Research Review: Older and inflamed? Try exercise
Cast your mind back – way back. All the way to the 19th century. People walked, rode horses, or drove buggies to get around. Roads were made of dirt. Sewers didn’t exist in many towns. Coal fumes belched from the chimneys. And without running water, flushing toilets, weekly garbage pickup, and anti-bacterial soap, people’s homes and communities were a lot grubbier. Plagues abounded. Cholera, diphtheria, tuberculosis, and other infectious diseases ran rampant. Many people died in infancy. In fact, just making it to your second birthday was an achievement that testified to the strength of your immune system. Check the headstones in an old cemetery if you doubt this.
CHRONIC INFLAMMATION: A MODERN DISEASE
Fast forward to today. Our homes and public spaces are (relatively) clean. Infectious diseases are almost unknown. We take it for granted that most kids will live past their second birthdays. Hurray for progress! But before we get too carried away, let’s take a closer look. Because – let’s face it – while we’ve been so busy scrubbing and polishing, we’ve also been polluting and contaminating our environment and ourselves. And all that pollution and contamination contributes to the chronic inflammation that tends to make us ill today.
Comparing the top ten causes of death in 1900 to the top ten causes of death in 2010, you will quickly notice that in 1900, most deaths were caused by pathogens (bacteria or viruses) while in 2010, most non-accidental deaths are caused by heart disease, cancer, chronic lower respiratory diseases, and stroke. Guess what? All of these – plus diabetes, Alzheimer’s, and even suicide are rooted in chronic inflammation.
Top 10 causes of death: 1900 vs 2010. Source: The New England Journal of Medicine
What causes chronic inflammation?
For a long time, we faced some threats from inflammatory substances and situations – but overall we were doing okay. Then, as industrialization took hold, we started to face new threats to immune health, such as:
- outdoor and indoor air pollution
- endocrine disruptors and environmental chemicals
- less daily activity
- sleep deprivation and artificial lighting
- chronic stress
- too many omega-6 fats, not enough omega-3s
- fast foods
These days, faced with so many threats from our environment, our immune systems are always on red alert. And that in turn becomes a new problem for us.
The immune system: From protector to assailant
To understand what went wrong, we need to understand the difference between acute (short-term or classical) and low level chronic (long-term) inflammation.
Our great-grandparents’ immune systems battled bacteria, viruses, and parasites on a regular basis. And one side effect of that constant skirmish was acute inflammation. The classic signs of acute inflammation: heat, redness, swelling, pain, and loss of function. All these signs of inflammation are caused by your immune system’s attempt to fight off the invader – whether that “invader” is a species of bacteria or a simple injury. And fighting takes energy, so classical inflammation increases metabolism.
The good news is that this whole process lasts for a few days or weeks at most. Meanwhile, modern medicine offers many tools to help us control this type of inflammation if it happens to go on for too long. Antibiotics kill off bacteria, vaccines can protect us from viruses, and surgery can remove severely infected areas (for example, with appendicitis).
The cardinal signs of inflammation — heat, redness, swelling, pain and loss of function.
“COLD” INFLAMMATION OR CHRONIC INFLAMMATION
Acute inflammation was the only kind of inflammation anyone recognized for thousands of years. Then doctors and researchers started noticing a new kind of inflammation: low-level, chronic, and systemic. Researchers started calling this new inflammation “chronic” or “cold” inflammation. That’s because it doesn’t have the typical hallmarks of acute inflammation. There’s no heat, redness, swelling, pain, or loss of function. What’s more, it’s linked to metabolic dysfunction. In fact, instead of speeding your metabolism up, this type of inflammation actually decreases metabolism.
What’s going on? As near as we can understand, chronic inflammation is an immune response similarto classical inflammation but not nearly as intense. Acute inflammation increases inflammatory markers over a hundred-fold, while chronic inflammation increases inflammatory markers two to four-fold. Instead of a short, vicious, site-specific burst of fighting as in classical inflammation, chronic inflammation involves a long, relatively mild, systemic grind. It’s like the difference between an explosion and a smoldering fire.
Chronic inflammation: obesity offender or accomplice?
Let’s go back and take a closer look at the modern immune system threats listed above. When you look at that list, what strikes you? If you’re like me, when you read: high energy intake, inactivity, sleep deprivation, chronic stress, and fast food your first thought is probably “weight gain” rather than “inflammation.” What’s going on?
Chronic inflammation is a metabolic inflammatory response. Your immune system responds to distress from adipocytes (fat cells) and other metabolic cells (liver, brain, muscle). And visceral fat (the fat around your internal organs) plays a larger role in chronic inflammation than subcutaneous fat (the fat under your skin).
Visceral fat triggers inflammation, and that’s why it has such a powerful effect on metabolic disease.
Here’s how this works:
- Excess fat from the cells oozes out, triggering an immune response.
- Fat cells undergo mechanical stress, triggering an immune response.
What this means is that macrophages (the foot soldiers of the immune system) make their way into fat tissue to see what all the fuss is about (macrophage adipose infiltration).
Everybody has some macrophages in their fat tissue. But the proportion varies considerably – from 10 % macrophages in lean people, to 50% macrophages in obese people. Lean people also have a different type of macrophage (the M2 macrophage) compared to obese people (who harbor the M1 macrophage).As the macrophages make their way into fat tissue, the body shows a small, but important increase in markers of inflammation, such as:
- tumor necrosis factor-α (TNF- α);
- interleukin-6 (IL-6); and
- C-reactive protein (CRP).
Exhibit A: If you inject TNF- α into a healthy, lean mouse, it will become insulin resistant. And while obesity is central to chronic inflammation and disease, pro-inflammatory factors such as stress, lack of sleep, and pollution can alsobe linked to disease – even in the absence of obesity.
The important point is that chronic inflammation isn’t just another a side effect of obesity. Instead, it appears to be the link between obesity and disease.
To recap: Chronic inflammation is bad for your health. Decreasing chronic inflammation is the key to improving health. So… what’s the role of exercise in all of this? First off, it’s not as simple as you might think. Yes, activity is a good thing. But if you exercise at all, you know that exercise can trigger classical inflammation. (DOMS, anyone?) Based on that, you might assume that exercise would also trigger chronic inflammation, right?
This week’s Research Review probes that assumption, studying the role of resistance exercise training in obese postmenopausal women—a population susceptible to chronic inflammation. Phillips MD, Patrizi RM, Cheek DJ, Wooten JS, Barbee JJ, Mitchell JB. Resistance training reduces subclinical inflammation in obese, postmenopausal women. Med Sci Sports Exerc. 2012 Nov;44(11):2099-110.
Subjects and methods
The subjects included 23 post-menopausal women (60-70 years old) who were obese (with BMIs ranging from 30 to 40) and had not participated in regular exercise for at least 6 months. None of the subjects suffered from severe arthritis, nervous system disorders, previous stroke, infections, immune disorders (autoimmune or viral), or metabolic disorders (i.e. diabetes). They were not smoking, or taking antidepressants, steroids, or hormone replacements. In other words, for their age and BMI, these women were very healthy. About half the women were randomly assigned to the exercise group (11 women) and the other half became the control group (12 women).
EXERCISE ACCLIMATION: PRE-TRAINING BASELINE
Both groups underwent an exercise acclimation or pre-training baseline that took 3 days. During this period, researchers showed the women how to do the exercises and tested their strength before and after learning (to make sure any gains weren’t due to simply learning the movements).
CONTROL GROUP: 12 WEEKS OF SOCIALIZING & STRETCHING
While this group didn’t exercise, they did go to the lab for one hour, twice a week forcontrol activities. Why bother? Just in case the social component of exercise and not the exercise itself made a difference. The idea was to limit the confounding factors. Social activities included:
- health education
- safety talks
I think we’d all agree that these activities wouldn’t increase strength or aerobic capacity, but the stretching may have some physical impact, and some of the others could reduce stress. Except maybe the safety talks, which could have raised stress. Note that unlike the exercise group, they came in to the lab only twice a week – perhaps on the exercise group’s days off.
EXERCISE GROUP: 12 WEEKS OF SWEATING & STRAINING
The exercise group trained for 12 weeks, 3 times a week, with a day of rest in between each training session, for a total of 36 training sessions. Each training session involved 10 exercises done on Nautilus or Cybex machines.
|EXERCISE||SET 1||SET 2||SET 3|
|A1||Chest press||8 reps||8 reps||As many as possible (failure)|
|A2||Lat pull-down||8 reps||8 reps||As many as possible (failure)|
|B1||Seated rows||8 reps||8 reps||As many as possible (failure)|
|B2||Shoulder press||8 reps||8 reps||As many as possible (failure)|
|C1||Leg abduction||8 reps||8 reps||As many as possible (failure)|
|C2||Leg adduction||8 reps||8 reps||As many as possible (failure)|
|D1||Chest flyes||8 reps||8 reps||As many as possible (failure)|
|D2||Leg press||8 reps||8 reps||As many as possible (failure)|
|E1||Leg curls||8 reps||8 reps||As many as possible (failure)|
|E2||Leg press||8 reps||8 reps||As many as possible (failure)|
The researchers didn’t mention if there was any rest between sets or exercises, but the exercises were paired (see table, exercise A1 & A2 were paired with each other, B1 & B2 were paired, etc.) Over the 12 weeks, if a woman could lift a weight more than 12 times in a given exercise, the researchers increased the weight for that exercise.
Why this study matters
The biggest strength of the study is the population the researchers chose. We don’t really know much about post-menopausal women and exercise. Most exercise physiology research is done on young males (typically university students, who are easily available to researchers) whose results may not translate to older women or older populations in general. The other reason the researchers chose well, in this case, is that obese post-menopausal women are very likely to be suffering from chronic inflammation! So if exercise will do anything to reduce or increase chronic inflammation, you’d expect to find that out by studying this group.
Finally, obese post-menopausal women are probably the least likely to engage in resistance training. I can convince my mom to walk, go to stretching classes, and even dance classes – but when it comes to resistance training, I’ve gotten nowhere. Show these women some real evidence that resistance training can improve their health, and maybe we’ll be able to persuade them.
BODY COMPOSITION: NO CHANGE
As you’ll see from the table below, the 12-week program led to no significant change in body composition for either the control or the exercise group. In other words, there was no change in weight, fat, lean mass, or percent body fat. Note that the women were not asked to make nutritional changes as part of their program, and that probably explains the lack of change. But keep this in mind when you look at the rest of the results. (And by the way, if you’re a 60+ woman — or anyone else — reading this, and you’re frustrated by seeing no body composition changes despite hard work in the gym, check out our Lean Eating coaching program. We might be able to help.)
|BEFORE TRAINING||AFTER TRAINING||BEFORE TRAINING||AFTER TRAINING|
|Age (years)||64.8 ± 2.4||n/a||66.4 ± 2.8||n/a|
|Height (cm)||161.3 ± 5.5||n/a||159.6 ± 7.7||n/a|
|Body weight (kg)||83.8 ± 8.8||83.2 ± 8.5||86.0 ± 13.4||86.1 ± 12.8|
|Body Fat (%)||35.1 ± 2.7||34.8 ± 2.5||36.4 ± 3.3||36.0 ± 3.0|
|BMI (kg/m2)||32.2 ± 3.3||32.0 ± 3.5||33.7 ± 4.4||33.7 ±4.0|
|Fat-free (Lean) mass (kg)||54.4 ± 5.8||54.5 ± 7.5||54.2 ± 5.3||54.9 ± 7.0|
|Fat mass (kg)||29.4 ± 4.3||29.0 ± 4.3||31.6 ± 6.9||31.2 ± 6.5|
They may not have experienced changes in body composition, but the women in the exercise group did get stronger. Using changes in 8 RM, the exercise group increased strength by an average of 44% (ranging from 22-67%). There was no change in strength for the control group, but that’s no surprise. They weren’t doing anything different.
So let’s look at chronic inflammation, since that was the point of the study. While weight training can briefly increase acute inflammation (which is what causes the stiffness and soreness the day after a tough workout), what happens to chronicinflammation? In this study, researchers looked at tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), C-reactive protein (CRP), and leptin as chronic inflammation markers. Leptin is known primarily for its role in appetite suppression, but it can also show inflammation, and these two roles are related.
In this study, subjects showed a 29% decrease in TNF-α, 33% decrease in CRP, and an 18% decrease in leptin after resistance training for 12 weeks. The control group showed no similar change. Knitting and general socializing didn’t alter the inflammatory proteins.
In this study, exercisers showed a 40-60% increase in IL-6 immediately after exercise, which was expected. But training for 12 weeks didn’t result in an overall change. Here’s another interesting result: There was also a 20% increase in IL-10(interleukin-10), an anti-inflammatory protein.
Inflammatory markers: decrease
- TNF-α: 29% less
- CRP: 33% less
- Leptin: 18% less
Anti-inflammatory marker: increase
- IL-10: 20% more
Another cool finding:
There was an inverse relationship between strength and inflammation. The stronger the women were, the lower their CRP and leptin.
Understanding how chronic inflammation works and how to stop it is crucial, because chronic inflammation is at the root of most lifestyle disease, from Alzheimer’s to cancer to stroke to everything in between. This study sheds some light on the problem and also offers some hope.
STRENGTHS AND WEAKNESSES OF THE STUDY
Overall, I think this study did a good job getting at the question of whether or not strength training reduces chronic inflammation. Strengths of the study included:
1. Focusing on an under-studied population.
Weight-training studies in obese post-menopausal women are a rarity, with the vast majority of studies being on young males. Why does this matter? Because, as estrogen and progesterone decrease, post-menopausal women tend to show higher levels of inflammation. And obese post-menopausal women are likely to get the most health benefits from exercise, particularly weight training. Men have the advantage of testosterone, which does a good job and making and maintaining muscle. In comparison, women tend to have less muscle. Worse yet, as we age, we tend to lose muscle.
Having lower muscle mass is associated with lower personal independence, an increased risk of falls, and an increased risk of death. Weight-bearing activity is also important for bone health. In fact, it’s arguably more important than taking calcium supplements. Studies that investigate the effects of weight training on women’s health are therefore important.
2. Limiting confounding factors.
Ensuring that the control group engaged in stress-reducing activities helps to support the study’s findings about the specific effect of weight training on inflammation.
3. Choosing a weight-training program focused on increasing strength and muscle mass.
This program resulted in no cardiovascular benefit for the subjects. In fact, it turned out all changes were strength-related, with little change in muscle mass. But the strict focus on strength training is rare in studies. In the past, the medical community has largely minimized health improvements based exclusively on changes in strength. Understanding how increased strength affects our health is as crucial as understanding the role of cardiovascular improvements.
4. Examining factors other than body composition.
Being obese is bad for your health – no question. But there’s more to the problem than fat alone. And we need to understand this. Since the subjects in this study experienced no change in fat and muscle mass, any change in inflammation that they experienced cannot be attributed to changes in body composition. In other words, inflammation is responding to something other than fat.
Confused? Maybe an analogy will help. Compare lifestyle disease (Type 2 diabetes, cardiovascular disease, etc.) to a fire, and obesity to gasoline.Can you start a fire without gasoline? Absolutely. Can you have lifestyle disease without obesity? Of course! But gasoline can start a fire. And if you pour it on an existing blaze, you’ll get an explosion. Similarly, obesity can set off a lifestyle disease. And if you already have a lifestyle disease and you are also obese or become obese, obesity will likely make your condition a lot worse. Despite the study’s strengths, the researchers could have done a better job in a couple of key areas:
They could have devised a better training program.
Using free weights rather than machines may have required a longer training period. But the results would translate better to real world activities.
Measuring visceral fat.
It’s possible that any changes in inflammation were due to a reduction in visceral fat.I don’t think that’s the case, because any major change in visceral fat would show up on the scale. But without a specific measure of visceral fat before and after the 12-week program, minor changes could be missed.
The common denominator in most, if not all, modern disease is chronic or “cold” inflammation. Not enough exercise and sleep; too much body fat and stress – all contribute to this insidious form of inflammation. This week’s review showed that even in the absence of changes to weight and body composition, weight-bearing exercise decreased inflammation in post-menopausal subjects. In short, this study gives you one more reason to ignore the scale and keep up with your exercise routine.
Physical activity even without weight loss is anti-inflammatory.
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