Creatine supplementation increases muscle total creatine but not maximal intermittent exercise performance

1999 ◽  
Vol 87 (6) ◽  
pp. 2244-2252 ◽  
Author(s):  
Michael J. McKenna ◽  
Judith Morton ◽  
Steve E. Selig ◽  
Rodney J. Snow

This study investigated creatine supplementation (CrS) effects on muscle total creatine (TCr), creatine phosphate (CrP), and intermittent sprinting performance by using a design incorporating the time course of the initial increase and subsequent washout period of muscle TCr. Two groups of seven volunteers ingested either creatine [Cr; 6 × (5 g Cr-H2O + 5 g dextrose)/day)] or a placebo (6 × 5 g dextrose/day) over 5 days. Five 10-s maximal cycle ergometer sprints with rest intervals of 180, 50, 20, and 20 s and a resting vastus lateralis biopsy were conducted before and 0, 2, and 4 wk after placebo or CrS. Resting muscle TCr, CrP, and Cr were unchanged after the placebo but were increased ( P < 0.05) at 0 [by 22.9 ± 4.2, 8.9 ± 1.9, and 14.0 ± 3.3 (SE) mmol/kg dry mass, respectively] and 2 but not 4 wk after CrS. An apparent placebo main effect of increased peak power and cumulative work was found after placebo and CrS, but no treatment (CrS) main effect was found on either variable. Thus, despite the rise and washout of muscle TCr and CrP, maximal intermittent sprinting performance was unchanged by CrS.

2003 ◽  
Vol 13 (3) ◽  
pp. 294-302 ◽  
Author(s):  
Darren G. Burke ◽  
Philip D. Chilibeck ◽  
Gianni Parise ◽  
Mark A. Tarnopolsky ◽  
Darren G. Candow

α-lipoic acid has been found to enhance glucose uptake into skeletal muscle in animal models. Studies have also found that the co-ingestion of carbohydrate along with creatine increases muscle creatine uptake by a process related to insulin-stimulated glucose disposal. The purpose of this study was to determine the effect of α-lipoic acid on human skeletal muscle creatine uptake by directly measuring intramuscular concentrations of creatine, phosphocreatine, and ad-enosine triphosphate when creatine monohydrate was co-ingested with α-lipoic acid. Muscle biopsies were acquired from the vastus lateralis m. of 16 male subjects (18–32 y) before and after the experimental intervention. After the initial biopsy, subjects ingested 20 g · d−1 of creatine monohydrate, 20 g · d−1 of creatine monohydrate + 100 g · d−1 of sucrose, or 20 g · d−1 of creatine monohydrate + 100 g · d−1 of sucrose + 1000 mg · d−1 of α-lipoic acid for 5 days. Subjects refrained from exercise and consumed the same balanced diet for 7 days. Body weight increased by 2.1% following the nutritional intervention, with no differences between the groups. There was a significant increase in total creatine concentration following creatine supplementation, with the group ingesting α-lipoic acid showing a significantly greater increase (p < .05) in phosphocreatine (87.6 → 106.2 mmol · kg−1 dry mass [dm]) and total creatine (137.8 → 156.8 mmol · kg−1 dm). These findings indicate that co-ingestion of α-lipoic acid with creatine and a small amount of sucrose can enhance muscle total creatine content as compared to the ingestion of creatine and sucrose or creatine alone.


2003 ◽  
Vol 104 (2) ◽  
pp. 153-162 ◽  
Author(s):  
Luc J.C. van LOON ◽  
Audrey M. OOSTERLAAR ◽  
Fred HARTGENS ◽  
Matthijs K.C. HESSELINK ◽  
Rodney J. SNOW ◽  
...  

Most research on creatine has focused on short-term creatine loading and its effect on high-intensity performance capacity. Some studies have investigated the effect of prolonged creatine use during strength training. However, studies on the effects of prolonged creatine supplementation are lacking. In the present study, we have assessed the effects of both creatine loading and prolonged supplementation on muscle creatine content, body composition, muscle and whole-body oxidative capacity, substrate utilization during submaximal exercise, and on repeated supramaximal sprint, as well as endurance-type time-trial performance on a cycle ergometer. Twenty subjects ingested creatine or a placebo during a 5-day loading period (20g·day-1) after which supplementation was continued for up to 6 weeks (2g·day-1). Creatine loading increased muscle free creatine, creatine phosphate (CrP) and total creatine content (P<0.05). The subsequent use of a 2g·day-1 maintenance dose, as suggested by an American College of Sports Medicine Roundtable, resulted in a decline in both the elevated CrP and total creatine content and maintenance of the free creatine concentration. Both short- and long-term creatine supplementation improved performance during repeated supramaximal sprints on a cycle ergometer. However, whole-body and muscle oxidative capacity, substrate utilization and time-trial performance were not affected. The increase in body mass following creatine loading was maintained after 6 weeks of continued supplementation and accounted for by a corresponding increase in fat-free mass. This study provides definite evidence that prolonged creatine supplementation in humans does not increase muscle or whole-body oxidative capacity and, as such, does not influence substrate utilization or performance during endurance cycling exercise. In addition, our findings suggest that prolonged creatine ingestion induces an increase in fat-free mass.


2007 ◽  
Vol 17 (6) ◽  
pp. 624-634 ◽  
Author(s):  
Jeffrey J. Brault ◽  
Theodore F. Towse ◽  
Jill M. Slade ◽  
Ronald A. Meyer

Short-term creatine supplementation is reported to result in a decreased ratio of phosphocreatine (PCr) to total creatine (TCr) in human skeletal muscle at rest. Assuming equilibrium of the creatine kinase reaction, this decrease in PCr:TCr implies increased cytoplasmic ADP and decreased Gibbs free energy of ATP hydrolysis in muscle, which seems contrary to the reported ergogenic benefits of creatine supplementation. This study measured changes in PCr and TCr in vastus lateralis muscle of adult men (N = 6, 21–35 y old) during and 1 day after 5 d of creatine monohydrate supplementation (0.43 g·kg body weight−1·d−1) using noninvasive 31P and 1H magnetic-resonance spectroscopy (MRS). Plasma and red-blood-cell creatine increased by 10-fold and 2-fold, respectively, by the third day of supplementation. MRS-measured skeletal muscle PCr and TCr increased linearly and in parallel throughout the 5 d, and there was no significant difference in the percentage increase in muscle PCr (11.7% ± 2.3% after 5 d) vs. TCr (14.9% ± 4.1%) at any time point. The results indicate that creatine supplementation does not alter the PCr:TCr ratio, and hence the cytoplasmic Gibbs free energy of ATP hydrolysis, in human skeletal muscle at rest.


2004 ◽  
Vol 96 (1) ◽  
pp. 19-24 ◽  
Author(s):  
Timothy P. Gavin ◽  
Christopher B. Robinson ◽  
Robert C. Yeager ◽  
Justin A. England ◽  
L. Wiley Nifong ◽  
...  

We investigated whether acute systemic exercise increases vascular endothelial growth factor (VEGF), VEGF receptor (KDR and Flt-1) mRNA, and VEGF protein in sedentary humans. Twelve sedentary subjects were recruited and performed 1 h of acute, cycle ergometer exercise at 50% of maximal oxygen consumption. Muscle biopsies were obtained from the vastus lateralis before exercise and at 0, 2, and 4 h postexercise. Acute exercise significantly increased VEGF mRNA at 2 and 4 h and increased KDR and Flt-1 mRNA at 4 h postexercise. The sustained increase in VEGF mRNA through 4 h and the increases in KDR and Flt-1 at 4 h are different from their respective time course responses in rats. In contrast to the increase in VEGF mRNA postexercise, VEGF protein levels were decreased at 0 h postexercise. These results provide evidence in humans that 1) VEGF, KDR, and Flt-1 mRNA are increased by acute systemic exercise; 2) the time course of the VEGF, KDR, and Flt-1 mRNA responses are different from those previously reported in rats (Gavin TP and Wagner PD. Acta Physiol Scand 175: 201–209, 2002); and 3) VEGF protein is decreased immediately after exercise.


1998 ◽  
Vol 84 (5) ◽  
pp. 1687-1691 ◽  
Author(s):  
Mark Hargreaves ◽  
Michael J. McKenna ◽  
David G. Jenkins ◽  
Stuart A. Warmington ◽  
Jia L. Li ◽  
...  

Six men were studied during four 30-s “all-out” exercise bouts on an air-braked cycle ergometer. The first three exercise bouts were separated by 4 min of passive recovery; after the third bout, subjects rested for 4 min, exercised for 30 min at 30–35% peak O2 consumption, and rested for a further 60 min before completing the fourth exercise bout. Peak power and total work were reduced ( P < 0.05) during bout 3 [765 ± 60 (SE) W; 15.8 ± 1.0 kJ] compared with bout 1 (1,168 ± 55 W, 23.8 ± 1.2 kJ), but no difference in exercise performance was observed between bouts 1 and 4 (1,094 ± 64 W, 23.2 ± 1.4 kJ). Before bout 3, muscle ATP, creatine phosphate (CP), glycogen, pH, and sarcoplasmic reticulum (SR) Ca2+ uptake were reduced, while muscle lactate and inosine 5′-monophosphate were increased. Muscle ATP and glycogen before bout 4 remained lower than values before bout 1( P < 0.05), but there were no differences in muscle inosine 5′-monophosphate, lactate, pH, and SR Ca2+ uptake. Muscle CP levels before bout 4 had increased above resting levels. Consistent with the decline in muscle ATP were increases in hypoxanthine and inosine before bouts 3 and 4. The decline in exercise performance does not appear to be related to a reduction in muscle glycogen. Instead, it may be caused by reduced CP availability, increased H+ concentration, impairment in SR function, or some other fatigue-inducing agent.


2004 ◽  
Vol 106 (1) ◽  
pp. 99-106 ◽  
Author(s):  
Luc J. C. VAN LOON ◽  
Robyn MURPHY ◽  
Audrey M. OOSTERLAAR ◽  
David CAMERON-SMITH ◽  
Mark HARGREAVES ◽  
...  

It has been speculated that creatine supplementation affects muscle glucose metabolism in humans by increasing muscle glycogen storage and up-regulating GLUT-4 protein expression. In the present study, we assessed the effects of creatine loading and prolonged supplementation on muscle glycogen storage and GLUT-4 mRNA and protein content in humans. A total of 20 subjects participated in a 6-week supplementation period during which creatine or a placebo was ingested. Muscle biopsies were taken before and after 5 days of creatine loading (20 g·day-1) and after 6 weeks of continued supplementation (2 g·day-1). Fasting plasma insulin concentrations, muscle creatine, glycogen and GLUT-4 protein content as well as GLUT-4, glycogen synthase-1 (GS-1) and glycogenin-1 (Gln-1) mRNA expression were determined. Creatine loading significantly increased total creatine, free creatine and creatine phosphate content with a concomitant 18±5% increase in muscle glycogen content (P<0.05). The subsequent use of a 2 g·day-1 maintenance dose for 37 days did not maintain total creatine, creatine phosphate and glycogen content at the elevated levels. The initial increase in muscle glycogen accumulation could not be explained by an increase in fasting plasma insulin concentration, muscle GLUT-4 mRNA and/or protein content. In addition, neither muscle GS-1 nor Gln-1 mRNA expression was affected. We conclude that creatine ingestion itself stimulates muscle glycogen storage, but does not affect muscle GLUT-4 expression.


1995 ◽  
Vol 5 (2) ◽  
pp. 94-101 ◽  
Author(s):  
Ronald J. Maughan

Creatine phosphate allows high rates of adenosine triphosphate resynthesis to occur in muscle and therefore plays a vital role in the performance of high-intensity exercise. Recent studies have shown that feeding large amounts of creatine (typically 20 g per day for 5 days) increases muscle total creatine (and phosphocreatine) content. The extent of the increase that is normally observed is inversely related to the presupplementation level. Vegetarians, who have a very low dietary creatine intake, generally show the largest increases. Creatine supplementation has been shown to increase performance in situations where the availability of creatine phosphate is important; thus, performance is improved in very high-intensity exercise and especially where repeated sprints are performed with short recovery periods. Creatine supplementation is widely practiced by athletes in many sports and does not contravene current doping regulations. There are no reports of harmful side effects at the recommended dosage.


2007 ◽  
Vol 85 (6) ◽  
pp. 634-645 ◽  
Author(s):  
H.J. Green ◽  
T.A. Duhamel ◽  
G.P. Holloway ◽  
J. Moule ◽  
J. Ouyang ◽  
...  

The alterations in muscle metabolism were investigated in response to repeated sessions of heavy intermittent exercise performed over 16 h. Tissue samples were extracted from the vastus lateralis muscle before (B) and after (A) 6 min of cycling at approximately 91% peak aerobic power at repetitions one (R1), two (R2), nine (R9), and sixteen (R16) in 13 untrained volunteers (peak aerobic power = 44.3 ± 0.66 mL·kg–1·min–1, mean ± SE). Metabolite content (mmol·(kg dry mass)–1) in homogenates at R1 indicated decreases (p < 0.05) in ATP (21.9 ± 0.62 vs. 17.7 ± 0.68) and phosphocreatine (80.3 ± 2.0 vs. 8.56 ± 1.5) and increases (p < 0.05) in inosine monophosphate (IMP, 0.077 ± 0.12 vs. 3.63 ± 0.85) and lactate (3.80 ± 0.57 vs. 84.6 ± 10.3). The content (µmol·(kg dry mass)–1) of calculated free ADP ([ADPf], 86.4 ± 5.5 vs. 1014 ± 237) and free AMP ([AMPf], 0.32 ± 0.03 vs. 78.4 ± 31) also increased (p < 0.05). No differences were observed between R1 and R2. By R9 and continuing to R16, pronounced reductions (p < 0.05) at A were observed in IMP (72.2%), [ADPf] (58.7%), [AMPf] (85.5%), and lactate (41.3%). The 16-hour protocol resulted in an 89.7% depletion (p < 0.05) of muscle glycogen. Repetition-dependent increases were also observed in oxygen consumption during exercise. It is concluded that repetitive heavy exercise results in less of a disturbance in phosphorylation potential, possibly as a result of increased mitochondrial respiration during the rest-to-work non-steady-state transition.


2000 ◽  
Vol 278 (1) ◽  
pp. E118-E126 ◽  
Author(s):  
H. Green ◽  
R. Tupling ◽  
B. Roy ◽  
D. O'Toole ◽  
M. Burnett ◽  
...  

The purpose of this study was to investigate the hypothesis that a single, extended session of heavy exercise would be effective in inducing adaptations in energy metabolism during exercise in the absence of increases in oxidative potential. Ten healthy males [maximal aerobic power (V˙o 2 peak) = 43.4 ± 2.2 (SE) ml ⋅ kg−1 ⋅ min−1] participated in a 16-h training session involving cycling for 6 min each hour at ∼90% of maximal oxygen consumption. Measurements of metabolic changes were made on tissue extracted from the vastus lateralis during a two-stage standardized submaximal cycle protocol before (Pre) and 36–48 h after (Post) the training session. At Pre, creatine phosphate (PCr) declined ( P < 0.05) by 32% from 0 to 3 min and then remained stable until 20 min of exercise at 60%V˙o 2 peak before declining ( P < 0.05) by a further 35% during 20 min of exercise at 75%V˙o 2 peak. Muscle lactate (mmol/kg dry wt) progressively increased ( P < 0.05) from 4.59 ± 0.64 at 0 min to 17.8 ± 2.7 and 30.9 ± 5.3 at 3 and 40 min, respectively, whereas muscle glycogen (mmol glucosyl units/kg dry wt) declined ( P < 0.05) from a rest value of 360 ± 24 to 276 ± 31 and 178 ± 36 at similar time points. During exercise after the training session, PCr and glycogen were not as depressed ( P < 0.05), and increases in muscle lactate were blunted ( P < 0.05). All of these changes occurred in the absence of increases in oxidative potential as measured by the maximal activities of citrate synthase and malate dehydrogenase. These findings are consistent with other studies, namely, that muscle metabolic adaptations to regular exercise are an early adaptive event that occurs before increases in oxidative potential.


1992 ◽  
Vol 72 (5) ◽  
pp. 1999-2004 ◽  
Author(s):  
J. J. Widrick ◽  
D. L. Costill ◽  
G. K. McConell ◽  
D. E. Anderson ◽  
D. R. Pearson ◽  
...  

This study examined the time course of glycogen accumulation in skeletal muscle depleted by concentric work and subsequently subjected to eccentric exercise. Eight men exercised to exhaustion on a cycle ergometer [70% of maximal O2 consumption (VO2max)] and were placed on a carbohydrate-restricted diet. Approximately 12 h later they exercised one leg to subjective failure by repeated eccentric action of the knee extensors against a resistance equal to 120% of their one-repetition maximum concentric knee extension force (ECC leg). The contralateral leg was not exercised and served as a control (CON leg). During the 72-h recovery period, subjects consumed 7 g carbohydrate.kg body wt-1.day-1. Moderate soreness was experienced in the ECC leg 24–72 h after eccentric exercise. Muscle biopsies from the vastus lateralis of the ECC and CON legs revealed similar glycogen levels immediately after eccentric exercise (40.2 +/- 5.2 and 47.6 +/- 6.4 mmol/kg wet wt, respectively; P greater than 0.05). There was no difference in the glycogen content of ECC and CON legs after 6 h of recovery (77.7 +/- 7.9 and 85.1 +/- 4.9 mmol/kg wet wt, respectively; P greater than 0.05), but 18 h later, the ECC leg contained 15% less glycogen than the CON leg (90.2 +/- 8.2 vs. 105.8 +/- 8.9 mmol/kg wet wt; P less than 0.05). After 72 h of recovery, this difference had increased to 24% (115.8 +/- 8.0 vs. 153.0 +/- 12.2 mmol/kg wet wt; P less than 0.05). These data confirm that glycogen accumulation is impaired in eccentrically exercised muscle.(ABSTRACT TRUNCATED AT 250 WORDS)


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