CHAPTER TWO

How Intensity Works

Not everyone was convinced by the first few interval-training studies to come out of our lab. After the first study was published in 2005, we received a lot of incredulous responses from other physiologists. My laboratory group participates in an annual conference in which other scientists in the region get together to discuss their research. I remember that after one of my students had presented our results, another scientist stood up and essentially called our research BS. To paraphrase: “Come on—you’re going to sprint for a few minutes and you get these incredible performance benefits? In only two weeks? That’s hard to believe.”

On one level I could understand the skepticism. It seemed incredible to me, too. But soon after our study came out, we conducted additional experiments that verified our initial results. More editorials in prestigious journals followed. “For those looking to do the least possible work to be fit, the work of Gibala et al. presents hope,” Keith Baar wrote in the Journal of Physiology. “In as little as 3 min . . . we can improve our VO2max and performance.”

Other scientists around the world replicated our results. Interval training was for real. But why did it work? How was it possible that such small amounts of exercise could trigger such large benefits? That’s the question some of the best exercise scientists in the world were asking one another back in the mid-2000s, as people marveled at the results of our interval training studies. And I was no different. When I’d appear on TV shows or be interviewed in newspapers, the television host or reporter would ask me why intervals had the potency that they did. And I didn’t really know. But I knew one thing: I wanted to find out.

•   •   •

REMEMBER HOW I’d just begun my second three-year contract as an assistant professor when my lab started doing the HIIT research? Thanks to that Journal of Applied Physiology paper and other studies like it, I was promoted from assistant professor to associate professor with tenure. The 2005–2006 academic year provided the opportunity for my first-ever sabbatical. That’s a phenomenon common in academia in which a professor is freed from teaching and administrative commitments to devote a year to research. I could dig into whatever the heck I wanted. To some people that sounds wonderful, but it’s a lot of pressure, especially at the beginning of your career. I needed something high-impact to maintain my trajectory.

So I was looking for ways to push my research forward—and to do that, I just followed my intellectual curiosity. Here was my chance to answer the question that kept me up at night: Why did interval training work? Why was it so potent?

It was a tricky question to answer because the discipline of exercise physiology still hadn’t completely figured out how traditional endurance training triggered performance benefits. We knew that training—whether that entailed laps around a track or lots of cycling on the road—triggered adaptations on the entire body that made it possible to exercise faster and longer the next time around.

Some of the most exciting work involved looking at the molecular signals in muscles that were activated by endurance exercise. Scientists were learning that some of those proteins were, in fact, signals that prompted the body to change so it could more easily exercise the next time around.

Some of the best research into this process was happening in the laboratory of an Australian colleague named Mark Hargreaves. I wanted to do the same thing Mark was doing at his lab, but rather than studying the effects of endurance training, I wanted to look at how the body responded to interval training.

First, I had to pitch Mark on the idea. Conveniently, this was around the time that I started to get invited to conferences held by the Gatorade Sports Science Institute (GSSI). For exercise physiologists in the mid-2000s, the GSSI board was sort of like the top fraternity. Its members were some of the best minds and most respected scientists in the field.

Mark was on the GSSI Science Advisory Board, which would meet every year and invite a few newbies to speak on cutting-edge topics. Getting invited to one of these meetings was a big deal for your career—kind of like getting booked on The Tonight Show Starring Johnny Carson if you were a comedian. And then if you got invited to sit on the GSSI Science Advisory Board? That was like Johnny inviting you over after your set to sit in the chair next to him. You’d made it.

One of the first GSSI meetings that I attended took place at the Arizona Biltmore, an historic, beautifully designed hotel in Phoenix. The event went so well that afterward I was invited to join the board. That was the transition. I was in the club.

I believe that also was the meeting where I first asked Mark whether I could work in his Melbourne laboratory. Ever gracious, Mark was receptive to the idea. I soon found myself in Melbourne at the start of my sabbatical. The challenge now was to determine the mechanisms of why interval training was so potent. To stay at the forefront of this research, we had to do it before anyone else did. The race was on.

Physiology 101

To understand what happened next, it’s necessary to understand a few things about the physiology of fitness. One important aspect of fitness is the ability of your heart and lungs to pump blood and oxygen throughout your body. This is what most people mean when they talk about “cardio” fitness. Another component of fitness is the ability of your muscles to use the oxygen that gets delivered. Muscles use oxygen to burn fuels, such as sugars and fats, in a complex process that yields the energy-laden molecule known as adenosine triphosphate, or ATP.

Every movement we make requires ATP, and the body has a complex and remarkable system to ensure that we have ATP when we need it. While you’re sitting quietly, reading a book about interval training, say, your overall demand for ATP is relatively low. So all the things your body does to get ATP to your muscles tend to be relaxed and slow—including your heart rate, your breathing rate, the amount of oxygen you’re distributing to the muscles. But let’s say a smoke alarm goes off, there’s a fire, and you’ve got to sprint to safety as fast as you can. Your demand for ATP skyrockets, and so your heart pounds faster, and your breathing gets deeper and harder.

Let’s back up a minute and look at what happened to your body the moment you started to sprint from the fire. You heard the smoke alarm, got up off the couch, and started hightailing it out of your house. To allow you to do that, a whole bunch of things happened at once in the body. All of them involved the energy-laden molecule ATP.

Muscles store only a small amount of ATP. It’s a relatively heavy molecule and therefore just not efficient to keep on hand in large quantities. Instead of storing large amounts of ATP, your body stores energy in other ways. It’s similar to the way you keep your money. You could keep a lot of quarters around to spend, but those tend to be inconveniently heavy; it’s more efficient to store the funds in the more compact form of paper currency, in a diverse selection of denominations, such as one-, five-, and twenty-dollar bills. Rather than carrying around huge quantities of coins in your pockets, you keep a wad of bills in various denominations. Then you “convert” the bill when you need to spend the money.

Muscles do something similar with energy. One convenient form of energy is a molecule called phosphocreatine. Think of this molecule as dollar bills in your wallet. Phosphocreatine is easy to convert, but you tend not to keep it in large quantities. It’s used to immediately resupply ATP when your muscle starts to contract. Phosphocreatine fuels the lion’s share of the energy during your first few seconds of sprinting. This process is extremely fast, but the capacity is very limited.

Another process that can supply ATP relatively quickly is anaerobic glycolysis, which involves the partial breakdown of sugars stored in muscle. You can think of these as the fives in your wallet. The process is quick but rather inefficient, and can get bogged down by the formation of metabolic by-products. The classic by-product is lactic acid, which accumulates in the muscles of sprinters and is part of the reason why they eventually slow down during a race. The role of lactic acid formation in fatigue is actually quite a controversial topic that could be the focus of a separate chapter or an entire book. For our purposes here, suffice it to say that anaerobic glycolysis is a limited capacity system.

By far, the most efficient way to supply energy is through a process called oxidative metabolism, which involves the use of oxygen to burn fuels such as sugars and fats—the large-denomination bills in your wallet. While slower than the other two processes, oxidative metabolism provides the capacity to utilize many different fuels. The other nice thing about it is that, given adequate fuel availability, the capacity is almost limitless.

Oxidative metabolism really is an ingenious process. It’s pretty complex stuff, and one of the scientists who helped figure it out won a Nobel Prize. But what happens in the muscle cell when the oxygen gets in there? The lion’s share of this ATP-production process happens in specialized structures in the cell called mitochondria, which suck in oxygen and fuels to generate high-energy ATP molecules. The more mitochondria a cell has, the greater its capacity to produce ATP for energy. For example, spermatozoa are comparatively small cells, but their midpoint is packed with mitochondria, the better to power the tail thrashing that propels the sperm toward the egg.

To summarize, the key to aerobic metabolism is all about getting oxygen and fuel to the mitochondria in the muscles. This ability largely determines our capacity to perform exercise and, in turn, our overall fitness level. When we exercise regularly, the body gets better at each step in the process. This is the process of training. The challenge for me on my sabbatical was to determine why intervals were so effective at boosting aerobic metabolism. Quite literally, how did the intervals “signal” to the body that it needed to make changes?

Our Response to Exercise

Exercise is traditionally grouped into two broad categories. Endurance exercise typically refers to long-duration, low- to moderate-intensity activity that increases the body’s ability to use oxygen to produce energy for sustained movement. Many people think of jogging when they think of this type of exercise, although it also encompasses everything from long-distance swimming to cycling.

The other category features short-duration intense exercise that is usually associated with building muscle strength and size. Many people refer to this type as resistance training, and it encompasses everything from bodyweight push-ups to heavy barbell squats as well as the many exercises that can be done on the pulley-equipped machines found in fitness centers.

What is so fascinating about interval training is that it seems to occupy a middle ground between the two broad categories. It’s short duration and high intensity, like strength training, but triggers effects on the body we’d previously associated with endurance training—in a lot less time.

Before we get to why interval training is so effective, let’s first consider how the body responds to any type of exercise, which scientists like me consider a stress on the body. A physician named Hans Selye in the 1930s developed a theory about the way the body responds when stressed. Selye’s general adaptation syndrome says that the body responds in a manner intended to reduce the stress the next time we experience it.

When you’re at rest, you’re in a state called homeostasis. Your heart rate and breathing rate are relatively low and constant, and there is a good match between the body’s demand for energy and its capacity to supply it. But once you start exercising, the disturbance to homeostasis throws the body out of whack. The body needs more oxygen than you’re giving it. The body responds by increasing heart rate and breathing faster to get more oxygen to the muscles. Then, once the stressor is gone and the body is recovering, the body adapts so that the next time the same stressor presents itself, it disturbs the body to a lesser degree.

Take cycling. If you mash your pedals so hard that you struggle for breath, and you do it long enough and frequently enough, your body changes so that the next time you hop on a bike, you don’t struggle for breath so much. “Hey!” the body says to itself when it experiences a stressful bout of exercise. “This stuff hurts! We need to make some changes to ensure it doesn’t hurt so much next time!”

The concept is pretty simple, but the remodeling that takes place is incredibly complex. Repeated over time, exercise provokes a response in the body similar to a major building renovation—except that the normal work going on inside needs to continue during construction. The body’s like an airport terminal that is completely modernized while it remains operational. The response to endurance exercise involves changes in every element of the pathway that controls the supply and utilization of oxygen to produce energy.

Over time your heart becomes a better and stronger pump, so that it ejects more blood with each beat. The arteries become more flexible—the better to propel blood through the system. Tiny blood vessels called capillaries grow through muscle tissue to more efficiently deliver the blood-borne oxygen to the muscle fibers. And the muscles grow more mitochondria—the powerhouses that actually use the oxygen to burn the fuel to produce ATP. Highly trained endurance athletes have about twice the mitochondria in their muscles as your average couch potato does.

It’s really an amazing process. Think of a garden hose. If your garden hose had the same response to stress as your blood vessels, then it would grow wider and more flexible each time you watered your lawn. Not only that—it might even sprout smaller hoses snaking out from the main conduit, the better to distribute moisture to each individual blade of grass.

So how does the body know to trigger all these physiological adaptations? Discovering the precise mechanisms involved has for decades been one of the holy grails of our field. When it comes to muscle cells, scientists believe that certain proteins serve as molecular fuel gauges. Just as a warning light on your car dashboard turns on when the gas in your tank gets low, proteins in your muscles are activated when fuel levels drop. Remember that our most important fuel is ATP. One of the most important fuel-sensing molecules is activated when ATP levels drop.

The energy stored in ATP is a bit like a rechargeable battery. As you exercise, your muscles use up the available energy—the ATP. That ATP gets converted into two metabolic by-products called adenosine diphosphate (ADP) and adenosine monophosphate (AMP). These molecules are like spent batteries that can be recharged. When the body senses a lot of spent batteries lying around, other protein signals get activated.

AMP in particular triggers the activation of a protein with the unwieldy name of 5’-adenosine monophosphate-activated protein kinase, or AMPK. In turn, AMPK activates a protein called—bear with me here, because it, too, is a mouthful—peroxisome proliferator-activated receptor gamma coactivator-1alpha, which most physiologists refer to by its short form, PGC-1α—that last symbol is pronounced “alpha.”

PGC-1α turns out to be a pretty special molecule. Some people refer to it as the “master regulator” because of its crucial role in building more mitochondria—important because those additional mitochondria increase the capacity to build more ATP molecules by using oxygen to burn sugars and fats. Some scientists also believe that PGC-1α helps stave off age-related muscle decay. The bottom line for our purposes is that PGC-1α is a key signal that triggers skeletal muscle remodeling, allowing the body to perform exercise for longer than it did before.

What’s Different About Interval Training

So here’s where we are so far: Exercise, the theory goes, uses up ATP, creating lots of AMP, which then turns on a series of signals, including the PGC-1 or master switch. But how much exercise does it take to trigger this process? A 2005 study out of Switzerland suggested that the PGC-1α master switch could be turned on only with contractions that were repeated and sustained for over an hour at a time.

That’s a lot of roadwork.

And yet we were seeing similar muscle remodeling triggered by just a few minutes of exercise a week. Really hard exercise, admittedly. An effort that required you to cycle as hard as you could. But still!

That year, we submitted a study to the Journal of Physiology in which sixteen college-age students performed six training sessions over two weeks. In each training session, half the subjects cycled continuously for 90 to 120 minutes at a moderate-intensity pace. The other eight subjects performed four to six 30-second sprints at an all-out pace, separated by 4 minutes of recovery. The endurance training group’s total time commitment was 10.5 hours over the two-week period. In contrast, the total training commitment for the sprint group was about 2.5 hours, including the recovery periods—although the total amount of hard exercise for the sprint group was just 18 minutes.

Once the two weeks were up, testing revealed that the two groups had improved to a virtually identical extent in every measure we tested. Both groups improved their cycling time-trial performance by the same amount and also demonstrated remarkably similar changes in the molecular makeup of their muscles. Considering the difference in the amount of time the two groups trained, it was an incredible result. A total of just 18 minutes of very intense exercise produced the same benefits as 10.5 hours of traditional endurance training.

To physiologists and just about anyone else who followed exercise science, interval training seemed like a miraculous shortcut. But how did it work?

That’s what I was trying to figure out in Mark Hargreaves’s Melbourne laboratory, where I was working alongside a postdoctoral researcher named Sean McGee, who was an expert at analyzing the molecular changes that exercise prompted.

We took muscle biopsies from subjects who performed a single session of interval training, involving four 30-second all-out cycling efforts, with each burst separated by several minutes of rest. Our analyses revealed two remarkable things.

First, we discovered that a series of short, hard intervals could really ramp up the production of PGC-1α. That is, just a few minutes of sprints had activated the PGC-1α master switch. People were absolutely blown away by this. Remember, some scientists thought that the PGC-1α switch could be turned on only by more than an hour at a time of endurance training. In fact the total amount of exercise done by our subjects was just one-twentieth of that performed in some previous endurance studies—and less than one-third the total training time. We’d shown that this master switch, PGC-1α, could be activated by a lot less total exercise than anyone ever thought possible.

The second important thing that we discovered in the Melbourne lab involved how the PGC-1α switch was activated. It turned out that several of the signals believed to crank up PGC-1α after endurance exercise could also be turned on by a few short, hard intervals. For example, one of the proteins activated was our old friend AMPK—the same one that responds to long bouts of endurance-type exercise.

In Melbourne, we established that interval training could activate the same pathways that triggered adaptations to endurance training. Remember the doubters who previously called the results of our initial research into question? The fact that we now had molecular evidence of the potency of interval training silenced them. It legitimized our research. That felt pretty good. It also went a long way toward selling the rest of the field on the power of interval training. We’d not only shown this shortcut to fitness benefits existed; now we’d also taken an important step toward showing how it worked.

Why All This Matters to You

Mysteries persist regarding the physiology of interval training. What regulates the cardiovascular side of things? For example, why does the heart become a better pump, and how do we grow more blood vessels after a few short, hard intervals? My McMaster colleague Maureen MacDonald, a cardiovascular physiologist, and other bright minds across the world are working on these important questions.

I’ll tell you what I suspect is going on in the muscle, though. And if what I suspect is true, then it’ll go a long way toward helping you choose the sort of workouts that you do.

It all comes back to the concept of fuel gauges. The traditional thinking is that endurance exercise leads to a progressive decrease in ATP and a gradual emptying of the fuel reservoirs needed to replenish ATP. The gradual reduction in fuel stores that happens during prolonged exercise activates the molecular signals that regulate adaptation and muscle remodeling. So for endurance exercise, the longer the exercise bout and the greater the fuel depletion, the larger the adaptive response. Exercise for longer, get more fit.

The situation is different with intervals, however. With a few short sprints of twenty or thirty seconds, the total amount of fuel depletion is modest, especially when compared with what can happen over a prolonged period of moderate-intensity continuous exercise. And yet, we have shown that a series of short, hard intervals can activate molecular signaling pathways to the same extent as traditional endurance training does. How can this be?

Here’s what I think: With interval exercise, it’s the dramatic rate at which fuel stores in the muscle are changing. Not the absolute level. It’s the rate of fuel depletion that’s key. Interval exercise is also different from endurance training because more of the muscle is involved in the exercise.

Muscle fibers are generally grouped into two broad categories. Smaller type I fibers, also called slow-twitch fibers, make up about half the overall muscle tissue. These tend to be “recruited” for relatively easy movements that don’t require a lot of force. These fibers also are the ones used mainly during moderate-intensity endurance exercise.

Type II muscle fibers, also known as fast-twitch fibers, tend to be recruited for fast, powerful movements that require a lot of force. The effort demanded during high-intensity interval exercise recruits type I muscle fibers and the larger type II fibers. Sprinting is hard work, and it takes all the muscle fibers to do it. Because interval training recruits the entirety of the muscle, the muscle uses up available fuel at a much faster rate—so fast, in fact, that even short durations of the most intense flavors of interval training trigger training adaptations. Remember the theory based on Hans Selye’s stress-adaptation theory, that the effects of exercise stemmed from the body’s disturbance from homeostasis? Interval training may be so effective because it creates big changes from homeostasis—a.k.a. a high degree of stress—in a small amount of time.

Other studies have illustrated the benefits of a technique called exercise snacking—breaking a workout into multiple chunks spread throughout a day. In a 2014 study conducted out of New Zealand’s University of Otago, researchers tracked blood sugar in subjects who performed two different exercise interventions. The traditional group performed 30 minutes of continuous exercise once a day. The snacking group performed a quick interval workout before each meal—specifically, six hard reps of minute-long incline walking. The interval workout proved much more effective at reducing subjects’ blood sugar, even though the total time spent exercising was the same. Perhaps breaking up exercises into these snacks creates more disturbances in the body’s equilibrium. And that’s why it’s so effective.

The other thing we’re learning from interval training studies is that the size of the disturbance matters, too. Generally the lesson is, the bigger the disturbance, the better; the bigger the disturbance from homeostasis, the greater the adaptation. So going from homeostasis at rest to a light jog is good. But going from rest to a full run is better. And best of all is going from rest to an all-out sprint. And even better than all that, if you’re really looking to cram the biggest performance benefits into the smallest amount of time? Repeat the number of disturbances in a single workout by doing intervals—whether they’re light-jogging intervals or as-hard-as-you-can Wingate tests.

In the old endurance-training way of thinking, what was most important was exhausting ourselves through long, slow exercise, which in turn caused a slow and steady absolute decrease in fuel reserves. That suggested it was less about intensity and more about duration—not so much how hard we exercised but that we exercised long enough to drain the batteries. But who has infinite free time to exercise?

Now, the new interval-way of thinking suggests that exercise duration is a lot less important than exercise intensity. The trick is to drop the fuel levels as quickly as possible. Doing it once is great. Doing it more frequently is better. The volatile nature of the stimulus is what’s key. Mix it up! Disturb homeostasis! Traditional endurance training sees one main disturbance from homeostasis, right at the beginning. In contrast, interval training gives you as many disturbances as you have repetitions. You harness the power of the disturbance that happens at the start of aerobic exercise, only it’s more pronounced. And then you do it again and again and again.

So it’s not just the absolute amount of fuel in the cell; it’s also the rate at which the stuff is falling. That’s important to people who don’t have much time. Intervals provide a shortcut. You can drop the fuel gauges really fast by going as hard as possible, particularly if you repeat that a few times. And you’ll gain in minutes the benefits that once were thought possible only with hours of exercise.