Let me introduce myself. My name is Mark Sisson. I’m 63 years young. I live and work in Malibu, California. In a past life I was a professional marathoner and triathlete. Now my life goal is to help 100 million people get healthy. I started this blog in 2006 to empower people to take full responsibility for their own health and enjoyment of life by investigating, discussing, and critically rethinking everything we’ve assumed to be true about health and wellness...Tell Me More
A couple weeks ago, I wrote about how becoming an efficient fat-burner helps mitochondrial function, and last week I went over some of the nutrients and supplements most important for your mitochondria. All good and all useful, but today I’m going to talk about another route: exercise. It makes intuitive sense that mitochondria are profoundly affected by exercise, doesn’t it? They are the power plants of the cells (and that goes for muscle cells), they are the organelles that convert fat, protein, and glucose into usable energy – and continuously producing ample amounts of cellular energy to lift heavy things, run really fast (or really far at a slower pace), or jump high is what exercise is all about. What I like about exercise is that it’s an entirely self-contained lifestyle modification. Modifying your energy pathways from sugar to fat and obtaining certain nutrients requires eating different foods and different amounts of those foods, and supplementing (obviously) requires taking supplements. But exercise is entirely up to you. If you want to. It’s a subtle distinction, but an important one. And an empowering one, if you ask me.
If your interest in mitochondria was piqued over the last few weeks, and you’re the type to focus on lifestyle modifications before supplementations, this post is for you. If you want to improve your exercise performance by increasing the effectiveness of your muscle mitochondria, this post is for you. If you want to reduce age-related muscle atrophy and promote better, more robust health, this post is for you. In other words, this post is for you. All of you. Now, exercise may not be sufficient to keep your mitochondria happy and healthy, but it’s a vital piece of the whole picture.
How does it work?
Remember how I mentioned that getting your body to create new mitochondria requires a stressor, a challenge to the system? Well, the presence of AMPK, or amp-activated protein kinase, is how we know that such a stressor has been applied. What’s AMPK? AMPK is a metabolic regulator that increases mitochondrial biogenesis (in addition to a number of other roles that I won’t discuss). Many things can stimulate AMPK, like caloric restriction, fasting, ketosis, and exercise. What do you notice about all four? CR requires restricted caloric intake, fasting removes caloric intake entirely, ketosis restricts glucose intake, and exercise depletes stored energy; the common thread is that these are all energy-depleted states. So, AMPK increases mitochondrial biogenesis as a response to the lack of cellular energy and an adaption to the applied stress. AMPK is the marker to look for when assessing mitochondrial enhancement potential.
Today’s about exercise, though, so let’s dig into the research and see how specific types and intensity levels of exercise influence AMPK expression. Shall we?
Most research into exercise and mitochondria has revolved around traditional endurance training. Classic stuff – long slow distance, jogging, cycling. And endurance exercise works, don’t get me wrong. I’m no fan of long slow cardio anymore, but it does have the ability to increase mitochondria. I’ll give it that. In fact, though I’m biting my lip as I type this, “cardio” is the best way to increase AMPK and induce mitochondrial biogenesis. It’s quite basic, actually. Slow twitch muscle fibers, the ones employed in endurance training, contain the most mitochondria, so it’s natural that training that targets slow twitch fibers will also target more muscle mitochondria.
It even works in elderly patients with old, presumably creaky muscles, for whom performing between four and six light-medium cardio sessions (cycling, treadmill, or brisk outdoor walking) per week for 12 weeks increased mitochondrial content of muscles. And more recently, here (although trained elderly individuals exhibited less of an AMPK response than untrained elderly).
Just be wary (as always) of chronic cardio. One of cycling’s greats, Greg Lemond attributes his degenerative mitochondrial myopathy to overtraining. I suppose training for the Tour’ll do that.
Of course, who ever said that cardio had to be chronic?
High-intensity interval training is just as, if not more effective than regular endurance training, and sprint training works great, too. Now, a word on sprinting and HIIT. Most studies blur the lines between high intensity interval training and sprinting. The language blends into itself. What I’d call a series of all-out sprints with plenty of recovery time in between, they might call high intensity interval training. Without full texts and full study set-up descriptions for everything, we can’t know whether the training was true sprinting or HIIT. Thus, in lieu of better information I’ll discuss both together.
From Gibala et al comes an interesting study in which four 30 second “all-out” cycling sprints interspersed with four minutes of rest activated AMPK signaling. The authors speculate (but don’t test) that the increased AMPK probably resulted in mitochondrial biogenesis and improved glucose and fat oxidation. In another study earlier this year, that same crew of researchers confirmed that the same sprint training protocol – 30 sec on, four minute rest, four times – does increase mitochondrial biogenesis through activation of AMPK. They called it high intensity, but it sounds like sprinting to me.
HIIT is probably best for certain populations, like the time-strapped, the impatient, the former marathoner-living-in-Malibu-with-a-burning-desire-to-get-work-over-with-so-he-can-play, the obese, and those with type 2 diabetes. Yes, in type 2 diabetics and the obese, activating AMPK and spurring biogenesis requires higher exercise intensities. The mitochondria are slower to respond, probably because their ability to tap into fat for energy is blunted. If your mitochondria aren’t burning energy, you’re not sending the “low energy” signal that stimulates AMPK. If you’re not releasing AMPK… well, you get the point.
How about strength training? Lifting heavy things is good for you. On that, we can agree. And when you tack it onto an endurance training regimen, the degree of mitochondrial biogenesis surpasses that of endurance training alone. But in and of itself? The evidence is mixed. Hypertrophy training, which employs higher reps (10-12 reps), more volume (4-5 sets), and less weight (because, well, you’re lifting the weight more times), decreases muscle mitochondrial density. You are literally expanding the size of your existing muscle fibers without generating a commensurate number of new mitochondria, so they become more “spread out.” This is because hypertrophy training specifically, and strength training generally, doesn’t stimulate as much AMPK expression. If it did, hypertrophy training wouldn’t really result in any actual hypertrophy, since AMPK inhibits mTOR (mammalian target of rapamycin), the premier muscle building agent in the mammalian body. (This is why excessive cardio can inhibit lean mass accumulation.)
On the other hand, strength training does stimulate AMPK in some studies. For example, 10 sets of 10 reps of leg extensions at 70% of 1-rep max increased AMPK for over an hour post-workout, after which mTOR increased and muscle protein synthesis upregulated. So lifting gets you a quick AMPK boost, though not as acute as with extended endurance training. The upside is that strength training also boosts mTOR, which preserves and builds muscle, whereas endurance training is inherently catabolic. You still should lift – especially if you’re during endurance work. As Jamie so eloquently explains, resistance training can actually improve endurance performance, most likely via the boost to mitochondrial function and growth explained in the study above.
Whoops, I almost forgot walking. Now, I love walking, as you already know, and it does improve health, but it doesn’t appear to do much for the mitochondria (at least in type 2 diabetics, who, as you remember, require greater intensity to ramp up AMPK). Casual walking just isn’t physically-demanding enough to force adaptation from the mitochondria. Of course, it’s all about context. If walking around the block leaves you breathless, you might be working your mitochondria. Keep walking regardless. I’m just sticking this here to be as thorough as possible.
Try not to hone in too much on the mitochondria issue, though. I often decry “nutritionism” for its attempts to reduce the worth of a food to a single constituent micro- or macro-nutrient, and I don’t want you chasing mitochondria. Remember: this stuff is supposed to be fun. It’s supposed to enhance your life on a subjective (and objective, lab-verified, if you wanna go that route) level. You could happily go about your life and enjoy fantastic athletic performance without ever learning about mitochondria, let alone tailoring your training to wring every last drop of performance out of every last organelle in your muscle fibers.
Besides, if you want an idea of what being a mitochondria-chaser might be like, just visit the treadmills next time you’re at the gym. Watch the folks that are putting in upwards of 30 minutes. Do they look happy? How’s their body comp? How are their lifts – if they even lift weights at all?
Exactly. The proof is in the pudding, regardless of what a study tells you is optimal. But that doesn’t mean it’s not good to know.
Me? I’ll pass on the extended bouts of cardio (and its numerous drawbacks), max out my mitos through a Primal eating plan and actually enjoy my workouts.
So, will this change how you exercise?