The effects of whey, pea, and collagen protein supplementation beyond the recommended dietary allowance on integrated myofibrillar protein synthetic rates in older males: a randomized controlled trial.

aging muscle anabolism nutrient requirements plant-based protein protein nutrition sarcopenia stable isotope tracers

Journal

The American journal of clinical nutrition
ISSN: 1938-3207
Titre abrégé: Am J Clin Nutr
Pays: United States
ID NLM: 0376027

Informations de publication

Date de publication:
16 May 2024
Historique:
received: 01 12 2023
revised: 09 05 2024
accepted: 13 05 2024
medline: 19 5 2024
pubmed: 19 5 2024
entrez: 18 5 2024
Statut: aheadofprint

Résumé

Skeletal muscle mass is determined predominantly by feeding- and activity-induced fluctuations in muscle protein synthesis (MPS). Older individuals display a diminished MPS response to protein ingestion, referred to as age-related anabolic resistance, that contributes to the progression of age-related muscle loss - sarcopenia. We aimed to determine the impact of consuming higher- versus lower-quality protein supplements above the recommended dietary allowance (RDA) on integrated MPS rates. We hypothesized that increasing total protein intake above the RDA, regardless of the source, would support higher integrated rates of myofibrillar protein synthesis. Thirty-one healthy older males (72 ± 4 y) underwent a controlled diet with protein intake set at the RDA - control phase (CON; days 1-7). In a double-blind, randomized controlled fashion, participants were assigned to consume an additional 50g (2x25g) of Whey (WHEY, n=10), Pea (PEA, n=11), or collagen (COLL, n=10) protein each day (25 g at breakfast and lunch) during the supplemental phase (SUPP; days 8-15). Deuterated water ingestion and muscle biopsies assessed integrated MPS and acute anabolic signaling. Postprandial blood samples were collected to determine feeding-induced aminoacidemia. Integrated-MPS was increased during SUPP with WHEY (1.59 ± 0.11 %/d, p<0.001) and PEA (1.59 ± 0.14 %/d, p<0.001) when compared with RDA (1.46 ± 0.09 %/d WHEY; 1.46 ± 0.10 %/d PEA); however, it remained unchanged with COLL. Supplemental protein was sufficient to overcome anabolic signaling deficits (mTORC1 and rpS6), corroborating the greater postprandial aminoacidemia. Our findings demonstrate that supplemental protein provided at breakfast and lunch over the current RDA enhanced anabolic signaling and integrated MPS in older males; however, the source of additional protein may be an important consideration in overcoming age-related anabolic resistance. Clinical Trial Registry number and website where it was obtained This trial (NCT04026607) was registered clinicaltrials.gov.

Sections du résumé

BACKGROUND BACKGROUND
Skeletal muscle mass is determined predominantly by feeding- and activity-induced fluctuations in muscle protein synthesis (MPS). Older individuals display a diminished MPS response to protein ingestion, referred to as age-related anabolic resistance, that contributes to the progression of age-related muscle loss - sarcopenia.
OBJECTIVE OBJECTIVE
We aimed to determine the impact of consuming higher- versus lower-quality protein supplements above the recommended dietary allowance (RDA) on integrated MPS rates. We hypothesized that increasing total protein intake above the RDA, regardless of the source, would support higher integrated rates of myofibrillar protein synthesis.
METHODS METHODS
Thirty-one healthy older males (72 ± 4 y) underwent a controlled diet with protein intake set at the RDA - control phase (CON; days 1-7). In a double-blind, randomized controlled fashion, participants were assigned to consume an additional 50g (2x25g) of Whey (WHEY, n=10), Pea (PEA, n=11), or collagen (COLL, n=10) protein each day (25 g at breakfast and lunch) during the supplemental phase (SUPP; days 8-15). Deuterated water ingestion and muscle biopsies assessed integrated MPS and acute anabolic signaling. Postprandial blood samples were collected to determine feeding-induced aminoacidemia.
RESULTS RESULTS
Integrated-MPS was increased during SUPP with WHEY (1.59 ± 0.11 %/d, p<0.001) and PEA (1.59 ± 0.14 %/d, p<0.001) when compared with RDA (1.46 ± 0.09 %/d WHEY; 1.46 ± 0.10 %/d PEA); however, it remained unchanged with COLL. Supplemental protein was sufficient to overcome anabolic signaling deficits (mTORC1 and rpS6), corroborating the greater postprandial aminoacidemia.
CONCLUSIONS CONCLUSIONS
Our findings demonstrate that supplemental protein provided at breakfast and lunch over the current RDA enhanced anabolic signaling and integrated MPS in older males; however, the source of additional protein may be an important consideration in overcoming age-related anabolic resistance. Clinical Trial Registry number and website where it was obtained This trial (NCT04026607) was registered clinicaltrials.gov.

Identifiants

pubmed: 38762187
pii: S0002-9165(24)00472-6
doi: 10.1016/j.ajcnut.2024.05.009
pii:
doi:

Banques de données

ClinicalTrials.gov
['NCT04026607']

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest ☒ The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:Stuart Phillips reports financial support was provided by Roquette Frères. Stuart Phillips reports a relationship with Nestlé SA that includes: speaking and lecture fees and travel reimbursement. Stuart Phillips reports a relationship with Enhanced Recovery that includes: non-financial support. Stuart Phillips has patent #11504413 issued to Exerkine Corporation. Chair, Publications Committee, American Society for Nutrition If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

James McKendry (J)

Department of Kinesiology, Exercise Metabolism Research Group, McMaster University, Hamilton, Ontario, Canada.

Caroline V Lowisz (CV)

Department of Kinesiology, Exercise Metabolism Research Group, McMaster University, Hamilton, Ontario, Canada.

Arraksana Nanthakumar (A)

Department of Kinesiology, Exercise Metabolism Research Group, McMaster University, Hamilton, Ontario, Canada.

Meaghan MacDonald (M)

Department of Kinesiology, Exercise Metabolism Research Group, McMaster University, Hamilton, Ontario, Canada; School of Human Kinetics, Faculty of Health Sciences, University of Ottawa, Ottawa, Ontario, Canada.

Changhyun Lim (C)

Department of Kinesiology, Exercise Metabolism Research Group, McMaster University, Hamilton, Ontario, Canada.

Brad S Currier (BS)

Department of Kinesiology, Exercise Metabolism Research Group, McMaster University, Hamilton, Ontario, Canada.

Stuart M Phillips (SM)

Department of Kinesiology, Exercise Metabolism Research Group, McMaster University, Hamilton, Ontario, Canada. Electronic address: phillis@mcmaster.ca.

Classifications MeSH