Does Creatine Supplementation Increase Muscle Strength in Women?

The purpose of this study was to see if creatine supplementation increased muscular strength in women. Ten females were assigned to either a creatine (CG) or a placebo (PG) group with five subjects in each. The study lasted five weeks with one week of pre-testing, three weeks of creatine use which included one week of loading (12-13 g/day for seven days) and two weeks of maintenance (3-4 g/day for 14 days), and one week of post testing. Pre- and post-test strength were measured with a one repetition maximal lift (1RM) on the bench press and the leg press. All subjects were required to perform a 20-minute warm-up before 1RM measurements to help avoid injury. Each subject then completed two warm-up sets with the bench press or leg press to prepare the working muscle for the 1RM test. After warm-up sets, each subject then completed one repetition lifts until their max lift was attained. Subjects were required to rest a minimum of two minutes in between lifts. No subject performed more than four, one repetition lifts. Over the course of the three-week study, all subjects performed similar workout routines. The results of the post-test 1RM values were not significant between the two groups. The CG increased their mean leg press 1RM (70 ± 47.2 lbs.) and mean bench press 1RM (12 ± 2.2 lbs.). The PG increased their mean leg press 1RM (56 ± 12.7 lbs) and mean bench press 1RM (8 ± 2.8 lbs). Although the PG started and ended with a greater 1RM, the CG displayed a larger mean relative average than did the PG. The CG increased their relative average for the bench press and leg press by 11.3% and 18.6%, respectively compared to the PI increases of 6.5%, 13.2%, respectively. It is concluded that three weeks of creatine supplementation in women failed to significantly increase leg press and bench press strength greater than a placebo

Does Creatine Supplementation Increase Muscle Strength in Women?

The purpose of this study was to see if creatine supplementation increased muscular strength in women. Ten females were assigned to either a creatine (CG) or a placebo (PG) group with five subjects in each. The study lasted five weeks with one week of pre-testing, three weeks of creatine use which included one week of loading (12-13 g/day for seven days) and two weeks of maintenance (3-4 g/day for 14 days), and one week of post testing. Pre- and post-test strength were measured with a one repetition maximal lift (1RM) on the bench press and the leg press. All subjects were required to perform a 20-minute warm-up before 1RM measurements to help avoid injury. Each subject then completed two warm-up sets with the bench press or leg press to prepare the working muscle for the 1RM test. After warm-up sets, each subject then completed one repetition lifts until their max lift was attained. Subjects were required to rest a minimum of two minutes in between lifts. No subject performed more than four, one repetition lifts. Over the course of the three-week study, all subjects performed similar workout routines. The results of the post-test 1RM values were not significant between the two groups. The CG increased their mean leg press 1RM (70 ± 47.2 lbs.) and mean bench press 1RM (12 ± 2.2 lbs.). The PG increased their mean leg press 1RM (56 ± 12.7 lbs) and mean bench press 1RM (8 ± 2.8 lbs). Although the PG started and ended with a greater 1RM, the CG displayed a larger mean relative average than did the PG. The CG increased their relative average for the bench press and leg press by 11.3% and 18.6%, respectively compared to the PI increases of 6.5%, 13.2%, respectively. It is concluded that three weeks of creatine supplementation in women failed to significantly increase leg press and bench press strength greater than a placebo

Effects of creatine supplementation on muscle weakness in patients with rheumatoid arthritis

Background and objectives. Patients with rheumatoid arthritis (RA) frequently suffer from muscle weakness. Oral administration of creatine has been shown to improve muscle strength in healthy subjects. The objective of this study was to examine the effect of oral creatine supplementation on muscle weakness, disease activity and activities of daily living in patients with RA. Methods. During a period of 3 weeks, 12 patients with RA were treated with creatine monohydrate (20 g/day for 5 days followed by 2 g/day for 16 days). They were examined on entry and at the end of the study. The patients were investigated clinically, blood and urine samples were obtained, muscle biopsies were performed before and after treatment, muscle strength was determined, and self‐administered patient questionnaires were completed. Results. From all patients we were able to obtain full clinical and questionnaire data, while biopsies were taken from 12 patients at the start and from nine patients at the end of the study. Muscle strength, as determined by the muscle strength index, increased in eight of 12 patients. In contrast, physical functional ability and disease activity did not change significantly. The creatine concentration in serum and skeletal muscle increased significantly, while creatine phosphate and total creatine did not increase in skeletal muscle. The skeletal muscle creatine content was associated with muscle strength at baseline but not after administration of creatine. The changes in muscle strength were not associated with the changes in skeletal muscle creatine or creatine phosphate. Conclusion. Although the skeletal muscle creatine content and muscle strength increased with creatine administration in some patients with RA, a clear clinical benefit could not be demonstrated for this treatment when the patients were considered as one grou

Progressive, Irreversible Loss of Vision: Gyrate Atrophy of the Choroid and Retina

In our highly visual society, a genetic disease that gradually dims one’s vision must be seen as a cruel and debilitating disease. One such disease is the gyrate atrophy of the choroid and retina (GA), an autosomal recessive disease caused by mutations in the gene encoding the mitochondrial enzyme ornithine aminotransferase (OAT). GA is characterized by early onset myopia and night-blindness followed by cataracts and progressive loss of peripheral vision culminating in complete blindness. More than 60 mutations in the gene coding for OAT cause the 150 known cases of GA by an unknown mechanism. Clinical genetic tests are available and should be carried out if there is a family history of the disease, as early dietary restriction of arginine and clinical doses of vitamin B6 slow its progression. Experiments in cultured epidermal keratinocytes show promise towards gene therapy for GA. Future research should be geared towards understanding the molecular basis of GA and finding a permanent cure

Safety of Creatine Supplementation in Active Adolescents and Youth: A Brief Review

Creatine has been extensively researched and is well-supported as one of the most effective dietary supplements available. There is overwhelming support within the literature regarding the ability of creatine to augment performance following short term (5–7 days) and long-duration supplementation periods. There is also strong support for creatine regarding its safety profile and minimal risk for adverse events or any negative influence on markers of clinical health and safety. Recent research has also highlighted the ability of creatine to confer several health-related benefits in select clinical populations in addition to offering cognitive benefits. Creatine is also a popular supplement of choice for adolescent athletes; however, research in this area is extremely limited, particularly when examining the safety and efficacy of creatine supplementation in this population. Therefore, the purpose of this review was to highlight the limited number of studies available in adolescent populations and systematically discuss the topic of safety of creatine supplementation in a younger population

Comparison of Different Forms of Creatine on Creatine Availability, Retention, and Training Adaptations

The purpose of this study was to determine if a buffered creatine monohydrate (KA) that has been purported to promote greater creatine retention and training adaptations with fewer side effects at lower doses is more efficacious than creatine monohydrate (CrM) supplementation in resistance-trained individuals. In a double-blind manner, 36 resistance-trained participants (20.2±2 years, 181±7 cm, 82.1±12 kg, and 14.7±5 % body fat) were randomly assigned to supplement their diet with CrM or KA at two different dosages. Muscle biopsies from the vastus lateralis, fasting blood samples, body weight, DEXA determined body composition, and Wingate Anaerobic Capacity (WAC) tests were performed at 0, 7, and 28-days while 1RM strength tests were performed at 0 and 28-days. Data were analyzed by a repeated measures multivariate analysis of variance (MANOVA) and are presented as mean ± SD changes from baseline after 7 and 28-days, respectively. Muscle free creatine content obtained in a subgroup of 25 participants increased in all groups over time (p=0.03) after 7 and 28-days, respectively, with no significant differences among groups (p=0.46). Although some significant time effects were observed, no significant group x time interactions (p>0.05) were observed in changes in body mass, fat free mass, fat mass, percent body fat, or total body water; bench press and leg press 1RM strength; WAC mean power, peak power, or total work; serum blood lipids, markers of catabolism and bone status, and serum electrolyte status; or, whole blood markers of lymphocytes and red cells. Neither manufacturers recommended doses (1.5 g/d) or KA with equivalent loading (20 g/d for 7-days) and maintenance doses (5 g/d for 21-days) of CrM promoted greater changes in muscle creatine content, body composition, strength, or anaerobic capacity than CrM (20 g/d for 7-days, 5 g/d for 21-days). There was no evidence that supplementing the diet with a buffered form of creatine resulted in fewer side effects than CrM. These findings do not support claims that consuming a buffered form of creatine is a more efficacious and/or safer form of creatine to consume than creatine monohydrate

Sintesi e caratterizzazione di nuovi derivati della creatina per la terapia del deficit del trasportatore SLC6A8 e nuova procedura sintetica per l'ottenimento della fosfocreatina

Parte 1 Il Deficit del trasportatore della creatina \ue8 una rara malattia genetica dovuta al malfunzionamento della proteina denominata SLC6A8 e deputata al trasporto della creatina attraverso le barriere biologiche. Il mancato funzionamento del trasportatore della creatina comporta l\u2019assenza di creatina a livello cerebrale con la conseguenza di gravissimi danni neurologici. La creatina infatti \ue8 una molecola polare che attraversa le barriere biologiche solo per mezzo del suo trasportatore. Ad oggi non esiste nessuna terapia per tale patologia. Una possibilit\ue0 terapeutica potrebbe essere rappresentata da profarmaci della creatina in grado di attraversare le membrane cellulari e la barriera ematoencefalica (BEE) in modo indipendente dal trasportatore della creatina stessa. Questo potrebbe ripristinare il contenuto di creatina all'interno delle cellule nervose. Per raggiungere tale scopo, in questo progetto di tesi, si sono messe a punto due diverse strategie di sviluppo di derivati della creatina: 1. modificare la struttura della creatina in modo tale da ottenere una molecola maggiormente lipofila che possa attraversare le membrane biologiche per diffusione passiva. 2. realizzare derivati ottenuti dalla coniugazione della creatina con molecole che possano utilizzare un trasportatore diverso dall\u2019SLC6A8. I derivati sintetizzati secondo tali strategie sono stati ottenuti in buona resa e caratterizzati mediante HPLC e spettrometria di massa; alcuni di loro sono stati anche valutati dal punto di vista della stabilit\ue0 in mezzo fisiologico e degli effetti neurobiologici.Parte 2 La fosfocreatina esogena viene prodotta con il nome di \u201cNeoton\u201d dalla casa farmaceutica Alfa Wasserman S.p.A. (Italia), e fa parte del gruppo di farmaci metabolici utilizzati nella protezione del miocardio in aggiunta alle soluzioni cardioplegiche. La fosfocreatina infatti esercita un duplice effetto che la rende un potenziale agente terapeutico cardioprotettivo: l\u2019attivit\ue0 di conservazione dell\u2019energia miocardica mediante il ripristino delle riserve di ATP e l\u2019azione protettiva verso le membrane biologiche. Quasi tutti i metodi pubblicati finora per la sintesi della fosfocreatina portano nella maggior parte dei casi ad una molecola ottenuta in bassa resa e dopo molteplici step di purificazione.La bassa resa \ue8 dovuta ad una scarsa reattivit\ue0 dell\u2019agente guanilante utilizzato, soprattutto quando esso \ue8 costituito da un derivato della cianoammide. Parte del lavoro svolto ha riguardato la messa a punto di una metodica alternativa ai metodi convenzionali che ha permesso di ottenere la fosfocreatina in buona resa e purezza.Part 1 Creatine transporter deficiency is a rare hereditary disease due to the loss of function of the SLC6A8 (creatine transporter). Creatine is a polar molecule, able to cross the biological barriers exclusively using its own transporter and therefore this disease causes the lack of cerebral creatine and leads to dramatic neurological symptoms. To date there is no therapy available for this disorder. A therapeutic strategy could be represented by creatine prodrugs able to cross the cellular membranes and the blood brain barrier (BBB) in an independent way from using the creatine transporter and releasing creatine once inside the cells to exert its biological activities. Two different strategies have been developed to synthesized creatine derivatives: 1.The modification of the creatine molecular skeleton in order to obtain more lipophilic prodrugs that could cross the BBB and the biological membranes by passive diffusion. 2. The conjugation of creatine with a molecule able to exploit a different transporter than SLC6A8, i.e. the glucose transporters, creating a chimeric molecule able to use an alternative way The synthesized derivatives have been obtained in high yield and purity and characterized by means of HPLC and mass spectrometry. Some of them have been evaluated for their stability in physiological conditions and neurobiological effects.Part 2 The exogenous phosphocreatine is currently marketed as \u201cNeoton\u201d by Alfa Wasserman Industry S.p.A. (Italy) and is part of the therapy in the myocardial protection in addition to the cardioplegic solutions. Phosphocreatine exerts a twofold effect as a cardioprotective agent: the regeneration of the ATP reserves and the protective effects of the biological membranes. Most of the methods published so far to synthesize phosphocreatine lead to a low-yielded molecule and involve several purification steps. Low yield is due to the poor reactivity of the guanilating agent used, especially when it is a cyanamide derivative. Part of this job was to develop an alternative method to conventional methods ,that allowed to obtain phosphocreatine with good yeld and purity

Creatine Supplementation for Health and Clinical Diseases

Creatine plays a critical role in cellular metabolism, primarily by binding with phosphate to form phosphocreatine (PCr) as well as shuttling high-energy phosphate compounds in and out of the mitochondria for metabolism. Increasing the dietary availability of creatine increases the tissue and cellular availability of PCr, and thereby enhances the ability to maintain high-energy states during intense exercise. For this reason, creatine monohydrate has been extensively studied as an ergogenic aid for exercise, training, and sport. Limitations in the ability to synthesize creatine and transport and/or store dietary creatine can impair metabolism and is a contributor to several disease states. Additionally, creatine provides an important source of energy during metabolically stressed states, particularly when oxygen availability is limited. Thus, researchers have assessed the role of creatine supplementation on health throughout the lifespan, as well as whether creatine availability may improve disease management and/or therapeutic outcomes. This book provides a comprehensive overview of scientific and medical evidence related to creatine's role in metabolism, health throughout the lifespan, and our current understanding of how creatine can promote brain, heart, vascular and immune health; reduce the severity of musculoskeletal and brain injury; and may provide therapeutic benefits in glucose management and diabetes, cancer therapy, inflammatory bowel disease, and post-viral fatigue