Ammonia as an Indicator of Exercise Stress Implications of Recent Findings to Sports Medicine

Banister, E. W.; Rajendra, Wudayagiri; Mutch, Barbara J. C.

doi:10.2165/00007256-198502010-00004

Cited by 41 publications

(16 citation statements)

References 64 publications

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“…This increasing ammonia concentration in blood starts to affect the liver and brain, generating fatigue due to excess cerebral ammonia and the inability of peripheral organs to detoxify ammonia. According to Banister et al (1985) and Bianchi et al (1997), hyperammonemia reduces ATP resynthesis, with a consequent increase in the activity of the purine nucleotide cycle (deamination of AMP into IMP). However, deamination of BCAA, and the consequent oxidation of their carbon skeletons for ATP synthesis, occurs due to depletion of muscle and hepatic glycogen stores when fatigue is probably already installed (Jakeman, 1998;Wagenmakers, 1998).…”

Section: Discussionmentioning

confidence: 99%

Effect of chronic supplementation with branched-chain amino acids on the performance and hepatic and muscle glycogen content in trained rats

et al. 2006

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Section: Discussionmentioning

confidence: 99%

Effect of chronic supplementation with branched-chain amino acids on the performance and hepatic and muscle glycogen content in trained rats

et al. 2006

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“…However, the specific site of fatigue within active skeletal muscle during submaximal dynamic contractions is unclear in light of a recent investigation by Kayser et al (1993), who observed no evidence of local muscle fatigue during exercise in conditions of severe hypoxia, and suggested that limitations to performance were likely to be central. Furthermore, much attention has been focused on the possible effects of hypoxia-induced hyperammonia on central mechanisms (Bannister et al 1985).…”

Section: Introductionmentioning

confidence: 99%

Myoelectric evidence of peripheral muscle fatigue during exercise in severe hypoxia: some references to m. vastus lateralis myosin heavy chain composition

Taylor

Bronks

Smith

et al. 1997

European Journal of Applied Physiology

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Integrated electromyography (iEMG) of the m. vastus lateralis was analysed during cycle ergometry in male subjects (n = 8). Two work trials were conducted, one under normoxia (N), the other under environmental normobaric hypoxia (EH in which the oxygen fraction in inspired gas = 0.116), each trial lasting 10 min. The absolute power output (180 W) was the same for both trials and was equivalent to 77 (4)% of maximum heart rate in trial N. Maximal voluntary isometric contractions were performed after each trial to assess changes in force, muscle fibre conduction velocity (MFCV), electromechanical delay (EMD), median frequency of EMG (MF) and maximal iEMG (iEMGmax). Biopsy samples of muscle were obtained from the m. vastus medialis before testing. Myosin heavy chain (MHC) differences were determined through sodium dodecyl-polyacrylamide gel electrophoresis followed by densitometric analysis. No differences in submaximal iEMG were observed between EH and N trials during the first minute of work. At the end of both work trials iEMG was significantly elevated compared with starting values, however the iEMG recorded in EH exceeded N values by 15%. At the end of the EH trials the following were observed: a decrease in isometric force, MFCV and MF with an increase in EMD and the iEMGmax/force ratio. The iEMGmax was unchanged. No differences in any of these variables were observed after the N trial. Mean (SD) lactate concentrations following EH and N trials were 9.2 (4.4) mmol x 1(-1) and 3.5 (1.1) mmol x 1(-1), respectively. Results indicate that an increased motor unit recruitment and rate coding was needed in EH to maintain the required power output. The increased motor unit recruitment and rate coding were associated with myoelectric evidence of "peripheral" muscle fatigue. Subjects with higher compositions of type II MHC accumulated more lactate and displayed greater reductions in MF and MFCV during fatigue.

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“…Plasm a am m onia values, re¯ecting adenosine m onophosphate (AM P) deam ination, m easured in the 8´50 yard test, m ay provide fur ther inform ation regarding the m echanism s responsible for the im provem ents in perform ance observed in the creatine group during the later repetitions (Banister et al, 1985;Greenhaþ et al, 1993b). This reaction is accelerated in extrem e, highintensity exercise bouts (such as in this study) to support high AT P turnover rates.…”

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confidence: 99%

The effects of oral creatine supplementation on performance in single and repeated sprint swimming

Peyrebrune

Nevill²,

Donaldson³

et al. 1998

Journal of Sports Sciences

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We studied the effects of oral creatine supplementation on sprint swimming performance in 14 elite competitive male swimmers. The subjects performed a single sprint (1 x 50 yards [45.72 m]) and repeated sprint set (8 x 50 yards at intervals of 1 min 30 s) before and after a 5 day period of either creatine (9 g creatine + 4.5 g maltodextrin + 4.5 g glucose day(-1)) or placebo (18 g glucose day(-1); double-blind protocol) supplementation. Venous and capillary blood samples were taken for the determination of plasma ammonia, blood pH and lactate. Mean times recorded for the single 50 yard sprint were unchanged as a result of supplementation (creatine vs control, N.S.). During the repeated sprint test, mean times increased (P< 0.01, main effect time) during all trials, but performance was improved as a result of creatine supplementation (sprints 1-8: control pre-, 23.35+/-0.68 to 26.32+/-1.34 s; control post-, 23.59+/-0.66 to 26.19+/-1.48 s; creatine pre-, 23.20+/-0.67 to 26.85+/-0.42 s; creatine post-, 23.39+/-0.54 to 25.73+/-0.26 s; P < 0.03, group x trial interaction). Thus the percentage decline in performance times was reduced after creatine supplementation (control, 12.7+/-5.7% vs 11.0+/-5.5%; creatine, 15.7+/-4.3% vs 10.0+/-2.5%; P< 0.05, group x trial interaction). The metabolic response was similar before and after supplementation, with no differences in the blood lactate or pH response. Plasma ammonia was lower on the second trial (P< 0.05, main effect trial), but this could not be attributed to the effect of supplementation (group x trial interaction, N.S.). A further urinary analysis study supported these findings by demonstrating an approximately 67% (approximately 26 g) retention of the administered creatine in this group of swimmers after an identical supplementation regimen. In summary, our results suggest that ingesting 9 g creatine per day for 5 days can improve swimming performance in elite competitors during repeated sprints, but appears to have no effect on a single 50 yard sprint.

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Ammonia as an Indicator of Exercise Stress Implications of Recent Findings to Sports Medicine

Cited by 41 publications

References 64 publications

Effect of chronic supplementation with branched-chain amino acids on the performance and hepatic and muscle glycogen content in trained rats

Effect of chronic supplementation with branched-chain amino acids on the performance and hepatic and muscle glycogen content in trained rats

Myoelectric evidence of peripheral muscle fatigue during exercise in severe hypoxia: some references to m. vastus lateralis myosin heavy chain composition

The effects of oral creatine supplementation on performance in single and repeated sprint swimming

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