Abstract

BackgroundRecent studies in rodents indicate that a combination of exercise training and supplementation with nicotinamide adenine dinucleotide (NAD+) precursors has synergistic effects. However, there are currently no human clinical trials analyzing this.ObjectiveThis study investigates the effects of a combination of exercise training and supplementation with nicotinamide mononucleotide (NMN), the immediate precursor of NAD+, on cardiovascular fitness in healthy amateur runners.MethodsA six-week randomized, double-blind, placebo-controlled, four-arm clinical trial including 48 young and middle-aged recreationally trained runners of the Guangzhou Pearl River running team was conducted. The participants were randomized into four groups: the low dosage group (300 mg/day NMN), the medium dosage group (600 mg/day NMN), the high dosage group (1200 mg/day NMN), and the control group (placebo). Each group consisted of ten male participants and two female participants. Each training session was 40–60 min, and the runners trained 5–6 times each week. Cardiopulmonary exercise testing was performed at baseline and after the intervention, at 6 weeks, to assess the aerobic capacity of the runners.ResultsAnalysis of covariance of the change from baseline over the 6 week treatment showed that the oxygen uptake (VO2), percentages of maximum oxygen uptake (VO2max), power at first ventilatory threshold, and power at second ventilatory threshold increased to a higher degree in the medium and high dosage groups compared with the control group. However, there was no difference in VO2max, O2-pulse, VO2 related to work rate, and peak power after the 6 week treatment from baseline in any of these groups.ConclusionNMN increases the aerobic capacity of humans during exercise training, and the improvement is likely the result of enhanced O2 utilization of the skeletal muscle.Trial registration numberChiCTR2000035138.

Highlights

  • Nicotinamide adenine dinucleotide (NAD+) is pivotal to physiological processes, as the coenzyme of cellular oxidation–reduction reactions and for the activation of NAD+-consuming enzymes, such as sirtuins, poly-ADP-ribose polymerases (PARPs), cADP-ribose synthases, NADase (CD38), and mono-ADP-ribose transferases (ARTs) [1]

  • The combination of nicotinamide mononucleotide (NMN) and exercise increases VT but not VO2max or O2−pulse No significant changes in HRmax, RERmax, heart rate reserve (HRR), O2pulse, peak power, peak workload, ΔO2/ΔWR, or VO2max were shown between the control and any of the NMN treatment groups

  • The VO2@VT1, %VO2max@VT1, HR@ VT1, power@VT1, and power@VT2 (Tables S1 and S2; Table 3) were increased significantly from the NMN supplementation compared with baseline, and the positive effect was in a dosedependent manner (Table 4)

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Summary

Introduction

Nicotinamide adenine dinucleotide (NAD+) is pivotal to physiological processes, as the coenzyme of cellular oxidation–reduction reactions and for the activation of NAD+-consuming enzymes, such as sirtuins, poly-ADP-ribose polymerases (PARPs), cADP-ribose synthases, NADase (CD38), and mono-ADP-ribose transferases (ARTs) [1]. Supplementation with NR and supplementation with NMN have shown a dose-dependent increase in cellular NAD+ levels in a variety of tissues in rodents and humans [4,5,6]. Clinical studies have shown that the effects of NR (dosages from 500 mg/d to 2000 mg/d; durations of 1 day to 3 months) on skeletal muscle, cardiovascular function, and physical function in the elderly and obese are limited [4]. The NAD+ precursor nicotinic acid (NA), an effective pharmacological drug with indications for lowering triacylglycerol levels and dilating blood vessels [9], significantly improved skeletal muscle function in healthy individuals [10] and in patients with adult-onset mitochondrial myopathy [11, 12]. Recent studies in rodents indicate that a combination of exercise training and supplementation with nicotinamide adenine dinucleotide (NAD+) precursors has synergistic effects. There are currently no human clinical trials analyzing this

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