Article

Building muscle: Nutrition to maximize bulk and strength adaptations to resistance exercise training

Wiley
European Journal of Sport Science
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Abstract

Several nutritional strategies can optimize muscle bulk and strength adaptations and enhance recovery from heavy training sessions. Adequate energy intake to meet the needs of training and carbohydrate intake sufficient to maintain glycogen stores (>7 g carbohydrate·kg·day for women; >8 g carbohydrate·kg·day for men) are important. Dietary protein intake for top sport athletes should include some foods with high biological value, with a maximum requirement of approximately 1.7 g·kg·day being easily met with an energy sufficient diet. The early provision of carbohydrate (>1 g·kg) and protein (>10 g) early after an exercise session will enhance protein balance and optimize glycogen repletion. Creatine monohydrate supplementation over several days increases body mass through water retention and can increase high-intensity repetitive ergometer performance. Creatine supplementation can enhance total body and lean fat free mass gains during resistance exercise training; however, strength gains do not appear to be enhanced versus an optimal nutritional strategy (immediate post-exercise protein and carbohydrate). Some studies have suggested that β-OH-methyl butyric acid (β-HMB) can enhance gains made through resistance exercise training; however, it has not been compared “head to head” with optimal nutritional practices. Overall, the most effective way to increase strength and bulk is to perform sport-specific resistance exercise training with the provision of adequate energy, carbohydrate, and protein. Creatine monohydrate and β-HMB supplementation may enhance the strength gains made through training by a small margin but the trade-off is likely to be greater bulk, which may be ergolytic for any athlete participating in a weight-supported activity.

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... Berikut ini adalah tanda-tanda klinis yang mengindikasikan bahwa seseorang mengalami kekurangan zat gizi. (Houston, 1999;Kloby Nielsen et al., 2020;Tarnopolsky, 2008;Tipton & Ferrando, 2008). Rekomendasi umum untuk asupan protein dalam meningkatkan massa otot adalah 1,6-2,2 g/kgBB/hari. ...
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... 2,4 Some studies also suggest to the possibility of an even higher intake. 9 The majority of dietary carbohydrate should come from complex carbohydrates with a low to moderate glycemic index (named "slow carbs"). Appropriate sources are whole grains, fruit, vegetables, legumes, etc. ...
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... Research over the last decade has indicated that athletes engaged in intense training need to ingest about two times the usual recommended daily allowance (RDA) of protein in their diet to maintain protein balance. 4,9 An insufficient amount of protein in the diet leads to the negative nitrogen balance, which can increase protein catabolism and can slow post-workout recovery. This may lead to muscle wasting, training intolerance and, certainly, overtraining. ...
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... Another factor contributing to the changes observed in body weight and body composition over time is the use of improved nutritional intake. This is especially true as it relates to adequate carbohydrate and protein intake during training (53). Numerous studies have demonstrated the importance of adequate carbohydrate and protein intake during training for the purpose of increasing body weight and muscle mass (53). ...
... This is especially true as it relates to adequate carbohydrate and protein intake during training (53). Numerous studies have demonstrated the importance of adequate carbohydrate and protein intake during training for the purpose of increasing body weight and muscle mass (53). Furthermore, an appropriate macronutrient intake is especially important during periods of heavy training when attempting to increase muscle mass (53). ...
... Numerous studies have demonstrated the importance of adequate carbohydrate and protein intake during training for the purpose of increasing body weight and muscle mass (53). Furthermore, an appropriate macronutrient intake is especially important during periods of heavy training when attempting to increase muscle mass (53). ...
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... However, recent reviews discussing this aspect conclude that it still seems unclear if there is a real benefi t for athletes following this strategy (8,12). Even if studies show different fi ndings, a protein-carbohydrate snack or meal after strenuous workout seems to be a possible choice for muscle repair, adaptation to training and to provide carbohydrate fuel to restore muscle glycogen levels (11). Nevertheless, in general this does not make a carbohydrate-protein bar, drink or powder necessary, it can be provided by a food based snack or meal. ...
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... Carbohydrate intakes greater than 7.0 g · kg -1 day -1 for women and greater than 8.0 g kg -1 · day -1 for men is probably sufficient for the maintenance of carbohydrate store during repetitive training sessions (Burke, Loucks & Board, 2006). The sport-specific and periodization training, optimal nutrition intake, genetic factors, and equipment are the main determinants of athletic performance ( (Tarnopolsky, 2008). ...
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Eight highly trained cyclists were studied during exercise after glycogen depletion (test A) and during carbohydrate (CHO) loading (test B). In test B subjects were able to complete 2 h of exercise at 70-75% maximal workload (Wmax), whereas the initial intensity of 70% Wmax had to be reduced to 50% in test A. Plasma ammonia increased more rapidly, and plasma alanine, glutamate, and glutamine were lower in test A. Exercise caused a 3.6-fold increase in the proportion of active branched-chain 2-oxoacid dehydrogenase (BC) complex in muscle in test A. No activation occurred in test B. There was an inverse correlation between the activity of the BC complex and the glycogen content of the postexercise biopsies. Exercise did not cause changes in the muscle content of ATP, ADP, AMP, IMP, hypoxanthine, and lactate. It is concluded that CHO loading abolishes increases in branched-chain amino acid (BCAA) oxidation during exercise and that part of the ammonia production during prolonged exercise originates from deamination of amino acids. The data appear to confirm the hypothesis (A.J. M. Wagenmakers, J.H. Coakley, and R.H.T. Edwards. Int. J. Sports Med. 11: S101-S113, 1990) that acceleration of the BCAA aminotransferase reaction may drain the tricarboxylic acid cycle and that glycogen is a carbon chain precursor of tricarboxylic acid cycle intermediates and glutamine.
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The kinetics of urea metabolism were measured in children recovering from severe malnutrition. For a period of up to 10 d they received one of four diets which provided 711 kJ (170 kcal)/kg per d. Two groups received a diet with a high protein:energy (P:E) ratio of 10-6% (HP), enriched with either fat (HP/F) or maize starch and sucrose (HP/C). Two groups received a diet with a low P:E ratio of 8.8% (LP), enriched with either fat (LP/F) or maize starch and sucrose (LP/C). The rate of weight gain on the HP diets was significantly greater than on the LP diets. There was no difference in urea production between any of the four diets: HP/F 1.23 (SE 0.12), HP/C 1.37 (SE 0.14), LP/F 1.64 (SE 0.22), LP/C 1.15 (SE 0.15) mmol nitrogen/kg per h. On the HP diets urea excretion was 0.77 (SE 0.07) mmol N/kg per h, 61% of production. There was significantly less urea excreted in the urine on diet LP/C than on LP/F (0.36 (SE 0.05) and 0.64 (SE 0.04) mmol N/kg per h respectively). A significantly greater percentage of the urea production was hydrolysed on the LP diets (61%) compared with the HP diets (39%), with the consequence that 50% of urea-N produced was available for synthetic activity on the LP diets compared with 30% on the HP diets. The increase in the urea hydrolysed on the LP diets was equivalent in magnitude to the decreased intake of N, so that overall intake plus hydrolysis did not differ between the LP and the HP diets. Crude N balance was similar on diets HP/F, HP/C and LP/C, but was significantly reduced on diet LP/F. These results show that there is an accommodation in urea kinetics during rapid catch-up weight gain, which becomes evident when the P:E ratio of the diet falls to 8.8%. It is proposed that, for a P:E ratio of 8.8%, protein is limiting for catch-up growth. When the intake has a P:E ratio of 8.8% the pattern of urea kinetics can be modified by the relative proportions of fat and carbohydrate in the diet. The measurement of urea kinetics provides a useful approach to the definition of the adequacy of the protein in the diet.
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Field studies during the Tour de France indicated that cyclists consume 30% of daily energy intake as liquid carbohydrate (CHO)-enriched nutrition with the goal of maintaining energy and CHO balance. The aim of the present investigation was to study the effect of such dietary manipulation during 2 days of long-lasting exhausting cycling on food and fluid intake, energy balance, nitrogen balance, and nutrient oxidation. Thirteen highly trained cyclists were divided into two subgroups receiving ad libitum either a primarily maltodextrin-based beverage (Mf) (20% w/v, 85% maltodextrin, 15% fructose) or a 50/50% composed fructosemaltodextrin (FM) beverage in addition to their normal diet. The study was performed during a 7-day stay in a respiration chamber (2 preparation days, 1 standardized resting day, 2 cycling days, 1.5 standardized recovery days), allowing for continuous gas analysis, weighed food and fluid intake procedure, and collection of excretes. The data of this study were compared with data from the same subjects receiving a normal CHO-rich diet (N) (60 En%) in a separate experiment. The results showed that the cyclists receiving Mf were able to maintain EB during sustained exercise days in contrast to when receiving N and to subjects receiving FM. With Mf treatment CHO intake increased, up to 80 En% (17.5 ± 1.0 g · kg⁻¹ BW) and carbohydrate balance remained positive. The subjects receiving FM had the largest CHO oxidation, calculated from R. Protein oxidation significantly increased in N and FM as a result of exercise but not in Mf. The latter subjects were in slighly negative nitrogen balance at a protein intake level of 1.4 g · kg⁻¹ BW. The results show that supplementation with maltodextrin beverages is an adequate measure to maintain EB and CHO balance and furthermore that increased CHO intake induces protein sparing. The protein requirement while being in energy and carbohydrate balance during days of sustained exhausting cycling was in the range of 1.5-1.8 g · kg⁻¹ BW.
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L-Arginine-glycine amidinotransferase (transamidinase) is the first and rate-limiting step in creatine biosynthesis. Rats fed a creatine-supplemented diet or hypophysectomized rats have only 20% of the kidney transamidinase activity as intact rats fed a creatine-free diet. A cDNA clone corresponding to transamidinase was isolated by immunoscreening of a lambda gt11 expression library prepared from rat kidney mRNA. The transamidinase cDNA had an open reading frame containing the known sequence of the amino-terminal peptide of transamidinase. Based on the cDNA sequence, transamidinase is synthesized as a precursor with an amino-terminal extension of 50 amino acids, consistent with its mitochondrial localization. Comparison of the transamidinase sequence with the protein data base identified only a single, related protein. Remarkably, this protein, which has a 37% amino acid identity with transamidinase, is also an amidinotransferase, catalyzing streptomycin biosynthesis in Streptomyces griseus. Transamidinase cDNA was used to investigate the regulation of mRNA levels by creatine and growth hormone. Hypophysectomized rats were fed a creatine-free or a creatine-supplemented diet and maintained with and without injections of growth hormone. An excellent correlation was found between changes in transamidinase activity and mRNA levels in response to creatine and growth hormone. Thus, the regulation of transamidinase by creatine and growth hormone is at a pretranslational level. In addition, the two effectors do not act independently but interact at a pretranslational level to control transamidinase gene expression.
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The effects of dietary supplementation with the leucine metabolite beta-hydroxy-beta-methylbutyrate (HMB) were studied in two experiments. In study 1, subjects (n = 41) were randomized among three levels of HMB supplementation (0, 1.5 or 3.0 g HMB/day) and two protein levels (normal, 117 g/day, or high, 175 g/day) and weight lifted for 1.5 h 3 days/wk for 3 wk. In study 2, subjects (n = 28) were fed either 0 or 3.0 g HMB/day and weight lifted for 2-3 h 6 days/wk for 7 wk. In study 1, HMB significantly decreased the exercise-induced rise in muscle proteolysis as measured by urine 3-methylhistidine during the first 2 wk of exercise (linear decrease, P < 0.04). Plasma creatine phosphokinase was also decreased with HMB supplementation (week 3, linear decrease, P < 0.05). Weight lifted was increased by HMB supplementation when compared with the unsupplemented subjects during each week of the study (linear increase, P < 0.02). In study 2, fat-free mass was significantly increased in HMB-supplemented subjects compared with the unsupplemented group at 2 and 4-6 wk of the study (P < 0.05). In conclusion, supplementation with either 1.5 or 3 g HMB/day can partly prevent exercise-induced proteolysis and/or muscle damage and result in larger gains in muscle function associated with resistance training.
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We determined the effect of the timing of glucose supplementation on fractional muscle protein synthetic rate (FSR), urinary urea excretion, and whole body and myofibrillar protein degradation after resistance exercise. Eight healthy men performed unilateral knee extensor exercise (8 sets/approximately 10 repetitions/approximately 85% of 1 single maximal repetition). They received a carbohydrate (CHO) supplement (1 g/kg) or placebo (Pl) immediately (t = 0 h) and 1 h (t = +1 h) postexercise. FSR was determined for exercised (Ex) and control (Con) limbs by incremental L-[1-13C]leucine enrichment into the vastus lateralis over approximately 10 h postexercise. Insulin was greater (P < 0.01) at 0.5, 0.75, 1.25, 1.5, 1.75, and 2 h, and glucose was greater (P < 0.05) at 0.5 and 0.75 h for CHO compared with Pl condition. FSR was 36.1% greater in the CHO/Ex leg than in the CHO/Con leg (P = not significant) and 6.3% greater in the Pl/Ex leg than in the Pl/Con leg (P = not significant). 3-Methylhistidine excretion was lower in the CHO (110.43 +/- 3.62 mumol/g creatinine) than P1 condition (120.14 +/- 5.82, P < 0.05) as was urinary urea nitrogen (8.60 +/- 0.66 vs. 12.28 +/- 1.84 g/g creatinine, P < 0.05). This suggests that CHO supplementation (1 g/kg) immediately and 1 h after resistance exercise can decrease myofibrillar protein breakdown and urinary urea excretion, resulting in a more positive body protein balance.
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The effects of oral creatine supplementation on muscle phosphocreatine (PCr) concentration, muscle strength, and body composition were investigated in young female volunteers (n = 19) during 10 wk of resistance training (3 h/wk). Compared with placebo, 4 days of high-dose creatine intake (20 g/day) increased (P < 0.05) muscle PCr concentration by 6%. Thereafter, this increase was maintained during 10 wk of training associated with low-dose creatine intake (5 g/day). Compared with placebo, maximal strength of the muscle groups trained, maximal intermittent exercise capacity of the arm flexors, and fat-free mass were increased 20-25, 10-25, and 60% more (P < 0. 05), respectively, during creatine supplementation. Muscle PCr and strength, intermittent exercise capacity, and fat-free mass subsequently remained at a higher level in the creatine group than in the placebo group during 10 wk of detraining while low-dose creatine was continued. Finally, on cessation of creatine intake, muscle PCr in the creatine group returned to normal within 4 wk. It is concluded that long-term creatine supplementation enhances the progress of muscle strength during resistance training in sedentary females.
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To determine the effects of 28 d of creatine supplementation during training on body composition, strength, sprint performance, and hematological profiles. In a double-blind and randomized manner, 25 NCAA division IA football players were matched-paired and assigned to supplement their diet for 28 d during resistance/agility training (8 h x wk[-1]) with a Phosphagen HP (Experimental and Applied Sciences, Golden, CO) placebo (P) containing 99 g x d(-1) of glucose, 3 g x d(-1) of taurine, 1.1 g x d(-1) of disodium phosphate, and 1.2 g x d(-1) of potassium phosphate (P) or Phosphagen HP containing the P with 15.75 g x d(-1) of HPCE pure creatine monohydrate (HP). Before and after supplementation, fasting blood samples were obtained; total body weight, total body water, and body composition were determined; subjects performed a maximal repetition test on the isotonic bench press, squat, and power clean; and subjects performed a cycle ergometer sprint test (12 x 6-s sprints with 30-s rest recovery). Hematological parameters remained within normal clinical limits for active individuals with no side effects reported. Total body weight significantly increased (P < 0.05) in the HP group (P 0.85 +/- 2.2; HP 2.42 +/- 1.4 kg) while no differences were observed in the percentage of total body water. DEXA scanned body mass (P 0.77 +/- 1.8; HP 2.22 +/- 1.5 kg) and fat/bone-free mass (P 1.33 +/- 1.1; HP 2.43 +/- 1.4 kg) were significantly increased in the HP group. Gains in bench press lifting volume (P -5 +/- 134; HP 225 +/- 246 kg), the sum of bench press, squat, and power clean lifting volume (P 1,105 +/- 429; HP 1,558 +/- 645 kg), and total work performed during the first five 6-s sprints was significantly greater in the HP group. The addition of creatine to the glucose/taurine/electrolyte supplement promoted greater gains in fat/bone-free mass, isotonic lifting volume, and sprint performance during intense resistance/agility training.
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We examined the effect of glycogen availability and branched-chain amino acid (BCAA) supplementation on branched-chain oxoacid dehydrogenase (BCOAD) activity during exercise. Six subjects cycled at approximately 75% of their maximal oxygen uptake to exhaustion on three occasions under different preexercise conditions: 1) low muscle glycogen (LOW), 2) low muscle glycogen plus BCAA supplementation (LOW+BCAA), and 3) high muscle glycogen (CON). The LOW trial was performed first, followed by the other two conditions in random order, and biopsies for all trials were obtained at rest, after 15 min of exercise (15 min), and at the point of exhaustion during the LOW trial (49 min). BCOAD activity was not different among the three conditions at rest; however, at 15 min BCOAD activity was higher (P < or = 0.05) for the LOW (31 +/- 5%) and LOW+BCAA (43 +/- 11%) conditions compared with CON (12 +/- 1%). BCOAD activity at 49 min was not different from respective values at 15 min for any condition. These data indicate that BCOAD is rapidly activated during submaximal exercise under conditions associated with low carbohydrate availability. However, there was no relationship between BCOAD activity and glycogen concentration or net glycogenolysis, which suggests that factors other than glycogen availability are important for BCOAD regulation during exercise in humans.
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Creatine supplementation has been shown to augment muscle PCr content and increase the rate of ATP resynthesis. Thus, we hypothesized that creatine supplementation might enhance sprinting performance. Eighteen subjects completed both of two testing sessions (control and postsupplement) 1 week apart, wherein they sprinted three 60-m distance trials that were recorded with videotape. Following the control session, for 7 days, subjects in the treatment group ingested a creatine-glucose mixture, while the placebo group consumed a glucose powder, followed by the postsupplementation session. Velocities of the subjects through three testing zones within the 60-m sprint were calculated from the videotape. Resultant velocities were analyzed using a MANOVA with a2x2x3x3 (Group x Session x Trial x Zone) design. Results indicated that there were no statistically significant main or interaction effects on velocity between groups for session, trial, or zone. These data do not support the hypothesis that supplementary c...
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Nutrient intake before, during, and after training will influence the adaptations that occur in response to the training stimulus. The influence of protein on training adaptations is receiving increasing attention from researchers. Methodological issues should be carefully considered when evaluating evidence of nutritional influence on training adaptations. Evidence suggests that adaptations to training are due to changes in the types and activities of various proteins in response to each exercise bout. Thus, study of the acute metabolic and molecular responses to exercise plus nutrition may provide valuable information about the expected influence on training adaptations. The type of protein, timing of protein ingestion relative to exercise, concurrent ingestion of other nutrients with protein, as well as the type of exercise training performed will impact the adaptations to training with the intake of protein. Protein is an important nutrient for muscle hypertrophy with training, but there is little support for the need for very high (e.g. >2.5–3.0 grams of protein per kilogram of body weight) intakes. Traditionally, endurance athletes have focused on carbohydrate intake, but recently protein has been touted to be critical during and after endurance exercise. There is evidence for and against the importance of protein for endurance exercise and more, well-controlled studies are required to delineate the importance of protein for endurance exercise adaptations. Whereas nutritional manipulations have customarily been focused on preventing protein degradation, muscle damage, and oxidative stress, recent evidence suggests that these processes may be critical for the optimal adaptive response to training.
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The effects of supplementation of the leucine metabolite β-hydroxy-β-methylbutyrate (HMB) were examined in a resistance training study. Thirty-nine men and 36 women between the ages of 20–40 y were randomized to either a placebo (P) supplemented or HMB supplemented (3.0 g HMB/d) group in two gender cohorts. All subjects trained three times per week for 4 wk. In the HMB group, plasma creatine phosphokinase levels tended to be suppressed compared to the placebo group following the 4 wk of resistance training (HMB:174.4 ± 26.8 to 173.5 ± 17.0 U/L; P:155.0 ± 20.8 to 195.2 ± 23.5 U/L). There were no significant differences in strength gains based on prior training status or gender with HMB supplementation. The HMB group had a greater increase in upper body strength than the placebo group (HMB:7.5 ± 0.6 kg; P:5.2 ± 0.6 kg; P = 0.008). The HMB groups increased fat-free weight by 1.4 ± 0.2 kg and decreased percent fat by 1.1% ± 0.2% while the placebo groups increased fat-free weight by 0.9 ± 0.2 kg and decreased percent fat by 0.5% ± 0.2% (fat-free weight P = 0.08, percent fat P = 0.08, HMB compared to placebo). In summary, this is the first short-term study to investigate the roles of gender and training status on the effects of HMB supplementation on strength and body composition. This study showed, regardless of gender or training status, HMB may increase upper body strength and minimize muscle damage when combined with an exercise program.
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Plasma characteristics at high pressure YBa2Cu3O7−δ reactive magnetron sputtering were investigated with a probe technique and in situ film resistance measurements. The experimental features of probe measurements in oxygen plasma are discussed. Electron energy distribution is the sum of two Maxwell distributions with kTe ≈ 1.5 eV and kTe ≈ 0.3 eV. N2O addition to a gas mixture results in the generation of negative ions with a density virtually equal to the density of positive ions. The energies of ions, impinging the film surface under film biasing, are discussed in collisionless and drift approximations. Low energy ion bombardment of the film surface at temperatures ≈ 400 °C results in a reduction of film oxygen content. © 1997 American Institute of Physics.
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The aim of this study was to examine the effects of short-term creatine monohydrate supplementation on multiple sprint running performance. Using a double-blind research design, 42 physically active men completed a series of 3 indoor multiple sprint running trials (15 3 30 m repeated at 35-second intervals). After the first 2 trials (familiarization and baseline), subjects were matched for fatigue score before being randomly assigned to 5 days of either creatine (4[middle dot]d-1 x 5 g creatine monohydrate 1 1g maltodextrin) or placebo (4[middle dot]d-1 x 6 g maltodextrin) supplementation. Sprint times were recorded via twin-beam photocells, and earlobe blood samples were drawn to evaluate posttest lactate concentrations. Relative to placebo, creatine supplementation resulted in a 0.7 kg increase in body mass (95% likely range: 0.02 to 1.3 kg) and a 0.4% reduction in body fat (95% likely range: 20.2 to 0.9%). There were no significant (p > 0.05) between-group differences in multiple sprint measures of fastest time, mean time, fatigue, or posttest blood lactate concentration. Despite widespread use as an ergogenic aid in sport, the results of this study suggest that creatine monohydrate supplementation conveys no benefit to multiple sprint running performance. (C) 2006 National Strength and Conditioning Association
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1. We investigated the effect of oral creatine supplementation during leg immobilization and rehabilitation on muscle volume and function, and on myogenic transcription factor expression in human subjects. 2. A double-blind trial was performed in young healthy volunteers (n = 22). A cast was used to immobilize the right leg for 2 weeks. Thereafter the subjects participated in a knee-extension rehabilitation programme (3 sessions week _1 , 10 weeks). Half of the subjects received creatine monohydrate (CR; from 20 g down to 5 g daily), whilst the others ingested placebo (P; maltodextrin). 3. Before and after immobilization, and after 3 and 10 weeks of rehabilitation training, the cross- sectional area (CSA) of the quadriceps muscle was assessed by NMR imaging. In addition, an isokinetic dynamometer was used to measure maximal knee-extension power (W max), and needle biopsy samples taken from the vastus lateralis muscle were examined to asses expression of the myogenic transcription factors MyoD, myogenin, Myf5, and MRF4, and muscle fibre diameters. 4. Immobilization decreased quadriceps muscle CSA (~10 %) and W max (~25 %) by the same magnitude in both groups. During rehabilitation, CSA and Wmax recovered at a faster rate in CR than in P (P < 0.05 for both parameters). Immobilization changed myogenic factor protein expression in neither P nor CR. However, after rehabilitation myogenin protein expression was increased in P but not in CR (P < 0.05), whilst MRF4 protein expression was increased in CR but not in P (P < 0.05). In addition, the change in MRF4 expression was correlated with the change in mean muscle fibre diameter (r = 0.73, P < 0.05). 5. It is concluded that oral creatine supplementation stimulates muscle hypertrophy during rehabilitative strength training. This effect may be mediated by a creatine-induced change in MRF4 and myogenin expression.
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1. The present study was undertaken to test whether creatine given as a supplement to normal subjects was absorbed, and if continued resulted in an increase in the total creatine pool in muscle. An additional effect of exercise upon uptake into muscle was also investigated. 2. Low doses (1 g of creatine monohydrate or less in water) produced only a modest rise in the plasma creatine concentration, whereas 5 g resulted in a mean peak after 1 h of 795 (sd 104) μmol/l in three subjects weighing 76–87 kg. Repeated dosing with 5 g every 2 h sustained the plasma concentration at around 1000 μmol/l. A single 5 g dose corresponds to the creatine content of 1.1 kg of fresh, uncooked steak. 3. Supplementation with 5 g of creatine monohydrate, four or six times a day for 2 or more days resulted in a significant increase in the total creatine content of the quadriceps femoris muscle measured in 17 subjects. This was greatest in subjects with a low initial total creatine content and the effect was to raise the content in these subjects closer to the upper limit of the normal range. In some the increase was as much as 50%. 4. Uptake into muscle was greatest during the first 2 days of supplementation accounting for 32% of the dose administered in three subjects receiving 6 × 5 g of creatine monohydrate/day. In these subjects renal excretion was 40, 61 and 68% of the creatine dose over the first 3 days. Approximately 20% or more of the creatine taken up was measured as phosphocreatine. No changes were apparent in the muscle ATP content. 5. No side effects of creatine supplementation were noted. 6. One hour of hard exercise per day using one leg augmented the increase in the total creatine content of the exercised leg, but had no effect in the collateral. In these subjects the mean total creatine content increased from 118.1 (sd 3.0) mmol/kg dry muscle before supplementation to 148.5 (sd 5.2) in the control leg, and to 162.2 (sd 12.5) in the exercised leg. Supplementation and exercise resulted in a total creatine content in one subject of 182.8 mmol/kg dry muscle, of which 112.0 mmol/kg dry muscle was in the form of phosphocreatine.
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Leucine kinetic and nitrogen balance (NBAL) methods were used to determine the dietary protein requirements of strength athletes (SA) compared with sedentary subjects (S). Individual subjects were randomly assigned to one of three protein intakes: low protein (LP) = 0.86 g protein.kg-1.day-1, moderate protein (MP) = 1.40 g protein.kg-1.day-1, or high protein (HP) = 2.40 g protein.kg-1.day-1 for 13 days for each dietary treatment. NBAL was measured and whole body protein synthesis (WBPS) and leucine oxidation were determined from L-[1-13C]leucine turnover. NBAL data were used to determine that the protein intake for zero NBAL for S was 0.69 g.kg-1.day-1 and for SA was 1.41 g.kg-1.day-1. A suggested recommended intake for S was 0.89 g.kg-1.day-1 and for SA was 1.76 g.kg-1.day-1. For SA, the LP diet did not provide adequate protein and resulted in an accommodated state (decreased WBPS vs. MP and HP), and the MP diet resulted in a state of adaptation [increase in WBPS (vs. LP) and no change in leucine oxidation (vs. LP)]. The HP diet did not result in increased WBPS compared with the MP diet, but leucine oxidation did increase significantly, indicating a nutrient overload. For S the LP diet provided adequate protein, and increasing protein intake did not increase WBPS. On the HP diet leucine oxidation increased for S. These results indicated that the MP and HP diets were nutrient overloads for S. There were no effects of varying protein intake on indexes of lean body mass (creatinine excretion, body density) for either group. In summary, protein requirements for athletes performing strength training are greater than for sedentary individuals and are above current Canadian and US recommended daily protein intake requirements for young healthy males.
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The present study was conducted to investigate the metabolic regulation of the oxidation of branched-chain amino acids (BCAA) by exercise in human skeletal muscle. Five trained male volunteers were exercised on a cycle ergometer at 70% +/- 10% (mean +/- SD) of their maximal oxygen consumption (VO2max). Percutaneous quadriceps muscle biopsies were obtained under local anaesthesia at rest and after 30 and 120 min of exercise. In the muscle samples the active and total amount of the branched-chain 2-oxo acid dehydrogenase complex (BC-complex), the regulatory enzyme in the oxidative pathway of the BCAA, were measured. Glycogen content and activity of mitochondrial marker enzymes were also measured. Blood samples were obtained every 20 min for the measurement of metabolites. Heart rate and rated perceived exertion on the Borg scale were recorded every 10 min. At rest 4.0% +/- 2.5% of the BC complex was active, after 30 min of exercise 9.9% +/- 9.0% and after 120 min 17.5% +/- 8.5% (mean +/- SD). Exercise did not change the total activity. The largest activation was seen in two of the subjects who developed higher blood lactates early on during exercise and decreased their muscle glycogen more (indications of anaerobic metabolism). These data demonstrate that in trained individuals significant increases in the activity of the BC-complex occur only after prolonged intense exercise. In spite of the 4-fold activation, the data support the classical view that amino acids and protein do not contribute substantially as an energy source during exercise, since VO2 increased more than 20-fold.
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On two separate occasions, five well-trained endurance runners (VO2max = 71 +/- 5 ml/kg/min; means +/- SD) consumed a meat-free diet for 6 days. For one trial the subjects consumed the recommended dietary allowance (RDA) of protein (REC-PRO = 0.86 +/- 0.23 g/kg body wt/day). Protein intake for the other trial was 1.7 times higher (HI-PRO = 1.49 +/- 0.29 g/kg body wt/day). Each subject followed his regular training program (12-16 km running/day), and on day 5 of each diet completed a treadmill run at a similar intensity and duration (75 min at 72% VO2max). Seventy-two hour urinary urea N loss (days 4, 5, and 6 of each diet) and day 5 exercise sweat urea N excretion were measured. Serum urea N and creatinine increased significantly during the treadmill run under both dietary conditions (P less than 0.05). No significances between diet differences were observed in sweat or urinary urea N excretion; however, excretion of both tended to be higher on the REC-PRO diet than on the HI-PRO diet. The differences in protein intake combined with the nitrogen excretion measures resulted in significant differences in estimated whole-body nitrogen retention between the two treatments. Nitrogen retention (means +/- SE) remained positive during the HI-PRO trial (2.41 +/- 1.99 g/day) but was significantly (P less than 0.005) reduced to -5.29 +/- 2.58 g/day during the REC-PRO trial. These results suggest that the current protein RDA may be inadequate for athletes engaging in chronic high-intensity endurance exercise. Future studies are needed to confirm this observation.
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Strength performance depends not only on the quantity and quality of the involved muscles, but also upon the ability of the nervous system to appropriately activate the muscles. Strength training may cause adaptive changes within the nervous system that allow a trainee to more fully activate prime movers in specific movements and to better coordinate the activation of all relevant muscles, thereby effecting a greater net force in the intended direction of movement. The evidence indicating neural adaptation is reviewed. Electromyographic studies have provided the most direct evidence. They have shown that increases in peak force and rate of force development are associated with increased activation of prime mover muscles. Possible reflex adaptations related to high stretch loads in jumping and rapid reciprocal movements have also been revealed. Other studies, including those that demonstrate the "cross-training" effect and specificity of training, provide further evidence of neural adaptation. The possible mechanisms of neural adaptation are discussed in relation to motor unit recruitment and firing patterns. The relative roles of neural and muscular adaptation in short- and long-term strength training are evaluated.
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Resistance training results in a wide spectrum of adaptations in various physiological systems. Increases in muscle size and strength, changes in body composition, neuroendocrine function and cardiovascular responses have been observed following resistance training. Additionally, resistance training may be an effective means by which the incidence of sports injuries can be reduced. The physiological alterations induced by resistance training appear to be specific to the number of sets and repetitions and exercises performed. Thus, special attention is required when developing the exercise prescription for resistance training.
Article
The present study examined the effects of training status (endurance exercise or body building) on nitrogen balance, body composition, and urea excretion during periods of habitual and altered protein intakes. Experiments were performed on six elite bodybuilders, six elite endurance athletes, and six sedentary controls during a 10-day period of normal protein intake followed by a 10-day period of altered protein intake. The nitrogen balance data revealed that bodybuilders required 1.12 times and endurance athletes required 1.67 times more daily protein than sedentary controls. Lean body mass (density) was maintained in bodybuilders consuming 1.05 g protein.kg-1.day-1. Endurance athletes excreted more total daily urea than either bodybuilders or controls. We conclude that bodybuilders during habitual training require a daily protein intake only slightly greater than that for sedentary individuals in the maintenance of lean body mass and that endurance athletes require daily protein intakes greater than either bodybuilders or sedentary individuals to meet the needs of protein catabolism during exercise.
Article
Two studies were conducted to investigate the effects of mild exercise on nitrogen balance in men given diets supplying adequate or slightly limiting energy. In experiment A the diet supplied 91 mg N/kg body weight (0.57 g protein/kg, the FAO/WHO safe level of intake) as egg white; in experiment B the same source was used to provide the 1980 NRC-RDA for adult males, 128 mg N/kg body weight (0.8 g protein/kg). By adjusting energy intake and activity, periods of energy equilibrium and negative energy balance (-15%) were achieved at three levels of activity (X for exercise): no programmed work (0.85X), 1 hour of treadmill walking (1.0X) and 1 hour each of treadmill and cycle ergometry (1.15X). "True" nitrogen balance (TNbal) was more positive or less negative during periods of energy equilibrium as compared to those of energy deficit. This effect of energy balance on TNbal increased with physical activity. At the lower protein intake the mean difference in TNbal between the period of energy equilibrium and that of energy deficit at 1.0X was 0.19 g N/day (nonsignificant difference) and 0.54 g N/day at 1.15X. When protein intake was increased, the difference in TNbal between periods of equilibrium and deficit was significant at all levels of activity: 0.65 g N/day at 0.85X, 0.93 g N/day at 1.0X and 1.09 g N/day at 1.15X. Physical activity was anabolic when energy balance was maintained. In experiment A the addition of 1 hour of exercise (1.0X to 1.15X) spared 2.5 mg N/kg body weight; reducing activity by 1 hour (1.0X to 0.85X) cost 1.4 mg N/kg body weight. In experiment B, TNbal was more positive with increased activity (by 5.9 mg N/kg body weight) and more negative (by 11.5 mg N/kg body weight) when the men were sedentary. During periods of energy deficit, the anabolic effect of activity was also present, although less markedly. When activity increased from 1 to 2 hours in experiment A, TNbal improved by 2.1 mg N/kg body weight and in experiment B, by 3.5 mg N/kg body weight. Thus, circumstances of negative energy balance with adequate protein intake are better tolerated when the energy deficit is generated by physical activity than when it derives from reduced intake; the picture when protein intake is marginal requires further investigation.
Article
Twelve patients who had undergone colon operations were randomized prospectively in the postoperative recovery room. Seven received a hypocaloric intravenous solution consisting of 3.5% amino acids plus 2.5% glucose and five received 3.5% amino acids plus 10% fat. Nitrogen balance data indicated that isocaloric amounts of glucose and fat seem equally effective when combined with amino acids. Although the albumin synthesis rates (measured by the 14C technique on the fourth postoperative day) were not significantly different between the two groups, when the results were included with pooled data from previous similar studies, there was a statistically significant difference which indicated a higher rate of albumin synthesis in patients who received the combination of amino acids and fat compared with those who received amino acids and glucose P < 0.05). In this clinical setting, fat may favor the uptake and synthesis of amino acids into visceral proteins, while glucose may have a more direct role in the synthesis of skeletal muscle protein.
Article
Phosphocreatine (PCr) availability is likely to limit performance in brief, high-power exercise because the depletion of PCr results in an inability to maintain adenosine triphosphate (ATP) resynthesis at the rate required. It is now known that the daily ingestion of four 5-g doses of creatine for 5 days will significantly increase intramuscular creatine and PCr concentrations prior to exercise and will facilitate PCr resynthesis during recovery from exercise, particularly in those individuals with relatively low creatine concentrations prior to feeding. As a consequence of creatine ingestion, work output during repeated bouts of high-power exercise has been increased under a variety of experimental conditions. The reduced accumulation of ammonia and hypoxanthine in plasma and the attenuation of muscle ATP degradation after creatine feeding suggest that the ergogenic effect of creatine is achieved by better maintaining ATP turnover during contraction.
Article
The rates of protein synthesis and degradation and of amino acid transport were determined in the leg muscle of untrained postabsorptive normal volunteers at rest and approximately 3 h after a resistance exercise routine. The methodology involved use of stable isotopic tracers of amino acids, arteriovenous catheterization of the femoral vessels, and biopsy of the vastus lateralis muscle. During postexercise recovery, the rate of intramuscular phenylalanine utilization for protein synthesis increased above the basal value by 108 +/- 18%, whereas the rate of release from proteolysis increased by 51 +/- 17%. Muscle protein balance improved (P < 0.05) after exercise but did not become positive (from -15 +/- 12 to -6 +/- 3 nmol phenylalanine.min-1.100 ml leg volume-1). After exercise, rates of inward transport of leucine, lysine, and alanine increased (P < 0.05) above the basal state from 132 +/- 16 to 208 +/- 29, from 122 +/- 8 to 260 +/- 8, and from 384 +/- 71 to 602 +/- 89 nmol.min-1.100 ml leg-1, respectively. Transport of phenylalanine did not change significantly. These results indicate that, during recovery after resistance exercise, muscle protein turnover is increased because of an acceleration of synthesis and degradation. A postexercise acceleration of amino acid transport may contribute to the relatively greater stimulation of protein synthesis.
Article
The effect of dietary creatine (Cr) supplementation on performance during 3, 30 s bouts maximal isokinetic cycling and on plasma ammonia and blood lactate accumulation during exercise was investigated. Placebo (P) ingestion had no effect on peak power output (PPO), mean power output (MPO) and total work output during each bout of exercise. Cr ingestion (4 x 5 g.day-1 for 5 days) significantly increased PPO in exercise bout 1 (p < 0.05) and MPO and total work output in exercise bouts 1 (p < 0.05, p < 0.05, respectively) and 2 (p < 0.05, p < 0.05, respectively). Cr ingestion had no effect on any of the measures of performance during exercise bout 3. No difference was observed in peak plasma ammonia accumulation before (146 + 30 mumol.l-1) and after (122 +/- 17 mumol.l-1) P ingestion, however the corresponding concentration was lower following Cr ingestion (129 +/- 22 mumol.l-1) compared with before Cr ingestion (160 +/- 18 mumol.l-1, p < 0.05), despite subjects performing more work. No difference in peak blood lactate accumulation was observed before and after P or Cr ingestion. The results demonstrate that Cr ingestion can increase whole body exercise performance during the initial two, but not a third, successive bout of maximal exercise lasting 30 s. The lower accumulation of plasma ammonia under these conditions suggests this response is achieved by an effect on muscle ATP turnover.
Article
A family of homologous, Na+/Cl- dependent plasma membrane transporters catalyze the uptake of a number of neurotransmitters and structurally related compounds into cells. Here, we report the cDNA cloning, sequencing and functional characterization of a non-mammalian member of this transporter family. A creatine transporter from the electric ray, Torpedo marmorata, displays 64% amino acid identity with its rabbit counterpart and has a similar substrate affinity and specificity. Sequence similarity generally is lowest in those regions where also the sequences of other members of the family, transporting different substrates, diverge. Only a few amino acids are better conserved between the two creatine transporters than with the other family members and are candidates for a role in conferring substrate specificity.
Article
Biopsy samples were obtained from the vastus lateralis muscle of eight subjects after 0, 20, 60, and 120 s of recovery from intense electrically evoked isometric contraction. Later (10 days), the same procedures were performed using the other leg, but subjects ingested 20 g creatine (Cr)/day for the preceding 5 days. Muscle ATP, phosphocreatine (PCr), free Cr, and lactate concentrations were measured, and total Cr was calculated as the sum of PCr and free Cr concentrations. In five of the eight subjects, Cr ingestion substantially increased muscle total Cr concentration (mean 29 +/- 3 mmol/kg dry matter, 25 +/- 3%; range 19-35 mmol/kg dry matter, 15-32%) and PCr resynthesis during recovery (mean 19 +/- 4 mmol/kg dry matter, 35 +/- 6%; range 11-28 mmol/kg dry matter, 23-53%). In the remaining three subjects, Cr ingestion had little effect on muscle total Cr concentration, producing increases of 8-9 mmol/kg dry matter (5-7%), and did not increase PCr resynthesis. The data suggest that a dietary-induced increase in muscle total Cr concentration can increase PCr resynthesis during the 2nd min of recovery from intense contraction.
Article
The current Canadian Recommended Nutrient Intake (RNI) for protein (0.86 g.kg-1.day-1) makes no allowance for an effect of habitual physical activity. In addition, Tarnopolsky et al. (J. Appl. Physiol. 68: 302-308, 1990) showed that males may catabolize more protein than females consequent to endurance exercise. We examined nitrogen (N) balance and leucine kinetics during submaximal endurance exercise to determine the adequacy of the current Canadian RNI for protein for male and female endurance athletes. Athletes were matched for equal training volume, competitive status, and conditioning and were fed diets isoenergetic with their habitual intake, containing protein at the Canadian RNI. Subjects were adapted to the diet for 10 days before completing a 3-day measurement of N balance. N balance showed that the RNI was inadequate for females (-15.9 +/- 6.0 mg.kg-1.day-1) and males (-26.3 +/- 11.0 mg.kg-1.day-1). Leucine kinetics during exercise were determined for each subject on day 3 of the N balance experiment by use of a primed continuous infusion of L-[1-13C]leucine and the reciprocal pool model. Exercise resulted in a significant (P < 0.01) increase in leucine oxidation for both groups. Males oxidized a greater amount of leucine during the infusion than females (P < 0.01). Leucine flux also increased significantly (P < 0.01) during exercise in both groups. We conclude that the current Canadian RNI for protein is inadequate for those who chronically engage in endurance exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
Article
1. The present experiment was undertaken to investigate the influence of oral creatine supplementation, shown previously to increase the total creatine content of human skeletal muscle (Harris RC, Soderlund K, Hultman E. Clin Sci 1992; 83: 367–74), on skeletal muscle isokinetic torque and the accumulation of plasma ammonia and blood lactate during five bouts of maximal exercise. 2. Twelve subjects undertook five bouts of 30 maximal voluntary isokinetic contractions, interspersed with 1 min recovery periods, before and after 5 days of placebo (4 × 6 g of glucose/day, n = 6) or creatine (4 × 5 g of creatine plus 1 g of glucose/day, n = 6) oral supplementation. Muscle torque production and plasma ammonia and blood lactate accumulation were measured during and after exercise on each treatment 3. No difference was seen when comparing muscle peak torque production during exercise before and after placebo ingestion. After creatine ingestion, muscle peak torque production was greater in all subjects during the final 10 contractions of exercise bout 1 (P <0.05), throughout the whole of exercise bouts 2 (P <0.01), 3 (P <0.05) and 4 (P = 0.057) and during contractions 11–20 of the final exercise bout (P <0.05), when compared with the corresponding measurements made before creatine ingestion. Plasma ammonia accumulation was lower during and after exercise after creatine ingestion. No differences were found when comparing blood lactate levels. 4. There is evidence to suggest that the decrease in the degree of muscle torque loss after dietary creatine supplementation may be a consequence of a creatine-induced acceleration of skeletal muscle phosphocreatine resynthesis. It is postulated that an increased availability of phosphocreatine would maintain better the required rate of ATP demand during contraction. This is supported by the observed lower accumulation of plasma ammonia during exercise after creatine ingestion.
Article
This study examined the influence of oral creatine monohydrate supplementation on repeated 10 s cycle ergometer sprint performance. Seventeen recreationally active males (mean +/- SD age, body mass, height, and peak oxygen uptake = 20.5 +/- 1.2 yr, 72.1 +/- 10.3 kg, 176.8 +/- 6.6 cm and 3.87 +/- 0.91 l.min-1, respectively) participated in the 16 day experiment. All subjects initially completed a VO2peak test and were then administered glucose (4 x 10 g per day) in a single blind fashion for four days, after which they completed the first series of multiple sprints (7 x 10 s). Following the sprints, subjects were matched on sprint performance and divided into two groups (n = 8, placebo (Pl); and n = 9, creatine (Cr)). For the following four days, diets were supplemented with either Cr (4 x 70 mg.kg-1 body mass per day mixed with 5 g glucose) or glucose (4 x 10 g per day); supplementation during this phase was double-blind. Subjects then repeated the multiple sprint and VO2peak tests. Measures of peak power output (PPO), mean power output (MPO), end-power output (EPO), and percent power decline were recorded during the sprints. Each 10 s sprint was separated by 30 s of passive recovery except for sprints five and six which were separated by five minutes. Venous blood was sampled at rest, immediately after sprint five, before sprint six, and following sprint seven for the analysis of plasma lactate and blood pH. Expired air was sampled for five minutes following sprint seven for the calculation of post-exercise VO2. Analysis of variance revealed that four days of Cr supplementation did not influence multiple sprint performance, plasma lactate, blood pH and excess post-sprint oxygen consumption. Furthermore, VO2peak was unchanged following Cr supplementation. The data suggest that either the four day period of Cr supplementation failed to significantly raise resting muscle [Cr], or that multiple sprint performance was not enhanced by increases in resting muscle [Cr].
Article
The effect of dietary creatine and supplementation on skeletal muscle creatine accumulation and subsequent degradation and on urinary creatinine excretion was investigated in 31 male subjects who ingested creatine in different quantities over varying time periods. Muscle total creatine concentration increased by approximately 20% after 6 days of creatine supplementation at a rate of 20 g/day. This elevated concentration was maintained when supplementation was continued at a rate of 2 g/day for a further 30 days. In the absence of 2 g/day supplementation, total creatine concentration gradually declined, such that 30 days after the cessation of supplementation the concentration was no different from the presupplementation value. During this period, urinary creatinine excretion was correspondingly increased. A similar, but more gradual, 20% increase in muscle total creatine concentration was observed over a period of 28 days when supplementation was undertaken at a rate of 3 g/day. In conclusion, a rapid way to "creatine load" human skeletal muscle is to ingest 20 g of creatine for 6 days. This elevated tissue concentration can then be maintained by ingestion of 2 g/day thereafter. The ingestion of 3 g creatine/day is in the long term likely to be as effective at raising tissue levels as this higher dose.
Article
Creatine supplementation has been shown to augment muscle PCr content and increase the rate of ATP resynthesis. Thus, we hypothesized that creatine supplementation might enhance sprinting performance. Eighteen subjects completed both of two testing sessions (control and postsupplement) 1 week apart, wherein they sprinted three 60-m distance trials that were recorded with videotape. Following the control session, for 7 days, subjects in the treatment group ingested a creatine-glucose mixture, while the placebo group consumed a glucose powder, followed by the postsupplementation session. Velocities of the subjects through three testing zones within the 60-m sprint were calculated from the videotape. Resultant velocities were analyzed using a MANOVA with a 2 x 2 x 3 x 3 (Group x Session x Trial x Zone) design. Results indicated that there were no statistically significant main or interaction effects on velocity between groups for session, trial, or zone. These data do not support the hypothesis that supplementary creatine ingestion will enhance velocity during the early or latter segments of a 60-m sprint.
Article
We examined the effect of glycogen availability and branched-chain amino acid (BCAA) supplementation on branched-chain oxoacid dehydrogenase (BCOAD) activity during exercise. Six subjects cycled at approximately 75% of their maximal oxygen uptake to exhaustion on three occasions under different preexercise conditions: 1) low muscle glycogen (LOW), 2) low muscle glycogen plus BCAA supplementation (LOW+BCAA), and 3) high muscle glycogen (CON). The LOW trial was performed first, followed by the other two conditions in random order, and biopsies for all trials were obtained at rest, after 15 min of exercise (15 min), and at the point of exhaustion during the LOW trial (49 min). BCOAD activity was not different among the three conditions at rest; however, at 15 min BCOAD activity was higher (P < or = 0.05) for the LOW (31 +/- 5%) and LOW+BCAA (43 +/- 11%) conditions compared with CON (12 +/- 1%). BCOAD activity at 49 min was not different from respective values at 15 min for any condition. These data indicate that BCOAD is rapidly activated during submaximal exercise under conditions associated with low carbohydrate availability. However, there was no relationship between BCOAD activity and glycogen concentration or net glycogenolysis, which suggests that factors other than glycogen availability are important for BCOAD regulation during exercise in humans.
Article
Few studies examine ammonia and amino acid metabolism in response to endurance training. Trained humans generally experience less increase in plasma ammonia during either prolonged or intense exercise. This is probably a reflection of reduced ammonia production and release from the active muscle; it could be a reflection of decreased AMP deaminase activity, decreased glutamate dehydrogenase activity, and/or increased alanine and glutamine formation. Little is known regarding the associated enzyme systems in humans, but in experiments with animal models, aerobic training decreases AMP deaminase and increases the enzymes of amino acid transamination and oxidation.
Article
Six normal untrained men were studied during the intravenous infusion of a balanced amino acid mixture (approximately 0.15 g.kg-1.h-1 for 3 h) at rest and after a leg resistance exercise routine to test the influence of exercise on the regulation of muscle protein kinetics by hyperaminoacidemia. Leg muscle protein kinetics and transport of selected amino acids (alanine, phenylalanine, leucine, and lysine) were isotopically determined using a model based on arteriovenous blood samples and muscle biopsy. The intravenous amino acid infusion resulted in comparable increases in arterial amino acid concentrations at rest and after exercise, whereas leg blood flow was 64 +/- 5% greater after exercise than at rest. During hyperaminoacidemia, the increases in amino acid transport above basal were 30-100% greater after exercise than at rest. Increases in muscle protein synthesis were also greater after exercise than at rest (291 +/- 42% vs. 141 +/- 45%). Muscle protein breakdown was not significantly affected by hyperminoacidemia either at rest or after exercise. We conclude that the stimulatory effect of exogenous amino acids on muscle protein synthesis is enhanced by prior exercise, perhaps in part because of enhanced blood flow. Our results imply that protein intake immediately after exercise may be more anabolic than when ingested at some later time.
Article
Mixed muscle protein fractional synthesis rate (FSR) and fractional breakdown rate (FBR) were examined after an isolated bout of either concentric or eccentric resistance exercise. Subjects were eight untrained volunteers (4 males, 4 females). Mixed muscle protein FSR and FBR were determined using primed constant infusions of [2H5]phenylalanine and 15N-phenylalanine, respectively. Subjects were studied in the fasted state on four occasions: at rest and 3, 24, and 48 h after a resistance exercise bout. Exercise was eight sets of eight concentric or eccentric repetitions at 80% of each subject's concentric 1 repetition maximum. There was no significant difference between contraction types for either FSR, FBR, or net balance (FSR minus FBR). Exercise resulted in significant increases above rest in muscle FSR at all times: 3 h = 112%, 24 h = 65%, 48 h = 34% (P < 0.01). Muscle FBR was also increased by exercise at 3 h (31%; P < 0.05) and 24 h (18%; P < 0.05) postexercise but returned to resting levels by 48 h. Muscle net balance was significantly increased after exercise at all time points [(in %/h) rest = -0.0573 +/- 0.003 (SE), 3 h = -0.0298 +/- 0.003, 24 h = -0.0413 +/- 0.004, and 48 h = -0.0440 +/- 0.005], and was significantly different from zero at all time points (P < 0.05). There was also a significant correlation between FSR and FBR (r = 0.88, P < 0.001). We conclude that exercise resulted in an increase in muscle net protein balance that persisted for up to 48 h after the exercise bout and was unrelated to the type of muscle contraction performed.
Article
In a double-blind and randomized manner, 18 male and female junior competitive swimmers supplemented their diets with 21 g.day-1 of creatine monohydrate (Cr) or a maltodextrin placebo (P) for 9 days during training. Prior to and following supplementation, subjects performed three 100-m freestyle sprint swims (long course) with 60 s rest/recovery between heats. In addition, subjects performed three 20-s arm ergometer maximal-effort sprint tests in the prone position with 60 s rest/recovery between sprint tests. Significant differences were observed among swim times, with Cr subjects swimming significantly faster than P subjects following supplementation in Heat 1 and significantly decreasing swim time in the second 100-m sprint. There was also some evidence that cumulative time to perform the three 100-m swims was decreased in the Cr group. Results indicate that 9 days of Cr supplementation during swim training may provide some ergogenic value to competitive junior swimmers during repetitive sprint performance.
Article
Effects of a 10-week progressive strength training program composed of a mixture of exercises for increasing muscle mass, maximal peak force, and explosive strength (rapid force production) were examined in 8 young (YM) (29+/-5 yrs) and 10 old (OM) (61+/-4 yrs) men. Electromyographic activity, maximal bilateral isometric peak force, and maximal rate of force development (RFD) of the knee extensors, muscle cross-sectional area (CSA) of the quadriceps femoris (QF), muscle fiber proportion, and fiber areas of types I, IIa, IIb, and IIab of the vastus lateralis were evaluated. Maximal and explosive strength values remained unaltered in both groups during a 3-week control period with no training preceding the strength training. After the 10-week training period, maximal isometric peak force increased from 1311+/-123 N by 15.6% (p <.05) in YM and from 976+/-168 N by 16.5% (p <.01) in OM. The pretraining RFD values of 4049+/-791 N*s(-1) in YM and 2526+/-1197 N*s(-1) in OM remained unaltered. Both groups showed significant increases (p < .05) in the averaged maximum IEMGs of the vastus muscles. The CSA of the QF increased from 90.3+/-7.9 cm2 in YM by 12.2% (p <.05) and from 74.7+/-7.8 cm2 in OM by 8.5% (p <.001). No changes occurred in the muscle fiber distribution of type I during the training, whereas the proportion of subtype IIab increased from 2% to 6% (p < .05) in YM and that of type IIb decreased in both YM from 25% to 16% (p < .01) and in OM from 15% to 6% (p < .05). The mean fiber area of type I increased after the 10-week training in YM (p < .001) and OM (p < .05) as well as that of type IIa in both YM (p < .01) and OM (p < .01). The individual percentage values for type I fibers were inversely correlated with the individual changes recorded during the training in the muscle CSA of the QF (r=-.56, p < .05). The present results suggest that both neural adaptations and the capacity of the skeletal muscle to undergo training-induced hypertrophy even in older people explain the gains observed in maximal force in older men, while rapid force production capacity recorded during the isometric knee extension action remained unaltered during the present mixed strength training program.