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Effects of creatine supplementation on aerobic power and cardiovascular structure and function

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Abstract

This project aimed to determine 1) whether creatine (Cr) supplementation affects cardiovascular structure and function and 2) to examine its effect on aerobic power. Eighteen males undertook aerobic testing on a cycle ergometer and echocardiographic assessment of the heart. The experimental group (N = 9) ingested 20g x day(-1) of Cr for seven days followed by l0g x day(-1) for a further 21 days. The control group (N = 9) followed an identical protocol ingesting a placebo for the same period. Assessment was performed pre-, mid- (seven days) and post-testing (28 days). A MANOVA with repeated measures was used to test for group differences before and after supplementation. The Cr group demonstrated a significant increase in body mass for the pre-mid (1.0 +/- 0.6 kg) and the pre-post (1.5 +/- 0.7 kg) testing occasions. Submaximal VO2 decreased significantly from the pre-mid and pre-post testing occasions by between 4.8% to 11.4% with Cr supplementation at workloads of 75 W and 150 W. Other oxygen consumption measures and exercise time to exhaustion, for the Cr group, showed decreasing trends that approached significance. Additionally, there was a significant pre-post decrease in maximum heart rate of 3.7%. There were no changes in any of the echocardiographic or blood pressure measures for either group. The present results suggest short term Cr supplementation has no detectable negative effect on cardiac structure or function. Additionally, Cr ingestion improves submaximal cycling efficiency. These results suggest that the increase in efficiency may be related to peripheral factors such an increase in muscle phosphocreatine, rather than central changes.

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... Consequently, 41 eligible studies were included for the fulltext screening. Finally, 13 articles were considered to be included in this SRMA, involving 277 participants [37][38][39][40][41][42][43][44][45][46][47][48][49]. Figure 1 displays the information concerning the PRISMA flow diagram. ...
... All relevant information regarding studies meeting the inclusion criteria is summarized in Table 1. Nine studies reported a loading supplementation protocol [37-39, 41, 44-48], while six studies reported a maintenance supplementation protocol [40,42,43,45,48,49]. Two studies started with a loading protocol and continued with the maintenance protocol [45,48]. ...
... Nine studies reported a loading supplementation protocol [37-39, 41, 44-48], while six studies reported a maintenance supplementation protocol [40,42,43,45,48,49]. Two studies started with a loading protocol and continued with the maintenance protocol [45,48]. In the studies that completed the loading supplementation protocol, ingested dosages ranged from 5 g [39] to 30 g per day [47]. ...
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Background There is robust evidence that creatine monohydrate supplementation can enhance short-term high-intensity exercise in athletes. However, the effect of creatine monohydrate supplementation on aerobic performance and its role during aerobic activities is still controversial. Objective The purpose of this systematic review and meta-analysis was to evaluate the supplementation effects of creatine monohydrate on endurance performance in a trained population. Methods The search strategy in this systematic review and meta-analysis was designed following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, and PubMed/MEDLINE, Web of Science, and Scopus databases were explored from inception until 19 May, 2022. Only human experimental trials, controlled with a placebo group, evaluating the effects of creatine monohydrate supplementation on endurance performance in a trained population were analyzed in this systematic review and meta-analysis. The methodological quality of included studies was evaluated using the Physiotherapy Evidence Database (PEDro) scale. Results A total of 13 studies satisfied all the eligibility criteria and were included in this systematic review and meta-analysis. The results for the pooled meta-analysis showed a non-significant change in endurance performance after creatine monohydrate supplementation in a trained population (p = 0.47), with a trivial negative effect (pooled standardized mean difference = − 0.07 [95% confidence interval − 0.32 to 0.18]; I² = 34.75%). Further, after excluding the studies not evenly distributed around the base of the funnel plot, the results were similar (pooled standardized mean difference = − 0.07 [95% confidence interval − 0.27 to 0.13]; I² = 0%; p = 0.49). Conclusions Creatine monohydrate supplementation was shown to be ineffective on endurance performance in a trained population. Clinical Trial Registration The study protocol was registered in the Prospective Register of Systematic Review (PROSPERO) with the following registration number: CRD42022327368.
... It also has a role in increasing glycogen storage with an increase in GLUT4 transporters (Ju et al. 2005;Eijnde et al. 2001) and changes in cell volume with the osmotic effect of Cr (Loon et al. 2004). In addition to its role in the regulation and homeostasis of energy metabolism, CS could improve muscle activation (Da Silva Azevedo et al. 2019) and VO 2 kinetics at the same workloads (Murphy et al. 2005;Hickner et al. 2010), which may be beneficial for endurance performance. Besides its common use in sports, CS has also been evaluated in the elderly and certain pathological conditions (Canete et al. 2006;Carvalho et al. 2012). ...
... All the studies were monocentric. Five studies were conducted in Europe (Germany (Kuethe et al. 2006), Netherlands (Van Loon et al. 2003;Bert O. Eijnde et al. 2003), Poland (Sterkowicz et al. 2012) and Sweden (Balsom et al. 1993 Canete et al. 2006;Villanueva, He, and Schroeder 2014)), and four in Australia (Barnett, Hinds, and Jenkins 1996;Lawrence et al. 1997;Murphy et al. 2005;Reardon et al. 2006). The duration between baseline and after supplementation ranged from 4 (Barnett, Hinds, and Jenkins 1996) to 180 days (Carvalho et al. 2012). ...
... The duration between baseline and after supplementation ranged from 4 (Barnett, Hinds, and Jenkins 1996) to 180 days (Carvalho et al. 2012). The nineteen included studies aimed to evaluate the effect of CS on performance or quality of life in elderly and patients with heart failure (Canete et al. 2006;Carvalho et al. 2012;Kuethe et al. 2006;Villanueva, He, and Schroeder 2014), among which nine studies aimed specifically at assessing aerobic performance (Balsom et al. 1993;Nelson et al. 2000;Murphy et al. 2005;Hickner et al. 2010;Smith et al. 2011;Reardon et al. 2006;Forbes et al. 2017;Graef et al. 2009;Lawrence et al. 1997). Seventeen studies recruited healthy individuals, while two studies recruited patients with heart failure (Carvalho et al. 2012;Kuethe et al. 2006) ( Table 1). ...
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Although creatine supplementation is well-known to increase exercise performance in acute high-intensity exercises, its role in aerobic performance based on VO2max is more controversial. Thus, we performed a systematic review and meta-analysis on the effects of creatine supplementation on VO2max. PubMed, Cochrane, Embase, and ScienceDirect were searched for randomized controlled trials (RCTs) reporting VO2max in creatine supplementation and placebo groups before and after supplementation. We computed a random-effects meta-analysis on VO2max at baseline, within groups following supplementation, on changes on VO2max between groups, and after supplementation between groups. Sensitivity analyses and meta-regression were conducted. We included 19 RCTs for a total of 424 individuals (mean age 30 years old, 82% men). VO2max did not differ at baseline between groups (creatine and placebo). Participants in both groups were engaged in exercise interventions in most studies (80%). Using changes in VO2max, VO2max increased in both groups but increased less after creatine supplementation than placebo (effect size [ES] = −0.32, 95%CI = −0.51 to −0.12, p = 0.002). Comparisons after creatine supplementation confirmed a lower VO2max in the creatine group compared to the placebo group (ES= −0.20, 95%CI = −0.39 to −0.001, p = 0.049). Meta-analysis after exclusion from meta-funnel resulted in similar outcomes in a subgroup of young and healthy participants. Meta-regressions on characteristics of supplementation, physical training, or sociodemographic were not statistically significant. Creatine supplementation has a negative effect on VO2max, regardless of the characteristics of training, supplementation, or population.
... While the HIIT program was effective in improving VO 2PEAK by 9%, creatine supplementation had no further influence on aerobic capacity. These results are in agreement with the few studies that have examined the effects of Cr supplementation on VO 2PEAK [30,[42][43][44]. Cr has been shown to be effective in improving short-duration, intense activities, but few studies have examined the effects of Cr on longer duration, endurance-type activities. ...
... However, in the current study, significant improvements in VT were only observed in the Cr group (16%), although the Pl group demonstrated a trend for improved VT (10%). The increased VT in the Cr group is in agreement with previous studies that demonstrated improved VT following Cr supplementation but without training [30,42,44]. Improved exercise efficiency at submaximal workloads following Cr supplementation may be attributed to an increase in muscle PCr levels, which may augment the ratio of ATP/ADP, stimulating mitochondrial respiration [42] and delaying reliance on anaerobic glycolysis [51,52]. ...
... where creatine supplementation and exercise for a month did not change cardiac structure or function as measured echocardiographically [Murphy et al 2005]. However, Fenning et al [2003] showed increased HW: BW ratios after 6 and 12 weeks of treadmill exercise training (5 days per week, 30 mins per day). ...
... year lowered body weight along with insulin, HbA1c's and cholesterol levels and increased HDL but did not have an effect on systolic blood pressure or heart rate at rest [Loimaala et al 2007]. Murphy et al [2005] presented work which showed that creatine supplementation and exercise in humans had no detectable effects on cardiac structure or function as determined by echocardiography. Resting LVDP, heart rate and coronary flow were not influenced by creatine supplementation in rats [Horn et al 1998]. ...
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ENGLISH ABSTRACT: Background: There has been a dramatic increase in the use of dietary creatine supplementation among sports men and women, and by clinicians as a therapeutic agent in muscular and neurological diseases. The effects of creatine have been studied extensively in skeletal muscle, but knowledge of its myocardial effects is limited. Objectives: To investigate the effects of dietary creatine supplementation with and without exercise on 1) basal cardiac function, 2) susceptibility to ischaemia/reperfusion injury and 3) myocardial protein expression and phosphorylation and 4) mitochondrial oxidative function. Methods: Male Wistar rats were randomly divided into control or creatine supplemented groups. Half of each group was exercise trained by swimming for a period of 8 weeks, 5 days per week. At the end of the 8 weeks the open field test was performed and blood corticosterone levels were measured by RIA to determine whether the swim training protocol had any effects on stress levels of the rats. Afterwards hearts were excised and either freeze-clamped for biochemical and molecular analysis or perfused on the isolated heart perfusion system to assess function and tolerance to ischaemia and reperfusion. Five series of experiments were performed: (i) Mechanical function was documented before and after 20 minutes global ischaemia using the work heart model, (ii) A H2O filled balloon connected to a pressure transducer was inserted into the left ventricle to measure LVDP and ischaemic contracture in the Langendorff model, (iii) The left coronary artery was ligated for 35 minutes and infarct size determined after 30 minutes of reperfusion by conventional TTC staining methods. (iv) Mitochondrial oxidative capacity was quantified. (v) High pressure liquid chromatography (HPLC) and Western Blot analysis were performed on blood and heart tissue for determination of high energy phosphates and protein expression and phosphorylation. Results: Neither the behavioural studies nor the corticosterone levels showed any evidence of stress in the groups investigated. Hearts from creatine supplemented sedentary (33.5 ± 4.5%), creatine supplemented exercised rats (18.22 ± 6.2%) as well as control exercised rats (26.1 ± 5.9%) had poorer aortic output recoveries than the sedentary control group (55.9 ± 4.35% p < 0.01) and there was also greater ischaemic contracture in the creatine supplemented exercised group compared to the sedentary control group (10.4 ± 4.23 mmHg vs 31.63 ± 4.74 mmHg). There were no differences in either infarct size or in mitochondrial oxygen consumption between the groups. HPLC analysis revealed elevated phosphocreatine content (44.51 ±14.65 vs 8.19 ±4.93 nmol/gram wet weight, p < 0.05) as well as elevated ATP levels (781.1 ±58.82 vs 482.1 ±75.86 nmol/gram wet weight, p<0.05) in blood from creatine supplemented vs control sedentary rats. These high energy phosphate elevations were not evident in heart tissue and creatine tranporter expression was not altered by creatine supplementation. GLUT4 and phosphorylated AMPK and PKB/Akt were all significantly higher in the creatine supplemented exercised hearts compared to the control sedentary hearts. Conclusion: This study suggests that creatine supplementation has no effects on basal cardiac function but reduces myocardial tolerance to ischaemia in hearts from exercise trained animals by increasing the ischaemic contracture and decreasing reperfusion aortic output. Exercise training alone also significantly decreased aortic output recovery. However, the exact mechanisms for these adverse myocardial effects are unknown and need further investigation. AFRIKAANSE OPSOMMING: Agtergrond: Die gebruik van kreatien as dieetaanvulling het in die afgelope aantal jaar dramaties toegeneem onder sportlui, sowel as mediese praktisyns wat dit as ‘n terapeutiese middel vir die behandeling van spier- en neurologiese siektes aanwend. Die effekte van kreatien op skeletspier is reeds deeglik ondersoek, maar inligting aangaande die miokardiale effekte van die preperaat is beperk. Doelwitte: Om die effekte van kreatien dieetaanvulling met of sonder oefening ten opsigte van die volgende aspekte te ondersoek: 1) basislyn miokardiale funksie, 2) vatbaarheid vir iskemie/herperfusie besering, 3) proteïenuitdrukking en -fosforilering in die miokardium en 4) mitochondriale oksidatiewe funksie. Metodes: Manlike Wistar rotte is ewekansig in kontrole of kreatien aanvullings groepe verdeel. Helfte van elke groep is aan oefening in die vorm van swemsessies, vir ‘n periode van 8 weke, 5 dae per week blootgestel. Gedrags- en biochemiese toetse is aangewend om die moontlike effek van die swemprotokol op die rotte se stres vlakke te bepaal. In hierdie verband is die oop area toets gebruik, asook bloed kortikosteroon vlakke gemeet deur radioaktiewe immuunessais. Harte is daarna uit die rotte gedissekteer en gevriesklamp vir biochemiese en molekulêre analise, of geperfuseer op die geïsoleerde werkhart perfusiesisteem om sodoende funksie en weerstand teen iskemie en herperfusie beskadeging te bepaal. Vyf eksperimentele reekse is uitgevoer: (i) Meganiese funksie is noteer voor en na 20 minute globale isgemie in die werkhart model; (ii) ‘n Water gevulde plastiek ballon, gekoppel aan ‘n druk omsetter, is in die linker ventrikel geplaas om sodoende linker ventrikulêre ontwikkelde druk (LVDP), asook iskemiese kontraktuur te meet; (iii) Linker koronêre arterie afbinding is vir ‘n periode van 35 minute toegepas en die infarktgrootte bepaal na 30 minute herperfusie deur gebruik te maak van standaard kleuringsmetodes; (iv) Mitochondriale oksidatiewe kapasiteit is gemeet; (v) Hoë druk vloeistof chromatografie (HPLC) en Western Blot analises is uitgevoer op bloed en hartweefsel vir die bepaling van hoë energie fosfate (HEFe), sowel as proteïenuitdrukking en -fosforilering. Resultate: Beide gedragsstudies en kortikosteroonvlakke het geen teken van stres in die betrokke groepe getoon nie. Die groep blootgestel aan kreatienaanvulling en oefening se harte het na iskemie funksioneel swakker herstel as harte van die onaktiewe kontrole groep (18.22±6.2% vs 55.9±4.35%; p<0.01), asook ‘n groter ikgemiese kontraktuur in vergelyking met die onaktiewe kontrole groep ontwikkel (31.63±4.74 mmHg vs 10.4±4.23 mmHg). Daar was geen verskille in infarktgrootte of mitochondriale suurstofverbruik tussen die verskillende groepe waargeneem nie. HPLC analise het verhoogde fosfokreatien (44.51±14.65 vs 8.19±4.93 nmol/gram nat gewig, p<0.05) en adenosientrifosfaat (ATP) bloedvlakke (781.1±58.82 vs 482.1±75.86 nmol/gram nat gewig, p<0.05) in kreatien aanvullings vergelyk met die kontrole groepe getoon. Daar was egter geen meetbare veranderings in HEF vlakke in hartweefsel nie. Gepaardgaande hiermee het kreatienaanvulling geen effek gehad op die uitdrukking va die kreatien transporter nie. In vergelyking met onaktiewe kontrole harte was GLUT4, en fosforileerde AMPK en PKB/ Akt beduidend hoër in harte van geoefende rotte met kreatienaangevulling. Gevolgtrekking: Hierdie data dui daarop dat kreatienaanvulling geen effek op basislyn miokardiale funksie het nie. Kreatienaanvulling het egter die miokardium se weerstand teen iskemiese skade verlaag in harte van rotte blootgestel aan oefening: iskemiese kontraktuur is verhoog en aorta-uitset tydens herperfusie is verlaag. Die presiese meganismes hierby betrokke is egter onbekend en vereis dus verdere studie. Thesis (PhD (Biomedical Sciences. Medical Physiology))--University of Stellenbosch, 2010. Division of Medical Physiology (University of Stellenbosch), The National Research Foundation and the Harry Crossley Fund for financial support.
... 25,26 Further evidence to suggest that cardiopulmonary function during exhaustive exercise was unaffected by creatine supplementation was provided by the similarity in heart rate and net oxygen uptake responses before and after supplementation. In support of this conclusion, most previous studies that evaluate similar outcomes have failed to identify any effect of creatine supplementation on aerobic capacity in healthy [27][28][29][30][31] and diseased populations. [32][33][34] Nevertheless, some studies have demonstrated that creatine supplementation can influence other parameters that have the potential to contribute to improved endurance performance. ...
... [32][33][34] Nevertheless, some studies have demonstrated that creatine supplementation can influence other parameters that have the potential to contribute to improved endurance performance. For example, creatine-induced hyperhydration has been shown to attenuate heart rate responses to prolonged exercise in the heat 26 and creatine supplementation has been demonstrated to increase lactate threshold, 27 improve submaximal effeciency, 31 and enhance peak work capacity at fatigue during discontinuous exercise in elderly participants. 35 It has been repeatedly demonstrated that the current creatine monohydrate supplementation regime is effective in increasing circulatory creatine concentrations 2,3 and pharmacokinetic analysis of plasma creatine concentrations following a 5-g oral bolus of creatine monohydrate showed that plasma creatine decayed with a half-life of approximately 2 h. ...
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Many degenerative diseases are associated with increased oxidative stress. Creatine has the potential to act as an indirect and direct antioxidant; however, limited data exist to evaluate the antioxidant capabilities of creatine supplementation within in-vivo human systems. This study aimed to investigate the effects of oral creatine supplementation on markers of oxidative stress and antioxidant defenses following exhaustive cycling exercise. Following preliminary testing and two additional familiarization sessions, 18 active males repeated two exhaustive incremental cycling trials (T1 and T2) separated by exactly 7 days. The subjects were assigned, in a double-blind manner, to receive either 20 g of creatine (Cr) or a placebo (P) for the 5 days preceding T2. Breath-by-breath respiratory data and heart rate were continually recorded throughout the exercise protocol and blood samples were obtained at rest (preexercise), at the end of exercise (postexercise), and the day following exercise (post24 h). Serum hypdroperoxide concentrations were elevated at postexercise by 17 +/- 5% above pre-exercise values (P = 0.030). However, supplementation did not influence lipid peroxidation (serum hypdroperoxide concentrations), resistance of low density lipoprotein to oxidative stress (t1/2max LDL oxidation) and plasma concentrations of non-enzymatic antioxidants (retinol, alpha-carotene, beta-carotene, alpha-tocopherol, gamma-tocopherol, lycopene, and vitamin C). Heart rate and oxygen uptake responses to exercise were not affected by supplementation. These findings suggest that short-term creatine supplementation does not enhance non-enzymatic antioxidant defence or protect against lipid peroxidation induced by exhaustive cycling in healthy males.
... While the HIIT program was effective in improving VO 2PEAK by 9%, creatine supplementation had no further influence on aerobic capacity. These results are in agreement with the few studies that have examined the effects of Cr supplementation on VO 2PEAK [30,424344. Cr has been shown to be effective in improving short-duration, intense activities, but few studies have examined the effects of Cr on longer duration, endurance-type activities. ...
... However, in the current study, significant improvements in VT were only observed in the Cr group (16%), although the Pl group demonstrated a trend for improved VT (10%). The increased VT in the Cr group is in agreement with previous studies that demonstrated improved VT following Cr supplementation but without training [30,42,44] . Improved exercise efficiency at submaximal workloads following Cr supplementation may be attributed to an increase in muscle PCr levels, which may augment the ratio of ATP/ADP, stimulating mitochondrial respiration [42] and delaying reliance on anaerobic glycolysis [51,52]. ...
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High-intensity interval training has been shown to be a time-efficient way to induce physiological adaptations similar to those of traditional endurance training. Creatine supplementation may enhance high-intensity interval training, leading to even greater physiological adaptations. The purpose of this study was to determine the effects of high-intensity interval training (HIIT) and creatine supplementation on cardiorespiratory fitness and endurance performance (maximal oxygen consumption (VO2PEAK), time-to-exhaustion (VO2PEAKTTE), ventilatory threshold (VT), and total work done (TWD)) in college-aged men. Forty-three recreationally active men completed a graded exercise test to determine VO2PEAK, VO2PEAKTTE, and VT. In addition, participants completed a time to exhaustion (TTE) ride at 110% of the maximum workload reached during the graded exercise test to determine TWD (TTE (sec) x W = J). Following testing, participants were randomly assigned to one of three groups: creatine (creatine citrate) (Cr; n = 16), placebo (PL; n = 17), or control (n = 10) groups. The Cr and PL groups completed four weeks of HIIT prior to post-testing. Significant improvements in VO2PEAK and VO2PEAKTTE occurred in both training groups. Only the Cr group significantly improved VT (16% vs. 10% improvement in PL). No changes occurred in TWD in any group. In conclusion, HIIT is an effective and time-efficient way to improve maximal endurance performance. The addition of Cr improved VT, but did not increase TWD. Therefore, 10 g of Cr per day for five days per week for four weeks does not seem to further augment maximal oxygen consumption, greater than HIIT alone; however, Cr supplementation may improve submaximal exercise performance.
... In the current pilot study, no changes in resting SBP, DBP, or HR following CrM supplementation were observed. This lack of effect on hemodynamics in response to CrM has been similarly reported in other studies [39,[41][42][43][44]. While this lack of influence on hemodynamics is not a negative outcome, it may explain the lack of impact of CrM on PWA variables. ...
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Background/Objectives: A pilot study was conducted to investigate the effect of four weeks of creatine monohydrate (CrM) on vascular endothelial function in older adults. Methods: In a double-blind, randomized crossover trial, twelve sedentary, healthy older adults were allocated to either the CrM or placebo (PL) group for four weeks, at a dose of 4 × 5 g/day for 5 days, followed by 1 × 5 g/day for 23 days. Macrovascular function (flow-mediated dilation [FMD%], normalized FMD%, brachial-ankle pulse wave velocity [baPWV], pulse wave analysis [PWA]), microvascular function (microvascular reperfusion rate [% StO2/sec]), and biomarkers of vascular function (tetrahydrobiopterin [BH4], malondialdehyde [MDA], oxidized low-density lipoprotein [oxLDL], glucose, lipids) were assessed pre- and post-supplementation with a four-week washout period. Results: CrM significantly increased FMD% (pre-CrM, 7.68 ± 2.25%; post-CrM, 8.9 ± 1.99%; p < 0.005), and normalized FMD% (pre-CrM, 2.57 × 10⁻⁴ ± 1.03 × 10⁻⁴%/AUCSR; post-CrM, 3.42 × 10⁻⁴ ± 1.69 × 10⁻⁴%/AUCSR; p < 0.05), compared to PL. Microvascular reperfusion rates increased following CrM (pre-CrM, 2.29 ± 1.42%/sec; post-CrM, 3.71 ± 1.44%/sec; p < 0.05), with no change following PL. A significant reduction in fasting glucose (pre-CrM, 103.64 ± 6.28; post-CrM, 99 ± 4.9 mg/dL; p < 0.05) and triglycerides (pre-CrM, 99.82 ± 35.35; post-CrM, 83.82 ± 37.65 mg/dL; p < 0.05) was observed following CrM. No significant differences were observed for any other outcome. Conclusions: These pilot data indicate that four weeks of CrM supplementation resulted in favorable effects on several indices of vascular function in older adults.
... Along the same lines, there was a group effect on average exercising HR, as the CM group experienced an overall increase, but no effect of time (P = 0.47). In comparison to our study, others have reported reductions in submaximal and maximal HR after a brief loading period through decreases in the muscle metaboreflex [31,32]. It is important to note that this was not a mechanistic study, thus rationale for these discrepancies are speculative. ...
... One of the main side effects of Creatinine is an increase in body weight which is due to water retention in muscles, which causes weight gain up to 0.8 to 2.9 percent. The water retention in the muscles is because Creatinine is a molecule that attracts water (18) . It has seen that Creatinine has some minor side effects that are digestive problems in 5 to 7 percent of people. ...
... There have been no systematic reviews on blood pressure changes or adverse cardiovascular effects of creatine supplementation in relatively healthy male or mix-sex populations. However, our finding is consistent with no reported blood pressure effect in three published male only placebo-controlled trials with creatine [160][161][162] and one mix-sex study [144]. There has been one systematic review on the use of creatine and creatine analogues in hypertension and cardiovascular disease, which also concluded no change in blood pressure with creatine supplementation in myocardial infarction or heart failure trials [163]. ...
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Creatine Monohydrate (CrM) is a dietary supplement routinely used as an ergogenic aid for sport and training, and as a potential therapeutic aid to augment different disease processes. Despite its increased use in recent years, studies reporting potential adverse outcomes of CrM have been mostly derived from male or mixed sex populations. A systematic search was conducted, which included female participants on CrM, where adverse outcomes were reported, with meta-analysis performed where appropriate. Six hundred and fifty-six studies were identified where creatine supplementation was the primary intervention; fifty-eight were female only studies (9%). Twenty-nine studies monitored for adverse outcomes, with 951 participants. There were no deaths or serious adverse outcomes reported. There were no significant differences in total adverse events, (risk ratio (RR) 1.24 (95% CI 0.51, 2.98)), gastrointestinal events, (RR 1.09 (95% CI 0.53, 2.24)), or weight gain, (mean difference (MD) 1.24 kg pre-intervention, (95% CI −0.34, 2.82)) to 1.37 kg post-intervention (95% CI −0.50, 3.23)), in CrM supplemented females, when stratified by dosing regimen and subject to meta-analysis. No statistically significant difference was reported in measures of renal or hepatic function. In conclusion, mortality and serious adverse events are not associated with CrM supplementation in females. Nor does the use of creatine supplementation increase the risk of total adverse outcomes, weight gain or renal and hepatic complications in females. However, all future studies of creatine supplementation in females should consider surveillance and comprehensive reporting of adverse outcomes to better inform participants and health professionals involved in future trials.
... p0150 Time to exhaustion (enhanced resistance to fatigue) is another way to measure endurance capacity. Cr supplementation has been shown to be most effective for time to exhaustion with shorter-duration exercise [17,43À46] and the least effective in longer-duration exercise [37,39,40]. The anaerobic metabolic pathways of shorter-duration exercise may once again explain these results. ...
Article
Creatine (methylguanidino acetic acid) is one of the safest, most extensively studied, and popular supplements in the sports science community. Its primary role is to improve bioenergetics; by mediating phosphagen metabolism, creatine improves the availability of ATP for the myosin motor and improves force and power production. With resistance training, creatine-loaded muscle allows for a higher quality of training (e.g., more reps at a given weight, higher power output) that leads to more rapid training performance gains and muscle fiber hypertrophy. Creatine has therefore allowed an enhancement of muscle function and more rapid training gains within the genetic capabilities of the individual. Its role in endurance exercise is not well described but shows potential benefits for increased exercise economy at submaximal intensities. Finally, creatine supplementation may have important implications for aging as well as for muscle wasting and insulin resistance.
... Corroborating these findings, a work by Zhang (2007b) showed that resting heart rate and systolic blood pressures were not affected by exercise training in healthy individuals. Murphy et al. (2005) too showed that creatine supplementation and exercise in humans had no detectable effects on cardiac structure or function. Resting LVDP, HR and CF were influenced neither by exercise (Brown et al. 2003) nor by creatine supplementation in rats (Horn et al. 1998), and Lennon et al. (2004) also found unchanged baseline cardiac function (HR, CF, RPP or cardiac work) in hearts from moderate and high-intensity exercise-trained rats. ...
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There has been a dramatic increase in the use of dietary creatine supplementation among sports men and women, and by clinicians as a therapeutic agent in muscular and neurological diseases. The effects on skeletal muscles have been documented and reviewed extensively. However, this review looks at another important muscle - the heart - and both the advantages and disadvantages to creatine supplementation, exercise, and the combination. The proposed mechanisms of each are examined and explained.
... In humans, creatine supplementation for 4 weeks during high intensity interval training improved ventilatory threshold but had no additional benefits on the cardiorespiratory outcomes [56]. Furthermore, short term Cr supplementation improved submaximal cycling efficiency with no detectable negative effect on cardiac structure or function [57]. ...
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Creatine is a principle component of the creatine kinase (CK) phosphagen system common to all vertebrates. It is found in excitable cells, such as cardiomyocytes, where it plays an important role in the buffering and transport of chemical energy to ensure that supply meets the dynamic demands of the heart. Multiple components of the CK system, including intracellular creatine levels, are reduced in heart failure, while ischaemia and hypoxia represent acute crises of energy provision. Elevation of myocardial creatine levels has therefore been suggested as potentially beneficial, however, achieving this goal is not trivial. This mini-review outlines the evidence in support of creatine elevation and critically examines the pharmacological approaches that are currently available. In particular, dietary creatine-supplementation does not sufficiently elevate creatine levels in the heart due to subsequent down-regulation of the plasma membrane creatine transporter (CrT). Attempts to increase passive diffusion and bypass the CrT, e.g. via creatine esters, have yet to be tested in the heart. However, studies in mice with genetic overexpression of the CrT demonstrate proof-of-principle that elevated creatine protects the heart from ischaemia-reperfusion injury. This suggests activation of the CrT as a major unmet pharmacological target. However, translation of this finding to the clinic will require a greater understanding of CrT regulation in health and disease and the development of small molecule activators.
... Estudos realizados em indivíduos com deficiência da síntese de creatina não apontaram efeitos colaterais em períodos prolongados de utilização 67,82 . Já estudos com outras populações sugerem que a suplementação de creatina não prejudica a função renal 30,55,73,74,90 , hepática 83 e do sistema cardiovascular 48 , bem como inúmeros marcadores de saúde 12,62,65 . ...
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Creatine was discovered more than one century ago, but its use became importantin sports scenario in the 70’s. Since then, the improvement in knowledge and utilization protocolsmade this substance the licit ergogenic aid most studied and used by athletes nowadays. Thebenefits of supplementation in athletes served as a model for studies in diseased individuals,that present ATP synthesis or ressynthesis deficiency, neurological and muscular diseases,or that suffer from muscular atrophy or impairment of muscular metabolism
... Since the high-intensity efforts were likely well above the subject's lactate threshold, it is not necessarily a good indicator of the effects of Cr on lactate accumulation during graded exercise. At the same time, others have found improved efficiency and lower levels of oxygen consumption during submaximal exercise after Cr supplementation (Murphy, Watsford, Coutts, & Richards, 2005;Nelson et al., 2000).The proposed mechanisms for improved O 2 utilization in relation to the PCr:Cr ratio have been described by Walsh et al. (2001), who did not find that oral Cr supplementation altered these mechanisms in vitro. Given that we did not measure oxygen consumption during our current study, we are unable to conclude whether altered oxygen uptake could explain any of the changes in lactate accumulation. ...
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Purpose: To determine the effects of creatine supplementation on blood lactate during incremental cycling exercise. Methods: Thirteen male subjects (M ± SD 23 ± 2 yr, 178.0 ± 8.1 cm, 86.3 ± 16.0 kg, 24% ± 9% body fat) performed a maximal, incremental cycling test to exhaustion before (Pre) and after (Post) 6 d of creatine supplementation (4 doses/d of 5 g creatine + 15 g glucose). Blood lactate was measured at the end of each exercise stage during the protocol, and the lactate threshold was determined as the stage before achieving 4 mmol/L. Lactate concentrations during the incremental test were analyzed using a 2 (condition) × 6 (exercise stage) repeated-measures ANOVA. Differences in power at lactate threshold, power at exhaustion, and total exercise time were determined by paired t tests and are presented as M ± SD. Results: Lactate concentrations were reduced during exercise after supplementation, demonstrating a significant condition effect (p = .041). There was a tendency for increased power at the lactate threshold (Pre 128 ± 45 W, Post 143 ± 26 W; p = .11). Total time to fatigue approached significant increases (Pre 22.6 ± 3.2 min, Post 23.3 ± 3.3 min; p = .056), as did maximal power output (Pre 212.5 ± 32.5 W, Post 220 ± 34.6 W; p = .082). Conclusions: Our findings demonstrate that creatine supplementation decreases lactate during incremental cycling exercise and tends to raise lactate threshold. Therefore, creatine supplementation could potentially benefit endurance athletes.
... We also found that body fat percentage decreased. These results were expected and support previous findings of those studies in which there were reported increases in muscle mass and total body mass (Balsom et al., 1995; Becque, Lochmann, & Melrose, 2000; Bermon et al., 1998; Burke et al., 2001; Dawson et al., 1995; Green et al., 1996; Greenhaff et al., 1994; Harris, Soderlund, & Hultman, 1992; Kreider et al., 1998; Maganaris & Maughan, 1998; Mihic et al., 2000; Murphy et al., 2005; Peyrebrune et al., 1998; Preen et al., 2001; Rossiter, Cannell, & Jakeman, 1996; Snow et al., 1998; Vandenberghe et al., 1997; Volek et al., 1999; Volek et al., 2000). In a study in the elderly (Gotshalk et al., 2002), it was demonstrated that Cr supplementation increased total and lean mass significantly. ...
... Since the high-intensity efforts were likely well above the subject's lactate threshold, it is not necessarily a good indicator of the effects of Cr on lactate accumulation during graded exercise. At the same time, others have found improved efficiency and lower levels of oxygen consumption during submaximal exercise after Cr supplementation (Murphy, Watsford, Coutts, & Richards, 2005;Nelson et al., 2000).The proposed mechanisms for improved O 2 utilization in relation to the PCr:Cr ratio have been described by Walsh et al. (2001), who did not find that oral Cr supplementation altered these mechanisms in vitro. Given that we did not measure oxygen consumption during our current study, we are unable to conclude whether altered oxygen uptake could explain any of the changes in lactate accumulation. ...
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Purpose: To determine the effects of creatine supplementation on blood lactate during incremental cycling exercise. Methods: Thirteen male subjects (M ± SD 23 ± 2 yr, 178.0 ± 8.1 cm, 86.3 ± 16.0 kg, 24% ± 9% body fat) performed a maximal, incremental cycling test to exhaustion before (Pre) and after (Post) 6 d of creatine supplementation (4 doses/d of 5 g creatine + 15 g glucose). Blood lactate was measured at the end of each exercise stage during the protocol, and the lactate threshold was determined as the stage before achieving 4 mmol/L. Lactate concentrations during the incremental test were analyzed using a 2 (condition) × 6 (exercise stage) repeated-measures ANOVA. Differences in power at lactate threshold, power at exhaustion, and total exercise time were determined by paired t tests and are presented as M ± SD. Results: Lactate concentrations were reduced during exercise after supplementation, demonstrating a significant condition effect (p = .041). There was a tendency for increased power at the lactate threshold (Pre 128 ± 45 W, Post 143 ± 26 W; p = .11). Total time to fatigue approached significant increases (Pre 22.6 ± 3.2 min, Post 23.3 ± 3.3 min; p = .056), as did maximal power output (Pre 212.5 ± 32.5 W, Post 220 ± 34.6 W; p = .082). Conclusions: Our findings demonstrate that creatine supplementation decreases lactate during incremental cycling exercise and tends to raise lactate threshold. Therefore, creatine supplementation could potentially benefit endurance athletes.
... Murphy et al. 32 subsequently found that Cr ingestion improved submaximal cycling efficiency with no effect on cardiovascular structure and function in male athletes. In this study, V0 2 max was measured (pre-, mid-, and post-) at increased cycling increments to volitional exhaustion after creatine ingestion at 20 g· day -1 for seven days followed by a 10 g· day -1 maintenance dose for 21 days. ...
... Acta Physiologica Hungarica 96, 2009 supplementation on isometric and dynamic strength (4,12,20,22,41), on running speed (36), swimming perfomance (17,39), aerob (30), and anaerob endurance variables during running (32) swimming (1,25,35), cycling (3,34,42) and jumping (6,13,38). ...
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The objective of this study was to determine whether creatine supplementation (CrS) could improve mechanical power output, and swimming performance in highly trained junior competitive fin swimmers. Sixteen male fin swimmers (age:15.9+/-1.6 years) were randomly and evenly assigned to either a creatine (CR, 4x5 g/day creatine monohydrate for 5 days) or placebo group (P, same dose of a dextrose-ascorbic acid placebo) in a double-blind research. Before and after CrS the average power output was determined by a Bosco-test and the swimming time was measured in two maximal 100 m fin swims. After five days of CrS the average power of one minute continuous rebound jumps increased by 20.2%. The lactate concentration was significantly less after 5 minutes restitution at the second measurement in both groups. The swimming time was significantly reduced in both first (pre: 50.69+/-1.41 s; post: 48.86+/-1.34 s) and second (pre: 50.39+/-1.38 s; post: 48.53+/-1.35 s) sessions of swimming in CR group, but remained almost unchanged in the P group.The results of this study indicate that five day Cr supplementation enhances the dynamic strength and may increase anaerobic metabolism in the lower extremity muscles, and improves performance in consecutive maximal swims in highly trained adolescent fin swimmers.
Article
Creatine monohydrate supplementation (CrM) is a safe and effective intervention for improving certain aspects of sport, exercise performance, and health across the lifespan. Despite its evidence-based pedigree, several questions and misconceptions about CrM remain. To initially address some of these concerns, our group published a narrative review in 2021 discussing the scientific evidence as to whether CrM leads to water retention and fat accumulation, is a steroid, causes hair loss, dehydration or muscle cramping, adversely affects renal and liver function, and if CrM is safe and/or effective for children, adolescents, biological females, and older adults. As a follow-up, the purpose of this paper is to evaluate additional questions and misconceptions about CrM. These include but are not limited to: 1. Can CrM provide muscle benefits without exercise? 2. Does the timing of CrM really matter? 3. Does the addition of other compounds with CrM enhance its effectiveness? 4. Does CrM and caffeine oppose each other? 5. Does CrM increase the rates of muscle protein synthesis or breakdown? 6. Is CrM an anti-inflammatory intervention? 7. Can CrM increase recovery following injury, surgery, and/or immobilization? 8. Does CrM cause cancer? 9. Will CrM increase urine production? 10. Does CrM influence blood pressure? 11. Is CrM safe to consume during pregnancy? 12. Does CrM enhance performance in adolescents? 13. Does CrM adversely affect male fertility? 14. Does the brain require a higher dose of CrM than skeletal muscle? 15. Can CrM attenuate symptoms of sleep deprivation? 16. Will CrM reduce the severity of and/or improve recovery from traumatic brain injury? Similar to our 2021 paper, an international team of creatine research experts was formed to perform a narrative review of the literature regarding CrM to formulate evidence-based responses to the aforementioned misconceptions involving CrM.
Thesis
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The aim of the present study was to investigate the effect of a high dose, short-duration oral creatine supplementation on anaerobic power and morfofunctional profile of 20 (n=20) male off-road cyclists. A double-blind design was used and the athletes were randomly assigned into 2 groups: placebo (PLA = 10) and creatine (CRE = 10). The tests were split in two days. On the first day, subjects performed two tests, heart rate variability and aerobic power output. On the second day they were submitted to anthropometric evaluation, underwater weighing and Wingate Anaerobic Test. The oral supplements (creatine and malthodextrine) were taken in sweetened vehicle, during 7 days, in three equal doses per day (0, 1 g/kg body mass/dose). After seven-day period, the athletes returned to the laboratory to post-treatment tests (PÓS). Student t-test showed significant differences on skinfold sum between PRÉ and PÓS tests (P<0,05), without differences between groups. Total body mass (MCT) and lean tissue mass (MCM) increased in CRE group (0,5% and 1,1%), while the PLA group showed decreases (-0,7% and -1,1%). The percentual of fat (GORD%) and fat mass (GORD) decreased for both groups (CRE, 9,2% and 15,4%) and (PLA, 4,0% and 10,1%). The CRE group showed increases for power output (P<0,01) and decreases for fatigue index (P<0,05) between PRÉ and PÓS tests, however, no significant differences were observed between groups for power output, mean power and fatigue index. The only variable that differs between groups was the peak power moment (P<0, 01). The results of the present study indicates that the short-term creatine supplementation leads to significant improvements on power output (CRE, PRÉ 11,26 ± 0,46 / PÓS 11,69 ± 0,51 ∆% =3,81) and (PLA, PRÉ 11,28 ± 0,74 /11,27 ± 0,51 ∆% =-1,24%), fatigue index (CRE, PRÉ 36,06± 6,53/ PÓS 33,33 ± 7,52 ∆% = -7,57%) and (PLA, PRÉ 36,71 ± 5,41/ 36,61 ± 6,06 ∆% = -0,27) and peak power moment in off-road cyclists. Attention must be paid to the high values for both aerobic and anaerobic power as well as for anaerobic threshold obtained by these athletes
Chapter
Creatine (Cr) is a compound that is synthesized endogenously in the kidneys, liver, and pancreas by the transamidination and subsequent transmethylation of three constituent amino acids: glycine, agrinine, and methionine (1). As a result of its amino acid origin, Cr can also be manufactured and consumed as a nutritional supplement. Consequently, Cr is currently regarded as a true ergogenic aid, owing to many well-controlled clinical trials that have demonstrated increases in muscle strength, power output, and muscle mass in response to exogenous Cr consumption (1–6). In fact, aside from the potential ergogenic benefits of caffeine, Cr is the most widely marketed nutritional supplement in the world.
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To investigate the effects of dietary creatine supplementation alone and in combination with exercise on basal cardiac function, susceptibility to ischaemia/reperfusion injury and mitochondrial oxidative function. There has been an increase in the use of creatine supplementation among sports enthusiasts, and by clinicians as a therapeutic agent in muscular and neurological diseases. The effects of creatine have been studied extensively in skeletal muscle, but not in the myocardium. Male Wistar rats were swim-trained for 8 weeks, 5 days per week. Hearts were excised and either freeze-clamped for biochemical analysis or perfused on the isolated heart perfusion system to assess function and ischaemia/reperfusion tolerance. Mechanical function was documented in working heart and retrograde mode. The left coronary artery was ligated and infarct size determined. Mitochondrial oxidative capacity was quantified. Aortic output recovery of hearts from the sedentary controls (CSed) was significantly higher than those from creatine-supplemented sedentary (CrSed), creatine-supplemented exercised (CrEx) as well as control exercised (CEx) groups. Ischaemic contracture of hearts from CrEx was significantly higher than that of CSed. There were no differences in infarct size and mitochondrial oxygen consumption. This study suggests that creatine supplementation has no effects on basal cardiac function but reduces myocardial tolerance to ischaemia in hearts from exercise-trained animals, by increasing the ischaemic contracture and decreasing reperfusion aortic output. Exercise training alone also significantly decreased aortic output recovery. However, the exact mechanisms for these adverse myocardial effects are unknown and need further investigation.
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Arterial stiffness and hemodynamics may be increased following a bout of resistance exercise. Oral creatine supplementation (Cr) may attenuate cardiovascular responses after exercise via improved anaerobic metabolism. This study was aimed to determine the effect of Cr on hemodynamic and arterial stiffness responses after acute isokinetic exercise. Sixteen healthy males (22.6 ± 0.6 year) were randomly assigned to either placebo (Pl, n = 8) or Cr (n = 8) (2 × 5 g/day) for 3 weeks. Brachial systolic blood pressure (SBP), heart rate (HR), brachial-ankle pulse wave velocity (baPWV), and leg PWV were measured in the supine position at rest before and after the interventions. After the supplementation period, parameters were also measured 5 min (PE5) and 15 min (PE15) after two sets of leg isokinetic exercise. There was no difference between the groups in resting measurements before and after the supplementation. Compared with the Pl group, the Cr group had attenuated (P < 0.05) increases in SBP at PE5 (Pl 14.0 ± 2.5, Cr 5.6 ± 2.3 mmHg), HR at both P5 (Pl 28 ± 4 vs. Cr 16 ± 2 beats/min) and PE15 (Pl 21 ± 3, Cr 11 ± 2 beats/min) and rate pressure product at P5 (Pl 45.8 ± 6.4, Cr 24.8 ± 2.2) and P15 (Pl 34.2 ± 5.0, Cr 15.9 ± 6.0). Compared with the Pl group, the Cr group had suppressed increases in baPWV at PE5 (Pl 1.5 ± 0.4, Cr -0.1 ± 0.4 m/s) and PE15 (Pl 1.1 ± 0.2, Cr -0.3 ± 0.3 m/s) and returned SBP to pre-exercise values at PE15 (Pl 10.6 ± 2.8, Cr 2.1 ± 2.6 mmHg). PWV in the exercised leg decreased at PE5 in both groups. These findings suggest that Cr supplementation attenuates the hemodynamic and baPWV responses after acute isokinetic exercise.
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Com o objetivo de investigar os efeitos da suplementação aguda com creatina no desempenho da potência anaeróbia de atletas de elite do mountain bike, 20 atletas em período básico do macrociclo de treinamento foram distribuídos aleatoriamente (duplo-cego) em dois grupos: placebo (PLA, n = 10) e creatina (CRE, n = 10). Foram avaliados quanto à composição corporal (pesagem hidrostática) e potência anaeróbia (teste de Wingate - TW) antes (PRÉ) e depois (PÓS) de sete dias de suplementação. A creatina ou maltodextrina foi usada em três doses diárias de 0,3g/kg de massa corporal diluídos em meio líquido adoçado. Não foram observadas diferenças significativas nas variáveis morfológicas após sete dias de suplementação (PRÉ x PÓS), e os grupos não diferiram apesar da variação percentual (Δ%) contrária (positiva para o grupo CRE e negativa para o PLA). A potência anaeróbia pico (PP) e o instante da potência pico (IPP) aumentaram e o índice de fadiga diminuiu do PRÉ para o PÓS-testes no grupo CRE, enquanto que o grupo PLA não apresentou diferenças significantes. A PP apresentou forte tendência em ser maior e o IPP foi maior no grupo CRE comparado com o PLA. Conclui-se que existem evidências de que a suplementação com creatina (0,3g/kg) em curto prazo (sete dias) pode retardar o IPP (CRE 3,0 ± 0,5/3,6 ± 0,8 Δ%= 20%) no teste de Wingate em atletas de elite do mountain bike, sugerindo que a suplementação com creatina pode melhorar o desempenho físico quanto à potência anaeróbia durante o trabalho de alta intensidade e curta duração.
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To determine the effects of creatine supplementation on cardiorespiratory responses during a graded exercise test (GXT) 36 trained adults (20 male, 16 female; 21–27 years old) performed two maximal GXTs on a cycle ergometer. The first GXT was done in a non-supplemented condition, and the second GXT was done following 7 days of ingesting either 5 g creatine monohydrate, encased in gelatin capsules, four times daily (CS, 13 male, 6 female), or the same number of glucose capsules (PL, 7 male, 10 female). CS significantly (P < 0.05) improved total test time [pre-CS=1217 (240) s, mean (std. dev.) versus post-CS=1289 (215) s], while PL administration had no effect (P > 0.05) on total test time [pre-PL=1037 (181) s versus post-PL=1047 (172) s]. In addition, both oxygen consumption (V˙ O2) and heart rate at the end of each of the first five GXT stages were significantly lower after CS, but were unchanged after PL. Moreover, the ventilatory threshold occurred at a significantly greater V˙ O2 for CS [pre-CS=2.2 (0.4) l · min−1 or 66% of peak V˙ O2 versus post-CS=2.6 (0.5) l · min−1 or 78% of peak V˙ O2; pre-PL=2.6 (0.9) l · min−1 or 70% peak V˙ O2 versus post-PL=2.6 (1.1) l · min−1 or 68% of peak V˙ O2]. Neither CS nor PL had an effect on peak V˙ O2 [pre-CS=3.4 (0.7) l · min−1 versus post-CS=3.3 (0.7) l · min−1; pre-PL=3.7 (1.1) l · min−1 versus post-PL=3.7 (1.1) l · min−1]. Apparently, CS can alter the contributions of the different metabolic systems during the initial stages of a GXT. Thus, the body is able to perform the sub-maximal workloads at a lower oxygen cost with a concomitant reduction in the work performed by the cardiovascular system.
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The observation that increased muscular activity leads to muscle hypertrophy is well known, but identification of the biochemical and physiological mechanisms by which this occurs remains an important problem. Experiments have been described (5, 6) which suggest that creatine, an end product of contraction, is involved in the control of contractile protein synthesis in differentiating skeletal muscle cells and may be the chemical signal coupling increased muscular activity and the increased muscular mass. During contraction, the creatine concentration in muscle transiently increases as creatine phosphate is hydrolyzed to regenerate ATP. In isometric contraction in skeletal muscle for example, Edwards and colleagues (3) have found that nearly all of the creatine phosphate is hydrolyzed. In this case, the creatine concentration is increased about twofold, and it is this transient change in creatine concentration which is postulated to lead to increased contractile protein synthesis. If creatine is found in several intracellular compartments, as suggested by Lee and Vissher (7), local changes in concentration may be greater then twofold. A specific effect on contractile protein synthesis seems reasonable in light of the work of Rabinowitz (13) and of Page et al. (11), among others, showing disproportionate accumulation of myofibrillar and mitochondrial proteins in response to work-induced hypertrophy and thyroxin-stimulated growth. Previous experiments (5, 6) have shown that skeletal muscles cells which have differentiated in vitro or in vivo synthesize myosin heavy-chain and actin, the major myofibrillar polypeptides, faster when supplied creatine in vitro. The stimulation is specific for contractile protein synthesis since neither the rate of myosin turnover nor the rates of synthesis of noncontractile protein and DNA are affected by creatine. The experiments reported in this communication were undertaken to test whether creatine selectively stimulates contractile protein synthesis in heart as it does in skeletal muscle.
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These experiments provide evidence that creatine, an end product of contraction unique to muscle, is involved in the control of muscle-protein synthesis. Skeletal muscle cells formed both in vitro and in vivo synthesize myosin heavy chain faster when supplied creatine in vitro. The response is apparent within four hours after addition of creatine to the culture medium, and is dependent on concentration over a range of 10-100 muM creatine. The effect seems to be selective for cell-specific proteins(s), since the rate of total protein synthesis is unaffected.
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Ciliary neurotrophic factor (CNTF) has been described as a neuro-active cytokine that shares functional similarities with the leukemia inhibitory factor (LIF). We demonstrate here that, like LIF, CNTF stimulates expression of acute phase plasma proteins in rat H-35 hepatoma cells. Transfection of the LIF receptor into Hep3B hepatoma cells reconstituted LIF and oncostatin M regulation of acute phase plasma protein genes. Co-expression of the LIF receptor and the CNTF receptor, but not expression of either subunit alone, generated CNTF responsiveness in Hep3B cells, suggesting cooperativity of these receptor subunits. Evidence is presented for direct interaction of the LIF receptor with the intracellular signal transduction machinery.
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A cDNA has been cloned from rabbit brain that is a new member of the emerging family of Na(+)-dependent plasma membrane transporters for several neurotransmitters and structurally related compounds. Functional expression of this cDNA in COS-7 cells identifies its product as a Na(+)- and Cl(-)-dependent creatine transporter with a Km of approximately 35 microM. Its creatine transporter activity is efficiently antagonized by 3-guanidinopropionate, a well characterized alternative substrate of creatine transport in several tissues, and by 4-guanidinobutyrate. More distant structural analogues of creatine are much less efficient or inactive as antagonists, indicating a high substrate specificity of the transporter. Northern blot hybridization detects the expression of its mRNA in most tissues tested, most prominently in kidney, heart, and muscle, but not in liver and intestine. A full-length cDNA clone was also isolated from a muscle cDNA library and found to contain the same coding sequence. Substrate affinity and specificity of the cloned transporter are very similar to the endogenous creatine transporter of the COS-7 cells and to the creatine transport activities of several cell types described in the literature. Moreover, its mRNA is most abundant in the tissues known to possess high creatine uptake capacity.
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Nine male subjects performed two bouts of 30-s maximal isokinetic cycling before and after ingestion of 20 g creatine (Cr) monohydrate/day for 5 days. Cr ingestion produced a 23.1 +/- 4.7 mmol/kg dry matter increase in the muscle total creatine (TCr) concentration. Total work production during bouts 1 and 2 increased by approximately 4%, and the cumulative increases in both peak and total work production over the two exercise bouts were positively correlated with the increase in muscle TCr. Cumulative loss of ATP was 30.7 +/- 12.2% less after Cr ingestion, despite the increase in work production. Resting phosphocreatine (PCr) increased in type I and II fibers. Changes in PCr before exercise bouts 1 and 2 in type II fibers were positively correlated with changes in PCr degradation during exercise in this fiber type and changes in total work production. The results suggest that improvements in performance were mediated via improved ATP resynthesis as a consequence of increased PCr availability in type II fibers.
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To assess cardiac structure and function in elite cross-trained male and female athletes (Alpine skiers). Sixteen athletes (10 male, six female) and 19 healthy sedentary control subjects (12 male, seven female) volunteered to take part in the study. Basic anthropometry determined height, body mass, body surface area, and fat free mass. Cardiac dimensions and function were determined by two dimensional, M mode, and Doppler echocardiography. Absolute data and data corrected for body size (allometrically determined) were compared by two way analysis of variance and post hoc Scheffé tests. Absolute left ventricular internal dimension in diastole (LVIDd), septal and posterior wall thickness and left ventricular mass were larger in athletes than controls (p < 0.05) and also increased in the men (p < 0.05) compared with women (except for septal thickness in controls). An increased LVIDd, septal thickness, posterior wall thickness, and left ventricular mass in athletes persisted after correction for body size except when LVIDd was scaled by fat free mass. Cardiac dimensions did not differ between the sexes after correction for body size. All functional indices were similar between groups. There is evidence of both left ventricular chamber dilatation and wall enlargement in cross trained athletes compared with controls. Differences in absolute cardiac dimensions between the sexes were primarily due to greater body dimensions in the men.
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The purpose of this study was to test the effect of creatine supplement on the size of the extra- and intracellular compartments and on the increase of isokinetic force during a strength training-program. Twenty-five healthy male subjects (age 22.0+/-2.9 years) participated in this experiment. Seven subjects formed the control-group. They did not complete any training and did not have any dietary supplement. The eighteen other subjects were randomly divided into a creatine- (n = 8) and a placebo-group (n = 10). They were submitted to a controlled strength-training program for 42 days followed by a detraining period of 21 days. Creatine and placebo were given over a period of 9 weeks. The size of the body water compartments was assessed by bioimpedance spectroscopy and the isokinetic force was determined during a single squat by means of an isokinetic dynamometer. These measurements were completed beforehand, at the end of the training period, and after the determining period. Both placebo- and creatine-group increased the isokinetic force by about 6% after the training period, showing that creatine ingestion does not induce a higher increase of the force measured during a single movement. No change in body mass was observed in the control- and placebo-groups during the entire experiment period while the body mass of the creatine-group was increased by 2 kg (P < 0.001). This change can be attributed partially to an increase (P = 0.039) in the body water content (+1.11), and more specifically, to an increase (P < 0.001) in the volume of the inter-cellular compartment (+0.61). Nevertheless, the relative volumes of the body water compartments remained constant and therefore the gain in body mass cannot be attributed to water retention, but probably to dry matter growth accompanied with a normal water volume.
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While creatine has been known to man since 1835, when a French scientist reported finding this constitutent of meat, its presence in athletics as a performance enhancer is relatively new. Amid claims of increased power and strength, decreased performance time and increased muscle mass, creatine is being hailed as a true ergogenic aid. Creatinine is synthesised from the amino acids glycine, arginine and methionine in the kidneys, liver and pancreas, and is predominantly found in skeletal muscle, where it exists in 2 forms. Approximately 40% is in the free creatine form (Crfree), while the remaining 60% is in the phosphorylated form, creatine phosphate (CP). The daily turnover rate of approximately 2 g per day is equally met via exogenous intake and endogenous synthesis. Although creatine concentration (Cr) is greater in fast twitch muscle fibres, slow twitch fibres have a greater resynthesis capability due to their increased aerobic capacity. There appears to be no significant difference between males and females in Cr, and training does not appear to effect Cr. The 4 roles in which creatine is involved during performance are temporal energy buffering, spatial energy buffering, proton buffering and glycolysis regulation. Creatine supplementation of 20 g per day for at least 3 days has resulted in significant increases in total Cr for some individuals but not others, suggesting that there are 'responders' and 'nonresponders'. These increases in total concentration among responders is greatest in individuals who have the lowest initial total Cr, such as vegetarians. Increased concentrations of both Crfree and CP are believed to aid performance by providing more short term energy, as well as increase the rate of resynthesis during rest intervals. Creatine supplementation does not appear to aid endurance and incremental type exercises, and may even be detrimental. Studies investigating the effects of creatine supplementation on short term, high intensity exercises have reported equivocal results, with approximately equal numbers reporting significant and nonsignificant results. The only side effect associated with creatine supplementation appears to be a small increase in body mass, which is due to either water retention or increased protein synthesis.
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Creatine (Cr) supplementation has become a common practice among professional, elite, collegiate, amateur, and recreational athletes with the expectation of enhancing exercise performance. Research indicates that Cr supplementation can increase muscle phosphocreatine (PCr) content, but not in all individuals. A high dose of 20 g x d(-1) that is common to many research studies is not necessary, as 3 g x d(-1) will achieve the same increase in PCr given time. Coincident ingestion of carbohydrate with Cr may increase muscle uptake; however, the procedure requires a large amount of carbohydrate. Exercise performance involving short periods of extremely powerful activity can be enhanced, especially during repeated bouts of activity. This is in keeping with the theoretical importance of an elevated PCr content in skeletal muscle. Cr supplementation does not increase maximal isometric strength, the rate of maximal force production, nor aerobic exercise performance. Most of the evidence has been obtained from healthy young adult male subjects with mixed athletic ability and training status. Less research information is available related to the alterations due to age and gender. Cr supplementation leads to weight gain within the first few days, likely due to water retention related to Cr uptake in the muscle. Cr supplementation is associated with an enhanced accrual of strength in strength-training programs, a response not independent from the initial weight gain, but may be related to a greater volume and intensity of training that can be achieved. There is no definitive evidence that Cr supplementation causes gastrointestinal, renal, and/or muscle cramping complications. The potential acute effects of high-dose Cr supplementation on body fluid balance has not been fully investigated, and ingestion of Cr before or during exercise is not recommended. There is evidence that medical use of Cr supplementation is warranted in certain patients (e.g.. neuromuscular disease); future research may establish its potential usefulness in other medical applications. Although Cr supplementation exhibits small but significant physiological and performance changes, the increases in performance are realized during very specific exercise conditions. This suggests that the apparent high expectations for performance enhancement, evident by the extensive use of Cr supplementation, are inordinate.
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To determine the effects of creatine (Cr) supplementation (20 g x d(-1) during 5 d) on maximal strength, muscle power production during repetitive high-power-output exercise bouts (MRPB), repeated running sprints, and endurance in handball players. Nineteen trained male handball players were randomly assigned in a double-blind fashion to either creatine (N = 9) or placebo (N = 10) group. Before and after supplementation, subjects performed one-repetition maximum half-squat (1RM(HS) and bench press (1RM(BP)), 2 sets of MRPB consisting of one set of 10 continuous repetitions (R10) followed by 1 set until exhaustion (R(max)), with exactly 2-min rest periods between each set, during bench-press and half-squat protocols with a resistance equal to 60 and 70% of the subjects' 1RM, respectively. In addition, a countermovement jumping test (CMJ) interspersed before and after the MRPB half-squat exercise bouts and a repeated sprint running test and a maximal multistage discontinuous incremental running test (MDRT) were performed. Cr supplementation significantly increased body mass (from 79.4 +/- 8 to 80 +/- 8 kg; P < 0.05), number of repetitions performed to fatigue, and total average power output values in the R(max) set of MRPB during bench press (21% and 17%, respectively) and half-squat (33% and 20%, respectively), the 1RM(HS) (11%), as well as the CMJ values after the MRPB half-squat (5%), and the average running times during the first 5 m of the six repeated 15-m sprints (3%). No changes were observed in the strength, running velocity, or body mass measures in the placebo group during the experimental period. Short-term Cr supplementation leads to significant improvements in lower-body maximal strength, maximal repetitive upper- and lower-body high-power exercise bouts, and total repetitions performed to fatigue in the R(max) set of MRPB, as well as enhanced repeated sprint performance and attenuated decline in jumping ability after MRPB in highly trained handball players. Cr supplementation did not result in any improvement in upper-body maximal strength and in endurance running performance.
Article
The use of creatine (Cr) in its supplemental form, Cr monohydrate, has become rather widespread. The discovery that the Cr and phosphocreatine (PCr) content in human muscle can be increased by oral ingestion of supplemental Cr has led to numerous studies examining its benefits on exercise performance. Cr monohydrate supplementation appears to result in an increased ability to maintain power output during high-intensity exercise and increase the rate of PCr resynthesis during the recovery phase of intermittent high-intensity exercise. Subjects supplemented with Cr monohydrate demonstrate a reduction in the accumulation of plasma lactate, ammonia, and hypoxanthine, indicating an alteration in energy metabolism and an attenuation of ATP degradation. Thus, higher concentrations of Cr seem to enhance the muscle's ability to sustain the high ATP turnover rates encountered during strenuous exercise. Another potential benefit is an increase in body mass which results from the ingestion of Cr monohydrate; however, the composition of the weight gain remains undetermined. This article discusses the theoretical basis for Cr supplementation and reviews what is known about its effects on performance.
Article
The use of creatine (Cr) in its supplemental form, Cr monohydrate, has become rather widespread. The discovery that the Cr and phosphocreatine (PCr) content in human muscle can be increased by oral ingestion of supplemental Cr has led to numerous studies examining its benefits on exercise performance. Cr monohydrate supplementation appears to result in an increased ability to maintain power output during high-intensity exercise and increase the rate of PCr resynthesis during the recovery phase of intermittent high-intensity exercise. Subjects supplemented with Cr monohydrate demonstrate a reduction in the accumulation of plasma lactate, ammonia, and hypoxanthine, indicating an alteration in energy metabolism and an attenuation of ATP degradation. Thus, higher concentrations of Cr seem to enhance the muscle's ability to sustain the high ATP turnover rates encountered during strenuous exercise. Another potential benefit is an increase in body mass which results from the ingestion of Cr monohydrate; however, the composition of the weight gain remains undetermined. This article discusses the theoretical basis for Cr supplementation and reviews what is known about its effects on performance. (C) 1996 National Strength and Conditioning Association
Article
We investigated the effect of oral creatine supplementation (20 g d−1 for 7 days) on metabolism during a 1-h cycling performance trial. Twenty endurance-trained cyclists participated in this double-blind placebo controlled study. Five days after familiarization with the exercise test, the subjects underwent a baseline muscle biopsy. Thereafter, a cannula was inserted into a forearm vein before performing the baseline maximal 1-h cycle (test 1 (T1)). Blood samples were drawn at regular intervals during exercise and recovery. After creatine (Cr) loading, the muscle biopsy, 1-h cycling test (test 2 (T2)) and blood sampling were repeated. Resting muscle total creatine (TCr), measured by high performance liquid chromatography, was increased (P < 0.001) in the creatine group from 123.0 ± 3.8 − 159.8 ± 7.9 mmol kg−1 dry wt, but was unchanged in the placebo group (126.7 ± 4.7 − 127.5 ± 3.6 mmol kg−1 dry wt). The extent of Cr loading was unrelated to baseline Cr levels (r=0.33, not significant). Supplementation did not significantly improve exercise performance (Cr group: 39.1 ± 0.9 vs. 39.8 ± 0.8 km and placebo group: 39.3 ± 0.8 vs. 39.2 ± 1.1 km) or change plasma lactate concentrations. Plasma concentrations of ammonia (NH3) (P < 0.05) and hypoxanthine (Hx) (P < 0.01) were lower in the Cr group from T1 to T2. Our results indicate that Cr supplementation alters the metabolic response during sustained high-intensity submaximal exercise. Plasma data suggest that nett intramuscular adenine nucleotide degradation may be decreased in the presence of enhanced intramuscular TCr concentration even during submaximal exercise.
Article
These experiments test whether creatine, a product of muscular contraction, stimulates myofibrillar protein synthesis. It was found that skeletal muscle cells formed both in vitro and in vivo and cardiac muscle cells formed in vivo synthesize myofibrillar proteins faster when supplied creatine in vitro. The rates of synthesis and/or accumulation of three myofibrillar proteins-myosin heavy chain actin, and creatine kinase-were stimulated by creatine. In contrast, the rates of synthesis of total protein and of deoxyribonucleic acid (DNA) and the activities of several nonmyofibrillar enzymes were not altered by creatine. These include lactic dehydrogenase, cathepsin D, acid phosphatase, and beta-acetylglucosaminidase. It is concluded that creatine selectively stimulated the rate of synthesis of contractile proteins in skeletal and cardiac muscle in vitro and may play a role in muscle hypertrophy.
Article
The observation that increased muscular activity leads to muscle hypertrophy is well known, but identification of the biochemical and physiological mechanisms by which this occurs remains an important problem. The hypothesis has been proposed that creatine, an end product of contraction, may be the chemical signal coupling increased muscular activity and increased contractile mass. Two muscle models have been used in experimental tests of this hypothesis: differentiating skeletal muscle cells in culture and the fetal mouse heart in organ culture. Using these culture models, it is possible to alter the intracellular creatine concentration and to measure the effect of increased creatine concentrations on the rates of synthesis and accumulation of both muscle-specific and nonspecific proteins. The results show that muscle-specific protein synthesis in both skeletal and cardiac muscle is selectively stimulated by creatine.
Article
To ascertain the effect of anabolic steroids (AS) on left ventricle size and function, M-mode and 2D echocardiographic evaluation was carried out in 14 body builders at the end of a phase of AS self-administration (8 +/- 3 weeks, mean +/- S.D.) and after a period (9 +/- 2 weeks, mean +/- S.D.) of drug withdrawal, as well as in 14 other body builders who had never made use of AS, and in 14 sedentary individuals. All the subjects were also examined anthropometrically. Ventricular septal thickness index was slightly greater in athletes using AS, compared to the other two groups (p less than 0.05), while left ventricle mass, the end-diastolic volume indexes and isovolumetric relaxation time, (a parameter of left ventricle diastolic function) were significantly increased (p less than 0.001) as well as the fat free mass (FFM), a marker of skeletal muscle mass. The non-users showed no differences in echocardiographic parameters, compared to sedentary controls. During the off treatment phase, the percentage of adipose mass increased and FFM decreased, while echocardiographic parameters did not vary significantly from on treatment values. The findings indicate that AS can induce an unfavourable enlargement and thickening of the left ventricle, which loses its diastolic properties with the mass increase. These modifications tend to persist following a short period of drug withdrawal.
Article
Percutaneous muscle biopsies were obtained from the vastus lateralis of physically active men (n = 12) 1) at rest, 2) immediately after an exercise bout consisting of 30 maximal voluntary knee extensions of constant angular velocity (3.14 rad/s), and 3) 60 s after termination of exercise. Creatine phosphate (CP) content was analyzed in pools of freeze-dried fast-twitch (FT) and slow-twitch (ST) muscle fiber fragments, and ATP, CP, creatine, and lactate content were assayed in mixed pools of FT and ST fibers. CP content at rest was 82.7 +/- 11.2 and 73.1 +/- 9.5 (SD) mmol/kg dry wt in FT and ST fibers (P less than 0.05). After exercise the corresponding values were 25.4 +/- 19.8 and 29.7 +/- 14.4 mmol/kg dry wt. After 60 s of recovery CP increased (P less than 0.01) to 41.3 +/- 12.6 and 49.6 +/- 11.7 mmol/kg dry wt in FT and ST fibers, respectively. CP content after recovery, relative to initial level, was higher in ST compared with FT fibers (P less than 0.05). ATP content decreased (P less than 0.05) and lactate content rose to 67.4 +/- 28.3 mmol/kg dry wt (P less than 0.001) in response to exercise. It is concluded that basal CP content is higher in FT fibers than in ST fibers. CP content also appears to be higher in ST fibers after a 60-s recovery period after maximal short-term exercise. These data are consistent with the different metabolic profiles of FT and ST fibers.
Article
The relation between induced increases in cardiac work and phosphate metabolites was investigated in the canine heart in vivo to evaluate the role of ATP hydrolysis products, ADP and inorganic phosphate (Pi), in the control of myocardial oxygen consumption (MVO2). In these studies, myocardial blood flow and oxygen consumption were simultaneously measured with the 31P-nuclear magnetic resonance (NMR)-detected phosphate metabolites. Three protocols were used to increase myocardial work: pacing, epinephrine, and phenylephrine infusions. When these protocols were used, no or only slight changes in myocardial ATP, Pi, and creatine phosphate were observed with a greater than threefold increase in MVO2. The calculated intracellular free Mg concentration, ADP, and pH were also only slightly affected by these increases in work. These data indicate that a simple model involving the feedback of cytosolic ADP and Pi to the mitochondria regulating respiration is inadequate to explain respiratory control in vivo. These data suggest that some other parameters or cooperativity effects involving the phosphate metabolites must play a role in the feedback between respiration and work in the heart in vivo.
Article
Cardiac creatine levels are depressed in chronic heart failure. Oral supplementation of creatine to healthy volunteers has been shown to increase physical performance. To evaluate the effects of creatine supplementation on ejection fraction, symptom-limited physical endurance and skeletal muscle strength in patients with chronic heart failure. With a double-blind, placebo-controlled design 17 patients (age 43-70 years, ejection fraction < 40) were supplemented with creatine 20 g daily for 10 days. Before and on the last day of supplementation ejection fraction was determined by radionuclide angiography as was symptom-limited 1-legged knee extensor and 2-legged exercise performance on the cycle ergometer. Muscle strength as unilateral concentric knee extensor performance (peak torque, Nm at 180 degrees/s) was also evaluated. Skeletal muscle biopsies were taken for the determination of energy-rich phosphagens. Ejection fraction at rest and at work did not change. Performance before creatine supplementation did not differ between placebo and creatine groups. While no change was seen in the placebo group compared to baseline, creatine supplementation increased skeletal muscle total creatine and creatine phosphate by 17 +/- 4% (P < 0.05) and 12 +/- 4% (P < 0.05), respectively. Increments were seen only in patients with < 140 mmol total creatine/kg d.w. (P < 0.05). One-legged performance (21%, P < 0.05), 2-legged performance (10%, P < 0.05), and peak torque, Nm (5%, P < 0.05) increased. Both peak torque and 1-legged performance increased linearly with increased skeletal muscle phosphocreatine (P < 0.05). The increments in 1-legged, 2-legged and peak torque were significant compared to the placebo group, (P < 0.05). One week of creatine supplementation to patients with chronic heart failure did not increase ejection fraction but increased skeletal muscle energy-rich phosphagens and performance as regards both strength and endurance. This new therapeutic approach merits further attention.
Article
1. Muscle biopsy samples were obtained from the vastus lateralis of six healthy volunteers before and after 30 s of treadmill sprinting. A portion of each biopsy sample was used for mixed-fibre metabolite analysis. Single fibres were dissected from the remaining portion of each biopsy and were used for ATP, phosphocreatine (PCr) and glycogen determination. 2. Before exercise, PCr and glycogen contents were higher in type II fibres (79.3 +/- 2.7 and 472 +/- 35 mmol (kg dry matter (DM)-1, respectively) compared with type I fibres (71.3 +/- 3.0 mmol (kg DM)-1, P < 0.01 and 375 +/- 25 mmol (kg DM)-1, P < 0.001, respectively). 3. Peak power output was 885 +/- 66 W and declined by 65 +/- 3% during exercise. Phosphocreatine and glycogen degradation in type II fibres during exercise (74.3 +/- 2.5 and 126.3 +/- 15.8 mmol (kg DM)-1, respectively) was greater than the corresponding degradation in type I fibres (59.1 +/- 2.9 mmol (kg DM)-1, P < 0.001 and 77.0 +/- 14.3 mmol (kg DM)-1, P < 0.01, respectively). The decline in ATP during exercise was similar when comparing fibre types (P > 0.05). 4. Compared with previous studies involving similar durations of maximal cycling exercise, isokinetic knee extension and intermittent isometric contraction, the rates of substrate utilization recorded in type I fibres were extremely high, being close to the rapid rates observed in this fibre type during intense contraction with limb blood flow occluded.
Article
To determine whether there is a difference in cardiac size and function as well as in body composition, aerobic capacity, and blood lipids between resistance trained athletes who use anabolic steroids and those who do not, and to compare them to university cross country athletes. Four groups of men were evaluated: recreational lifters, n = 11, lifting < 10 h.week-1; heavy lifters, n = 16, lifting > 10 h.week-1; steroid users, n = 8, same as heavy lifters and used steroids; runners, n = 8, university track members. Echocardiograms, body composition (hydrostatic weighing), maximum oxygen consumption (Vo2), and lipids were studied. As expected, Vo2 (ml.kg-1.min-1), was greatest in the runners, with no difference among the lifting groups. High density lipoprotein cholesterol in the steroid user group was lower than in heavy lifters or runners. Left ventricular internal diastolic dimension was similar among the groups. The left ventricular mass index of the steroid user group was significantly greater than recreational lifters, at 161 v 103. There was no difference among heavy lifters (127), runners (124), and steroid users. There was no compromise in diastolic function in any group. There were no differences among groups in resting or exercise blood pressure. Resistance training in the absence of steroid use results in the same positive effects on cardiac dimensions, diastolic function, and blood lipids as aerobic training.
Article
To investigate the hypothesis that an increase in plasma volume (PV) is obligatory in reducing the cardiovascular drift that is associated with prolonged exercise following training, a plasma expander (Macrodex) was used to acutely elevate PV. Eight untrained volunteers [maximal oxygen consumption; V˙O2max 45.2 (2.2) ml · kg−1 · min−1, mean (SE)] cycled for 2 h [at 46 (4)% V˙O2max ] in ambient conditions either with no PV expansion (CON) or following PV expansions of either 14% (LOW) or 21% (HIGH). During CON, heart rate (HR) increased (P<0.05) from 147 (2.4) beats · min−1 to 173 (3.6) beats · min−1 from 15 to 120 min of exercise. Both LOW and HIGH conditions depressed (P<0.05) HR, an effect that was manifested following 15 min of exercise. In contrast, stroke volume (SV) was elevated following PV expansion, with values (ml) of 89.6 (6.8), 97.8 (5.9) and 104 (4.6) noted by 15 min of exercise for CON, LOW and HIGH conditions, respectively. Acute PV expansion, regardless of magnitude, also resulted in elevations in cardiac output (Q˙ c). These differences between conditions persisted throughout the exercise, as did the elevation in Q˙ c that was noted with LOW and HIGH conditions. No difference between Q˙ c, HR or SV was found between LOW and HIGH. In addition, neither LOW nor HIGH conditions altered the change in rectal temperature that was observed during exercise. These results demonstrate that, at least for moderate exercise performed in ambient conditions, PV expansion serves only to alter cardiac function (Q˙ c, HR, SV) early in exercise, and not to attenuate the drift that occurs as the exercise is prolonged.
Article
Creatine is a physiologically active substance indispensable to muscle contraction. The increase in creatine phosphate obtained by supplementation is greater than the increase in total creatine achieved by specific sports training. Less well-trained people can produce an immediate energy store when supplementing creatine such as is otherwise achieved by top athletes on normal nutrition by means of speed and power training. The publications so far available indicate that creatine accumulation in muscle was accomplished using relatively high doses (20 g daily over 5 d). The objective of our study was to investigate the alterations in creatine and creatinine concentrations following lower dosages. As intermediate and finishing spurts under anaerobic conditions are gaining in importance in endurance sports, we created a special exercise test for triathletes combining endurance and interval performance. After a pretreatment exercise test was performed, the athletes ingested 6 g of creatine daily, divided into two portions for 5 d. On day 6, another exercise test was performed. Creatine supplementation was found to have no influence on the cardiovascular system, oxygen uptake, and blood lactate concentration. The fall in blood glucose during the exercise test was significantly reduced after consumption of creatine. Although interval power performance was significantly increased by 18%, endurance performance was not influenced. We conclude that creatine supplementation at doses of 6 g daily has positive effects on short-term exercise included into aerobic endurance exercise.
Article
The main purpose of the present study was to measure the total oxygen consumed, accumulation of blood metabolites, and performance during alternating intensity exercise before and after a period of creatine (Cr) loading in well-trained humans. Fourteen males were randomly assigned to two groups of seven males and were tested before and after 5 d of placebo (PL) or Cr monohydrate (CR) loading (20 g x d(-1)). Oxygen uptake was measured using a breath-by-breath system during bicycle exercise alternating every 3 min between bouts at 30%(-30%) and 90% (-90%) of the maximal power output to exhaustion. Blood samples were also obtained at rest, before the end of each cycling load, at exhaustion, and 5-min postexercise. The oxygen consumed during 1-90% (5.08 +/- 0.39 L) and 2-90% (5.32 +/- 0.30 L) was larger after CR (5.67 +/- 0.34 and 5.78 +/- 0.35 L, P < 0.01 and P < 0.05, respectively). Blood ammonia accumulation at the end of 1-90% (23.1 +/- 6.5 micromol x L(-1)) and 3-30% (64.7 +/- 15.2 micromol x L(-1)) was lower after CR (P < 0.05), whereas plasma uric acid accumulation was lower at exhaustion (P < 0.05) and 5-min postexercise (P < 0.01). Time to exhaustion increased (P < 0.05) from 29.9 +/- 3.8 to 36.5 +/- 5.7 min after CR, whereas it remained the same after PL. The results indicate that Cr feeding increases the capacity of human muscle to perform work during alternating intensity contraction, possibly as a consequence of increased aerobic phosphorylation and flux through the creatine kinase system.
Article
We investigated the effect of oral creatine supplementation (20 g d(-1) for 7 days) on metabolism during a 1-h cycling performance trial. Twenty endurance-trained cyclists participated in this double-blind placebo controlled study. Five days after familiarization with the exercise test, the subjects underwent a baseline muscle biopsy. Thereafter, a cannula was inserted into a forearm vein before performing the baseline maximal 1-h cycle (test 1 (T1)). Blood samples were drawn at regular intervals during exercise and recovery. After creatine (Cr) loading, the muscle biopsy, 1-h cycling test (test 2 (T2)) and blood sampling were repeated. Resting muscle total creatine (TCr), measured by high performance liquid chromatography, was increased (P < 0.001) in the creatine group from 123.0 +/- 3.8 - 159.8 +/- 7.9 mmol kg(-1) dry wt, but was unchanged in the placebo group (126.7 +/- 4.7 - 127.5 +/- 3.6 mmol kg(-1) dry wt). The extent of Cr loading was unrelated to baseline Cr levels (r=0.33, not significant). Supplementation did not significantly improve exercise performance (Cr group: 39.1 +/- 0.9 vs. 39.8 +/- 0.8 km and placebo group: 39.3 +/- 0.8 vs. 39.2 +/- 1.1 km) or change plasma lactate concentrations. Plasma concentrations of ammonia (NH(3)) (P < 0.05) and hypoxanthine (Hx) (P < 0.01) were lower in the Cr group from T1 to T2. Our results indicate that Cr supplementation alters the metabolic response during sustained high-intensity submaximal exercise. Plasma data suggest that nett intramuscular adenine nucleotide degradation may be decreased in the presence of enhanced intramuscular TCr concentration even during submaximal exercise.
Article
Creatine is a nutritional supplement with major application as ergogenic and neuroprotective substrate. Varying supplementation protocols differing in dosage and duration have been applied but systematic studies of total creatine (creatine and phosphocreatine) content in the various organs of interest are lacking. We investigated changes of total creatine concentrations in brain, muscle, heart, kidney, liver, lung and venous/portal plasma of guinea pigs, mice and rats in response to 2-8 weeks oral creatine-monohydrate supplementation (1.3-2 g/kg/d; 1.4-2.8% of dietary intake). Analysis of creatine and phosphocreatine content was performed by high performance liquid chromatography. Total creatine was determined as the sum of creatine and phosphocreatine. Presupplementation total creatine concentrations were high in brain, skeletal and heart muscle (10-22 micromol/g wet weight), and low in liver, kidney and lung (5-8 micromol/g wet weight). During creatine supplementation, the relative increase of total creatine was low (15-55% of presupplementation values) in organs with high presupplementation concentrations, and high (260-500% of presupplementation values) in organs with low presupplementation concentrations. The increase of total creatine concentrations was most pronounced after 4 weeks of supplementation. In muscle, brain, kidney and lungs, an additional increase (p<0.01) was observed between 2-4 and 2-8 weeks of supplementation. Absolute concentrations of phosphocreatine increased, but there was no increase of the relative (percentual) proportion of phosphocreatine (14-45%) during supplementation. Statistical comparison of total creatine concentrations across the species revealed no systematically differences in organ distribution and in time points of supplementation. Results suggest that in organs with low presupplementation creatine levels (liver, kidney), a major determinant of creatine uptake is an extra-intracellular concentration gradient. In organs with high presupplementation total creatine levels like brain, skeletal and heart muscle, the maximum capacity of creatine accumulation is low compared to other organs. A supplementation period of 2 to 4 weeks is necessary for significant augmentation of the creatine pool in these organs.
Article
This study investigated the effect of creatine monohydrate (Cr) supplementation on performance and training volume in rowers. Twenty-two rowers trained with continuous and interval rowing and resistance training 4 and 2 days/week, respectively, for 6 weeks. Cr supplementation consisted of a 5-day load (0.3 g/kg(-1) x day(-1)) followed by a 5-week maintenance dose (0.03 g/kg(-1) x day(-1)) while training. Five days of Cr loading did not change body composition, repeated interval rowing performance, 2,000-m rowing times, or strength performance. Five additional weeks of training with a maintenance dose of Cr or placebo significantly improved body composition, VO2max, 2,000-m rowing times, repeated power interval performance, and strength to a similar extent in both groups. Subjects training with Cr did not perform more repetitions per set of strength exercise nor produce or maintain higher power outputs during repeated rowing sessions. Cr supplementation did not increase performance or training volume over a placebo condition in rowers that performed a combined high intensity rowing and strength program.
Article
Creatine is the object of growing interest in the scientific literature. This is because of the widespread use of creatine by athletes, on the one hand, and to some promising results regarding its therapeutic potential in neuromuscular disease on the other. In fact, since the late 1900s, many studies have examined the effects of creatine supplementation on exercise performance. This article reviews the literature on creatine supplementation as an ergogenic aid, including some basic aspects relating to its metabolism, pharmacokinetics and side effects. The use of creatine supplements to increase muscle creatine content above approximately 20 mmol/kg dry muscle mass leads to improvements in high-intensity, intermittent high-intensity and even endurance exercise (mainly in nonweightbearing endurance activities). An effective supplementation scheme is a dosage of 20 g/day for 4-6 days, and 5 g/day thereafter. Based on recent pharmacokinetic data, new regimens of creatine supplementation could be used. Although there are opinion statements suggesting that creatine supplementation may be implicated in carcinogenesis, data to prove this effect are lacking, and indeed, several studies showing anticarcinogenic effects of creatine and its analogues have been published. There is a shortage of scientific evidence concerning the adverse effects following creatine supplementation in healthy individuals even with long-term dosage. Therefore, creatine may be considered as a widespread, effective and safe ergogenic aid.
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