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Tissue-specific effects of exercise as NAD+ -boosting strategy: Current knowledge and future perspectives
David Walzik1, Wiebke Jonas1, Niklas Joisten1
1Division of Performance and Health (Sports Medicine), Institute for Sport and Sport Science, TU Dortmund University, Dortmund, Germany.
Exercise impacts nicotinamide adenine dinucleotide (NAD+) metabolism, influencing energy and cellular health. Both acute exercise and training alter NAD+ levels, suggesting exercise
Area of Science:
- Cellular Biology
- Metabolic Science
- Exercise Physiology
Background:
- Nicotinamide adenine dinucleotide (NAD+) is a crucial coenzyme involved in energy metabolism, signaling, epigenetics, and DNA repair.
- Declining NAD+ levels are linked to aging and various diseases, prompting research into NAD+-boosting strategies.
- Exercise is a potential lifestyle intervention to restore NAD+ homeostasis via metabolic adaptations to energy demands.
Purpose of the Study:
- To review the impact of acute exercise and exercise training on tissue-specific NAD+ metabolism in rodents and humans.
- To highlight exercise as a potential NAD+-boosting strategy.
- To explore the implications of tissue-specific NAD+ alterations for whole-body NAD+ homeostasis.
Main Methods:
- Review of existing scientific literature on exercise and NAD+ metabolism.
- Analysis of studies investigating acute exercise effects on NAD+ metabolism.
- Examination of research on the effects of exercise training on NAD+ levels and enzyme activity.
Main Results:
- Acute exercise induces significant, modality-dependent changes in intracellular NAD+ metabolism.
- Exercise training generally increases NAD+ levels and related enzyme activity across various tissues.
- Findings emphasize tissue-specific responses to exercise interventions.
Conclusions:
- Exercise, both acute and chronic, significantly modulates NAD+ metabolism.
- Understanding the molecular mechanisms linking acute exercise to chronic adaptations is crucial.
- Further research into exercise as an NAD+-modifying intervention could reveal therapeutic potential for NAD+-related pathologies.
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