Humans were born to run. Exoskeletons might make us better at it.

New research on ankle exoskeletons show promising results.

Photo: Getty Images
  • New research from Stanford finds that motor-powered ankle exoskeletons conserve 15 percent of energy expenditure when running.
  • Spring-powered exoskeletons without motors actually made running harder.
  • The researchers hope to develop better spring-powered models moving forward.

Humans were born to run, as journalist and running fanatic Christopher McDougall phrased it. Bipedalism offers many advantages over quadrupeds, including the ability to better communicate over longer distances and improved cardiovascular skills. Humans are relatively lackluster over short distances; since our organs don't crash into our lungs when we run, as they do with quadrupeds, we are master marathoners.

There are still trade-offs. Thanks to our upright posture, we have weak necks—misbalances in our ankles and knees often lead to neck problems. Further down the chain, running can lead to chronic knee problems and labrum tears; I've suffered both while training for half-marathons. The impact force of repetitive striking can result in chronic lower back problems, especially if runners don't stretch and practice mobility routines. We expend a lot of energy when running; our body pays the toll.

Still, running is a natural activity that, according to McDougall, excite evolutionary senses of fear and pleasure deeply embedded in our biology. Too bad our anatomy doesn't always agree.

Researchers have long sought new means for alleviating energy output while running. A fascinating new study on exoskeleton emulators, published in the journal Science Robotics, might have gotten us one step closer.

When McDougall's book was published in 2009, more Americans were running. As the researchers (based at Stanford but including experts from Carnegie Mellon, Ghent University, and Nike) in this new study note, only 25 percent of Americans aged 18-29 reported running even once in 2018. Participation for adults aged 30-49 dropped 20 percent that year. They cite time commitments and negative associations to exercise as two leading causes. Given the high likelihood of injury due to running, it makes sense that there's hesitancy.

Stanford researchers find ankle exoskeleton makes running easier

Mindset matters. Running is a birthright and offers great cardiovascular conditioning. Yet there has to be some excitement around it. As McDougall writes, "if you thought [running] was only a means to an end—an investment in becoming faster, skinnier, richer—then why stick with it if you weren't getting enough quo for your quid?"

You have to love running to dedicate yourself to it. If you're in pain, that's a tall order.

The researchers tested two modes of running assistance: motor-powered and spring-based exoskeletons. An exoskeleton is an external skeleton that supports an animal's body, such as insects and mollusks. In human terms, they are expensive devices designed to slow down fatigue. In this study, ankle exoskeletons were tethered to motors as volunteers ran on a treadmill.

Eleven competitive runners were divided into three groups: an "optimized power" group, the motor-based cohort that boosted the runners' strides; "optimized spring-like," the group wearing the exoskeleton sans motor power; and the control group, "zero torque mode," runners wearing an exoskeleton with none of the features initiated. A final control element was runners wearing a neutral running shoe with no exoskeleton.

Optimized spring-like and Optimized powered assistance resulted in metabolic reductions of 2.1 and 24.7%, respectively, compared with zero-torque mode, while running at 2.7 m s−1. Optimized powered assistance resulted in an improvement in running economy of 14.6% compared with running in normal shoes, whereas Optimized spring-like assistance resulted in an 11.1% increase in the energy cost of running. Error bars indicate SD. *P < 0.05.

Kirby A. Witte, et al.

The motors are an important component. Wearing an exoskeleton with the motor switched off actually increased physical demand by 13 percent. With the motors purring, the demand was 15 percent less than when running without an exoskeleton.

Spring-based exoskeletons did not fare nearly as well, as it increased energy output by 11 percent than running without the gear. Stanford's Steve Collins, lead author of the paper, was surprised by this result, noting,

"When people run, their legs behave a lot like a spring, so we were very surprised that spring-like assistance was not effective. We all have an intuition about how we run or walk but even leading scientists are still discovering how the human body allows us to move efficiently."

(A) Exoskeleton emulator testbed. A participant runs on a treadmill while wearing bilateral ankle exoskeletons actuated by motors located off-board with mechanical power transmitted through flexible Bowden cables. (B) Ankle exoskeleton. The ankle exoskeleton attaches to the user by a strap above the calf, a rope through the heel of the shoe, and a carbon fiber plate embedded in the toe of the shoe. The inner Bowden cable terminates on a 3D printed titanium heel spur that is instrumented with strain gauges for direct measurement of applied torque. A magnetic encoder measures ankle angle. (C) Participant running on the treadmill with bilateral ankle exoskeletons. Metabolic data are collected through a respiratory system by measuring the oxygen and carbon dioxide content of the participant's expired gasses.

Kirby A. Witte, et al.

On the plus side, spring-based exoskeletons are much cheaper than motor-based models. The researchers are hoping to design a more energy-efficient model. Motor-powered models work great when tethered to treadmills but are unrealistic for road and trail runners, so an affordable spring-based version would be a boon for outdoor runners.

Spring-based exoskeletons mimic the natural spring of running. As with our normal running pattern, it stores energy only to unleash it when pushing off from the toes. With the help of a motor, the foot is able to extend at the ankle at the end of the step. Not quite Iron Man, but as Stanford graduate student Delaney Miller says of these trials,

"Powered assistance took off a lot of the energy burden of the calf muscles. It was very springy and very bouncy compared to normal running. Speaking from experience, that feels really good. When the device is providing that assistance, you feel like you could run forever."

Collins says this is one of the biggest improvements in energy economy ever made in running. It will likely not affect pro marathoners that much, but for novice runners or those susceptible to injury, it could ease the pain and remove a few seconds from your mile time.

Yes, humans were born to run. As it turns out, some of us just do it a little better with assistance. If consumer-priced exoskeletons hit the market, the statistics on running enthusiasts might swing in an upward direction. If the result is decreased energy expenditure, which by extension lowers the risk of injury, it's a win for all of us bipeds.


Stay in touch with Derek on Twitter and Facebook. His next book is "Hero's Dose: The Case For Psychedelics in Ritual and Therapy."

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The surprise reason sleep-deprivation kills lies in the gut

New research establishes an unexpected connection.

Reactive oxygen species (ROS) accumulate in the gut of sleep-deprived fruit flies, one (left), seven (center) and ten (right) days without sleep.

Image source: Vaccaro et al, 2020/Harvard Medical School
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We don't have to tell you what it feels like when you don't get enough sleep. A night or two of that can be miserable; long-term sleeplessness is out-and-out debilitating. Though we know from personal experience that we need sleep — our cognitive, metabolic, cardiovascular, and immune functioning depend on it — a lack of it does more than just make you feel like you want to die. It can actually kill you, according to study of rats published in 1989. But why?

A new study answers that question, and in an unexpected way. It appears that the sleeplessness/death connection has nothing to do with the brain or nervous system as many have assumed — it happens in your gut. Equally amazing, the study's authors were able to reverse the ill effects with antioxidants.

The study, from researchers at Harvard Medical School (HMS), is published in the journal Cell.

An unexpected culprit

The new research examines the mechanisms at play in sleep-deprived fruit flies and in mice — long-term sleep-deprivation experiments with humans are considered ethically iffy.

What the scientists found is that death from sleep deprivation is always preceded by a buildup of Reactive Oxygen Species (ROS) in the gut. These are not, as their name implies, living organisms. ROS are reactive molecules that are part of the immune system's response to invading microbes, and recent research suggests they're paradoxically key players in normal cell signal transduction and cell cycling as well. However, having an excess of ROS leads to oxidative stress, which is linked to "macromolecular damage and is implicated in various disease states such as atherosclerosis, diabetes, cancer, neurodegeneration, and aging." To prevent this, cellular defenses typically maintain a balance between ROS production and removal.

"We took an unbiased approach and searched throughout the body for indicators of damage from sleep deprivation," says senior study author Dragana Rogulja, admitting, "We were surprised to find it was the gut that plays a key role in causing death." The accumulation occurred in both sleep-deprived fruit flies and mice.

"Even more surprising," Rogulja recalls, "we found that premature death could be prevented. Each morning, we would all gather around to look at the flies, with disbelief to be honest. What we saw is that every time we could neutralize ROS in the gut, we could rescue the flies." Fruit flies given any of 11 antioxidant compounds — including melatonin, lipoic acid and NAD — that neutralize ROS buildups remained active and lived a normal length of time in spite of sleep deprivation. (The researchers note that these antioxidants did not extend the lifespans of non-sleep deprived control subjects.)

fly with thought bubble that says "What? I'm awake!"

Image source: Tomasz Klejdysz/Shutterstock/Big Think

The experiments

The study's tests were managed by co-first authors Alexandra Vaccaro and Yosef Kaplan Dor, both research fellows at HMS.

You may wonder how you compel a fruit fly to sleep, or for that matter, how you keep one awake. The researchers ascertained that fruit flies doze off in response to being shaken, and thus were the control subjects induced to snooze in their individual, warmed tubes. Each subject occupied its own 29 °C (84F) tube.

For their sleepless cohort, fruit flies were genetically manipulated to express a heat-sensitive protein in specific neurons. These neurons are known to suppress sleep, and did so — the fruit flies' activity levels, or lack thereof, were tracked using infrared beams.

Starting at Day 10 of sleep deprivation, fruit flies began dying, with all of them dead by Day 20. Control flies lived up to 40 days.

The scientists sought out markers that would indicate cell damage in their sleepless subjects. They saw no difference in brain tissue and elsewhere between the well-rested and sleep-deprived fruit flies, with the exception of one fruit fly.

However, in the guts of sleep-deprived fruit flies was a massive accumulation of ROS, which peaked around Day 10. Says Vaccaro, "We found that sleep-deprived flies were dying at the same pace, every time, and when we looked at markers of cell damage and death, the one tissue that really stood out was the gut." She adds, "I remember when we did the first experiment, you could immediately tell under the microscope that there was a striking difference. That almost never happens in lab research."

The experiments were repeated with mice who were gently kept awake for five days. Again, ROS built up over time in their small and large intestines but nowhere else.

As noted above, the administering of antioxidants alleviated the effect of the ROS buildup. In addition, flies that were modified to overproduce gut antioxidant enzymes were found to be immune to the damaging effects of sleep deprivation.

The research leaves some important questions unanswered. Says Kaplan Dor, "We still don't know why sleep loss causes ROS accumulation in the gut, and why this is lethal." He hypothesizes, "Sleep deprivation could directly affect the gut, but the trigger may also originate in the brain. Similarly, death could be due to damage in the gut or because high levels of ROS have systemic effects, or some combination of these."

The HMS researchers are now investigating the chemical pathways by which sleep-deprivation triggers the ROS buildup, and the means by which the ROS wreak cell havoc.

"We need to understand the biology of how sleep deprivation damages the body so that we can find ways to prevent this harm," says Rogulja.

Referring to the value of this study to humans, she notes,"So many of us are chronically sleep deprived. Even if we know staying up late every night is bad, we still do it. We believe we've identified a central issue that, when eliminated, allows for survival without sleep, at least in fruit flies."

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