Connell 2021 J Nutr
Connell NJ, Grevendonk L, Fealy CE, Moonen-Kornips E, Bruls YMH, Schrauwen-Hinderling VB, de Vogel J, Hageman R, Geurts J, Zapata-Perez R, Houtkooper RH, Havekes B, Hoeks J, Schrauwen P (2021) NAD+-precursor supplementation with L-tryptophan, nicotinic acid, and nicotinamide does not affect mitochondrial function or skeletal muscle function in physically compromised older adults. J Nutr 151:2917-31 |
Connell NJ, Grevendonk L, Fealy CE, Moonen-Kornips E, Bruls YMH, Schrauwen-Hinderling VB, de Vogel J, Hageman R, Geurts J, Zapata-Perez R, Houtkooper RH, Havekes B, Hoeks J, Schrauwen P (2021) J Nutr
Abstract: Boosting NAD+ via supplementation with niacin equivalents has been proposed as a potential modality capable of promoting healthy aging and negating age-dependent declines of skeletal muscle mass and function.
We investigated the efficacy of NAD+-precursor supplementation (tryptophan, nicotinic acid, and nicotinamide) on skeletal muscle mitochondrial function in physically compromised older adults.
A randomized, double-blind, controlled trial was conducted in 14 (female/male: 4/10) community-dwelling, older adults with impaired physical function [age, 72.9 Β± 4.0 years; BMI, 25.2 Β± 2.3 kg/m2]. Participants were supplemented with 207.5 mg niacin equivalents/day [intervention (INT)] and a control product (CON) that did not contain niacin equivalents, each for 32 days. The primary outcomes tested were mitochondrial oxidative capacity and exercise efficiency, analyzed by means of paired Student's t-tests. Secondary outcomes, such as NAD+ concentrations, were analyzed accordingly.
Following supplementation, skeletal muscle NAD+ concentrations [7.5 Β± 1.9 compared with 7.9 Β± 1.6 AU, respectively] in INT compared with CON conditions were not significantly different compared to the control condition, whereas skeletal muscle methyl-nicotinamide levels were significantly higher under NAD+-precursor supplementation [INT, 0.098 Β± 0.063 compared with CON, 0.025 Β± 0.014; P = 0.001], suggesting an increased NAD+ metabolism. Conversely, neither ADP-stimulated [INT, 82.1 Β± 19.0 compared with CON, 84.0 Β± 19.2; P = 0.716] nor maximally uncoupled mitochondrial respiration [INT, 103.4 Β± 30.7 compared with CON, 108.7 Β± 33.4; P = 0.495] improved under NAD+-precursor supplementation, nor did net exercise efficiency during the submaximal cycling test [INT, 20.2 Β± 2.77 compared with CON, 20.8 Β± 2.88; P = 0.342].
Our findings are consistent with previous findings on NAD+ efficacy in humans, and we show in community-dwelling, older adults with impaired physical function that NAD+-precursor supplementation through L-tryptophan, nicotinic acid, and nicotinamide does not improve mitochondrial or skeletal muscle function. β’ Keywords: NAD+-Precursors, Metabolism, Mitochondrial function, Muscle health, Older adults, Skeletal muscle β’ Bioblast editor: Plangger M β’ O2k-Network Lab: NL Maastricht Schrauwen P
Labels: MiParea: Respiration, Exercise physiology;nutrition;life style, Pharmacology;toxicology
Organism: Human
Tissue;cell: Skeletal muscle
Preparation: Permeabilized tissue
Coupling state: LEAK, OXPHOS, ET
Pathway: F, N, NS
HRR: Oxygraph-2k
2021-07