Boosting the benefits of exercise

We all know exercise is beneficial to our health. Then why is it that ultramarathon runners may generate so many free radicals during a race that they can damage the DNA of a significant percentage of their cells? Researchers have looked at the exercise-induced increase in free radical production as a paradox: why would an apparently healthy act—exercise—lead to detrimental effects through damage to various molecules and tissues? This arises out of somewhat of a misunderstanding: exercise in and of itself is not necessarily the healthy act—it’s the recovery after exercise that is so healthy, the whole “that-which-doesn’t-kill-us-makes-us-stronger” notion. For example, exercise training has been shown to enhance antioxidant defenses by increasing the activities of our antioxidant enzymes. So, during the race ultra-marathoners may be taking hits to their DNA, but a week later they can experience great benefits, as shown in my video, Enhanced Athletic Recovery Without Undermining Adaptation.

In a recent study, researchers from Oregon State University looked at the level of DNA damage in athletes. Six days after a race, athletes didn’t just go back to the baseline level of DNA damage, but had significantly less, presumably because they had revved up their antioxidant defenses. So, maybe exercise-induced oxidative damage is beneficial, similar to vaccination. By freaking out the body a little, we might induce a response that’s favorable in the long run.

This concept, that low levels of a damaging entity can up-regulate protective mechanisms, is known as hormesis. For example, herbicides kill plants, but in tiny doses may actually boost plant growth, presumably by stressing the plant into rallying its resources to successfully fight back.

Wait a second, though. Could eating anti-inflammatory and anti-oxidant rich plant foods undermine this adaptation response? We know that berries may reduce inflammatory muscle damage (See Reducing Muscle Soreness with Berries), and greens may reduce free radical DNA damage (See Preventing Exercise Induced Oxidative Stress with Watercress). Dark chocolate and tomato juice appear to have similar effects. How it works is that flavonoid phytonutrients in fruits, vegetables, and beans seem to inhibit the activity of xanthine oxidase, considered the main contributor of free radicals during exercise. And the carbs in plant foods may also decrease stress hormone levels.

So in 1999, a theoretical concern was raised. Maybe all that free radical stress from exercise is a good thing, and increased consumption of some antioxidant nutrients might interfere with these necessary adaptive processes. If we decrease free radical tissue damage, maybe we won’t get that increase in activity of those antioxidant enzymes.

A group of researchers who performed a study on tart cherry juice and recovery following a marathon responded to this antioxidant concern by suggesting that, although it is likely that muscle damage, inflammation, and oxidative stress are important factors in the adaptation process, minimizing these factors may improve recovery so we can train more and perform better. So, there are theories on both sides, but what happens when we actually put it to the test?

While antioxidant or anti-inflammatory supplements may prevent these adaptive events, researchers found that blackcurrant extract – although packed with antioxidant and anti-inflammatory properties – actually boosted the health benefits of regular exercise.

If we take antioxidant pills—vitamin C and vitamin E supplements— we can also reduce the stress levels induced by exercise, but in doing so we block that boost in antioxidant enzyme activity caused by exercise. Now maybe we don’t need that boost if we don’t have as much damage, but vitamin C supplements seem to impair physical performance in the first place. With plant foods, though, we appear to get the best of both worlds.

For example, lemon verbena, an antioxidant-rich herbal tea, protects against oxidative damage and decreases the signs of muscular damage and inflammation, without blocking the cellular adaptation to exercise. In a recent study, researchers showed that lemon verbena does not affect the increase of the antioxidant enzyme response promoted by exercise. On the contrary: antioxidant enzyme activity was even higher in the lemon verbena group.

Reducing sedentary time protects DNA

Less time spent sitting may lengthen telomeres and protect DNA from age-related damage, a new study shows. However, the researchers found no significant association in telomere length with increased exercise in this small randomized trial.

"We're excited about this study," said lead author Mai-Lis Hellenius, MD, PhD, a professor of cardiovascular disease prevention in the Department of Medicine, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden. "Long telomeres are linked to a longer, healthier life."

Per Sjögren, PhD, from the Unit of Clinical Nutrition and Metabolism, Department of Public Health and Caring Sciences, Uppsala University, Sweden, and colleagues published the study online September 3 in the British Journal of Sports Medicine.

Telomeres are sections of DNA that protect the ends of chromosomes from damage during cell division. Telomeres tend to shorten with age, and previous research has linked shorter telomeres with shorter life spans and increased risk for some types of cancer and cardiovascular disease.

"Our DNA will be damaged during a lifetime," Dr. Hellenius said. "It's damaged by bad diets, smoking, infections, and so on. Our capability to copy and produce new DNA and new cells is so important."

Previous research has shown that people who exercise more tend to have longer telomeres.

In the current study, Dr. Sjögren and colleagues analyzed the length of telomeres a subset of people who had participated in a randomized exercise trial. The original study included 101 predominantly sedentary and overweight people adults aged 68 years at baseline. The investigators randomly assigned half of the participants to an exercise program and the other half to their regular behavior.

They asked the participants to keep a 7-day diary and to wear a pedometer to measure the number of steps taken every day. They also asked them to fill out a questionnaire tallying up the amount of time spent sitting down each day.

As the researchers reported previously, the time spent exercising, as well as the number of steps taken daily, increased significantly in the group assigned the exercise program, whereas the amount of time spent seated fell in both groups ( Br J Sports Med. 2011;45:158). Various risk factors for heart disease and stroke also improved in both groups, particularly those on the exercise program, who lost more weight than their counterparts left to their own devices.

In the current subset analysis, the researchers examined telomere length from blood samples drawn at baseline and after the 6-month intervention in 49 randomly chosen participants. They found that the number of daily steps taken was not associated with changes in telomere length.

An increase in moderate-intensity physical activity correlated to a shortening in telomere length in both groups, but this finding was not statistically significant. However, a reduction in the amount of time spent sitting in the exercise group was associated with telomere lengthening in blood cells.

"We hypothesise that a reduction in sitting hours is of greater importance than an increase in exercise time for elderly risk individuals," the researchers conclude.

Dr. Hellenius acknowledged that the study was a small one and needed to be replicated before drawing conclusions from it. However, she notes, other research has also shown that people who spend more time sitting have shorter lives, regardless of whether they also exercise regularly.

"So I think you can say to our patients yes, it's important to break up sedentary time and take a break for 1 or 2 minutes every 30 minutes," said Dr. Hellenius.