The Effects of Leucine-Enriched Branched-Chain Amino Acid Supplementation on Recovery After High-Intensity Resistance Exercise

2019 ◽  
Vol 14 (8) ◽  
pp. 1081-1088 ◽  
Author(s):  
Adam D. Osmond ◽  
Dean J. Directo ◽  
Marcus L. Elam ◽  
Gabriela Juache ◽  
Vince C. Kreipke ◽  
...  

Context: Of the 3 branched-chain amino acids (BCAA), leucine has arguably received the most attribution for the role of BCAA supplementation in alleviating symptoms of exercise-induced muscle damage and facilitation of acute performance recovery. Purpose: To examine whether enrichment of a standard BCAA supplement with additional leucine or a standalone leucine (LEU) supplement differentially affects exercise-induced muscle damage and performance recovery compared with a standard BCAA supplement. Methods: A total of 22 recreationally active male and female subjects were recruited and assigned to consume a BCAA, leucine-enriched BCAA (LBCAA), or LEU supplement for 11 d. On the eighth day, subjects performed eccentric-based resistance exercise (ECRE). Lower-body mean average and peak power, plasma creatine kinase, soreness, and pain threshold were measured before and 24, 48, and 72 h after ECRE. Results: LEU showed decreased mean average power (P = .02) and mean peak power (P = .01) from baseline to 48 h post-ECRE, whereas LBCAA and BCAA only trended toward a reduction at 24 hours post-ECRE. At 48 h post-ECRE, BCAA showed greater recovery of mean peak power than LEU (P = .04). At 24 h post-ECRE, LEU demonstrated a greater increase in plasma creatine kinase from baseline than BCAA (P = .04). Area under the curve for creatine kinase was greater in LEU than BCAA (P = .02), whereas BCAA and LBCAA did not differ. Only LEU demonstrated increased soreness during rest and under muscular tension at 24 and 48 h post-ECRE (P < .05). Conclusions: LBCAA failed to afford any advantages over a standard BCAA supplement for postexercise muscle recovery, whereas a LEU supplement was comparatively ineffective.

1991 ◽  
Vol 23 (9) ◽  
pp. 1028???1034 ◽  
Author(s):  
THOMAS G. MANFREDI ◽  
ROGER A. FIELDING ◽  
KEVIN P. O??REILLY ◽  
CAROL N. MEREDITH ◽  
HO YONG LEE ◽  
...  

2001 ◽  
Vol 62 (9) ◽  
pp. 1375-1380 ◽  
Author(s):  
Guillaume P. Chanoit ◽  
Herve P. Lefebvre ◽  
Karine Orcel ◽  
Valerie Laroute ◽  
Pierre-Louis Toutain ◽  
...  

2019 ◽  
Vol 126 (1) ◽  
pp. 30-43 ◽  
Author(s):  
Henning Wackerhage ◽  
Brad J. Schoenfeld ◽  
D. Lee Hamilton ◽  
Maarit Lehti ◽  
Juha J. Hulmi

One of the most striking adaptations to exercise is the skeletal muscle hypertrophy that occurs in response to resistance exercise. A large body of work shows that a mammalian target of rapamycin complex 1 (mTORC1)-mediated increase of muscle protein synthesis is the key, but not sole, mechanism by which resistance exercise causes muscle hypertrophy. While much of the hypertrophy signaling cascade has been identified, the initiating, resistance exercise-induced and hypertrophy-stimulating stimuli have remained elusive. For the purpose of this review, we define an initiating, resistance exercise-induced and hypertrophy-stimulating signal as “hypertrophy stimulus,” and the sensor of such a signal as “hypertrophy sensor.” In this review we discuss our current knowledge of specific mechanical stimuli, damage/injury-associated and metabolic stress-associated triggers, as potential hypertrophy stimuli. Mechanical signals are the prime hypertrophy stimuli candidates, and a filamin-C-BAG3-dependent regulation of mTORC1, Hippo, and autophagy signaling is a plausible albeit still incompletely characterized hypertrophy sensor. Other candidate mechanosensing mechanisms are nuclear deformation-initiated signaling or several mechanisms related to costameres, which are the functional equivalents of focal adhesions in other cells. While exercise-induced muscle damage is probably not essential for hypertrophy, it is still unclear whether and how such muscle damage could augment a hypertrophic response. Interventions that combine blood flow restriction and especially low load resistance exercise suggest that resistance exercise-regulated metabolites could be hypertrophy stimuli, but this is based on indirect evidence and metabolite candidates are poorly characterized.


Nutrients ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 744 ◽  
Author(s):  
Eduard Isenmann ◽  
Franziska Blume ◽  
Daniel Bizjak ◽  
Vera Hundsdörfer ◽  
Sarah Pagano ◽  
...  

Physical performance and regeneration after exercise is enhanced by the ingestion of proteins and carbohydrates. These nutrients are generally consumed by athletes via whey protein and glucose-based shakes. In this study, effects of protein and carbohydrate on skeletal muscle regeneration, given either by shake or by a meal, were compared. 35 subjects performed a 10 km run. After exercise, they ingested nothing (control), a protein/glucose shake (shake) or a combination of white bread and sour milk cheese (food) in a randomized cross over design. Serum glucose (n = 35), serum insulin (n = 35), serum creatine kinase (n = 15) and myoglobin (n = 15), hematologic parameters, cortisol (n = 35), inflammation markers (n = 27) and leg strength (n = 15) as a functional marker were measured. Insulin secretion was significantly stimulated by shake and food. In contrast, only shake resulted in an increase of blood glucose. Food resulted in a decrease of pro, and stimulation of anti-inflammatory serum markers. The exercise induced skeletal muscle damage, indicated by serum creatine kinase and myoglobin, and exercise induced loss of leg strength was decreased by shake and food. Our data indicate that uptake of protein and carbohydrate by shake or food reduces exercise induced skeletal muscle damage and has pro-regenerative effects.


1987 ◽  
Vol 73 (s17) ◽  
pp. 50P-50P
Author(s):  
S Page ◽  
MJ Jackson ◽  
J Coakley ◽  
RHT Edwards

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