Do Nike’s “Super Shoes” Really Enhance Performance?

*Photo source: https://www.self.com/review/nike-air-zoom-alphafly-next-shoe-review*

Elite and recreational runners train their bodies to run fast and far. This is typically accomplished through a variety of training stimuli including faster intervals, long runs, and tempo workouts. An effective training program will be designed to enhance three key variables that combine to determine running performance: VO2 max (aerobic capacity), lactate threshold (and speed at lactate threshold), and running economy.

The latter, running economy, is perhaps the variable that can change the most, especially in elite runners. Simply put — running more economically (i.e. using less energy to cover the same amount of distance) means you can run faster for longer.

Training isn’t the only thing that can improve running economy — technology can too. This became apparent when Nike, in 2017, released the first prototype of their “4%” shoe — named so because initial laboratory testing showed that wearing these shoes could save runners about 4% in terms of energy expenditure vs. other shoes.

What makes the shoes so special? Several technological advancements including a carbon-fiber plate with a unique curvature and an extremely thick midsole composed of innovative materials.

*https://www.believeintherun.com/a-breakdown-of-the-nike-kipchoge-prototype/*

The advent of these shoes has sparked controversy over their “fairness” and legality. Some think they should be banned, or otherwise that world records run in these shoes should be marked with an asterisk. Nonetheless, elite marathon runners (and many non-elites) are sporting the new “supershoes” at races around the world.

All of the hype surrounding the shoes (models which now include the 4%, Next%, VaporFly, and AlphaFly) begs the question — do they actually work?

A new study published in the Journal of Applied Physiology sought to answer this question using real-world marathon race data.

Primary objective

There were a few different aims to this study. First, the authors wanted to determine whether, overall, runners who wore the neoteric Nikes (this is what they call the Nike “supershoes” in the paper) run faster than runners in other shoe models (i.e. non-Nikes).

The authors of this paper also wanted to investigate whether performance improvements (if any) in the shoes were different among male and female marathoners. In addition, they performed a within-runner analysis to see whether a particular runner improved performance when they started wearing the neoteric Nikes.

Brief study methods

Marathon finish times and racing shoes worn by athletes were analyzed for the top 50 male and female finishers at four major marathon races: the Boston Marathon, Chicago Marathon, London Marathon, and New York City Marathon between 2010 and 2019.

Average finish times were compared among runners who wore the neoteric Nikes and those who wore other shoe types. Additionally, where data were available, the change in marathon performance was calculated for runners who ran races with and without the neoteric Nike shoes.

Results

Data were analyzed for 3,886 marathon performances during the period of interest. Here’s what they had to say on the performance effects of “supershoes.”

In 2019, more runners started wearing neoteric Nikes (66.3% of males and 58.4% of females)
In 2019, marathon performances were significantly faster when compared to times in 2010-2018 (when fewer runners were wearing Nike “supershoes”)

Marathon times were faster for runners wearing neoteric Nikes vs. other marathon racing shoes, consistent in both males and females
Males wearing Nike shoes ran ~2% faster (2.8 minutes faster) than non-Nike wearers
Females wearing Nike shoes ran ~2.6% faster (4.3 minutes faster) than non-Nike wearers
Females had a greater improvement in marathon performance while wearing Nike shoes compared to males (~2.6% vs. ~2% improvement, respectively)
Changing to neoteric Nike shoes improves performance — the between-race difference for a runner wearing vs. not wearing neoteric Nike shoes was 0.8% for males and 1.6% for females (corresponding to a 1.2 minute improvement for males and 3.7 minute improvement for females)
The performance advantage of neoteric Nike shoes was consistent across all of the marathon race courses analyzed

These data complement other real-world and laboratory data that confirm the “ergogenic” effect of wearing the technologically-advanced Nike “supershoes.” Don these shoes, evidence says, and you’ll run faster. While the improvements seen here are a bit less than the 4% claim that staked in the shoe’s name, the magnitude is still significant from a statistical and a performance perspective.

An elite runner gaining a 1-5 minute improvement in their marathon time from a shoe — that’s incredible. No extra training, no tweaks to nutrition required; just lace up a different pair of sneakers (those with a swoosh).

It should be noted that Nike is not the only company introducing new shoe technology — nearly all major running brands now have their own version of a carbon fiber-plated racing shoe. It has become a race (pun intended) to see who can design the chunkiest, cushiest, and springiest shoe on the market.

Personally, I think that the debate over whether these shoes should be banned is ludicrous. They clearly improve performance, but in general, most athletes now have access to this once-limited technology, meaning that there is no relative advantage for those who use them.

That being said — why not see how far (and how fast) technology can take us? Why constrain the limits of human performance because a shoe seems “unnatural” or ruins the “purity” of the sport? Advancements — in training, nutrition, psychology — are what allow us to redefine what is possible in the world of athletics. The way that I see it, shoe technology is just another aspect of natural progression in athletics, and we should enjoy the trajectory in which the sport is headed.

Study cited

Senefeld JW, Haischer MH, Jones AM, et al. Technological advances in elite marathon performance. Journal of Applied Physiology. Published online May 13, 2021.

Marathon Training Turns Back Biological Age of Blood Vessels

What is the single biggest risk factor for cardiovascular disease?

Elevated blood pressure? Obesity? High cholesterol?

Nope. Age.

That’s right. Age is the single biggest risk factor for developing cardiovascular disease — the older we get, the greater our risk.

Why does the passage of time confer such a drastic risk on our cardiovascular health? This has to do largely with one single process — the stiffening of our arteries, in particular, our aorta — the largest artery in the body with the most important functions. The aorta is the main valve through which blood is distributed from the heart to the rest of the body. A compliant (think “stretchy”) and powerful aorta is crucial for our cardiovascular performance and long-term health.

“Normal aging” does a number on our aorta — increasing the amount of collagen in the wall and reducing its elasticity. As a result, the aorta gets stiffer with age. This is traditionally seen as a “natural” consequence of aging.

But natural it might not be.

In fact, several studies show that lifestyle factors (mainly exercise) can drastically alter the trajectory of aortic aging.

Whether by preventing stiffening in the first place or reversing stiffness that has already occurred, exercise is “medicine” for the aged aorta.

A newly-published study lends more support to the profound anti-aging effects of aerobic exercise, showing that even in apparently “healthy” individuals, aerobic exercise training can seemingly reverse “biological age”of the arteries.

Running a marathon might be more than something to brag about on Instagram. Indeed, as summarized in the article “Training for a first-time marathon reverses age-related aortic stiffening”, adopting even a mild-volume marathon training program exerts impressive cardiovascular effects, and might even turn back the arterial clock.

Published in the Journal of the American College of Cardiology (JACC), this study analyzed a cohort of 138 individuals (average age of 37; 49% of whom were men) who signed up for and completed the London Marathon. These people had never seriously trained for (or finished) a marathon (their typical training was <2 hours/week). This fit with the goal of the study — which was to see how adopting a loosely structured training program impacts the arteries of “untrained” individuals.

The training program adopted here was indeed “loosely” structured. While this could be seen as a “limitation” of the study (a lack of control), it also complemented the study purpose; which was to investigate a “real world” scenario where participants could essentially choose their volume and intensity of training outside of a laboratory setting.

The general training paradigm called for at least 3 runs/week, with a progression over 17 weeks leading up to marathon race day. The explicit goal for the runners was “marathon completion” — the plan wasn’t designed to drastically improve their cardiovascular fitness (V02 max) or produce six-pack abs.

Measurements

Your standard health biomarkers like height, weight, blood pressure, and cardiovascular fitness were taken for all participants to gain insight into the demographics of the group as a whole and determine how exercise training would impact anthropometric variables. These and all other study measurements were taken before and after the marathon program.

To measure aortic stiffness, this study used cardiac magnetic resonance (CMR) — which is essentially an MRI of the aorta. Using MRI allows researchers to visualize in real time changes in the diameter and area of the aorta throughout the cardiac cycle. Using this data along with measurements of pressure (blood pressure), one can calculate how much the aorta distends or “stretches” in response to pressure; which gives us a measure of how elastic (distensible) the aorta is.

Example of aortic MRI. Source: http://cdt.amegroups.com/article/view/3630/4523

Accordingly, the two main outcome measures in this study were aortic distensibility and aortic beta-stiffness. A higher distensibility indicates less stiffness, and vice-versa for beta-stiffness — where higher is worse.

MRI was performed on three different segments or regions of the aorta. Another measurement called pulse-wave velocity (PWV) was also measured. PWV analyzes how fast a pressure wave travels from the aorta when the heart contracts — with a faster speed indicating a stiffer aorta.

Results

All “baseline” measurements were made an average of 176 days before the marathon, and “post” assessments occurred about 16 days after race day. Let’s take a look at the general “running statistics” for the group.

Average race completion time:

Men: 4.5 hours

Women: 5.4 hours

Estimated weekly training volume: 6–13 miles

We won’t judge here, but needless to say, these aren’t record-breaking stats. However, this makes the study all the more intriguing. Given the results, this implies that you need not engage in elite-level training or racing to achieve benefits of exercise. Just some will do.

Let’s talk blood pressure. On average, the training program reduced brachial artery systolic and diastolic BP by 4 mmHg (from 120 to 116 for SBP) and 3 mmHg (from 75 to 72 for DBP). Similar results were found for aortic systolic and diastolic BP, which fell 4 mmHg (from 110 to 106 for SBP) and 3 mmHg (from 76 to 74 for DBP). Interestingly, training had no effect on resting heart rate.

Even with the “low” amount of training in this study, aortic stiffness was reduced significantly. In two of the aortic segments analyzed (the proximal descending aorta and thoracic descending aorta), distensibility was increased by 9% and 16%, indicating that these arterial segments became less stiff with training.

Beta-stiffness (the opposite of distensibility) followed a similar but reverse pattern, with a reduction of 6% observed in each of the aortic regions mentioned above. Reductions in PWV were also observed in both regions of the descending aorta analyzed.

Interestingly, the benefits weren’t reaped equally by all. While older participants and those with higher blood pressure experienced greater improvements overall, it was older men with a slower marathon finishing time who received the most benefit from training.

Differences in BP and stiffness improvements by age category. Bhuva 2020

These stiffness improvements are impressive, but perhaps the most interesting finding was what happened to “biological age” of the participants’ arteries throughout the training study.

When various calculations were run by the researchers, it was shown that improved distensibility in the various regions of the aorta translated to a “reversal” of biological age by 1.5, 3.9, and 4 years! When the same calculations were made for beta-stiffness, biological age was estimated to be reversed by 0, 2.4, and 3.2 years, on average. In essence, training made the arteries of older participants more similar to people 4 years younger.

While not the main focus of the study, it is worthwhile to note that body fat % was reduced in after training and upon further analysis, it appears that the older participants experienced the bulk of the reduction — losing about 2% body fat throughout the study.

Not too shabby for just around 5 months of exercise training.

Change in “aortic age” with marathon training in older participants. Bhuva 2020

A few things stand out about this study.

The first, which I mentioned before, is the almost surprising fact (surprising to me at least) that such a “minor” amount of training could lead to the significant beneficial adaptations that it did.

Just ~5 weeks of training at right around the bare minimum exercise recommendations (which call for 150 minutes/week) was sufficient to reverse biological aging of the arteries and reduce blood pressure to a similar magnitude seen in people using blood pressure lowering medications!

What is even more interesting is the fact that these changes occurred without a substantial increase in V02 max (maximal aerobic capacity or cardiovascular “fitness”). While V02 max did change slightly and significantly (from 34.5 to 35.6 ml/kg/min, this isn’t a radical improvement by any means.

This implies that even without “training” your fitness, you can “train” your way to healthier arteries.

And it’s never too late to “turn back the clock”. Older participants in this study improved their arterial health to a greater extent than the younger participants. Perhaps they had more to improve upon…or perhaps the effects of aging are more malleable than we think.

References

Anish N. Bhuva et al. Training for a First-Time Marathon Reverses Age-Related Aortic Stiffening, Journal of the American College of Cardiology, Volume 75, Issue 1, 2020, Pages 60–71

Julio A. Chirinos, The Run Against Arterial Aging,
Journal of the American College of Cardiology,
Volume 75, Issue 1, 2020, Pages 72–75

Lifelong Exercise Prevents “Inflammaging”

There are many theories to why we age, why our bodies seem to decline inevitably with the passage of time.

One of the theories suggests that inflammation caused by aging leads to a progressive downward spiral into disease, frailty, and reduced quality of life.

Inflammation is a beneficial process, despite receiving generally negative publicity in the health and wellness sphere. Name any disease or ailment, and inflammation has likely been cited as the cause. Drugs, foods, and detoxes designed to abolish inflammation are marketed far and wide.

But we need inflammation — it’s our body’s response to infection, injury, or some sort of foreign virus that we need to fight off. The inflammatory response is a protective mechanism…in the short term.

However, chronic low-grade inflammation is the source of problems. In contrast to an acute inflammatory response, persistent levels of inflammation are known to cause damage to cells, tissues, and DNA within the body. If inflammation fails to resolve, damage accumulates over time. This leads to processes associated with aging and disease.

A critical driver of the age-associated increase in inflammation could be related to exercise (or a lack thereof). With aging and a lack of physical activity, muscle mass declines and fat mass increases. The effects on inflammation here are two-fold.

For one, adipose (fat) tissue is actually a source of pro-inflammatory cytokines. More fat tissue means more inflammation. Additionally, skeletal muscle can be a source of pro, but also anti-inflammatory cytokines. As lean mass goes down with age, we lose the beneficial anti-inflammatory effects of muscle.

For this reason, exercise is important…especially for aging individuals. It’s necessary to build (or at least maintain) muscle mass and prevent sarcopenia — the age-related decline in muscle mass.

The data are pretty conclusive: people who are considered “lifelong exercisers” have better cardiovascular and skeletal muscle health than couch potatoes of the same age. They also have lower levels of inflammation. Lower inflammation is likely both a cause and a consequence of the superior health and functional abilities observed in these individuals.

It’s pretty cut-and-dry — exercise staves off the inflammation associated with aging. It also may reduce inflammation in response to increased “stressors” like exercise, which would also be beneficial. Inflammation can actually interrupt adaptations to exercise. Thus, in older people who start to exercise, they might not get the most bang for their buck if high-levels of inflammation follow the exercise bout.

A new study published in the Journal of Applied Physiology took an interesting approach to study how aging, exercise, and inflammation interact.

Titled “Effects of Aging and Lifelong Aerobic Exercise on Basal and Exercise-Induced Inflammation”, the study investigated how levels of inflammation at rest and after exercise were different among groups of different ages and fitness levels.

They recruited groups of young healthy exercisers, old lifelong exercisers, and old sedentary people (all men).

Of particular interest in this study is the lifelong exercise (LLE) group. These men had been exercising for an average of 50 years, and reported doing 5 days (~7 hours) per week of exercise. This is pretty remarkable given the fact that they were 75 years old. Within this group, researchers created two subgroups — a lifelong exercise “performance” group and a “fitness” group. The performance group reported participating in “vigorous” training while the fitness group exercised for overall health (i.e. at a lower intensity).

In these groups, blood draws and muscle biopsies (from the thigh) were taken at two time points; once at rest and another 4 hours after the participants completed a bout of resistance training exercise (knee extensions). This exercise was designed to elicit a “stress” response in the muscle.

Blood and muscle samples were analyzed for a variety of pro- and anti-inflammatory factors. Of note: C-reactive protein (CRP), IL-6, TNF-alpha, insulin-like growth factor (IGF-1), and several components of the prostaglandin pathway.

Results: Basal Inflammation

One of the main findings for basal (resting) inflammation was that levels of IL-6, a pro-inflammatory cytokine, were significantly higher in the older sedentary men compared to young and old exercising groups.

In terms of anti-inflammatory factors, the lifelong exercisers were found to have 43% more IL-10 and 66% more TGF-beta compared to the young and old groups, respectively.

Both of these results support the fact that aging increases inflammation, and exercise reduces it.

Results: Exercise-Induced Inflammation

The theme of inflammation held consistent after exercise. The pro-inflammatory marker TNF-alpha increased in the older sedentary group after exercise, while remaining unchanged in the young and older exercising groups.

The authors note that TNF-alpha is involved in proteolytic (protein degrading) pathways within cells, and thus, could contribute to pathological responses in older muscle. An increase in inflammation after exercise could indicate an inability to “resolve” inflammation in this group, and perhaps a reduced adaptive response to exercise.

Overall, this study provides some obvious but also some novel conclusions.

For one, the idea that aging is pro-inflammatory in both the blood and muscle environment is strengthened by these findings. Furthermore, the beneficial “anti-aging” effects of exercise on inflammation were well-supported.

The authors place the findings in context by explaining that a failure to reduce inflammation after exercise could perhaps be detrimental; limiting older individuals’ ability to adapt to training.

I find small issue with this for one reason. This was an acute study, and it could well be expected that older individuals with zero exercise history would experience some sort of “negative” response to exercise. Exercise is a stress, and someone unaccustomed to it will, initially, have some side effects. In this case, the side effects were inflammation-related.

Train these people for a few weeks, and I’d bet the inflammatory response to exercise goes down.

I also wouldn’t expect young and old exercising individuals to mount an inflammatory response to the exercise in this study — it wasn’t that vigorous. A 3 x 10 set of knee extensions isn’t much of a stress for someone who has been training consistently for 50+ years.

I think the more important aspect of the exercise story here is that our ability to reduce inflammation at rest and with exercise is preserved with aging. Even more important may be the fact that starting exercise earlier is better. These people had been exercising since they were 30 years old. The benefits likely starting mounting early.

This might seem like just another study telling us that “exercise is good for you.” While true, I think the novelty lies in finding a potential mechanism by which exercise keeps us young.

Run for your life, literally.

A muscle stain from one of the lifelong exercisers

References

Lavin KM, Perkins RK, Jemiolo B, Raue U, Trappe SW, Trappe TA. Effects of Aging and Lifelong Aerobic Exercise on Basal and Exercise-Induced Inflammation. J Appl Physiol. 2019

de Lemos Muller, C.H., de Matos, J.R., Grigolo, G.B. et al. J. of SCI. IN SPORT AND EXERCISE (2019) 1: 97.

New Study: Previous High-Level Training Doesn’t Protect Against Cardiovascular Aging

I’ve written enough about the topic of cardiovascular aging and how exercise is beneficial in preventing it. There is little argument that exercise is good when you’re young, and perhaps even better as you age — helping to prevent the myriad of age-related changes to blood vessel structure and function that are major risk factors for cardiovascular disease (CVD) risk.

Master’s athletes and even older adults who engage in regular, consistent physical activity show significantly better cardiovascular function compared to age-matched peers who engage in little to no physical activity. In fact, if you exercise as you age, you can maintain similar levels of blood vessel health to that of younger adults.

A new study proposes a totally different and quite novel hypothesis related to exercise and aging. Rather than study the well-known benefits of exercise with age, the question was posed:

“Do older adults who were previously engaged in high-level activity and training demonstrate superior cardiovascular aging compared to non-athlete older adults?”

That is — if you were once an elite athlete, but then stopped training, do you maintain some of the benefits decades later?

The study, published in the Journal of the American Heart Association, tested the hypothesis that age-dependent changes in endothelial function and arterial stiffness (highly covered topics on this blog) — two strong predictors of CVD— would be delayed in former endurance- and sprint-trained athletes compared to age-matched controls (untrained).

Study population

A total of 94 men participated in this study — 47 old and 47 young men. Within the old and young groups, they were further stratified into three different categories based on activity — endurance-trained, sprint-trained, or untrained (the control group).

The older endurance- and sprint trained athletes, in contrast to the young athletes, were no longer actively engaged in training. In fact, they’d been “retired” for an average of 27 years and now reported engaging in low-level activity of around 120 minutes per week.

What’s super cool about this study population is that they represent the cream of the crop — the former and current athletes had all competed in their respective events at the national and international level (i.e. country or world championships and the Olympics). This means they didn’t just study recreational-level athletes, but people (men) who probably represent(ed) the peak of human physiology, especially in terms of cardiovascular performance.

Study measures

This study included a ton of measures related to cardiovascular and metabolic health — so I’ll only cover them briefly.

To assess cardiovascular health and aging, flow-mediated dilation (FMD) of the brachial artery, pulse-wave velocity, and augmentation index were measured. FMD is a measure of how well your blood vessel responds to an increase in blood flow (more relaxation = better endothelial function) and pulse-wave velocity and augmentation index measure the stiffness of your arteries (aging is typically associated with an increase in arterial stiffness). Central systolic, diastolic, and pulse pressure were also measured.

The study also assessed carotid intima-media thickness — the thickness of the wall of the carotid artery. Greater wall thickness is a sign of early atherosclerosis and positively correlates to cardiovascular disease risk.

Blood was analyzed for several different outcomes: inflammatory cytokines including TNF-alpha, interlekin-6 (IL-6), C-reactive protein (CRP), blood glucose and lipids (i.e. cholesterol), and other metabolites related to vascular function.

To assess how aging and exercise training influence all of these variables, comparisons were made among the young and old men, as well as within the subgroups (meaning they compared old and young endurance trained, sprint trained, and untrained athletes to each other).

Effect of Aging on Study Outcomes

Before discussing how training influenced the outcomes of this study, we’ll touch upon the independent effect of aging. Not surprisingly, the older group of men demonstrated significantly higher arterial stiffness, blood pressure, and carotid artery wall thickness compared to younger men. They also had reduced endothelial function (lower FMD), higher levels of blood glucose and lipids, and greater levels of low-grade inflammatory markers.

These data pretty much line up with any other study on aging and cardiovascular/metabolic outcomes, and don’t add much novel data to the discussion on mechanisms of aging.

The impact of aging and the professional physical training on arterial stiffness parameters, central arterial pressures, and carotid‐intima media thickness.

Effect of Previous Training on Cardiovascular Aging

Now on to the interesting part — and maybe the most surprising (or not) result from this study. How does previous training impact the trajectory of cardiovascular aging.

It turns out, when training was introduced as a variable, nothing changed.

That’s right, in the older athletes, previous elite-level training had no significant influence on age-related changes in arterial stiffness, endothelial function, blood parameters, or systemic inflammation. The older athletes had comparable levels of all outcomes to those of the untrained age-matched men.

Let’s Discuss

The major finding of this study was that, despite once being engaged in elite-level athletics, older athletes weren’t any more protected against the impairments in cardiovascular function that occur as a result of normal aging. This suggests that any benefits gained from training at a young age aren’t “maintained” into older age.

Olympic level training, while likely resulting in supreme fitness at a young age, inevitably withers with time.

While this doesn’t line up with the original study hypothesis, I can’t say I’m too surprised. Exercise is good, and the benefits can last a decent amount of time. However, we know from “detraining” studies that just 4–6 weeks of inactivity can erase most if not all of the benefits gained from an endurance training program.

The impact of aging and physical training on inflammatory markers.

In this study, it wasn’t just 6 weeks of inactivity — it was 27 years! These men weren’t “sedentary” for all of that time, but based on the study data, they barely engaged in 2 hours of exercise per week — not even meeting the baseline physical activity recommendations. Where before they reported engaging in nearly 1100 minutes of activity (in their “prime”), their current activity represent less than 1/5 of that.

One of the major reasons for that lack of maintained benefits, as the authors discuss, is probably the increase in body fat percent and BMI that also correlated with increasing age. In fact, a higher BMI and body fat % correlated with arterial stiffness, blood pressure, arterial wall thickness, and inflammatory cytokines in the entire study population.

It is well known that adipose tissues can lead to chronic low-grade inflammation, and inflammation is linked to endothelial dysfunction and arterial stiffness. Along with oxidative stress, inflammation is one of the more well-evidenced causes of aging. To put it crudely — getting “fatter” with age is probably one of the primary causes (in this study, at least) of cardiovascular aging.

Who knows how these results would be different if the former athletes had maintained a similar body composition, even in the absence of continuing to train. I propose that they might still experience a decline in many of the study outcomes simply due to their “inactivity.”

The moral of the story; we can’t “precondition” ourselves when we are younger and expect that the benefits will carry over into old age. While good habits and genetic programming are surely influenced by early-life factors, it seems like we need to maintain a robust (or at least adequate) physical activity regimen well into old age, so long as we wish to stave off the seemingly inevitable effects of aging on our cardiovascular system.

Brachial artery ultrasound. Source: http://ircmj.com/en/articles/16152.html

References

Seals DR, Nagy EE, Moreau KL. Aerobic exercise training and vascular function with ageing in healthy men and women. J Physiol (Lond). 2019

Majerczak J, Grandys M, Frołow M, et al. Age-Dependent Impairment in Endothelial Function and Arterial Stiffness in Former High Class Male Athletes Is No Different to That in Men With No History of Physical Training. J Am Heart Assoc. 2019;8(18):e012670.