Muscle ammonia and amino acid metabolism during dynamic exercise in man

Katz, Abram; Broberg, S.; Sahlin, Kent; Wahren, John

doi:10.1111/j.1475-097x.1986.tb00242.x

Cited by 113 publications

(98 citation statements)

References 33 publications

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“…Cycle ergometer exercise with a load of 70% maximum oxygen uptake (V ・ O2max) for 10 or 20 min increased glutamine and alanine levels, but decreased glutamate levels in muscles 18) . Cycle ergometer exercise with a load of 50% V ・ O2max, followed by a load of 97% of the V ・ O2max for 5.2 min to fatigue, increased alanine levels, but decreased glutamate levels 24) . Furthermore, isometric contraction exercise with two-thirds maximum voluntary contraction to fatigue decreased glutamate levels, but increased alanine and pyruvate levels in muscles 25) .…”

Section: Muscle Fiber Type Differencesmentioning

confidence: 91%

Exercise-induced changes in amino acid levels in skeletal muscle and plasma

Ishikura¹,

Ra²,

Ohmori³

2013

JPFSM

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During exercise, amino acid oxidation and protein breakdown are enhanced while protein synthesis is suppressed, even though protein does not constitute a quantitatively important energy source. In response to exercise-induced stimulation, various changes in free amino acids occur in skeletal muscle to meet physiological demands. Plasma amino acids are also under the influence of various types of stress, including exercise stress. For example, acute exercise increases alanine and glutamine levels, but decreases glutamate levels in skeletal muscle. At the same time, it increases tryptophan and taurine levels, but decreases glutamine levels in plasma. Prolonged exercise decreases glutamine and glutamate levels, while increasing tyrosine and phenylalanine levels in skeletal muscle. Furthermore, when prolonged exercise-induced changes in amino acid levels are compared between trained and untrained individuals, glutamate and taurine levels in skeletal muscle and phenylalanine, leucine, isoleucine, and tyrosine levels in plasma are higher in trained individuals. This review provides an overview of changes in amino acid levels in skeletal muscle and plasma, with a focus on changes induced by exercise.

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Section: Muscle Fiber Type Differencesmentioning

confidence: 91%

Exercise-induced changes in amino acid levels in skeletal muscle and plasma

Ishikura¹,

Ra²,

Ohmori³

2013

JPFSM

View full text Add to dashboard Cite

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“…In the present study 1 of the lactate produced was released to the blood during the exercise and the rate of release was as high as 27 mmol min-' for one subject. In ordinary two-legged exercise a rate of lactate entering the blood of 4-7 mmol min-' has been found (Jorfelt, Juhlin-Dannfelt & Karlsson, 1978;Katz et al 1986). Thus, the present data for anaerobic energy yield obtained during exhaustive exercise with a small muscle group in man cannot be extrapolated to the whole body, and values of 100 ml 02 (kg body wt)-1 are likely peak values.…”

Section: Discussionmentioning

confidence: 99%

“…t Spriet, Soderlund, Bergstrdm & Hultman (1987 b); Katz et al (1986). § Svedenhag, Henriksson & Sylven (1983).…”

Section: P6unclassified

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Anaerobic energy production and O2 deficit‐debt relationship during exhaustive exercise in humans.

Bangsbo¹,

Gollnick²,

Graham³

et al. 1990

The Journal of Physiology

302

248

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SUMMARY1. Eight subjects performed one-legged, dynamic, knee-extensor exercise, first at 10 W followed by 10 min rest, then at an intense, exhaustive exercise load (65 W) lasting 3-2 min. After 60 min recovery, exercise was performed for 8-10 min each at 20, 30, 40 and 50 W. Measurements of pulmonary oxygen uptake, heart rate, blood pressure, leg blood flow, and femoral arterial-venous differences of oxygen content and lactate were performed as well as determination of ATP, creatine phosphate (CP) inosine monophosphate (IMP) and lactate concentrations on biopsy material from the quadriceps muscle before and immediately after the intense exercise, and at 3, 10 and 60 min into recovery.2. Individual linear relations (r = 0-95-1-00) between the power outputs for submaximal exercise and oxygen uptakes (leg and pulmonary) were used to estimate the energy demand during intense exercise. Pulmonary and leg oxygen deficits determined as the difference between energy demand and oxygen uptake were 0-46 and 0-48 1 (kg active muscle)-', respectively. Limb and pulmonary oxygen debts (oxygen uptake during 60 min of recovery -pre-exercise oxygen uptake) were 0-55 and 1P65 1 (kg active muscle)-', respectively. J. BANGSBO AND OTHERS for less than 10 % of the leg oxygen debt, and lactate elimination including resynthesis of glycogen for another 25 %. 5. The anaerobic energy contribution during the first half-minute of intense exercise accounted for 80 % of the total energy turnover and this decreased to 30 % during the last phase of the exercise. The mean anaerobic energy contribution was 45 % for the 3-2 min of exhaustive exercise.6. The maximal anaerobic capacity of human muscle amounted to the equivalent of close to 051 02 kg-1. An extrapolation to whole-body anaerobic capacity cannot be made, as the magnitude of neither [ATP] and [CP] reduction nor lactate release from the muscle is likely to be comparable in all muscles when the human performs whole-body exercise.7. When exercising with a small muscle group the measurements of (i) oxygen deficit and (ii) energy yield, based on metabolic alterations of the active muscle, give similar values for the anaerobic energy release. The dominant fraction of the elevation in recovery oxygen uptake (i.e. oxygen debt) is not accounted for, as normalization of nucleotides, CP, muscle and blood lactate only amounted to about 3 of the debt measurement. Elevation in hormones such as adrenaline and noradrenaline as well as temperature do not appear to play a role in the high recovery oxygen uptake in the present study.

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“…It has been suggested that the upper limit for lactate efflux is 5 mmol min-' (Jorfeldt, Juhlin-Dannfelt & Karlsson, 1978). However, in more recent studies higher effluxes have been obtained and no saturation was apparent (Katz, Broberg, Sahlin & Wahren, 1986;.…”

Section: Introductionmentioning

confidence: 99%

Lactate and H+ effluxes from human skeletal muscles during intense, dynamic exercise.

Bangsbo

Johansen

Graham

et al. 1993

The Journal of Physiology

148

145

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SUMMARY1. Lactate and H+ efflux from skeletal muscles were studied with the one-legged knee extension model under conditions in which blood flow, arterial lactate and the muscle-blood lactate concentration gradient were altered. Subjects exercised one leg twice to exhaustion (EXI, EX2), separated by a 10 min recovery and a period of intense intermittent exercise. After 1 h of recovery the exercise protocol was repeated with the other leg. Low-intensity exercise was performed with one leg during the recovery periods, while the other leg was passive during its recovery periods.2. Prior to, and immediately after, EXI and EX2 and then 3 and 10 min after EXI, a biopsy was taken from the vastus lateralis of the exercised leg for lactate, pH, muscle water and fibre-type determinations. Measurements of leg blood flow and venous-arterial differences for lactate (whole blood and plasma), pH, partial pressure of CO2 (PC02) haemoglobin, saturation and base excess (BE) were performed at the end of exercise and regularly during the recovery period after EX1.3. The lactate release was linearly related (r = 0-96; P < 0-05) to the muscle lactate gradient over a range of muscle lactate from 0 to 45 mmol (kg wet wt)-1. The muscle lactate transport was evaluated from the net femoral venous-arterial differences (V-Adiff) for lactate. This rose with increases in the muscle lactate gradients, but as the gradient reached higher levels the V-Adiff lactate responded less than at smaller gradients. Thus, the lactate transport over the muscle membrane appears to be partly saturated at high muscle lactate concentrations. 4. The percentage of slow twitch (% ST) fibres was inversely related to the muscle lactate gradient, but it was not correlated to the lactate release at the end of the exercises. In spite of a significantly higher blood flow during active recovery, the lactate release was the same whether the leg was resting or performed low-intensity exercise in the recovery periods. In several other conditions the muscle lactate and H+ gradients would have predicted that the V-Adiff lactate would have been greater than it actually was. Thus, a variety of factors affect muscle lactate transport, including arterial lactate concentration, muscle perfusion, muscle contraction pattern and muscle morphology. respectively, and they increased to resting levels during 10 min of either passive or active recovery. The ratio between proton release and lactate efflux was estimated from the BE difference across the muscle, adjusted for changes in reduced haemoglobin. This was 1-4-1P6 at the end of each exercise and remained greater than unity during recovery. Thus, proton release appears to be faster than the lactate efflux both during exercise and recovery.

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Muscle ammonia and amino acid metabolism during dynamic exercise in man

Cited by 113 publications

References 33 publications

Exercise-induced changes in amino acid levels in skeletal muscle and plasma

Exercise-induced changes in amino acid levels in skeletal muscle and plasma

Anaerobic energy production and O2 deficit‐debt relationship during exhaustive exercise in humans.

Lactate and H+ effluxes from human skeletal muscles during intense, dynamic exercise.

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