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Nicotinamide riboside supplementation does not alter whole‐body or skeletal muscle metabolic responses to a single bout of endurance exercise
Author(s) -
Stocks Ben,
Ashcroft Stephen P.,
Joanisse Sophie,
Dansereau Linda C.,
Koay Yen Chin,
Elhassan Yasir S.,
Lavery Gareth G.,
Quek LakeEe,
O'Sullivan John F.,
Philp Ashleigh M.,
Wallis Gareth A.,
Philp Andrew
Publication year - 2021
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jp280825
Subject(s) - skeletal muscle , nad+ kinase , medicine , endocrinology , nicotinamide adenine dinucleotide , nicotinamide mononucleotide , glycogen , nicotinamide , biochemistry , biology , niacin , chemistry , enzyme
Key points Acute nicotinamide riboside (NR) supplementation does not alter substrate metabolism at rest, during or in recovery from endurance exercise. NR does not alter NAD + ‐sensitive signalling pathways in human skeletal muscle. NR supplementation and acute exercise influence the NAD + metabolome.Abstract Oral supplementation of the NAD + precursor nicotinamide riboside (NR) has been reported to alter metabolism alongside increasing sirtuin (SIRT) signalling and mitochondrial biogenesis in rodent skeletal muscle. However, whether NR supplementation can elicit a similar response in human skeletal muscle is unclear. This study assessed the effect of 7‐day NR supplementation on whole‐body metabolism and exercise‐induced mitochondrial biogenic signalling in skeletal muscle. Eight male participants (age: 23 ± 4 years,V ̇O 2 peak46.5 ± 4.4 ml kg –1 min –1 ) received 1 week of NR or cellulose placebo (PLA) supplementation (1000 mg day –1 ). Muscle biopsies were collected from the medial vastus lateralis prior to supplementation and pre‐, immediately post‐ and 3 h post‐exercise (1 h of 60% W max cycling) performed following the supplementation period. There was no effect of NR supplementation on substrate utilisation at rest or during exercise or on skeletal muscle mitochondrial respiration. Global acetylation, auto‐PARylation of poly ADP‐ribose polymerase 1 (PARP1), acetylation of Tumour protein 53 (p53) Lys382 and Manganese superoxide dismutase (MnSOD) Lys122 were also unaffected by NR supplementation or exercise. NR supplementation did not increase skeletal muscle NAD + concentration, but it did increase the concentration of deaminated NAD + precursors nicotinic acid riboside (NAR) and nicotinic acid mononucleotide (NAM) and methylated nicotinamide breakdown products (Me2PY and Me4PY), demonstrating the skeletal muscle bioavailability of NR supplementation. In summary, 1 week of NR supplementation does not alter whole‐body metabolism or skeletal muscle signal transduction pathways implicated in the mitochondrial adaptation to endurance exercise.