Wednesday, March 24, 2021

What’s the Minimum Dose of Training to Stay Fit?

A new review assesses what it takes to maintain endurance and strength when circumstances interfere with your usual training

by Alex Hutchinson, Mar 23, 2021

My college coach used to assign us a week of complete rest every November, after the conclusion of the cross-country season. But one of my teammates, an exercise science student, discovered the research of Robert Hickson, who did some classic studies in the early 1980s on maintaining fitness with reduced training. So, during our yearly week of sloth and bacchanalian revels, we would sneak out for two 30-minute bouts of hard running, hoping that would allow us to be both well-rested and still fit when we started training for indoor track.

Life as a grown-up is more complicated, and the reasons for temporarily reducing training are sometimes considerably more pressing—like a pandemic, say. But the question endures: what’s the smallest dose of training you can get away with temporarily while staying mostly fit? It’s particularly relevant for military personnel, whose ability to train while on deployment is often severely constrained, which is why a group of researchers at the United States Army Research Institute of Environmental Medicine, led by Barry Spiering, has just published an interesting review of the “minimum dose” literature in the Journal of Strength and Conditioning Research.

The review addresses three key training variables: frequency (how many days per week), volume (how long is your endurance workout, or how many sets and reps do you lift), and intensity (how hard or how heavy). It only includes studies in which the subjects reduced their training for at least four weeks, to distinguish it from research on tapering before big competitions—although some of the conclusions are similar. And it’s focused on athletic performance, not weight loss or health.

Maintain Your Endurance

The main conclusions about endurance are still based on those Hickson studies from the early 1980s, with a bit of confirmation from more recent studies. Hickson’s basic design was to put volunteers through ten weeks of fairly hellish training, involving six days a week of 40 minutes of cycling or running at intensities that reached 90 to 100 percent of max heart rate by the end. Then, for another 15 weeks, they reduced either the number of weekly sessions (to two or four), the duration of sessions (to 13 or 26 minutes), or the intensity of the sessions (to 61 to 67 percent or 82 to 87 percent of max heart rate).

Here’s the graph that got my college teammate so fired up, from Hickson’s 1981 study:

(Illustration: Medicine & Science in Sports & Exercise)

The vertical axis shows VO2 max, a measure of aerobic fitness. On the horizontal axis, you have baseline pre-training values on the left, for subjects who were recreationally active but untrained. After the ten-week period of hard six-day-a-week training, they’ve increased VO2 max by a very impressive 20 to 25 percent. Then, for the next 15 weeks, their VO2 max just stays at the new value, regardless of whether they drop down to only two or four days a week.

The overall conclusion of the new review, then, is that you can get away with as few as two sessions a week as long as you maintain volume and intensity of your workouts. But they caution that maintaining your VO2 max isn’t the same as maintaining your ability to perform long-duration endurance activities. Don’t expect to run your best marathon after a few months of twice-a-week training: your legs, if nothing else, won’t be able to handle it.

The picture was similar when Hickson’s volunteers reduced the duration of their training sessions to 13 or 26 minutes (i.e. reducing their baseline duration by one third or two thirds). Once again, VO2 max gains were preserved for 15 weeks. This study also included tests of short (~5-minute) and long (~2-hour) endurance. Short endurance was preserved in both groups, but the 13-minute group got worse in the two-hour test.

The third and final variable that Hickson manipulated was intensity—and here, finally, we get confirmation that training does matter. Dropping training intensity by a third (from 90 to 100 percent of max heart rate to 82-87 percent) led to declines in VO2 max and long endurance; dropping it by two-thirds (to 61 to 67 percent) wiped out most of the training gains. The takeaway: you can get away with training less often, or for shorter durations, but not with going easy.

There are a few important caveats here. Most notably, we’re drawing these conclusions based mostly on one specific, unusual, and probably unsustainable training protocol: hammering six days a week. If you have a more balanced training program that mixes hard and easy training, does it take more or less training to maintain fitness? It’s not obvious.

Also, the subjects in Hickson’s studies weren’t trained athletes or military personnel. If you’ve been training for years, you accrue some structural changes (a bigger heart and more extensive network of blood vessels, for example) that presumably take longer to fade away. Conversely, you probably reach a higher level of absolute fitness, which might fade away more quickly. One of the co-authors of the new review is Iñigo Mujika, a physiologist and coach at the University of the Basque Country in Spain who is among the world’s leading experts in tapering, in which athletes try to reduce their training enough to rest and recover for a few weeks without losing fitness before a big race. In tapering studies, athletes can reduce their training frequency by about 20 percent and their volume by 60 to 90 percent and maintain fitness as long as they keep their intensity high. That’s one good reality-check that suggests Hickson’s findings about the importance of intensity make sense.

Maintain Your Strength

The literature on resistance training is much more varied, which makes for a more complicated picture but hopefully more reliable conclusions. Surprisingly, the overall pattern turns out to be pretty similar to endurance training. You can reduce both the frequency and volume of workouts as long as you maintain the intensity, and you’ll preserve both maximum strength and muscle size for several months.

For exercise frequency, several studies find that even training just once a week is sufficient to maintain strength and muscle size. That fits with the conclusions of a study I wrote about recently that demonstrated impressive strength gains on a simple once-a-week routine. The exception is in older populations: for adults older than 60, there’s a bit of evidence that twice-a-week sessions are better at preserving muscle. There’s a similar picture for training volume: one set per exercise seems to be sufficient for younger populations, but older people may need two sets.

It’s worth noting that maintaining your existing strength is not the same as gaining strength: this review focuses on the minimum dose, not the optimaldose. Even in the broader strength training literature, there’s quite a bit of disagreement about how many sets or how many workouts per week it takes to fully max out your gains. But the basic finding here is that one set a week per exercise (or maybe a bit more for older adults) is probably enough to tread water for a while, as long as you don’t decrease how hard you lift. The review suggests aiming to approach failure by the end of each set, or at least to not decrease intensity compared to what you usually do.

In a perfect world, you’ll never need to apply any of this. But things happen, whether it’s related to work, travel, family, or global health. Over the years, as my own training has waxed and waned depending on the circumstances, the one non-negotiable element has remained a weekly tempo run—the spiritual descendant of those Hickson-inspired post-cross-country hammer sessions. It’s a shock to the system when my training has been patchy, but if that’s the minimum effective dose that ensures I never get truly out of shape, then I’m happy to swallow it.

For more Sweat Science, join me on Twitter and Facebook, sign up for the email newsletter, and check out my book Endure: Mind, Body, and the Curiously Elastic Limits of Human Performance.
Lead Photo: Mihajlo Ckovric/Stocksy

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Thursday, March 18, 2021

Brain’s ‘wiring insulation’ is one of the major factors of age-related brain deterioration

A new study led by the University of Portsmouth has identified that one of

the major factors of age-related brain deterioration is the loss of a substance

called myelin.

Myelin acts like the protective and insulating plastic casing around the

electrical wires of the brain - called axons. Myelin is essential for superfast

communication between nerve cells that lie behind the supercomputer

power of the human brain.

The loss of myelin results in cognitive decline and is central to several

neurodegenerative diseases, such as Multiple Sclerosis and Alzheimer’s

disease. This new study found that the cells that drive myelin repair become

less efficient as we age and identified a key gene that is most affected by

aging, which reduces the cell's ability to replace lost myelin.

The study, published this week in the journal Aging Cell, is part of  

an international collaboration led by Professor Arthur Butt at the University of

Portsmouth with Dr. Kasum Azim at the University of Dusseldorf in Germany,

together with Italian research groups of Professor Maria Pia Abbracchio in

Milan and Dr. Andrea Rivera in Padua.

Professor Butt said: “Everyone is familiar with the brain’s grey matter, but

very few know about the white matter, which comprises the insulated

electrical wires that connect all the different parts of our brains.

“A key feature of the aging brain is the progressive loss of white matter and

myelin, but the reasons behind these processes are largely unknown. The

brain cells that produce myelin - called oligodendrocytes – need to be

replaced throughout life by stem cells called oligodendrocyte precursors. If

this fails, then there is a loss of myelin and white matter, resulting in

devastating effects on brain function and cognitive decline. An exciting new

finding of our study is that we have uncovered one of the reasons that this

process is slowed down in the aging brain.”

By improving our understanding of aging brain stem cells, it gives

us a new target to help slow the progression of MS, and could have

important implications for future treatment.

Dr. Emma Gray, Assistant Director of Research at the MS Society

Dr. Rivera, lead author of the study while he was in the University of Portsmouth

and who is now a Fellow at the University of Padua, explained: “By

comparing the genome of a young mouse brain to that of a senile mouse, we

identified which processes are affected by aging. These very sophisticated

analysis allowed us to unravel the reasons why the replenishment of

oligodendrocytes and the myelin they produce is reduced in the aging


“We identified GPR17, the gene associated to these specific precursors, as

the most affected gene in the aging brain and that the loss of GPR17 is

associated to a reduced ability of these precursors to actively work to

replace the lost myelin.”

The work is still very much ongoing and has paved the way for new studies

on how to induce the ‘rejuvenation’ of oligodendrocyte precursor cells to

efficiently replenish lost white matter.

Dr. Azim of the University of Dusseldorf said: “This approach is promising for

targeting myelin loss in the aging brain and demyelination diseases,

including Multiple Sclerosis, Alzheimer’s disease and neuropsychiatric

disorders. Indeed, we have only touched the tip of the iceberg and future

investigation from our research groups aim to bring our findings into human

translational settings.”

The image shows myelin and specialized brain stem cells Oligodendrocyte

Progenitor Cells (OPCs) in the grey and white matter of the brain. 

The image depicts myelin (Cyan) and specialised brain stem cells Oligodendrocyte Progenitor Cells (OPCs) in the grey and white matter of the brain.
Credit: Dr. Andrea Rivera

Dr. Rivera performed the key experiments published in this study while at the

University of Portsmouth and he has been awarded the prestigious MSCA

Seal of Excellence @UniPD Fellowship to translate these findings and

investigate this further in the human brain, in collaboration with Professors

Raffele De Caro, Andrea Porzionato and Veronica Macchi at the Institute of

Human Anatomy of the University of Padua.

The study was funded by grants from the BBSRC and MRC to Professor Butt,

together with the UK and Italian MS Societies (to Professors Butt and

Abbracchio, respectively), and the Swiss National Funds Fellowship and

German Research Council (Dr. Azim). Dr. Andrea Rivera was supported by an

Anatomical Society Ph.D. Studentship (with Professor Butt), and the MSCA

Seal of Excellence @UniPD (Dr. Rivera).

Dr. Emma Gray, Assistant Director of Research at the MS Society, said: “MS

can be relentless and painful, and there are sadly still no treatments to stop

disability progression. We can see a future where no one has to worry about

MS getting worse but, for that to happen, we need to find ways to repair

damaged myelin. This research sheds light on why cells that drive myelin

repair becomes less efficient as we age, and we’re really proud to have helped

fund it. By improving our understanding of aging brain stem cells, it gives

us a new target to help slow the progression of MS, and could have

important implications for future treatment.”

Monday, March 15, 2021

The Enduring Mystery of Muscle Cramps? You’re not Alone - Alex Hutchinson

Any discussion of muscle cramps needs to start by revisiting retired baseball infielder Munenori Kawasaki’s detailed explanation of how he avoided a repeat of the cramp that had hobbled him the previous day.

Kawasaki: Monkey never cramps. Because a monkey eat every day banana. Two.

Interviewer: So how many did you have today?

Kawasaki: Three.

I love that interview so much that it pains me to cast doubt on his advice. It’s based on the traditional view of exercise-associated muscle cramps, which attributes them to dehydration and the loss of electrolytes like sodium and potassium (which bananas contain in abundance) from prolonged sweating. That theory dates back almost a century, and it remains dominant: a survey of 344 endurance athletes, published last year, found that 75 percent of them believed that taking extra sodium wards off muscle cramps.

The problem is that science keeps failing to back this theory up. Starting more than a decade ago, a series of studies have compared crampers with non-crampers at marathons, triathlons, and other endurance races and has failed to find any differences in the athletes’ hydration or electrolyte levels. Instead, a rival theory blaming cramps on “altered neuromuscular control” first proposed in the 1990s by Martin Schwellnus, a sports physician at the University of Cape Town in South Africa, has been gaining support. The basic idea: it’s a nerve problem that occurs in excessively fatigued muscles, essentially leaving a switch temporarily stuck in the on position.

But this theory, too, has a problem: unlike the electrolyte theory, it doesn’t give us an obvious solution or countermeasure to prevent cramps. The closest thing so far is a product called HotShot, a spicy drink developed by Flex Pharmaceuticals that triggers some of the same nerve receptors as pickle juice (long known as a folk cure for cramps) and hot peppers. There’s a bit of evidence from a HotShot-funded study published by Penn State researchers in 2017 that this jolt to the nerves makes your muscles a little more cramp-resistant and shortens the duration of cramps stimulated in the lab. But it’s hardly a panacea; even in that study, all the subjects still ended up cramping. Schwellnus himself warned that muscle cramps are a complex phenomenon with many different contributing factors, so we shouldn’t expect a simple solution.

What we’re left with is a search for factors we can control that might influence cramp risk. That’s the goal of a new study in the Journal of Strength and Conditioning Research from a research team at the University of Valencia and Jaume I University in Spain. It recruited 98 runners preparing for the Valencia Marathon, ran them through a series of tests before and after the race, and looked for differences between crampers and non-crampers. Some of the results were predictable, while others were surprising.

The good news, from the study’s perspective, is that 20 of the runners suffered muscle cramps during or immediately after the race. A total of 84 runners (72 men and 12 women) completed all the pre-and post-race testing, which means that 24 percent of them cramped, with similar rates in men and women. That’s roughly consistent with the stats from other races. Once again, urine and blood tests found no differences in dehydration or electrolyte levels before, during, or after the race.

Instead, the biggest difference was in the blood levels of creatine kinase and lactate dehydrogenase, both markers of muscle damage, which were significantly elevated immediately after the race and 24 hours later in the crampers. For example, day-after creatine kinase averaged 2,439 international units per liter. in the crampers compared to 1,167 in the non-crampers. This, too, is consistent with previous studies, suggesting that cramps occur in muscles that are fatigued to the point of damage.

The harder question is what predisposes some runners more than others to this kind of damage. One previous study suggested that crampers actually start the race with elevated muscle damage, perhaps because they didn’t back off their training enough. In this study, though, there was no sign of elevated muscle damage in the pre-race testing and no difference in the amount of time between the final training run and the start of the race.

In fact, most of the training variables the team assessed—the runners’ number of previous marathons, weekly training volume, and so on—were the same in both groups. Just one differed: 48 percent of the non-crampers reported regular lower-body resistance training compared with 25 percent of the crampers.

Another often discussed risk factor for cramps is pacing. A few previous studies have found that runners who end up cramping tend to have started the race more quickly compared to their eventual average pace, suggesting that they’re paying the price for overestimating their fitness. There’s a problem with this type of analysis, however: the cramp may cause the late-race slowdown rather than the other way around.

To get around this issue, the Valencia researchers brought all their subjects in for a VO2-max test prior to the marathon. This allowed them to assess their starting pace relative to their actual fitness instead of relative to their eventual finish time. Here’s what the average speed for each 5K segment looked like for the crampers (black circles) and non-crampers (white circles), as a fraction of speed at VO2 max:(Illustration: Journal of Strength and Conditioning Research)

There are no significant differences between the groups until after the 25K mark. If anything, the crampers started a little bit slower relative to their lab-measured fitness. This punctures the idea that cramps are a punishment for bad pacing. I apologize for any cramp-shaming I’ve done in the past: it wasn’t your fault after all. Unless you were neglecting your lower-body strength training, that is. The obvious news-you-can-use nugget from the new study is the apparent protective effect of resistance training. I got the same advice a few years ago from Juan Del Coso, the author of an earlier study that implicated muscle damage in late-race slowdowns: he suggested leg exercises such as squats with loads to up to 80 percent of max to protect your legs from damage.

But at this point, it’s probably worth recalling Schwellnus’s note of caution. People get cramps for all sorts of reasons, including underlying injury, disease, and medication side effects. The exercise-associated cramps you get during a running race may be influenced by some of these secondary factors. They may also be influenced by your genes: one of the best predictors of cramping is whether you’ve cramped in the past. And despite the paucity of evidence, it’s entirely possible that, in some people, traditional risk factors like dehydration or electrolyte depletion may play a role. So before I get too excited about squats as the new miracle cure, I’d like to see whether a few months of strength training actually reduces cramp risk in a randomized trial.

It’s tricky to get those sorts of studies funded, though—there’s no pharmaceutical money, no sports-drink money. So for now, if you’re struggling with recurring cramps, you’re left with trial and error. It’s worth giving strength training a shot (and not just for its cramp benefits). I’d be open to giving HotShot a try, too. And, hey, whatever the evidence says, I love bananas.

For more Sweat Science, join me on Twitter and Facebook, sign up for the email newsletter, and check out my book Endure: Mind, Body, and the Curiously Elastic Limits of Human Performance.