Renate Jonker1, Nicolaas E P Deutz1, Gerdien C Ligthart-Melis1, Anthony J Zachria2, Eugene A Veley3, Rajesh Harrykissoon2, Mariëlle P K J Engelen4. 1. Center for Translational Research in Aging & Longevity, Dept. of Health and Kinesiology, Texas A&M University, College Station, TX, USA. 2. Center for Pulmonary and Sleep Disorders, College Station Medical Center, College Station, TX, USA. 3. Dept. of Medicine, Div. of Pulmonary Critical Care, Baylor Scott & White Medical Center, College Station, TX, USA. 4. Center for Translational Research in Aging & Longevity, Dept. of Health and Kinesiology, Texas A&M University, College Station, TX, USA. Electronic address: mpkj.engelen@ctral.org.
Abstract
BACKGROUND & AIMS: Assessing the ability to respond anabolic to dietary protein intake during illness provides important insight in the capacity of lean body mass maintenance. We applied a newly developed stable tracer approach to assess in one session in patients with chronic obstructive pulmonary disease (COPD) and healthy older adults both the minimal amount of protein intake to obtain protein anabolism (anabolic threshold) and the efficiency of dietary protein to promote protein anabolism (anabolic capacity). METHODS: We studied 12 clinically and weight stable patients with moderate to very severe COPD (mean ± SE forced expiratory volume in 1 s: 36 ± 3% of predicted) and 10 healthy age-matched older adults. At 2-h intervals and in consecutive order, all participants consumed a mixture of 0.0, 0.04, 0.10 and 0.30 g hydrolyzed casein protein×kg ffm-1×2 h-1 and carbohydrates (2:1). We assessed whole body protein synthesis (PS), breakdown (PB), net PS (PS-PB) and net protein balance (phenylalanine (PHE) intake - PHE to tyrosine (TYR) hydroxylation) by IV primed and continuous infusion of L-[ring-2H5]PHE and L-[13C9,15N]-TYR. Anabolic threshold (net protein balance = 0) and capacity (slope) were determined on an individual basis from the assumed linear relationship between protein intake and net protein balance. RESULTS: We confirmed a linear relationship between protein intake and net protein balance for all participants (R2 range: 0.9988-1.0, p ≤ 0.0006). On average, the anabolic threshold and anabolic capacity were comparable between the groups (anabolic threshold COPD vs. healthy: 3.82 ± 0.31 vs. 4.20 ± 0.36 μmol PHE × kg ffm-1 × hr-1; anabolic capacity COPD vs. healthy: 0.952 ± 0.007 and 0.954 ± 0.004). At protein intake around the anabolic threshold (0.04 and 0.10 g protein×kg ffm-1×2 h-1), the increase in net PS resulted mainly from PB reduction (p < 0.0001) whereas at a higher protein intake (0.30 g protein×kg ffm-1×2 h-1) PS was also stimulated (p < 0.0001). CONCLUSIONS: The preserved anabolic threshold and capacity in clinically and weight stable COPD patients suggests no disease related anabolic resistance and/or increased protein requirements. TRIAL REGISTRY: ClinicalTrials.gov; No. NCT01734473; URL: www.clinicaltrials.gov.
BACKGROUND & AIMS: Assessing the ability to respond anabolic to dietary protein intake during illness provides important insight in the capacity of lean body mass maintenance. We applied a newly developed stable tracer approach to assess in one session in patients with chronic obstructive pulmonary disease (COPD) and healthy older adults both the minimal amount of protein intake to obtain protein anabolism (anabolic threshold) and the efficiency of dietary protein to promote protein anabolism (anabolic capacity). METHODS: We studied 12 clinically and weight stable patients with moderate to very severe COPD (mean ± SE forced expiratory volume in 1 s: 36 ± 3% of predicted) and 10 healthy age-matched older adults. At 2-h intervals and in consecutive order, all participants consumed a mixture of 0.0, 0.04, 0.10 and 0.30 g hydrolyzed casein protein×kg ffm-1×2 h-1 and carbohydrates (2:1). We assessed whole body protein synthesis (PS), breakdown (PB), net PS (PS-PB) and net protein balance (phenylalanine (PHE) intake - PHE to tyrosine (TYR) hydroxylation) by IV primed and continuous infusion of L-[ring-2H5]PHE and L-[13C9,15N]-TYR. Anabolic threshold (net protein balance = 0) and capacity (slope) were determined on an individual basis from the assumed linear relationship between protein intake and net protein balance. RESULTS: We confirmed a linear relationship between protein intake and net protein balance for all participants (R2 range: 0.9988-1.0, p ≤ 0.0006). On average, the anabolic threshold and anabolic capacity were comparable between the groups (anabolic threshold COPD vs. healthy: 3.82 ± 0.31 vs. 4.20 ± 0.36 μmol PHE × kg ffm-1 × hr-1; anabolic capacity COPD vs. healthy: 0.952 ± 0.007 and 0.954 ± 0.004). At protein intake around the anabolic threshold (0.04 and 0.10 g protein×kg ffm-1×2 h-1), the increase in net PS resulted mainly from PB reduction (p < 0.0001) whereas at a higher protein intake (0.30 g protein×kg ffm-1×2 h-1) PS was also stimulated (p < 0.0001). CONCLUSIONS: The preserved anabolic threshold and capacity in clinically and weight stable COPDpatients suggests no disease related anabolic resistance and/or increased protein requirements. TRIAL REGISTRY: ClinicalTrials.gov; No. NCT01734473; URL: www.clinicaltrials.gov.
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