Influence Of Branched-chain Aminoacids (BCAA) Supplementation On Free Fatty Acids Oxidation During Endurance Exercise After Muscle Glycogen Depletion

The interaction of substrates and hormones in response to ingestion of intact proteins during endurance exercise is unknown. This study characterized substrate and hormone responses to supplementation during endurance exercise. Nine male runners participated in 3 trials in which a non-fat (MILK), carbohydrate (CHO), or placebo (PLA) drink was consumed during a 2-hour treadmill >· run at 65% V̇O2max. Circulating levels of insulin, glucagon, epinephrine, norepi-nephrine, growth hormone, testosterone, and cortisol were measured. Plasma substrates included glucose, lactate, free fatty acids, and select amino acids. Except for insulin and cortisol, hormones increased with exercise. While post-exercise insulin concentrations declined similarly in all 3 trials, the glucagon increase was greatest following MILK consumption. CHO blunted the post-exercise increase in growth hormone compared to levels in MILK. Free fatty acids and plasma amino acids also were responsive to nutritional supplementation with both CHO and MILK attenuating the rise in free fatty acids compared to the increase observed in PLA. Correspondingly, respiratory exchange ratio increased during CHO. Essential amino acids increased significantly only after MILK and were either unchanged or decreased in CHO. PLA was characterized by a decrease in branched-chain amino acid concentrations. Modest nutritional supplementation in this study altered the endocrine response as well as substrate availability and utilization following and during an endurance run, respectively.

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The Metabolic Response of Glycogen and Free Fatty Acids to Endurance Exercise

Current Metabolomics ◽

10.2174/2213235x04666160801155231 ◽

2017 ◽

Vol 5 (1) ◽

pp. 68-75

Author(s):

Piero Ipata ◽

Francesco Balestri ◽

Rossana Pesi

Keyword(s):

Fatty Acids ◽

Free Fatty Acids ◽

Endurance Exercise ◽

Metabolic Response

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Branched-chain amino acid supplementation augments plasma ammonia responses during exercise in humans

Journal of Applied Physiology ◽

10.1152/jappl.1993.74.6.2711 ◽

1993 ◽

Vol 74 (6) ◽

pp. 2711-2717 ◽

Cited By ~ 33

Author(s):

D. A. MacLean ◽

T. E. Graham

Keyword(s):

Fatty Acids ◽

Amino Acid ◽

Free Fatty Acids ◽

Amino Acid Supplementation ◽

Placebo Administration ◽

Branched Chain Amino Acid ◽

Placebo Trial ◽

The Mean ◽

Branched Chain ◽

Exercise In Humans

This study examined the effects of branched-chain amino acid (BCAA) supplementation on amino acid and ammonia (NH3) responses during prolonged exercise in humans. Seven men cycled for 60 min at 75% of maximal O2 uptake after 45 min of either placebo (dextrose, 77 mg/kg) or BCAA (leucine + isoleucine + valine, 77 mg/kg) supplementation. Plasma samples (antecubital vein) were collected at rest and during exercise and analyzed for plasma NH3 and amino acids, whole blood glucose and lactate, and serum free fatty acids and glycerol. After BCAA administration, plasma BCAA levels increased from 375 +/- 22 to 760 +/- 80 microM (P < 0.05) by the onset of exercise and remained elevated throughout the experiment. Plasma NH3 concentrations increased continually during exercise for both trials and were higher (P < 0.05) after BCAA supplementation than after placebo administration. The mean plasma NH3 increase from rest to 60 min was 79 +/- 10 and 53 +/- 4 microM for BCAA and placebo trials, respectively. Plasma alanine and glutamine concentrations were elevated (P < 0.05) during exercise for both treatments. However, only glutamine concentrations were greater (P < 0.05) for BCAA trial than for placebo trial during exercise. There were no significant differences between treatments for glucose, lactate, free fatty acids, and glycerol or any other plasma amino acid. These data suggest that increased BCAA availability before exercise, when initial muscle glycogen is normal, results in significantly greater plasma NH3 responses during exercise than does placebo administration.

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Sparing effect of chronic high-altitude exposure on muscle glycogen utilization

Journal of Applied Physiology ◽

10.1152/jappl.1982.52.4.857 ◽

1982 ◽

Vol 52 (4) ◽

pp. 857-862 ◽

Cited By ~ 79

Author(s):

A. J. Young ◽

W. J. Evans ◽

A. Cymerman ◽

K. B. Pandolf ◽

J. J. Knapik ◽

...

Keyword(s):

Fatty Acids ◽

Free Fatty Acids ◽

High Altitude ◽

Muscle Glycogen ◽

Vastus Lateralis ◽

Venous Blood ◽

Vastus Lateralis Muscle ◽

Before And After ◽

Glycogen Utilization ◽

Sparing Effect

Substrate utilization during heavy [approximately 85% maximum O2 consumption (VO2max)] bicycle exercise was examined in eight low-altitude residents at sea level (SL) and after acute (2 h) and chronic (18 days) high-altitude (HA) exposure at 4,300 m. Mean VO2max was approximately 27% lower at acute HA than at SL and did not change significantly with continued HA exposure. Biopsies from the vastus lateralis muscle and venous blood samples were obtained before and after 30 min of exercise, whereas determinations of the respiratory exchange ratio (R) were made at 10-min intervals during each of the submaximal bouts. Resting levels of serum-free fatty acids at acute and chronic HA were, respectively, two and three times higher than SL but were unchanged with exercise. Exercise did not alter resting serum glycerol levels at SL or during acute HA, but during chronic HA resting glycerol levels were increased 11-fold. Although mean blood lactate concentrations following exercise at SL and acute HA were not significantly different, postexercise lactate concentrations were 87% lower after chronic HA. During exercise at SL and acute HA, muscle glycogen utilization and R were not different. At chronic HA, muscle glycogen utilization and R were 41 and 15% lower, respectively. These data suggest that after chronic HA exposure, increased mobilization and use of free fatty acids during exercise resulted in sparing of muscle glycogen.

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Enhanced plasma IL-6 and IL-1ra responses to repeated vs. single bouts of prolonged cycling in elite athletes

Journal of Applied Physiology ◽

10.1152/japplphysiol.01263.2001 ◽

2002 ◽

Vol 92 (6) ◽

pp. 2547-2553 ◽

Cited By ~ 49

Author(s):

Ola Ronsen ◽

Tor Lea ◽

Roald Bahr ◽

Bente Klarlund Pedersen

Keyword(s):

Receptor Antagonist ◽

Endurance Exercise ◽

Muscle Glycogen ◽

Plasma Levels ◽

Elite Athletes ◽

Cycle Ergometer ◽

Glycogen Depletion ◽

Single Bout ◽

The Impact

The impact of repeated bouts of exercise on plasma levels of interleukin (IL)-6 and IL-1 receptor antagonist (IL-1ra) was examined. Nine well-trained men participated in four different 24-h trials: Long [two bouts of exercise, at 0800–0915 and afternoon exercise (Ex-A), separated by 6 h]; Short (two bouts, at 1100–1215 and Ex-A, separated by 3 h); One (single bout performed at the same Ex-A as second bout in prior trials); and Rest (no exercise). All exercise bouts were performed on a cycle ergometer at 75% of maximal O2uptake and lasted 75 min. Peak IL-6 observed at the end of Ex-A was significantly higher in Short (8.8 ± 1.3 pg/ml) than One (5.2 ± 0.7 pg/ml) but not compared with Long (5.9 ± 1.2 pg/ml). Peak IL-1ra observed 1 h postexercise was significantly higher in Short (1,774 ± 373 pg/ml) than One (302 ± 53 pg/ml) but not compared with Long (1,276 ± 451 pg/ml). We conclude that, when a second bout of endurance exercise is performed after only 3 h of recovery, IL-6 and IL-1ra responses are elevated. This may be linked to muscle glycogen depletion.

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Effect of Exercise Intensity on Free Tryptophan to Branched-Chain Amino Acids Ratio and Plasma Prolactin During Endurance Exercise

Canadian Journal of Applied Physiology ◽

10.1139/h97-019 ◽

1997 ◽

Vol 22 (3) ◽

pp. 280-291 ◽

Cited By ~ 22

Author(s):

Heiko K. Strüder ◽

Wildor Hollmann ◽

Petra Platen ◽

Ronny Wöstmann ◽

Alexander Ferrauti ◽

...

Keyword(s):

Amino Acids ◽

Fatty Acids ◽

Free Fatty Acids ◽

Endurance Exercise ◽

Exercise Duration ◽

Cycle Ergometer ◽

Plasma Prolactin ◽

Free Tryptophan ◽

Energy Bar ◽

Intensity Of Exercise

The potential of exercise-induced changes in peripheral amino acids to alter blood prolactin levels through a seratonergic system modification was investigated in 8 male athletes. In two trials, subjects (N = 8) exercised on a cycle ergometer for 5 hr. The intensity of exercise corresponded to 55% VO2max (T55) or 75% VO2max (T75) respectively. In each trial, each subject received a 25-g energy bar (111 kcal) every 60 min, as well as 300 ml of a 6% carbohydrate solution (90 kcal) every 30 min of exercise duration. Plasma glucose and insulin declined (p ≤.05) in both trials during exercise. Ammonia was augmented (p ≤.05) above the baseline concentration after 120 min in both trials. During the last 2 hr of exercise, plasma free fatty acids were higher (p ≤.05) in T75, than in T55. During this time, the plasma free TRP/BCAA ratio was also augmented (p ≤.05) in T75 while no change was induced in T55. Plasma prolactin did not change in T55, while an increase (p ≤.05) was found in T75. The findings may further support the hypothesis that during endurance exercise changes in peripheral amino acid concentration may influence prolactin response via serotonergic system modifications. Key words: blood-brain barrier, serotonin, neuroendocrine system, free fatty acids, ammonia

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Unbalanced lipolysis results in lipotoxicity and mitochondrial damage in peroxisome-deficient Pex19 mutants

Molecular Biology of the Cell ◽

10.1091/mbc.e17-08-0535 ◽

2018 ◽

Vol 29 (4) ◽

pp. 396-407 ◽

Cited By ~ 19

Author(s):

Margret H. Bülow ◽

Christian Wingen ◽

Deniz Senyilmaz ◽

Dominic Gosejacob ◽

Mariangela Sociale ◽

...

Keyword(s):

Fatty Acids ◽

Free Fatty Acids ◽

Mitochondrial Damage ◽

Mitochondrial Abnormalities ◽

Peroxisomal Biogenesis ◽

Metabolic Functions ◽

Branched Chain ◽

The Many ◽

Key Aspects ◽

Chain Fatty Acids

Inherited peroxisomal biogenesis disorders (PBDs) are characterized by the absence of functional peroxisomes. They are caused by mutations of peroxisomal biogenesis factors encoded by Pex genes, and result in childhood lethality. Owing to the many metabolic functions fulfilled by peroxisomes, PBD pathology is complex and incompletely understood. Besides accumulation of peroxisomal educts (like very-long-chain fatty acids [VLCFAs] or branched-chain fatty acids) and lack of products (like bile acids or plasmalogens), many peroxisomal defects lead to detrimental mitochondrial abnormalities for unknown reasons. We generated Pex19 Drosophila mutants, which recapitulate the hallmarks of PBDs, like absence of peroxisomes, reduced viability, neurodegeneration, mitochondrial abnormalities, and accumulation of VLCFAs. We present a model of hepatocyte nuclear factor 4 (Hnf4)-induced lipotoxicity and accumulation of free fatty acids as the cause for mitochondrial damage in consequence of peroxisome loss in Pex19 mutants. Hyperactive Hnf4 signaling leads to up-regulation of lipase 3 and enzymes for mitochondrial β-oxidation. This results in enhanced lipolysis, elevated concentrations of free fatty acids, maximal β-oxidation, and mitochondrial abnormalities. Increased acid lipase expression and accumulation of free fatty acids are also present in a Pex19-deficient patient skin fibroblast line, suggesting the conservation of key aspects of our findings.

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