≤0.05, compared to the placebo group).
Daily vitamin C and E supplementation attenuated increases in markers of mitochondrial biogenesis following endurance training. However, no clear interactions were detected for improvements in VO2max and running performance. Consequently, vitamin C and E supplementation hampered cellular adaptions in the exercised muscles, and although this was not translated to the performance tests applied in this study, we advocate caution when considering antioxidant supplementation combined with endurance exercise.
Skeletal muscle plays a fundamental role in mobility, disease prevention, and quality of lif