Amino acid infusion fails to stimulate skeletal muscle protein synthesis up to 1 year after injury in children with severe burns

Craig Porter, Matthew Cotter, Eva C. Diaz, Kristofer Jennings, David Herndon, Elisabet Børsheim

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

BACKGROUND: Burn injury results in increased skeletal muscle protein turnover, where the magnitude of protein breakdown outweighs synthesis, resulting in muscle wasting. The effect of increased amino acid (AA) provision on skeletal muscle fractional synthesis rate (FSR) in severely burned patients during their convalescence after discharge from hospital is not known. Subsequently, the purpose of this study was to determine skeletal muscle FSR in response to AA infusion in severely burned pediatric patients at discharge from hospital and at 6 and 12 months after injury. METHODS: Stable isotope infusion studieswere performed in the fasted state and during intravenous AAinfusion. Skeletal muscle biopsies were obtained and isotope enrichment was determined to calculate skeletal muscle FSR. Patients were studied at discharge from hospital (n = 11) and at 6 (n = 15) and 12 months (n = 14) after injury. RESULTS: The cohorts of patients studied at each time point after injury were not different with regard to age, body mass, or burn size. AA infusion failed to stimulate FSR above basal values at discharge from hospital (mean [SEM]: 0.27% [0.04%] vs. 0.26% [0.06%] per hour), 6 months after injury (0.20% [0.04%] vs. 0.22% [0.03%] per hour), and 12 months after injury (0.16% [0.03%] vs. 0.15% [0.03%] per hour). Daily FSR was numerically lower at 6 months after burn (5.13% [0.78%] per day) and significantly (p G 0.05) lower at 12 months after burn (3.67% [0.65%] per day) relative to discharge group (6.32% [1.02%] per day). DISCUSSION: The findings of the current study suggest that the deleterious effect of burn injury on skeletal muscle AA metabolism persists for up to 1 year post burn. In light of these findings, nutritional and pharmacological strategies aimed at attenuating muscle protein breakdown post burn may be a more efficacious approach to maintaining muscle mass in severely burned patients. LEVEL OF EVIDENCE: Prognostic study, level II.

Original languageEnglish (US)
Pages (from-to)1480-1485
Number of pages6
JournalJournal of Trauma and Acute Care Surgery
Volume74
Issue number6
DOIs
StatePublished - Jun 2013

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Muscle Proteins
Burns
Skeletal Muscle
Amino Acids
Wounds and Injuries
Isotopes
Muscles
Patient Discharge
Pharmacology
Pediatrics
Biopsy

Keywords

  • Amino acids
  • Burn injury
  • Protein synthesis
  • Skeletal muscle

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine
  • Surgery

Cite this

Amino acid infusion fails to stimulate skeletal muscle protein synthesis up to 1 year after injury in children with severe burns. / Porter, Craig; Cotter, Matthew; Diaz, Eva C.; Jennings, Kristofer; Herndon, David; Børsheim, Elisabet.

In: Journal of Trauma and Acute Care Surgery, Vol. 74, No. 6, 06.2013, p. 1480-1485.

Research output: Contribution to journalArticle

Porter, Craig ; Cotter, Matthew ; Diaz, Eva C. ; Jennings, Kristofer ; Herndon, David ; Børsheim, Elisabet. / Amino acid infusion fails to stimulate skeletal muscle protein synthesis up to 1 year after injury in children with severe burns. In: Journal of Trauma and Acute Care Surgery. 2013 ; Vol. 74, No. 6. pp. 1480-1485.
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T1 - Amino acid infusion fails to stimulate skeletal muscle protein synthesis up to 1 year after injury in children with severe burns

AU - Porter, Craig

AU - Cotter, Matthew

AU - Diaz, Eva C.

AU - Jennings, Kristofer

AU - Herndon, David

AU - Børsheim, Elisabet

PY - 2013/6

Y1 - 2013/6

N2 - BACKGROUND: Burn injury results in increased skeletal muscle protein turnover, where the magnitude of protein breakdown outweighs synthesis, resulting in muscle wasting. The effect of increased amino acid (AA) provision on skeletal muscle fractional synthesis rate (FSR) in severely burned patients during their convalescence after discharge from hospital is not known. Subsequently, the purpose of this study was to determine skeletal muscle FSR in response to AA infusion in severely burned pediatric patients at discharge from hospital and at 6 and 12 months after injury. METHODS: Stable isotope infusion studieswere performed in the fasted state and during intravenous AAinfusion. Skeletal muscle biopsies were obtained and isotope enrichment was determined to calculate skeletal muscle FSR. Patients were studied at discharge from hospital (n = 11) and at 6 (n = 15) and 12 months (n = 14) after injury. RESULTS: The cohorts of patients studied at each time point after injury were not different with regard to age, body mass, or burn size. AA infusion failed to stimulate FSR above basal values at discharge from hospital (mean [SEM]: 0.27% [0.04%] vs. 0.26% [0.06%] per hour), 6 months after injury (0.20% [0.04%] vs. 0.22% [0.03%] per hour), and 12 months after injury (0.16% [0.03%] vs. 0.15% [0.03%] per hour). Daily FSR was numerically lower at 6 months after burn (5.13% [0.78%] per day) and significantly (p G 0.05) lower at 12 months after burn (3.67% [0.65%] per day) relative to discharge group (6.32% [1.02%] per day). DISCUSSION: The findings of the current study suggest that the deleterious effect of burn injury on skeletal muscle AA metabolism persists for up to 1 year post burn. In light of these findings, nutritional and pharmacological strategies aimed at attenuating muscle protein breakdown post burn may be a more efficacious approach to maintaining muscle mass in severely burned patients. LEVEL OF EVIDENCE: Prognostic study, level II.

AB - BACKGROUND: Burn injury results in increased skeletal muscle protein turnover, where the magnitude of protein breakdown outweighs synthesis, resulting in muscle wasting. The effect of increased amino acid (AA) provision on skeletal muscle fractional synthesis rate (FSR) in severely burned patients during their convalescence after discharge from hospital is not known. Subsequently, the purpose of this study was to determine skeletal muscle FSR in response to AA infusion in severely burned pediatric patients at discharge from hospital and at 6 and 12 months after injury. METHODS: Stable isotope infusion studieswere performed in the fasted state and during intravenous AAinfusion. Skeletal muscle biopsies were obtained and isotope enrichment was determined to calculate skeletal muscle FSR. Patients were studied at discharge from hospital (n = 11) and at 6 (n = 15) and 12 months (n = 14) after injury. RESULTS: The cohorts of patients studied at each time point after injury were not different with regard to age, body mass, or burn size. AA infusion failed to stimulate FSR above basal values at discharge from hospital (mean [SEM]: 0.27% [0.04%] vs. 0.26% [0.06%] per hour), 6 months after injury (0.20% [0.04%] vs. 0.22% [0.03%] per hour), and 12 months after injury (0.16% [0.03%] vs. 0.15% [0.03%] per hour). Daily FSR was numerically lower at 6 months after burn (5.13% [0.78%] per day) and significantly (p G 0.05) lower at 12 months after burn (3.67% [0.65%] per day) relative to discharge group (6.32% [1.02%] per day). DISCUSSION: The findings of the current study suggest that the deleterious effect of burn injury on skeletal muscle AA metabolism persists for up to 1 year post burn. In light of these findings, nutritional and pharmacological strategies aimed at attenuating muscle protein breakdown post burn may be a more efficacious approach to maintaining muscle mass in severely burned patients. LEVEL OF EVIDENCE: Prognostic study, level II.

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