Créditos da imagem: Marcos Ribolli
O futebol brasileiro tem falado cada vez mais sobre a necessidade de evoluir em termos de gestão, regras de governança e profissionalização de pessoas e processos. Mas é sempre muito difícil materializar os problemas de gestão e do sistema associativo brasileiro usando exemplos separados aqui e ali. Entretanto, na semana passado tivemos um caso recheado de problemas, e que acaba servindo quase como uma aula sobre exemplos de equívocos em clubes de futebol. Trata-se do caso Daniel Alves e São Paulo FC.
Antes de seguir, importante lembrar que quando falo dos problemas do modelo associativo não significa que eles não possam ocorrer no modelo corporativo, nem que não possam ser evitados pelas associações. O ponto é que os problemas do caso estão intimamente ligados às falhas do modelo de controle acionário mais comum no Brasil.
Vamos então elencar uma série de acontecimentos do caso.
O planejamento da contratação
Daniel Alves foi contratado em 2019, na janela de transferência de meio de temporada, saindo do PSG. Com a idade e a performance recente, claramente não teve propostas de clubes relevantes para seguir a carreira em alto nível na Europa. Não é um problema com ele, mas uma característica da indústria: atletas acima de 35 anos que não se chamam Cristiano Ronaldo ou Ibrahimovic tem dificuldades em seguirem em clubes grandes, porque custam caro e já não performam com a mesma intensidade de outros mais jovens.
No futebol brasileiro sempre existe a tese de que “aqui ele sobra” e “se jogar 10% do que já jogou será ótimo”. Papo de torcedor, mas que qualquer modelo de gestão eficiente deveria ignorar. No caso do São Paulo, o clube ainda tinha no elenco atletas como Pato, Hernanes e Juanfran, sempre com custos elevados.
E era uma oportunidade ter um atleta vencedor como Daniel Alves. Mesmo que esportivamente já não estivesse no auge, fizesse parte de um elenco caro e com graves problemas para honrar suas contas. O desejo foi maior que a capacidade de pagamento, que é um tema recorrente no futebol: o financeiro nunca apita no esportivo, mas é sempre chamado a pagar as contas.
Assim, temos o erro 1: contratar sem necessidade e análise, apenas pelo nome.
O pagamento
Precisamos apontar o caso Ronaldo-Corinthians como o maior responsável por inúmeras irresponsabilidades dos dirigentes brasileiros. Trata-se do único caso de sucesso efetivo do marketing pagando as contas do contratado, a partir do relacionamento direto do atleta com os patrocinadores. Mas Ronaldo só tem um! Depois dele houve inúmeras tentativas de contratações onde “buscaremos patrocinadores para ajudar no pagamento”. E isso obviamente nunca acontece, porque não funciona assim.
Depois da farsa da ideia de que contratações são pagas com vendas de camisas – e mesmo com inúmeras análises e reportagens mostrando que isso não é verdade, novamente nessa temporada ouvimos que “o PSG e o Manchester United praticamente pagaram as chegadas de Messi e Cristiano Ronaldo com a venda de camisas” – os dirigentes brasileiros escolheram o “faremos um projeto de marketing para ajudar a pagar a contratação” como a nova ideia brilhante a ser explorada. Pena que ela só existe na cabeça dos dirigentes e no coração dos torcedores desavisados.
Ou seja, erro 2: contratar baseado numa possibilidade de pagamento irreal.
Olho nas conquistas
Não é só a ideia do patrocinador que pagará as contas. Neste caso houve também a teoria de que reforçar o elenco melhora a competitividade, o clube pode conquistar títulos, melhorar sua posição na tabela, e isso significa mais dinheiro para o clube.
Pode acontecer. O próprio São Paulo conseguiu desempenho incomum na Copa do Brasil de 2020 ao chegar à semifinal e ocupar as primeiras posições da Série A do Brasileiro. Mas em 2019 a chegada de Daniel Alves não gerou nenhuma grande evolução, pois em Agosto o clube ocupava a 5ª colocação ao final da 13ª rodada e terminou a competição em 6º lugar.
É comum conversar com os clubes e os dirigentes dizerem que atrasaram salários e pagamentos porque previam conquistar competições, mas não conseguiram. Daí “perdemos” receitas e não foi possível pagar as contas em dia.
Erro 3: contar com desempenho esportivo num negócio tão imprevisível como o futebol. Em outras indústrias o empresário compra uma máquina nova, que produz mais e com menor custo, então é possível planejar aumento de margem. No futebol nem sempre a contratação resolve o problema, mas a conta fica ali pendurada para ser paga.
Elemento invisível: o atleta
Coitado do atleta. Todo mundo sabe que o clube está em dificuldades, com atrasos de todas as formas, dívidas imensas, mas ele vai lá realizar o sonho e jogar no clube do coração, e para isso aceita um salário milionário, acreditando no conto-da-carochinha de que encontrará um patrocinador para pagar sua conta.
Vale para o Daniel Alves e para qualquer atleta que assina contrato com clubes em dificuldades e que sabidamente atrasam salários. É comum, e eles fazem isso porque sabem que depois vem um acordo para pagar os atrasos em 5 anos, e isso se transforma numa poupança para ser recebida no futuro. Já vi casos de atletas que ganham mais de milhão mas recebem R$ 30/40 mil mensais de dois ou três clubes onde jogaram e não receberam, em acordos de longo prazo.
O atleta tem o direito de pedir o quanto quiser, mas tem que começar a saber do risco. E quanto mais ele incentiva este comportamento, menos os dirigentes se emendam.
Erro 4: achar que o atleta é vítima, especialmente em clubes de grande receita. No dia em que atletas e profissionais se recusarem a jogar em clubes que usualmente não honram seus pagamentos em dia, contribuirão muito para a recuperação do futebol.
O atleta veio de graça
Esta é outra ideia que os dirigentes vendem, mas raramente é verdade. No caso do Daniel Alves o jornalista André Plihal divulgou que o clube deve cerca de R$ 15 milhões para o atleta, sendo que R$ 12 milhões são de remuneração e R$ 3 milhões de comissões. Logo, não é “só pelo salário”. Não é à toa que nas dívidas dos clubes que estão nos balanços patrimoniais há muitos valores a serem pagos a agentes. Parte deles são comissões sobre negócios “sem custos”. E isso sem contar as luvas, também comuns.
Erro 5: vender a ideia de que contratações são “sem custo”.
Contratação da gestão anterior
Como o modelo associativo gera trocas de comando de tempos em tempos – normalmente curtos o suficiente para não permitirem projetos de planejamento eficientes – sempre que há a chegada da dita Oposição é comum falar que “pegamos um clube em dificuldade”. É um belo discurso, pena que não real.
Uma associação tem todos os associados e conselheiros como donos. São eles os responsáveis pelas aprovações de contas, pelo controle da gestão, por buscar formas legais e impedir movimentos temerários. E usam sempre o famoso estatuto para dizer que está tudo funcionando.
Associações são “bichos” políticos por natureza, e justamente por isso precisam de pesos e contrapesos para funcionar de maneira eficiente. Se uma associação se arrebenta financeiramente é responsabilidade de todos, seja porque não criaram modelos eficientes de governança e controle, seja porque aprovaram tudo. Mas é conveniente dizer que o problema é dos outros.
Erro número 6: empurrar o problema para o outro. Não resolve nada, e ainda coloca o clube em situação frágil em termos de imagem.
Mas está sempre errado?
Não necessariamente. É possível que os erros acima citados se transformem em acertos. Contratar veteranos nem sempre é um problema, desde que não haja muitos no elenco. Vale o mesmo para atletas caros. O problema não é o salário individual, mas a composição de elencos inchados com salários elevados.
Vale o mesmo para a ideia de reforçar e qualificar o elenco. Aliás, isso é óbvio. O problema é quando o óbvio esportivo não encontra a realidade financeira, nem a do equilíbrio de elenco. Reforça-se o ataque com um atleta caro, mas quem está capenga é a defesa.
Dessa forma os clubes jamais se reestruturam, e seguem empurrando o problema para as próximas gestões, que seguem culpando as anteriores, mas repetindo o comportamento. Os clubes precisam de manuais de gestão, mas não para deixar na estante atrás das câmeras, e sim para lê-los e aplicá-los.









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Moreover, the stimulation of Sirtuin 1 (SIRT1) and NRF2 signaling systems has been documented to mitigate mitochondrial harm and improve kidney activity, proteinuria, histological alterations, and irritation in aged mice. Further research is required to analyze the attainable influence of resveratrol on protein-energy wasting amongst people with CKD. This study supplies the first direct proof of metabolically beneficial effects of Urolithin A in major human skeletal muscle cells.
Delaying fatigue and selling recovery are current analysis priorities in sports medication. Exercise-induced fatigue can be categorized into central and peripheral fatigue, primarily based on the underlying mechanisms2. Research has indicated that extended vigorous exercise depletes power stores, causes extreme metabolite accumulation, disrupts redox balance, and disturbs internal homeostasis, leading to train fatigue and central nervous system imbalance3. The mind, nevertheless, an organ with a excessive oxygen consumption price, is especially susceptible to oxidative stress. Hypoxia, hypoglycemia, and oxidative stress brought on by extreme exercise can lead to damage to the hippocampal neurons, elevated cell dying, and impaired studying and reminiscence. The hippocampus, particularly, is a key space of the mind for studying and memory, grownup neurogenesis and development, and one of the sensitive tissues in the central nervous system.
In the endoplasmic reticulum, the MSTN precursor undergoes dimerization at the C-terminus, forming a posh generally known as promyostatin (proMSTN). This pro-form of MSTN has greater abundance and longevity than its active mature kind, which has a shorter temporal and spatial exercise window [20, 22]. MSTN is activated following the cleavage of its propeptides by bone morphogenetic protein-1 (BMP-1)/tolloid (TLD)-like metalloproteinases at an arginine residue. This motion releases the propeptides from the dimerized GF area, permitting mature MSTN to work together with non-specific activin receptors (ActRII) on the floor of goal cells (i.e., myoblasts) by way of a paracrine pathway [23, 24].
After performing in silico screening, the effects of MIF1 and MIF2 on C2C12 myoblasts had been evaluated, and both peptides were discovered to enhance myoblast proliferation and differentiation by inducing the expression of myogenic marker genes. C2C12 cells had been cultured in progress medium until 70% confluent and the medium was then switched to myogenic differentiation medium supplemented with MSTN-protein, Ac-MIF1 or Ac-MIF2-NH2 for three days. Fusion indices had been calculated for MSTN-protein-treated, Ac-MIF1-treated, Ac-MIF2-NH2-treated, MSTN-protein + Ac-MIF1-treated, and MSTN-protein + Ac-MIF2-NH2-treated cells. These data indicate that Ac-MIF1 and Ac-MIF2-NH2 peptides inhibit the effect of MSTN. Several strategies have been used to develop remedies for SM-related issues, and computational approaches present a powerful technique of designing and growing new therapeutics.
Thus, it might be argued that due to Flex’s unparalleled genetics, he didn’t should work as hard as his bodybuilding friends in order to achieve his success. In his training footage it’s additionally evident that Flex opted for simple workout routines, choosing to make use of workouts just like the leg press instead of squats. Belgian Blue and Piedmontese are two examples of cattle who also have myostatin poor genetics. Okay, you’re having a hard time believing anything I say proper now, however this genuinely is true (check out the references part on the finish of this article if you’re having trust issues).
In a mouse mannequin for rheumatoid arthritis, MSTN is extremely expressed in synovial tissues, and transgenic or antibody inhibition of MSTN ameliorates joint destruction and arthritis severity [149]. Although MSTN inhibition has shown promise in animal fashions for increasing bone mass and improving bone energy, no scientific trials concentrating on orthopedic ailments have been performed. The lately described increase in axon number together with delay in age-related neural degeneration in myostatin null mice have added assist to the investigation of myostatin inhibitors for the remedy of severe neuromuscular issues [54▪,55].
Additional analysis is needed to see if sulfo-polysaccharides or cystoseira canariensis have any helpful effect in humans in response to resistance coaching. Even if MSTN inhibition will increase muscle mass, it does not necessarily translate into improved useful power in muscle losing disorders. While MSTN inhibition could stimulate muscle hypertrophy, its effectiveness in bettering practical power depends closely on synergistic motor neuron activation and mechanical signaling induced by exercise. With Out adequate fusion of newly fashioned myotubes with present muscle fibers, facilitated by neural input, elevated muscle mass may not result in significant useful improvements [108]. This limitation is very related in circumstances like DMD, the place neuromuscular junction vulnerability and decreased neural enter contribute to impaired translation of neurological indicators to skeletal muscular tissues [109]. In distinction, mdx mice usually exhibit strong contractile perform and maintain ambulation all through their lifespan, which may elucidate why MSTN inhibition in these mice can lead to gains in each muscle mass and function [110].
MSTN inhibition is considered to be a doubtlessly effective technique of addressing the issue of muscle loss. Computational methods are widely used to discover novel inhibitors in a fast and cost-effective method, usually through peptide design and compound screening. Normally, peptides are generated primarily based on the 3D constructions of protein complexes (Baig et al., 2018). Peptide fragments are often created from the interacting residues of protein-protein interactions (PPIs), which are central issues in rational drug design (Baig et al., 2016). Computational screening of huge compound collections towards the binding websites of goal proteins usually results in the rapid identification of potential ligands. Virtual screening (VS.) is normally performed using structure- and ligand-based approaches (Baig et al., 2016).
Women usually begin with considerably smaller dosages, no more than 2 milligrammes per day as a place to begin. YK11 isn’t a quick repair for performance enhancement, and it is important to give your physique time to react. After a 4-week YK11 cycle, post-cycle therapy with drugs such as Clomid and Novaldex is beneficial to counteract these results. On its own, epicatechin is not a stimulant, so technically it can be taken at any time of day (provided there aren’t some other stimulants added into your chosen supplement). A lot of users prefer taking it pre-workout to maximize the enhanced vascularization and “pump” effects.
It was hoped that an examination of every dog could presumably be performed by the same investigator (MCH) at Weeks zero and 12; nevertheless, as acknowledged above, this was possible for under 24 dogs (16 canine from the therapy group and eight canines from the placebo group). Nonetheless, given that the canine have been seen solely twice, these assessments additionally lack quantifiable goal measurements. Including a purely quantifiable end result via exercise displays was initially attempted in sixteen dogs, however homeowners discovered these monitors tough to use and the information have been frequently incompatible with reported observed activity. Myostatin inhibitors are currently being investigated preclinically as potential adjunct remedy with these molecules [39▪,42,51–53]. Many approaches are being taken both preclinically and clinically to inhibit the myostatin signaling pathway (Fig. 1).
MSTN-deficient mice have been found to have 2 to three instances the SM mass of wild-type mice, which indicated MSTN acts as a unfavorable regulator of muscle cells in vivo (McPherron et al., 1997). MSTN inhibition can additionally be thought to be a crucial therapeutic target in the context of enhancing muscle strength and insulin sensitivity (Camporez et al., 2016). Myostatin (MSTN), also known as progress and differentiation factor 8 (GFD8), is a member of the remodeling progress issue β (TGF-β) superfamily of signaling proteins, and capabilities as a adverse regulator of skeletal muscle mass. It was first described by McPherron et al. in 1997, where MSTN-knockout mice displayed a super-muscled phenotype.
Another mice-based clinical research suggests that follistatin prevents the method of metastasis in lung and ovarian most cancers. Animal-based trials targeted on this glycoprotein suggest that it considerably improves muscle growth and provides a realm of secondary advantages. Kim and colleagues investigated the effects of the high-fat, high-energy food regimen (HFED) concerning average protein restriction in a rat mannequin. Their findings demonstrated that rats with giant kidney ablation using a high-fat, high-sucrose food plan might usually achieve weight and showed a lower in proteinuria and inhibition of oxidative stress in addition to inflammation in the remnant kidney [97]. Complete RNAs from cells muscle and adipose tissues were extracted using Trizol reagent (Thermo Fisher Scientific, Waltham, MA, USA).
Just Lately, Mak et al. examined the differential impacts of 25(OH)D3 versus 1,25(OH)2D3 repletion in a mice model of CKD. Intraperitoneal administration of 25(OH)D3 or 1,25(OH)2D3 (for 6 weeks) might elevate serum levels of 1,25(OH)2D3 or 25(OH)D3. The 25(OH)D3 could improve lean and fat mass, weight gain, urge for food, and muscle operate, and reduce an elevated resting metabolic rate compared to the 1,25(OH)2D3 repletion. Apart From, 25(OH)D3 decreased adipose tissue browning and enhanced power homeostasis in skeletal muscle and adipose tissue, whereas 1,25(OH)2D3 did present the same effects. Normalization of the molecular pathways linked with muscle fibrosis dysregulated gene expression of regulatory signaling in muscle mass, and muscle expression profile associated to skeletal muscle losing was additionally detected after 25(OH)D3 repletion. Taken all together, they concluded that the repletion of 25(OH)D3 was deemed to be advantageous over 1,25(OH)2D3 via decreasing muscle losing and adipose tissue browning in CKD mice [171].
Each can work to initiate signaling in the physique to advertise fats loss while keeping protein levels intact. GHRP-6, a peptide development hormone secretagogue (GHS), can also be used with follistatin 344 to extend muscle mass, enhanced power in addition to decrease ranges of body fats. One of the research involving mice with no myostatin recorded a 117% enhance in muscle fibers. This implies that follistatin 344 works to increase muscle mass in different methods as nicely. In human subjects, with growing older, SkM levels of myostatin and SA-β-Gal considerably increase (28%, 48%) whereas these of follistatin (30%), MyoD (41%) and myogenin (47%) decrease, adjustments largely in live performance with mouse results (figure 2A-C). Remedy for 7 days with Epi yielded a bilateral increase in hand strength of ~7% which was accompanied by a big increase (49.2 ± 16.6 %) in the ratio of plasma follistatin/myostatin ranges (data not shown).
This may be especially true for individuals utilizing myostatin inhibitors as exercise dietary supplements as an alternative of as a part of a medical remedy for muscular dystrophy or different problems [37]. Whereas the fitness world is abuzz with myostatin inhibitors’ promising muscle growth talents, they’ve therapeutic uses as properly. Myostatin dietary supplements like Follistatin are being researched for their capability to combat conditions like chronic kidney illness, Duchenne muscular dystrophy, spinal muscular atrophy, and combat muscle losing. Many bodybuilders and some scientists imagine that lowering myostatin can enhance muscular development, as nicely as stop growing older and improve total well being.[1] X Reliable Supply PubMed Central Journal archive from the U.S. Nationwide Institutes of Health Go to source Decreasing these ranges may assist folks with medical issues affecting muscle growth, like muscular dystrophy or different losing diseases. To lower myostatin levels, each cardiovascular (aerobic) train as well as resistance coaching (weight training) are useful. Taldefgrobep alfa, developed by Bristol-Meyers-Squibb and later by Biohaven Prescribed Drugs, is a novel anti-MSTN adnectin.
Equally, GYM-329 by Roche is designed to deal with FSHD by binding to latent MSTN, thus blocking its conversion to its mature type [61]. These antibodies are currently undergoing medical trials or awaiting the reporting of outcomes. The majority of clinically examined MSTN inhibitors have been MSTN-based antibodies.
Equally, earlier analysis exhibits that disuse leads to increased myostatin gene expression and signaling in humans25,36,37 and in rodents12,38,39. Nonetheless, much like fasting, disuse atrophy per se occurs even within the absence of practical myostatin signaling44. Additionally, muscle stretch reduces myostatin expression and will increase activation of protein synthesis pathways68,69 and partially counteracts muscle atrophy with unloading70.
Preclinical studies of ACE-083 demonstrated a dramatic increase in muscle mass and strength in wild-type, Charcot-Marie-Tooth disease (CMT), and DMD disease mannequin mice [81]. In a part 1 research, ACE-083 injected in to the rectus femoris muscle of healthy women resulted in approximately a 14.5% increase in local muscle mass however no change in muscle energy [82]. Part 2 research in sufferers with FSHD or CMT also revealed important localized will increase in muscle mass however failed to show any enchancment in muscle operate [83, 84].
This all natural complement is specially formulated to be highly bioavailable, so you take up more of the epicatechin for optimum results. Plus, customers seem to notice a significant difference in their training and appearance. In other words, epicatechin is a type of flavanol, flavanols are a kind of flavanoid, and flavanoids are a type of polyphenol. The primary thing to remember is these are all plant-based pure chemicals that can supply a bunch of benefits for your body. Analysis of post examine questionnaires revealed that subjects tolerated the supplementation protocol well with no stories of medical problems or signs. Myostatin reduces Akt/TORC1/p70S6K signaling, inhibiting myoblast differentiation and myotube size.
After you are accomplished along with your first cycle, take a break and enjoy the adjustments in your physique. You can alternatively use one other supplement before beginning another cycle of follistatin 344. Being an unlawful substance means no mounted dosage guidelines are available, however the general advice is to continuously administer between 50 mcg to one hundred mcg per day for 10 to 30 days. The reconstituted protein must be stored at minus 20 levels however ensure to use it inside 7 days of mixing. This glycoprotein also regulates the process of ovulation as a result of its interplay with granulosa cells to trigger the discharge of progesterone. Follistatin 344 acts on the granulosa cells to trigger the release of progesterone (3). As progesterone is amongst the primary hormones regulating the menstrual cycle, slight fluctuations in the hormonal levels can disturb the whole cycle.
Myostatin is a cytokine that works by inhibiting the proliferation of satellite cells and the differentiation of myoblasts [10]. Analysis in mice has proven that binding or blocking myostatin ends in dramatic increases in body mass, muscle mass, muscle measurement, and power following administration of antibodies which might be particular for the cytokine myostatin [11,12]. To date, just one human examine has administered sulfo-polysaccharides in conjunction with a resistance coaching protocol [13].
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