Older men (n = 12) and women (n = 18) 65–80 years of age completed twelve weeks of exercise and took either a placebo or resveratrol (500 mg/day) to test the hypothesis that resveratrol treatment combined with exercise would increase mitochondrial density, muscle fatigue resistance, and cardiovascular function more than exercise alone.
Contrary to our hypothesis, aerobic and resistance exercise coupled with resveratrol treatment did not reduce cardiovascular risk further than exercise alone. However, exercise added to resveratrol treatment improved the indices of mitochondrial density, and muscle fatigue resistance, more than placebo and exercise treatments.
In addition, subjects that were treated with resveratrol had an increase in knee extensor muscle peak torque (8%), average peak torque (14%), and power (14%) after training, whereas exercise did not increase these parameters in the placebo-treated older subjects. Furthermore, exercise combined with resveratrol significantly improved mean fiber area and total myonuclei by 45.3% and 20%, respectively, in muscle fibers from the vastus lateralis of older subjects.
Together, these data indicate a novel anabolic role of resveratrol in exercise-induced adaptations of older persons and this suggests that resveratrol combined with exercise might provide a better approach for reversing sarcopenia than exercise alone.
FULL TEXT: J Gerontol A Biol Sci Med Sci
EDITOR’S NOTE: ‘sarcopenia’ is muscle-wasting.
A chemical system in the brain, the cholinergic system, is primarily responsible for cognitive symptoms seen in people with dementia. It is not clear what role the cholinergic system (and a subset of receptors called the nicotinic system) plays in cognition during normal cognitive aging. This is critical because the ever-growing healthy aging population will show declines in cognition that fall short of dementia but still impact functional abilities and independence. Maintaining good nicotinic system functioning throughout adulthood might lessen the cognitive symptoms of aging.
This study will examine the role of the nicotinic system in the healthy aging brain, and examine its role in memory and thinking processes in older + younger adults.
NAD+ is a redox-active metabolite, the depletion of which has been proposed to promote aging and degenerative diseases in rodents. However, whether NAD+ depletion occurs in patients with degenerative disorders and whether NAD+ repletion improves their symptoms has remained open.
Here, we report systemic NAD+ deficiency in adult-onset mitochondrial myopathy patients. We administered an increasing dose of NAD+-booster niacin, a vitamin B3 form (to 750-1,000 mg/day; clinicaltrials.gov NCT03973203) for patients and their matched controls for 10 or 4 months, respectively.
Blood NAD+ increased in all subjects, up to 8-fold, and muscle NAD+ of patients reached the level of their controls. Some patients showed anemia tendency, while muscle strength and mitochondrial biogenesis increased in all subjects. In patients, muscle metabolome shifted toward controls and liver fat decreased even 50%.
Our evidence indicates that blood analysis is useful in identifying NAD+ deficiency and points niacin to be an efficient NAD+ booster for treating mitochondrial myopathy.
SOURCE: Cell Metabolism
EDITOR’S NOTE: Increased blood levels of NAD+ were achieved here with a readily available supplement, niacin (vitamin B3).