If you’re an older adult, a 30-minute workout may not be as effective, even at the cellular level, as it was when you were younger. According to a new study, age may play a significant role in cell’s ability to respond to that activity.
The study, led by Dr. Tinna Traustadóttir of Northern Arizona University, was recently published in Free Radical Biology and Medicine, a journal of the Society for Redox Biology and Medicine (SFRBM).
In the study, a group of men age 18-30 were tested against a group of older men 55 years of age and older. Study participants were generally healthy, non-smokers, who were not taking antioxidant supplements in excess of a multivitamin, or any non-steroidal anti-inflammatory drugs for two weeks leading up to their study visit.
The two groups cycled for 30-minutes, with blood being drawn at six time points to test cell function and antioxidant response. For this study, the exercise intensity was set relative to the individual’s maximal aerobic capacity as determined by a maximal oxygen consumption test during screening. It is known that older adults have a reduced aerobic capacity compared to young, thus this allowed the group to maintain the same relative workloads between young and old test groups.
“Through this study we were able to determine that an individual’s antioxidant response to exercise becomes suppressed with age,” said Dr. Traustadóttir an Associate Professor at Northern Arizona University and SFRBM Member. “Exercise is effective and critical for people of all ages, but this study shows that older adults do not achieve the same beneficial cellular responses as younger adults from a single bout of moderate exercise.”
The findings indicate a single session of submaximal aerobic exercise is sufficient to activate a important group of antioxidant genes at the whole cell level in both young and older adults. However, nuclear import of Nrf2, the regulator for this group of antioxidant genes, is impaired with aging. Nuclear import is required for Nrf2 to access the antioxidant gene targets. Together these data demonstrate for the first time the weakening of Nrf2 activity in response to exercise in older adults.
Traustadóttir’s ongoing research aims to identify molecular processes responsible for age-related cellular changes. By better understanding the molecular signals promoting beneficial effects of exercise, definitive recommendations could be made for improving the body’s reaction to oxidative stress, which could lower the risk for many chronic diseases.