Abstract
Background/Objective: Delaying muscle fatigue could alleviate economic and food security, and welfare concerns associated with transporting market-weight pigs to harvest. Previous research demonstrates barrow nicotinamide riboside (NR) supplementation at varying doses during the last 10 d of finishing shows to be a countermeasure to muscle fatigue by reducing muscle fiber recruitment and increasing mitochondrial DNA expression in a dose-dependent manner. Therefore, this study aims to determine if a greater NR dose further enhances barrow fatigue resistance and characterize muscle mitochondria content and efficiency. Methods: Barrows (N = 87) were assigned to one of two dietary NR supplementation doses (TRT): 0 (0NR) or 150 (150NR) mg/kg body weigh NR administered during the last 14 d of finishing. Muscle (MUS) biopsies were collected on supplementation d (DAY) 0, 7 and 14 from three hind-leg muscles for NAD+ quantification and mitochondrial DNA expression and efficiency. On days 15 and 16, barrows were subjected to a performance test until they were subjectively exhausted. Electromyography data collection during the performance test were divided into five periods (PER) and included normalized root mean square (nRMS) from the same muscles. Results: There were no three-way interaction for nRMS (p > 0.83), but there were MUS × TRT and PER × TRT interactions (p < 0.05). During performance testing, 150NR had greater nRMS than 0NR in the bicep femoris (BF) and tensor fasciae latae (TFL; p < 0.01), but there were no differences in the semitendinosus (ST; p = 0.77). Treatments did not differ during PER 1 and 2 (p > 0.14) but 150NR had greater nRMS than 0NR during PER 3, 4 and 5 (p < 0.01) across all muscles. There was no three-way interaction for normalized (nNAD+; p = 0.14), but there was a DAY × TRT interaction (p < 0.05). There were no differences between 0NR and 150NR at d 0 (p = 0.95); however, by d 7 and 14, 150NR muscles had greater nNAD+ than 0NR muscles (p < 0.01). There tended to be a three-way interaction for mitochondrial DNA expression (p = 0.09). At supplementation d 14, all 150NR muscles had greater mitochondrial DNA expression and electron transport chain complex I and II activities (p < 0.01). When normalized to citrate synthase activity, electron transport chain complex I and II activity did not differ (p > 0.05). Conclusions: Large-dose NR supplementation appears to support sustained muscle fiber recruitment during prolonged activity and enhance fatigue resilience, primarily through increased NAD+ and mitochondrial biomarkers abundance and not through mitochondrial efficiency.