PMID- 16631431
OWN - NLM
STAT- MEDLINE
DCOM- 20060601
LR  - 20180924
IS  - 0026-0495 (Print)
IS  - 0026-0495 (Linking)
VI  - 55
IP  - 5
DP  - 2006 May
TI  - Liquid carbohydrate/essential amino acid ingestion during a short-term bout of 
      resistance exercise suppresses myofibrillar protein degradation.
PG  - 570-7
AB  - A number of physiological events including the level of contractile activity, 
      nutrient status, and hormonal action influence the magnitude of exercise-induced 
      skeletal muscle growth. However, it is not the independent action of a single 
      mechanism, but the complex interaction between events that enhance the long-term 
      adaptations to resistance training. The purpose of the present investigation was 
      to examine the influence of liquid carbohydrate (CHO) and essential amino acid 
      (EAA) ingestion during resistance exercise and modification of the immediate 
      hormonal response on myofibrillar protein degradation as assessed by 
      3-methylhistidine (3-MH) excretion. After a 4-hour fast, 32 untrained young men 
      (18-29 years) performed a single bout of resistance exercise (complete body; 3 
      setsx10 repetitions at 75% of 1-repetition maximum; 1-minute rest between sets), 
      during which they consumed a 6% CHO (n=8) solution, a 6-g EAA (n=8) mixture, a 
      combined CHO+EAA (n=8) supplement, or placebo (PLA; n=8) beverage. Resistance 
      exercise performed in conjunction with CHO and CHO+EAA ingestion resulted in 
      significantly elevated (P<.001) glucose and insulin concentrations above 
      baseline, whereas EAA ingestion only increased the postexercise insulin response 
      (P<.05). Time matched at 60 minutes, the PLA group exhibited a peak cortisol 
      increase of 105% (P<.001) with no significant change in glucose or insulin 
      concentrations. Conversely, the CHO and CHO+EAA groups displayed a decrease in 
      cortisol levels of 11% and 7%, respectively. Coinciding with these hormonal 
      response patterns were significant differences in myofibrillar protein 
      degradation. Ingestion of the EAA and CHO treatments attenuated 3-MH excretion 48 
      hours after the exercise bout. Moreover, this response was synergistically 
      potentiated when the 2 treatments were combined, with CHO+EAA ingestion resulting 
      in a 27% reduction (P<.01) in 3-MH excretion. In contrast, the PLA group 
      displayed a 56% increase (P<.01) in 3-MH excretion. These data demonstrate that 
      not only does CHO and EAA ingestion during the exercise bout suppress 
      exercise-induced cortisol release; the stimulatory effect of resistance exercise 
      on myofibrillar protein degradation can be attenuated, most dramatically when the 
      treatments are combined (CHO+EAA). Through an "anticatabolic effect," this 
      altered balance may better favor the conservation of myofibrillar protein.
FAU - Bird, Stephen P
AU  - Bird SP
AD  - School of Human Movement Studies, Charles Sturt University, Bathurst, NSW 2795, 
      Australia. sbird@csu.edu.au
FAU - Tarpenning, Kyle M
AU  - Tarpenning KM
FAU - Marino, Frank E
AU  - Marino FE
LA  - eng
PT  - Journal Article
PT  - Randomized Controlled Trial
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Metabolism
JT  - Metabolism: clinical and experimental
JID - 0375267
RN  - 0 (Amino Acids, Essential)
RN  - 0 (Blood Glucose)
RN  - 0 (Dietary Carbohydrates)
RN  - 0 (Insulin)
RN  - 0 (Methylhistidines)
RN  - 0 (Muscle Proteins)
RN  - MEH8O8Y0H0 (3-methylhistidine)
RN  - WI4X0X7BPJ (Hydrocortisone)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Amino Acids, Essential/*administration & dosage
MH  - Area Under Curve
MH  - Blood Glucose/metabolism
MH  - Dietary Carbohydrates/*administration & dosage
MH  - Double-Blind Method
MH  - Exercise/*physiology
MH  - Humans
MH  - Hydrocortisone/blood
MH  - Insulin/blood
MH  - Male
MH  - Methylhistidines/urine
MH  - Muscle Proteins/*metabolism
MH  - Muscle, Skeletal/*metabolism
MH  - Regression Analysis
EDAT- 2006/04/25 09:00
MHDA- 2006/06/02 09:00
CRDT- 2006/04/25 09:00
PHST- 2005/06/13 00:00 [received]
PHST- 2005/11/15 00:00 [accepted]
PHST- 2006/04/25 09:00 [pubmed]
PHST- 2006/06/02 09:00 [medline]
PHST- 2006/04/25 09:00 [entrez]
AID - S0026-0495(05)00444-0 [pii]
AID - 10.1016/j.metabol.2005.11.011 [doi]
PST - ppublish
SO  - Metabolism. 2006 May;55(5):570-7. doi: 10.1016/j.metabol.2005.11.011.