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7 Hills of Kirkland Metric Century 2019

Normally, I start a ride report with a description of the ride, how much I like it, etcetera, etcetera, etcetera.

In this case, I’ve done 7 hills so often that it hardly seems worth the effort. If you want that information, there are plenty of examples here

I *will* note that this is the 12th time that I’ve done 7 hills, if you ignore the fact that I skipped a year or two when it was wet.

My typical approach for a ride like 7 hills is what I can the “make sure I finish” approach; start slowly and ride conservatively, and you can be confident that you are going to make it back for your serving of finish line strawberry shortcake, delta any mechanical issues with the bike or the rider.

This year I said, “the hell with that!”

I’ve been playing around with my training this year; I’ve been riding more hills earlier in the season than I have in the past and I’ve been feeling pretty good both aerobically and on climbs. So, the plan is to push a lot harder than I have in the past and see what happens.

That should provide more opportunity for humor and perhaps some pathos as well.

My big preparation for the ride was doing a one-hour recovery ride two days earlier that turned into a 25 minute recovery ride when it started 5% chance of precipationing on me and I headed for home.

Woke up at 5:30 due to my old dude internal clock, got my stuff together, and had a couple servings of SuperStarch. I’m put BioSteel hydration mix in my water bottle (no need for 2 on this ride), and headed for Kirkland about 6:50.

You may ask yourself why I drive to this ride when the route passes within about 3 miles of my house. I’ve ridden to the route and done the ride that way, riding the last few miles at the start of my day and skipping it later. I found it messed with my aesthetic appreciation of the route, so now I drive.

Parked on the waterfront, got out the bike, stuffed my pockets with stuff, and headed to the start. Joyously absent was any thought at all about what I would wear; it was already about 60 degrees and was forecast to get into the low 70s, so no arm warmers, no leg warmers, no jacket, no hat; just the usual minimal stuff.

Market street is the first hill; I climbed it in a little over 4 minutes at 211 watts. It’s just a warmup, as is hill 2, Juanita drive. Hit the light, turned down Holmes point, headed towards Seminary hill.

Seminary is one of the two hardest hills; Winery is steeper but gives you chances to rest, while Seminary is more of a constant annoyance. I rode easy on the first little blip, and then rode hard. The top came 8:42 later, more than a minute faster than last year’s effort and 16 seconds slower than my PR from 2016. But… averaging a fairly significant 270 watts for that time, which is pretty decent for me.

The usual descent and trip over to Norway hill, a nice 426’ hill that I’ve ridden up a lot and I backed off a little at climbed at 234 watts, which was pretty much my target.

Which brings us to Winery. I like to have some rabbits to chase up winery so I was okay when I got passed on the flat part before the climb, I was less okay when the blocked the whole lane on the little bump over the railroad track. I got around them and took off up the steepest first pitch, riding at about 420 watts. It’s a short pitch and I kept that power over it, and then slowed down to recover for the upcoming pitches. 5:26 later I was turning off at the top of the climb and listening to bagpipe music, a heartbreaking 4 seconds from my PR. I’m going to call this one a “virtual PR” because I lost more than that getting by the group at the bottom. 287 watts average was a great effort, but when I went back and looked at last year’s data, I did it in 5:22 but only averaged 250 watts. Not sure what is going on there, though I am in need of some drivetrain maintenance, and it would be good to do that on the bike as well. 

We then headed east and climbed a few more hills, then we came to Novelty Hill.

It would be fair to say that it’s not my favorite part of the ride; too much traffic and not really a very fun hill. This is compounded by the use of the lower part of the climb as an “out and back” route; as you are climbing up the hill there are riders who are ahead of you descending back down at a high rate of speed, not really the most motivating thing to see. Strava somewhat strangely didn’t match the whole climb for me, but I got PRs on various sections so I’m going to call a PR on that section.

After some flat roads, you end up coming back back over to Novelty for the descent, completing the circle of life. We learned about the circle of life from Disney’s “The Lion King” during the scene where Simba and Nala protected themselves from roving hyenas by building a impregnable perimeter from family-sized boxes of cereal.

Anyway, a couple climbs after that I hit the last rest stop and after a thoroughly pedestrian sandwich (turkey/cheese/green pepper slices on pita bread), headed out for the last climb. My intention was to spin up old redmond road at take it easy, but there was a guy right in front of me so I ended up pushing a bit and coming within my PR by about 10%. Then a couple of fun descents and a mostly-flat trip back to the starting line in which I missed every single traffic light.

Overall, a pretty good effort; I felt strong the whole day which has been an issue for me this spring; I’m not sure if it was the BioSteel or the SuperStarch or my smoked almonds or maybe that small oatmeal gluten free cookie I ate at the first food stop (it was *not* the cookie; that was a mistake).

I was about 15 minutes faster than 2018, averaging 14.7 mph rather than last year’s 14.1, finishing in 4:04:28 and burning 2538 calories for the effort.




Minicamp May 2019

My wife and I have done a few cycling vacations. The ones we’ve done don’t feature particularly long days – maybe 50 miles over the whole day – but they do involve riding for a bunch of days in a row. I’ve noticed that doing something like that helps my fitness; I just feel better overall.

And therefore I decided to conduct an experiment; I would ride 5 days in a row and see what happened. I wanted every ride to be at least 3 hours, but I wasn’t going for century lengths. And I would ride however I felt like that day.

I expected that I’d start out feeling okay and gradually get more tired as the days went by.

Day 1 was a big hills day; I rode a few of the Issaquah Alps. My speed on the first 3 (Squak, Talus, Zoo) was a conservative speed, but after Zoo I took a trip up Pinnacles and decided that I wasn’t up for Belvedeere, much less the trip up The Widowmaker. I crawled up the back side of Summit and headed for home.

Day 2 was supposed to be a ride all the way around Lake Washington, but after doing the south end I opted to take the 520 bridge back across for home. Felt okay but not great.

Day 3 was an evening ride that I lead. I chose the route to be a little hilly but not too hilly. On the ride down to the starting point, that seemed like a really good decision as my legs were hurting, but despite the hurting, they seemed to perform okay when I needed them. I have a 275’ hill on the way home from the ride with a couple of short 13-15% kickers, and those were not fun *at all*.

Day 4 was a ride in the country, specifically a ride out to Fall City. The intent was for it to be moderately hilly. My legs were tired from the night and I wanted to let the day warm up a bit, so I delayed my start until 11 AM. Legs were pretty sore but warmed up quickly. I had planned to ride up Sahalee (0.9 miles, 404’ of up) but that can be a long slog of a climb, so instead, I decided to head up “The Gate” (0.2 miles, 158’). That’s an average of 15%, with a top gradient of perhaps 21%. I didn’t have a lot of pop on it, but I rode up it okay with just a wee bit of paperboying. Worked my way east, the south, rode down Duthie, and then out to Fall City. Where I stopped at the grocer for a Coke Zero. My plan was to take Fall City –> Issaquah back, and take it I did, via the back way. Despite being on the 4th day and 25 miles into the ride, I was able to climb at about 250 watts pretty easy. Hit the top, finished my Coke Zero, did the bonus, and then worked my way to Issaquah and then back home.

Day 5 was the second evening ride for the week. I played with intensity as I spun through Marymoor, and my legs seemed fatigued but okay. The first climb was short but not a lot of fun. And then we hit Sahalee… I started slow, hit the steep spot, and found that my legs felt pretty good, so I rode the rest of ride at a bit more than 300 watts, averaging 280 for the whole climb. That put me close to my PR on the climb, which was a surprise. I did a sprint up a little steep hill on the route and managed somewhere in the mid 900 watts, though my legs *really really really* hurt at the top. I did notice that my aerobic recovery was pretty quick. After playing down the plateau we descended to East Lake Sam and pacelined back and I managed to “win” the fake sprint at the end by pulling out about 30 seconds from the end. My legs felt good, and the climb up to my house was considerably easier than on Tuesday.

Day 6 was designed just to warm up my legs and help them to recover a bit, so a 3.8 mile ride that took less than 20 minutes.



















































Day Distance Elevation Speed KJ
1 33.9 4177 10.9 1682
2 39.6 1575 14.3 1486
3 35.4 1788 14.5 1345
4 41.0 2470 13.6 1587
5 35.1 1903 14.3 1372
6 3.8 180 12.7 119
Total 188.8 12093 7591


The true test is going to be what my form is like after recovering for a few days, but early indications are that the minicamp did what I was hoping; I felt stronger in places where I hoped to feel stronger and my recovery seemed pretty good. I was mostly able to sleep quite well, and – somewhat surprisingly – my hunger didn’t seem to increase that much.


You meet the nicest people on the Zoo

Yes, “on the Zoo” is a strange wording; the reason for it might become apparent.

This afternoon I went on a bike ride. I go on a lot of bike rides; most of them don’t really warrant mention (got on the bike, rode, went home). This one might have showed up on Facebook as I sometimes do, so that my riding friends can “like” the ride as an indication of their recognition of my awesome cycling prowess (not really), and the rest of my facebook friends can… well, I’m not really sure what they think of those kind of rides, though “what a nutjob” is probably a good start…

You can look at the – which I cleverly named “A Grand Squaky Zoo” after the three hills I climbed (Grand Ridge, Squak Mountain, Zoo hill) – here. 38 miles, 4186’ of up, which is a lot for me in April.

But I digress…

The climb up Squak was a bit more painful than I had hoped, and I planned on skipping the Zoo hill climb, but I had to ride by it on the way home and turned up the hill on the spur of a moment. And immediately thought I’d made a mistake, as the bottom part up to the Zoo is steep. I came around the first turn, and noted a rider up ahead of me.

That’s a good thing; riders up in front of you are rabbits and you can focus on getting closer to them.

As I drew closer, I looked at his bike, because a bike can tell you a lot. Steel frame, fenders, pretty wide tires, and a handlebar bag in the front. That’s a touring setup. But many touring cyclists don’t ride hills, which meant it was most likely a Randonneur. Randonneur is a long-distance cycling discipline with events that are pass/fail based on elapsed time, so a 200 kilometer event (120 miles, or nearly 1000 furlongs) must be completed in 13.5 hours. Which isn’t really that out-of-the-ordinary, except that 200 km is the entry-level distance and the routes tend to be more than a bit hilly.

Where it gets to be a bit nuts is rides of 300, 400, or even 600 km; the local Seattle International Randonneurs 600k route involves nearly 22,000’ of climbing, is 383 miles long, and as a 600k has a time limit of 40 hours. There are also 1200k rides with a time limit of 90 hours; in that time you will climb 38,000’.

I like hills, but that seems a bit excessive…

As I pulled up next to the rider – why am I quite a bit faster than a randonneur rider? – I slow down to talk to him. Any distraction is welcome on a long climb, and this one is going to take me 36 minutes today – so we start talking, and he mentions that this is a training ride for him; he rode over from Freemont and he’s going to ride up this climb 6 times and then go home.

6 times. Well, if I was going to ride it 6 times (for about 7000’ of up total), I guess I’d be riding it fairly slowly as well.

Turns out his name is Doug Migden, and he’s training for the Transcontinental Race, a self-supported race across Europe. In 2015, he rode the 4200 km and climbed 35,000 *meters* in 446.5 hours. There’s a great writeup of his experience here.

I often wondered what you do if a 1200k ride isn’t long enough, and now I know. It’s always nice to run into people that are crazier than you as it lets you feel that you are sane.

We chatted and I learned a lot about long-distance self-supported riders. As we got about 3/4 of the way, I turned left to head to the classic top of the climb. Normally I don’t think you have done the Zoo if you don’t do the top, but a) Doug was going to an alternate top, and b) he was doing it 6 times, so I think I’m going to cut him a little slack.

And damn, was that descent cold.


The endurance athlete’s guide to fueling and weight loss part 6: Recommendations

This post will make considerably more sense if you have read the previous posts

After five long and sometimes tedious posts, I’m finally going to tell you exactly what your base diet should be and and how to fuel during exercise to achieve your goals.

Ha.

I sincerely wish I could do that, but the reality is that everybody is different (genetics, age, sex, metabolic condition) and we all have different goals (win that race/lose weight/have fun), so I’m not able to do that.

What I do think I can do is talk to you a bit about my philosophy of endurance eating and fueling and how you might apply it to your situation. And then I’m going to turn you loose to experiment/adapt/modify the recommendations to adapt them to your specific situation.

Philosophy

Based on the way our biochemistry works, here’s are the principles I advocate:

  • Train in ways to improve fat burning, and therefore improve the ability to use fat as a fuel so that more fat is burned and less glycogen is used, so there is less hunger.

  • Fuel in ways to support glycogen stores and therefore support endurance and performance without getting in the way of fat burning.

  • Eat in ways to support the first two goals and to leave us generally healthy.

The application of these principles is going to depend on your current weight, fitness state, goals, number of cats you own, etc. In the following sections I’m going to talk about some broad guidelines, but you will need to do experimentation and tuning yourself.

Train in ways to improve our fat burning

Doing training to specifically increase fat burning has been a thing for a long time; there was, for example, a big push towards LSD (either Long Steady Distance or Long Slow Distance) training in cycling in the early 2000s. And it worked okay, at least for some people.

But what it was missing was the dietary and fueling aspect; if you have a lot of glucose in your system during the training, you get improved endurance but you get little improved fat metabolism.

While thinking about this section, I remembered a mountain training ride I did with a couple of friends back in 2006 or so; it was scheduled for about 115 miles and around 8K of up. I was getting ready, stuffing my jersey pockets with little ziplocs of drink mix and other foods – probably 1500 calories worth – and I noticed one of my friends just standing there. I asked him what he was taking for food, and he pulled out a little bag of trail mix. He said, “I usually don’t eat much on rides, but I’ll have some of this if I get hungry”. Another paradox that the “you have to eat lots of carbs” model doesn’t explain.

The way that we improve our fat burning is exercise in situations where glucose is scarce. What does “scarce” mean in practice?

I don’t know.

Perhaps “scarcer” would be a better word to use, and in fact fits in better as I advocate an incremental approach. Take the amount of carbs that you eat before/during/after, and reduce it by some amount.

If you generally don’t eat on your workouts, pick one of your workouts – perhaps a longer weekend one – and do it fasted.

If you are a carbs before/during/after kind of athlete, look at the amount you are eating and cut them down. From a biochemical perspective, targeting the pre-workout carbs – so that you start with lower glycogen stores and steady blood glucose – is probably going to be more impactful, so maybe you cut down or eliminate that snack first. Or maybe you cut down all your carbs by 30%. And then go out and do your workout.

Generally speaking, longer steady workouts are much better for this than fast short ones. Use whatever definition of “long” that works for you.

Do that for a few weeks or even a month or two, evaluate how it’s working compared to your goals, and see if you want to make further changes.

Fuel in ways to support our glycogen stores

Didn’t I just tell you to reduce your carbs during training, and now I’m telling you to increase them?

Not quite.

While there are some athletes who eat full keto (very low carb) diets and use either no or very few carbs during workouts and races, there’s no prize for doing that nor is it a morally superior approach.

What we are trying to achieve biochemically is to have enough available glucose for our muscles to support us for the exercise so that we can achieve our goals, both from a weight perspective and from a performance perspective.

If we are doing the “better fat burning” training described in the last section, then the best approach can be described as “the minimal amount of carbs required to keep you from bonking”, as that will give you the most improvement in fat burning. We will deliberately eat in ways that put us close to running out of glycogen. Which is why it is absolutely essential during this training to carry carbs with you, especially if you are starting from a high-carb fueling strategy, because it is very hard to know exactly how close you are to bonking. If you start to get hungry and/or feel your energy dropping quickly, eat some carbs.

If you are in this purely for the fat burning side, then stick with this strategy. You will increase your fat burn during the ride and reduce the amount you eat during the ride. Both are good.

If your session is more performance/endurance sensitive – perhaps a goal event or a intense training session – then look at how long/hard it is going to be, make a guess at how many carbs you will burn, and plan a replacement strategy so that you have comfortable reserves at the end. If you are a better fat burner than before you won’t need as much as you did before, but you will likely need some. The pro cyclists who work to be very good fat burners still eat a *lot* of carbs during a hard day of racing.

Small amounts of carbs on an ongoing basis can be a pain to implement. If you want a simpler approach, consider UCAN’S SuperStarch, which acts like a time-release glucose. and is therefore quite convenient to use. Pricey, however. (note 1) I use it on my longer & harder events – say 4+ hours – but generally don’t on shorter events, where I just have water, even if fasted.

Recovery nutrition

Conventional wisdom says that you need to refill your glycogen stores as quickly as possible to take advantage of the brief window where glycogen replacement is increased when exercise is finished. The window does exist, but in most cases, we don’t really need our glycogen stores to be refilled especially soon, and those are extra calories that aren’t required. There’s an interesting study that shows that having the post exercise carbs reduces insulin sensitivity and glucose tolerance the next morning.

On the other hand, if you want to have something sweet, right after exercise that has depleted your glycogen stores is biochemically the best time to do so, and in particular, it’s a time when fructose likely doesn’t have the same downsides (note 2), so some fruit can be nice. I like peaches.

My general advice is to tend to not eat targeted recovery food, but if you find that you are ravenously hungry after long workouts, a bit of carbs after exercise can blunt that reaction.

Eat in ways to support the first two goals and to leave us generally healthy

Diet is a huge topic that I could write endless posts on. I will try to keep it simple and at least mostly related to the goals that we have been talking about.

Limit refined carbs and processed food

Refined sugar (sucrose) is an obvious target, and it’s bad for a lot of reasons – there is lots of glucose that you have to deal with, and lots of fructose that can lead to insulin resistance. Note that sucrose is added to a significant number of processed foods; this is a byproduct of the 1980/1990ss fat phobia, when manufacturers found that reducing fat made food taste awful but you can make it taste less awful if you add a lot of sugar. So, you’ll need to read labels.

And now for a bit of heresy… I think you should be careful with the amount of fruit you eat. There are many fruit advocates that assert that the sugars in fruit behave differently than refined sugars and therefore fruit is not an issue. It *is* true that:

  1. The sugar is bound up in the flesh of the fruit so that it takes longer to be absorbed than sugar outside of the flesh.
  2. A piece of fruit is much more filling than the equivalent amount of refined sugar.

But that just means that fruit is a gentler source of sugar, not that you can eat as much as you want. The impact of fruit hasn’t been well-studied in clinical trials, but I did find a study that looked at the relationship of fruit consumption to gestational diabetes, and the effect was significant (note 3).

If you have a lot of extra weight and/or type II diabetes, I would try to get rid of as much fructose as possible, from all sources.

And some more heresy… I think that other refined carbs are also important, though not as important as sugars. They lack fructose, but they still have a big load of glucose in them. This is mostly anything made with wheat flour (even whole wheat flour), so bread, pizza, pasta.

Yeah, I know, I like them all as well. I used to eat a lot of them when I was younger but they don’t agree with me now that I’m on the far side of 50. YMMV.

Alcohol is also something to limit, for the same reason as fructose.

And yes, I’ve totally killed the “ride and then celebrate” scene. Sorry to be such a buzzkill.

Choose an appropriate fat/carb ratio for your situation

From a general health perspective, the data I’ve seen suggests that if you are healthy in general and insulin sensitive, you will probably do fine on a moderate carb/low fat diet or a low carb/ moderate fat diet, as long as its a whole food diet (note 4). So just choose one that works for you.

If you are insulin resistant and/or have not being able to reduce your weight easily in the past, I’d recommend trying one of the low-carb approaches as they make more sense for that metabolic state. I usually recommend either Mark Sisson’s Primal, or the Duke University “No sugar No starch” diet.

Like the changes in fueling, I recommend that you make any dietary changes on an incremental basis.  If you end up going low carb, there is quite a bit of anecdotal data that suggests that endurance athletes are generally happier with diets that have a few more carbs in them (ie not keto), and an interesting study here where none of the participants stuck at a very-low-carb/keto diet but they all did eat a significantly lower-carb diet than they had in the past.

Case studies

Because my advice is non-specific, I thought I’d include a few case studies that have specific examples of what people have done.

One of the posts that started me on this journey was noted cycling coach Joe Friel’s blog post entitled “Aging: My Race Weight”.

My case study is in my blog post Down 20?

Chris Froome and other Team Sky cyclists use a low carb diet a their base diet – Froome famously tweeted this picture of a rest day breakfast that was very low carb. They do supplement with carbs based on the event. There’s a bit of insight into their approach here.

In Closing

I hope this has been helpful. If you have questions, please send me a comment; I’m planning on a follow-up post to clear up things that weren’t clear.

Notes

  1. SuperStarch is an interesting story. There is a disease called glycogen storage disease where a person is unable to store glucose as glycogen, and therefore is unable to regulate their blood glucose. The traditional treatment was corn starch every 2 hours, which was hugely impactful. SuperStarch is corn starch that has been modified so that the starch molecules become very long, which means that is slowly digested and therefore results in a slow release of glucose – exactly what is needed for people with this disorder. It also turns out to be quite useful as a carb replacement fuel for athletes. Here’s a paper with links to the clinical studies does with SuperStarch.
  2. Fructose in combination with high blood glucose preferentially metabolizes to fatty acids, which can accumulate in the liver. But if you have depleted glycogen stores, the glucose in the fruit goes straight into those stores and the fructose gets metabolized to more glucose.
  3. The odds ratio between the group that ate the most fruit and the group that ate the least was 4 – those who ate the most fruit were 4 times as likely to get gestational diabetes than those who ate the least. That is really a ridiculously high ratio for a nutritional study; it is uncommon to see anything above 1.5. It was still an observational study, however.
  4. Gardner’s DIETFITS study is a pretty good one. I recommend watching his video here.

The endurance athlete’s guide to fueling and weight loss part 5: Hunger etc..

Please read the previous posts if you haven’t seen them before…

We are moving closer to the post where I hope to give useful advice on the different tactics you might use to improve fueling or lose some weight. Or perhaps both.

This was going to be a short post as I was having trouble coming up with a good way to talk about hunger, but I came across some new (to me) information that I hope will be informative.

Hunger

Hunger lies at the intersection of energy balance, brain function, psychology, and group dynamics. Oh, and evolutionary biology. That makes it complex and hard to understand, and therefore not very amenable to easy explanations or simplification. It’s much more complex than – for example – how blood glucose is controlled. I’m therefore going to have to simplify quite a lot, and there will be a number of areas where it’s just not clear (to me) what is going on. That said, let’s get started.

The evolutionary purpose of hunger is to drive us to eat in ways that maintain our energy stores – and in particular, our fat stores – at a certain level. Or perhaps within a certain range. What factors could set the low and high limits of that range? (note 1).

Let’s start at the lower end – what drives the lower end of the fat storage range?

  • If we have too little stored energy, we won’t be able to survive when food becomes scarce.
  • If we are female, we need extra stored energy to be able to build and feed a child.
  • And at the upper range?

  • If we have too much stored energy, we may not be able to move around effectively, which could compromise our survival.
  • There may also be impact based upon climate, but I’m going to ignore that for this discussion.

    Another way to describe the range is “enough fat, but not too much fat”. Where “enough” and “too much” have definitions that are a bit squishy. But you get the idea…

    The regulation of hunger – and therefore the regulation of energy intake – is driven by two hormones, leptin and ghrelin. To oversimplify things:

    Leptin is produced by fat cells, and serves to reduce hunger. Generally speaking, the larger the fat storage, the higher the leptin levels will be. You can think of leptin levels like the gas gauge on a car; if your fat tank is empty, leptin reads low, if you fat tank is full, leptin reads high.

    Ghrelin is produced by the stomach, and serves to enhance hunger. It’s a shorter term signal.

    Based on a simple understanding of how the hormones work, we would expect that Ghrelin levels would be proportional to how long it was since we ate; the longer we went without food, the more hungry we would be.

    Here’s a graph of Ghrelin values over a typical day:

    (note 2)

    The solid line is the average while the dotted lines show the upper and lower range.

    That’s not what I expected. Ghrelin levels are lowest right when we get up, which is when we have gone the longest without eating and would therefore expect them to be highest. It turns out that ghrelin levels have a few somewhat interesting features:

  • They are adaptive based upon when we usually eat and our circadian rhythms.
  • They increase when we start to eat. This is familiar to most of us; not being really hungry but finding out that as we smell dinner or start eating, we are suddenly hungry.
  • There’s another strange feature of ghrelin related to fasting. Here’s a study (note 3) that looked at ghrelin levels over an 84 hour fast:

    image

    That’s just weird. The mean ghrelin levels decrease from day do day, which means you are actually quite a bit less hungry on day three of fast than you are in day one. While weird, this is pretty well established by research.

    Also note that there seems to be a greater reduction for women, for reasons that are not well understood.

    Why our bodies behave this way is not really known. The best theory I know is one from an evolutionary standpoint; while it is good to be hungry if food is available, it can quickly become counter-productive if food is scarce.

    Moving onto leptin, what do leptin levels look like? (note 4):

    image

    That is what we generally expect – at least there seems to be a decent linear relationship between BMI and leptin levels. It’s a bit messy, probably because BMI does not correlate perfectly to fat mass, and likely because of individual variations as well. The differences between male and female leptin levels are asserted to be caused by a) women having more fat mass at a given BMI and b) women having more of the kind of fat cells that produce more leptin than men, though I don’t think the question is truly settled.

    Disfunction

    Leptin is supposed to inhibit significant weight gain; if you gain excess fat, your leptin levels rise, your hunger drops, and you lose fat mass until your leptin levels drop. And that seems to work for some people, especially those who are young, choose their parents well, and male. But it’s pretty obvious it does not work well in a lot of cases.

    Is there anything known about the disfunction? Well, a bit…

    Leptin and ghrelin levels based on types of food

    I found a very nice experiment (note 5) that looks into leptin and ghrelin response based on different kinds of food. Take a group of people, have them fast overnight, and then give them one of three drinks:

  • 500 calories with 80%/10%/10% from carbs, fat, and protein
  • 500 calories with 10%/80%/10% from carbs, fat, and protein
  • 500 calories with 10%/10%/80% from carbs, fat, and protein
  • In other words, a carb-heavy (glucose-heavy), fat-heavy, and protein-heavy drink (note 6). This is done in what is called a “crossover” study, which means that each subject had all three drinks on different days.

    You sample their blood before they have the drink, and then every 30 minutes afterwards, and measure a bunch of different things. Based on how ghrelin works, I would expect that eating would suppress the ghrelin levels and then over time, they would rebound to their previous levels.

    What happens?

    image


    All three produce a significant suppression of ghrelin production, but carbohydrate produces the biggest reduction. Interestingly, however, after about two hours the carbohydrate ghrelin level goes shooting up and after 3 hours it is higher than the fat or protein curves and soon after becomes higher than the initial ghrelin level.

    Or, to put this another way, five hours after eating 500 calories of mostly glucose we would be *more hungry* than we were at the start.

    The authors write, “Our finding of a rebound of total and especially acyl-ghrelin above baseline after high-carbohydrate meals could provide some physiological basis for claims made by low-carbohydrate diet advocates that ingesting carbohydrates prompts an early hunger rebound”.

    Indeed.

    They did measure subjective appetite which showed no effect, though unfortunately they had technical difficulties with the appetite reporting system and that data was therefore not published.

    I’d also like to note that there are many experiments that measure satiety (the inverse of hunger) and show that carbohydrates lead to more satiety than fats or protein. And they do, if you only measure them for 2-3 hours.

    The experiment also measured blood glucose over time:

    image

    If I eyeball the two charts, it looks like ghrelin production starts to go up steeply about the time blood glucose drops quickly at 140 minutes, and is highest when the blood glucose is the lowest. The pattern here matches what is known as either “reactive hypoglycemia” or “postprandial hypoglycemia” – basically the blood glucose drops below initial levels a few hours after eating.

    It’s important to note that the drinks were dominated by a specific macro and drinks with mixed macros may show unexpected results. Though 500 calories is not really that much and these were consumed in a fasted state, and as we know that is the time when the body is best able to handle a lot of glucose.

    You can find the leptin chart in the paper if you’d like to see it; there were small drops over time but nothing very striking.

    Fructose vs Glucose

    Is there a difference between fructose and glucose? Let’s look at another experiment (note 7).

    In this experiment, we take 12 normal-weight women and feed them three meals containing 55%, 30%, and 15% of carbohydrate/fat/protein and take blood samples every 30-60 minutes.

    Of the 55% of the calories that come from carbs, 30% either comes from a fructose-sweetened or glucose-sweetened beverage.  Take a normal meal pattern and make the carbs either fructose heavy or glucose heavy. And sample their blood periodically:

    image

    Wow. Lunch and dinner show large spikes in ghrelin for both drinks, but the late-night spike of the fructose drink is much higher. Also notice the difference in levels at 8am the next day; the level of ghrelin in those who had glucose is quite low, but it’s pretty high for those who had fructose.

    Fructose gives us bigger positive ghrelin peak than glucose.

    They also measured blood glucose levels:

    image

    Based on what we know about glucose and fructose metabolism, that is what we would expect; because the fructose is processed in the liver, there is much less glucose. We would expect that the liver processes the fructose to triglycerides. Is there data to support that?

    image

    Yep. Vastly higher triglyceride levels show the fructose being converted to fat and released into the bloodstream, and those levels persist through the night.

    They also measured leptin levels:

    image

    Leptin levels rose much less for the high-fructose meal, which means there was less inhibition of appetite.

    Overall, fructose led to a greater increase in ghrelin (higher appetite) and a lesser increase in leptin (less appetite suppression).

    So, carbohydrates in general aren’t great, and fructose is worse.

    The best theory I’ve seen around why fructose behaves so differently is that significant fructose supplies were rare in historical times, and therefore it was advantageous for humans to eat as much as possible when they found them. That sounds reasonable, though like many studies in evolutionary biology they are hard to support.

    Leptin resistance

    The mystery of why leptin isn’t behaving as we would expect – why people still eat a lot even with high leptin levels – has been labeled “leptin resistance”, by analogy with insulin resistance; the idea is that for some reason the brain is not sensitive to the levels of leptin.

    Whether there is actual resistance or whether there are other factors that are overpowering the leptin signal is not clear.

    There are a number of theories round what is actually happening. Among them are:

  • There is a defect in transporting leptin from the bloodstream into brain cells across the blood/brain barrier.
  • The cells within the brain become less sensitive to leptin.
  • Dietary fructose leading to elevated triglycerides reducing leptin transport across the blood/brain barrier.
  • Here’s two papers if you want more information (note 8) (note 9).

    Dopamine

    I’m including this section for completeness. There is some research on how dopamine is affected by sugar ingestion, and while I think there something going on there that partially explains why sugar is addictive – at least for some people – I’m not confident enough in my understanding and the quality of the research to have much to offer.

    I do offer a few papers:

    Hunger Summary

    The main points from the preceding section on hunger:

    • Carbs – and especially fructose – seem to interfere with the hunger control system.

    • Hunger is not directly related to how long it’s been since you ate; it has a daily rhythm and decreases when fasting.

    Energy balance and weight loss

    If you have read official guidelines and advice about weight loss, you can generally boil them down to one bit of advice:

    Eat less and move more

    This is often summed up as the “Calories in / Calories out” (CICO) model; eat less means fewer calories in, move more means more calories out, and the result will be weight loss.

    It is also typical to see appeals toward the Laws of Thermodynamics. The more rabid adherents to the model treat it as if they have discovered one of the deep secrets of the universe.

    If you have read the earlier posts and have learned anything about biochemistry, I’m sincerely hoping that you suspect that the reality might just be a *tiny* bit more complicated than the simple world of “eat less and move more”. Especially since that advice fails for a large number of people, at least for the long term.

    There is truth to the CICO model in one sense, if you are losing weight you are burning more calories than you are taking in. And vice versa. But that’s the result, not the driver; the driver is the biochemistry at work.

    The key to understand how things really work – and why CICO isn’t very useful in many cases – is related to how the body responds to a reduction in food intake. The body essentially has three options to balance things out:

    1. It can burn stored fat.
    2. It can tear down muscles (ie “lean mass”) and burn that.
    3. It can reduce its energy use.

      We are hoping that it would do #1 – after all, the whole point of the fat storage system is to provide an energy reserve when food is scarce. But remembering the earlier posts, there are a couple of things that can get in the way of that. First off, we need to be good at burning fat in general. And second, we need to be in a hormonal state where fat burning is possible.

      If either of those aren’t true – or are true only to a limited extent – then we are stuck with tearing down muscle and reducing energy use. And, in fact, that is what we see in a lot of diet studies; people will lose lean mass – sometimes a significant amount – and people report being cold, tired, and hungry all the time.

      And they don’t really lose all that much weight.

      If we can get rid of the conditions that are blocking fat metabolism – and, since we are athletes, up the amount of fat we burn when exercising – then the body should naturally start burning more stored fat, and we should lose weight. Or, to put it another way, we are going to focus on the fat burning side of the house.

      This post is already quite long so I’ve tried to limit the detail in this section; if you want more I highly recommend Peter Attia’s post on fat flux.

      Summary

      There is a lot more that I could write about WRT hunger and energy balance, but I think this is enough for now.

      Our strategy is going to make dietary modifications to reduce hunger and improve our ability to use fat to generate energy while exercising, with a goal to lose weight/improve our ability to perform in long events.

      Which takes us to the tactics portion of the series. What do I think you should actually *do* to implement these strategies, so that you can – with any luck – see the benefits that I’m talking about.

      That will be post #6. When I get that done, I’m planning on doing at least one post to cover any questions.

      Post #6: Recommendations

      Notes:

      1. I’ve tried to base this section on what I’ve learned about evolutionary pressure, fat stores, and hunger.
      2. From Jason Fung’s excellent discussion on hunger and fasting here.
      3. Fasting unmasks a strong inverse association between ghrelin and cortisol in serum: studies in obese and normal-weight subjects
      4. Mechanisms behind gender differences in circulating leptin levels. This result is widely replicated in other studies.
      5. Acyl and Total Ghrelin Are Suppressed Strongly by Ingested Proteins, Weakly by Lipids, and Biphasically by Carbohydrates
      6. The beverages were mostly composed of a glucose beverage, whey protein/nonfat milk, and heavy whipping cream for the carb/protein/fat drinks.
      7. Dietary Fructose Reduces Circulating Insulin and Leptin, Attenuates Postprandial Suppression of Ghrelin, and Increases Triglycerides in Women
      8. Leptin resistance: a prediposing factor for diet-induced obesity
      9. Mechanisms of Leptin Action and Leptin Resistance
      10. MarksDailyApple, by Mark Sisson’s. Mark is an advocate for a way of eating named “Primal”.

      The endurance athlete’s guide to fueling and weight loss part 4: Better fat burning in actual athletes

      Please read the introduction and earlier posts if you haven’t…

      In the last post, I finished by asking what factor or factor might cause the difference between these two athletes:

      image_thumb2

      image_thumb5

      The differences might be genetic, differences in diet, or differences in training. Or maybe something else. What do you think is at play?

      We don’t know all the factors, but it turns out that this athlete does not have a sweet tooth, so he eats closer to the recommended cyclist diet; lots of carbs, but not a ton of sugar. At least in his base diet; I don’t know what he eats before/during/after training. And he’s better at burning fat.

      Hmm. It’s almost as if there might be a dietary effect here, that the availability of carbohydrate in the diet and on the bike might have an effect on fat burning ability. How could we test that?

      Well, let’s put two cyclists – how about these two cyclists? – in a situation where there is much less carbohydrate available, let them train for 10 weeks, remeasure their VO2Max, and see what changes. Since we want to maximize the effect, we’ll put them on a very low carb “keto” diet, which is something like 30 grams of carbs per day.

      What happens?

      Well, athlete #1 is not happy on the keto diet, and that’s really no surprise; he’s not good at producing energy from fat *at all*. If you take away his carbs he will feel horrible on the bike. He ends up making the following adjustments from has previous diet:

    1. He minimizes all sources of sugar
    2. He limits bread, rice, pasta, and potatoes to once or twice a week.
    3. He reduces the food he eats on the bike to an occasional banana plus water
    4. Not really a low-carb diet, but certainly a *lower than before carb* diet.

      Ten weeks of training go by, he retakes the test, and we generate a new graph (previous results are dotted):

      image

      This athlete is now a significantly better fat burner; rather than hitting only 25% of calories from fat, he’s averaging 40% or so across most of his range. His beta oxidation system is better.

      Athlete 2 started with the same very-low-carb diet, and he didn’t stick to it strictly either, but he did mostly get rid of grains and fruit from his diet, and he ended up lower-carb than athlete 1.

      10 weeks go by, and we get this:

      image 

      Yowsa! He nearly doubled the amount of energy he got from fat in parts of his range, and averages over 70% for most of the range. There is also a significant shift to the right, and he produces a higher maximum relative power. That’s great, the low carb diet made him much more powerful!

      Not so fast. Remember that this is *relative power*, and we know that he lost some weight as part of his 10 weeks training, so most of the improvement is likely from the reduction in weight. Though the training may also have helped.

      What did we see across these two athletes?

      First – and most importantly – we saw that a dietary switch made significant changes in the fat metabolism ability for both athletes. This really isn’t very surprising knowing what we know about the underlying biochemistry, but it does show very clearly that beta oxidation capability can be trained.

      Second, we saw a correlation between the amount of carbohydrate in the diet and the overall ability to metabolize fat.

      I do want to add a few caveats. The first is that two cyclists is a very low sample size, and the second is that we can’t tell the difference between changes due to base diet and changes due to food before/during/after. And there may be a genetic component at play here.

      Returning to my RAMROD example from the last post, let’s add in two more lines, corresponding to getting 50% of calories from carbs and supplementing 200 cal/hour (yellow) and getting 25% from carbs and supplementing 25 cal/hour (blue). These lines are closer to the “after” graphs of the two cyclists.

      image

      If I can get up to 50% fat utilization and supplement at 200 calories per hour, I should be able to go 12 hours without running out of glycogen. And if I can get up to 75% from fat, I can supplement at only 25 calories per hour and still easily make it to 12 hours.  I can almost get to 12 hours without eating anything at all…

      It may be better than that. Remembering back to the first post where we talked about triglycerides, and how those are composed of a glycerol backbone with three fatty acids attached to it. If we are burning lots of fatty acids in beta oxidation, that means the fat cells are breaking apart triglycerides, and that means we have a lot of extra glycerol around.

      Since the body doesn’t want to waste energy, it will try to use the glycerol for something useful, and it can turn it into glucose through gluconeogenesis. That means if we are burning a lot of fat, we will get some glucose out of it to support the glycolysis side. And no, I don’t know how much “some” turns out to be, this is hard to study.

      Some more data

      Is there more data out there that would be interesting?

      Jeff Volek and Stephen Phinney have done a number of studies looking at low-carb/keto diets and athletes (note 1), and here’s one that I think is relevant to this topic:

      Metabolic characteristics of keto-adapted ultra-endurance runners

      One of the problems with dietary studies is that the studies are expensive and time is limited, so it’s very hard to do studies where you change an athlete’s diet and check to see how it affects her for the next 12 months. That is why many of the studies around keto diets and athletes are extremely short; less than 3 weeks. Knowing what we know about how long it takes to achieve training gains in general, it’s pretty clear that 3 weeks is on the short side to see adaptations, so I don’t think most of those studies are very good.

      In this study, Volek and Phinney instead looked at two groups of elite ultra-endurance runners, 10 who followed a high-carb diet, and 10 who followed a low-carb diet. Since each group was on their habitual diet, it’s a pretty good bet they were adapted to it pretty well. I will note at the outset that this is an observational study and therefore there is the possibility that the runners who chose low-carb are genetically better at burning fat than the high-carb ones.

      From the hypothesis about trainability, what difference would we expect to see in fat burning rates between the two groups? Here’s the first graph:

      image

      The graph shows the peak fat oxidation during a 3-hour run for all of the athletes. Every low carb athlete is significantly better at burning fat than even the best fat-burning high carb athletes. If we look at the averages (circles to right), the average in the low carb group was 2.3 times higher than the high-carb group.

      I’d also like to note that the average for the low carb group was 1.54 grams/minute. That would be 92.4 grams/hour, or a whopping 92.4 * 9 = 832 calories / hour from fat burning alone.

      Where did that peak fat oxidation occur? Here’s another graph:

      image

      Here we are looking at the relative intensity of that fat peak for each runner; the HC group peak was at 54.9% of VO2max, and the LC group peak was at 70.3%. Not only are the low carb athletes burning more fat, they are hitting their peak at a higher intensity.

      It is pretty clear that the low carb athletes are burning vastly more fat during a long run than the high carb athletes. And this study was with elite athletes doing ultra-distance events, which means even the high-carb athletes are likely to be decent fat burners.

      There are some other interesting graphs in the paper that I recommend looking at (note 2), and we may come back to it later.

      Summary

      We found out that there seems to be a strong training effect and we can expect to improve the rate at which we burn fat through training. We also learned that if we can do that, it can make fueling more straightforward on long rides; we may need to still supplement, but likely not as much.

      In the next post, we’re going to take a little excursion into talking about weight loss and hunger.

      Part 5: Hunger etc.

      Notes:

      1. Phinney and Volek have written a couple of books that cover this same subject area: “The Art and Science of Low Carbohydrate Living” and “The Art and Science of Low Carbohydrate Performance”.
      2. Section 3.2 talks about submaximal substrate utilization, and features two charts that show the average oxidation rates (in grams/minute) for both fats and carbohydrates. The low carb group was very steady across the whole 180 minutes of the run; both fat and carbohydrate utilization is nearly a flat line. The high carb group saw a drop in carbohydrate and increase in fat over time; they also saw a slight reduction from 13.2 cal/minute at the start of the run to 12.0 cal/minute at the end.


      The endurance athlete’s guide to fueling and weight loss part 2: Energy Systems

      Please read the introduction and earlier posts before reading this one.

      In our last episode, we learned about how fat and carbohydrate get into our systems and the fundamental asymmetry between those two systems.

      In this episode, we will look at how fat and glucose are used for energy. My focus is going to be on muscles since these posts are for athletes; there are similar concepts that apply to other tissues but they are beyond the scope of this discussion (see note 1)

      I’m going to have to dive into some biochemistry to create a framework for further discussion; I have tried to simplify it as much as possible, and the post is relatively short.

      This is a summary of the overall processes at work for aerobic energy production; there are others that are at work for non-aerobic production.

      Each of the boxes is a complex series of chemical steps (note 2)

      image

      We’ll start at the bottom and work our way up.

      Citric acid cycle

      Our goal is to take fat and carbohydrates and create ATP, which is what powers our muscles. At the center of the diagram is a compound named acetyl coenzyme A, abbreviated as “Acetyl CoA”. You can think of Acetyl CoA as the common energy compound produced from either glucose or fatty acids. That’s not absolutely correct, but it’s correct enough.

      The Acetyl CoA feeds into the citric acid cycle (sometimes known as “Kreb’s Cycle” after one of the discoverers). If you want to see the details, here’s a link:

      Image result for don't press this button image

      You pressed it, didn’t you?

      Biochemistry is just ridiculously complex.

      All of this takes place inside of each of most of our cells. You probably studied cells when you were in biology class, and the diagrams looked something like this:

      Image result for simple cell nucleus mitochondria

      Specifically, the citric acid cycle happens within the mitochondria, which you can see are those oval-shaped structures within the cell. I generally think of cells as being these little spheres or flat discs, and some are, but muscle cells are a bit different:

      Image result for muscle cell nucleus mitochondria

      Not at all like a globule or a flat disc; I especially like the nucleus stuck on the side as an afterthought.

      Muscle cells need a lot of energy so they have tons of Mitochondria. Thousands of them.

      And how are we going to get all the Acetyl CoA that we need to drive those muscles?

      Glycolysis and Beta Oxidation

      Glycolysis is the the process that converts Glucose to Acetyl CoA. Beta oxidation is the process that convert fatty acids to Acetyl CoA. Both of these processes happen in the mitochondria.

      There is a very important point to be made about glycolysis and beta oxidation. Even though they both occur in the mitochondria and even though they both feed into the citric acid cycle, they use different chemical pathways and therefore use different machinery.

      The citric acid cycle, glycolysis, and beta oxidation can all be trained. Not only can the body build more mitochondria, it can improve the rate at which each bit of machinery in the mitochondria works. That is one of the adaptations that makes us better at aerobic exercise.

      But the body only makes improvement to the parts of the machinery that are being stressed, so if it’s glycolysis that is being stressed, improvements will be made in the glucose metabolism, and similarly if beta oxidation is stressed, improvements will show up in fat metabolism.

      This point is going to be fundamental to our next discussion, so I’ll state it again in a different way – you can be an athlete with a very powerful glycolysis pathway and a crappy beta oxidation pathway. And vice versa.

      Another interesting outcome is that to achieve higher performance, you need to improve either glycolysis or beta oxidation *and* the citric acid cycle. You can do a bunch of work to improve your beta oxidation and you’ll burn more fat and fewer carbs, but you won’t see higher performance if the citric acid cycle is unchanged (note 3).

      Summary

      This was a short post and I’m not sure I really need a summary, but the short one is that both fat burning and glucose burning have separate chemical reactions (glycolysis and beta oxidation) that feed into a shared set of chemical reactions (the citric acid cycle) that ultimately give the energy to drive the muscles.

      That’s all for this post. The next post will take this post and apply it in real-world situations.

      Part 3: Carbohydrate and fat use in actual athletes

      Notes

      1. That would take us into ketone bodies and their usage in different tissues.
      2. Like, ridiculously complex. In glycolysis, to get from glucose to pyruvate – which is fed into the citric acid cycle – takes a series of 10 different chemical transformations. Beta oxidation goes through 5 steps but repeats them for every two carbon atoms on the fatty acid, and it’s more complex for unsaturated fatty acids. The citric acid cycle has 9 steps.
      3. This depends a bit on what you mean by “performance” and it ties into fueling, which will come up very soon in a future post.


      The endurance athlete’s guide to fueling and weight loss introduction

      I’ve always been interested in nutrition for athletes, and as a serious recreational cyclist – whatever that means – I’ve played around with a number of different approaches. And I’ve read a lot of books that explain how to do the “standard athlete diet”, and done my best to follow them.

      But there were a couple of things that had me confused…

      The first was my inability to come up with a nutrition strategy that worked for me on very long and hard rides. Invariably, if I got beyond about 7 hours, I felt sick and weak, and sometimes it happened earlier.

      The second was just an observation at first; there were people I rode with who rode a *lot* more than I did but still carried a significant amount of extra weight – 30 or even 50 pounds. I knew from talking with them that they ate like I did, and they were already riding in excess of 5000 miles a year, so more exercise couldn’t be the answer. It was quite the puzzle, but it took getting into my 50s and finding that my weight was no longer easily controlled by cycling and that I was having energy issues in the afternoon to compel me to investigate a bit further.

      That led to a period of two years where I learned a lot more about physiology and taught myself enough biochemistry to be moderately dangerous. And changed both my diet and fueling strategy significantly.

      And, incidentally, I lost around 15 pounds. I was 178 pounds to start, and at 6’1”, that’s reasonably light, but at 163 pounds, I’m now “cycling light”, and that’s made a big difference on the rides I do.

      This series is my attempt to put down the important things that I’ve learned in a coherent manner so that others can benefit from it, and I can get clear in my head what I think I know.

      I’ll warn you at the outset; I’m going to be talking about biochemistry because that understanding is pretty critical when we get to talking about strategies and tactics. I have tried to make it “Just enough biochemistry”.

      The following is a list of the various posts. I really recommend reading them in order as the later posts build on the earlier posts.

      1. Part 1: Macronutrient intake and storage
      2. Part 2: Energy systems
      3. Part 3: Carbohydrate and fat use in actual athletes…
      4. Part 4: Better fat burning in actual athletes…
      5. Part 5: Hunger etc…
      6. Part 6: Recommendations

      The endurance athlete’s guide to fueling and weight loss part 1: macronutrient intake and storage

      If you haven’t already, I recommend reading the introduction

      We’re going to start by going into the biochemistry of how the various macronutrients – fat, protein, and carbohydrate – make it into our bloodstream and how they are stored.

      I’ve simplified the biochemistry as much as practical. If you want more details, you can start with the chapters about fat and carbohydrate metabolism in Marks Medical Biochemistry, but I’ll warn you that biochemistry is annoyingly complex.

      Digestion and Storage

      Fat

      When we eat fat, we are eating triglycerides, which look like this:

      Image result for triglyceride

      Triglycerides are simply 3 fatty acids hooked to a glycerol backbone. The fatty acids are just chains of carbons with hydrogens attached to them and then what’s called a hydroxyl group (pink in the image) at one end. Discussion of fats is imprecise; sometimes we talk about “fats”, sometimes “fatty acids”, and sometimes “triglycerides”. You can treat all those as equivalent for this discussion.

      The fatty acids shown here are saturated fatty acids; the differences are mostly immaterial for the purposes of this series, so I’m going to ignore them.

      After digestion, fatty acids end up in the bloodstream, our adipose (fat) tissue pulls them in, and stores the fatty acids away. Very simple and the system works quite well.

      The amount of energy you can store in fat cells is close to unlimited. Even only 10 pounds of fat stores about 35,000 calories, which is a ton of energy; that’s about 1000 miles of riding for the kinds of rides that I do.


      Protein

      The protein in the food we eat is broken apart into individual amino acids, absorbed into the bloodstream, and… Well, at that point it gets a little weird.

      There is no centralized storage for protein in the body. There is a what is called the “amino acid pool” in each of the cells, but generally speaking, if we eat more protein than is immediately usable by the cells, the rest is excess. Most of the excess amino acids can be converted to glucose through a process known as gluconeogenesis, so some of the excess energy becomes blood glucose, but if there is too much, it is just thrown away.

      Now, if you look at it another way, you can view muscles as a centralized storage for protein. There is something known as “protein sparing” where the body generally tries not to tear apart muscles to get energy, but if the need is great, the body will tear down protein, convert it to glucose, and burn it. If you’ve seen the pro cyclist upper body muscles, you can see this effect in action.


      Carbohydrate

      Carbohydrates are much more complex; unlike the fat system, where all fatty acids are treated equally, the different sugars are treated quite differently. I’m going to talk about how the various sugars get into the bloodstream and what form they take before I talk about storage.

      Glucose

      Image result for glucose

      Glucose is one of the common currencies for energy in the body. When you eat glucose, it is absorbed into the bloodstream.

      Starch/Maltodextrin/Dextrose

      These are sometimes known as “glucose polymers”, which is a fancy way of saying “chains of glucose”. The chains are broken apart into glucose in the digestive system before they are absorbed and that generally happens fairly fast.

      You can treat dextrose, maltodextrin, and most starches as if they were glucose from a nutritional perspective. There are a few exceptions; there is “resistant starch”, which doesn’t get digested easily and can be converted to fat in the digestive system by bacteria, and a cool product known as SuperStarch that I’ll talk about in a later post.

      Sucrose/Fructose

      Sucrose is a disaccharide, which means it’s a compound of one molecule of glucose and one of fructose. You can treat the glucose part just like any other glucose molecule.

      The fructose part is more complex. Some fructose may get digested into fat in the digestive system, but the fructose that makes it into the bloodstream cannot be used directly by the cells of the body. Rather than waste that energy, the liver takes the fructose molecules and does a bit of processing on them. If glucose is rare (blood glucose is not high), the resulting compounds will become glucose, and if glucose is common, it will convert those compounds into fatty acids, which is released (if you are lucky) or accumulates (if you are not lucky). More on that later.

      High fructose corn syrup is about 55% fructose and 45% glucose, so it’s pretty close to the same mixture as sucrose and from a dietary perspective, you can treat it the same.

      I should also note that some people have varying degrees of fructose intolerance; it can cause what is politely known as “digestive issues”. If I eat any fructose during exercise I will get immediate stomach issues. I mention this because it took me a long time to figure out.

      Lactose

      Lactose (milk sugar) is another disaccharide, in this case a combination of glucose and galactose. The glucose is like any other glucose, the galactose is like fructose in that it can only be handled by the liver.

      Alcohol

      What we call ‘alcohol’ – ethanol – is lumped together with other carbohydrates even though it is not a sugar. Ethanol can only be metabolized through the liver, and like fructose and galactose, it might end up as glucose or it might end up as fatty acids.

      Blood glucose levels and glucose storage

      Much of the physiology we’ll talk about is driven by blood glucose levels. There are two big things to know:

      Thing 1: There is a narrow range for healthy blood sugar levels

      When blood sugar is not in a narrow range, bad things happen. Normal fasting blood glucose levels are around 80 mg/dL (milligrams per deciliter). If you get below 50 or so, you can end up in a coma, which is bad; that is what happens to type I diabetics if they get too much insulin. If you get above about 215, you need to seek medical attention, and above 300 is an immediate risk. And moderately high levels on an ongoing mean that you have type II diabetes.

      Thing 2: The quantity of glucose in the bloodstream is small

      How much glucose is in the blood? Knowing that an average fasting blood glucose is 80 mg/DL and  that the average adult has about 5 liters of blood in their bloodstream – 50 dL – we can do some very simple math:

      glucose content of blood = 80 mg/dL * 50 dL = 4500 mg = 4 grams

      How much is that? About this much:

      Image result for sugar cube.

      One small sugar cube. There is a *tiny* amount of glucose in the bloodstream.

      The small range of normal blood glucose levels plus the small amount of glucose in the blood means that even a modest amount of glucose coming in from the outside could have a huge effect on blood glucose levels; a mere 4 grams of glucose would double the blood glucose level if there were no mechanism to deal with the extra glucose. The body therefore devotes significant amounts of machinery to try to keep blood glucose constant.

      Blood glucose level is regulated by the pancreas. As the cells of the body pull glucose out of the blood, the level drops, and the pancreas releases the hormone glucagon. The glucagon signals the liver to release some of its stored glucose into the blood stream to bring the blood level back to normal. The liver can store about 100 grams (400 calories) of glucose, which it stores as glycogen. If the liver glycogen stores are chronically low – if you aren’t eating many carbs on an ongoing basis – the liver can make glucose from other compounds – like lactate, the glycerol from triglycerides, and some amino acids from protein – using process known as gluconeogenesis – and it can also switch some tissues to use ketones rather than glucose to reduce the required amount. If you aren’t eating anything – if you are fasting or starving – your body can still make the carbs you need.

      Low blood sugar is the less interesting case, because the body is (generally) quite capable of dealing with it. The more problematic part is high blood glucose…

      If you eat something with carbs, as they are digested you will end up with glucose coming into the bloodstream. The pancreas detects the raised blood sugar, and starts releasing insulin, which is a signal to other tissues to do their best to pull glucose out of the blood. There are 3 main effects from the elevated insulin:

      First, the burning of fat is minimized so that as much glucose can be burned as quickly as possible. The more glucose being pulled out of the blood, the less the blood glucose level will rise.

    5. Second, the liver will start pulling glucose in and storing it as glycogen, as long as it has space. The muscles will also start pulling glucose in if they have space to store it, and the muscles can store around 400 grams (1600) calories. Conversion from glucose to glycogen is quick and there are a lot of liver and muscle cells, so if glycogen stores aren’t full, the glucose will quickly be pulled into those cells, and blood sugar won’t get very elevated. But compared to fat, the storage is quite limited, and it’s very rare that glycogen stores are low; muscle glycogen is only burned through activity, so it’s generally only the liver storage that is in play, so there’s often just not much space to store glycogen. 
    6. The third effect happens if the liver and muscle glycogen stores are full. There is no easy place to store the glucose but it’s still coming in from the digestive system, so the blood glucose level goes higher and the pancreas releases more insulin. There is only one place for this excess glucose to go, and that is fat, so the liver and the fat tissue pulls in glucose and converts it to fat. This is slower than the conversion to glycogen, so the elevated blood sugar and insulin levels persist for a few hours.

      Because that it is highly important to keep blood glucose low and limited storage space, there is a fundamental asymmetry between the fat and carbohydrate storage systems, and that asymmetry drives a lot of the physiological response.

      The big upshot of this – the reason I’ve talked so much about the underlying biochemistry – is that the two big effects of lots of carbs are a) converting excess carbs into fat and b) turning off fat burning while that process is happening. If you’ve ever “carb loaded”, you deliberately put yourself into this situation. It *does* push a little more glucose into your glycogen reserves, but most of the excess carbs just go straight to fat. Will they stay as fat? Well, that question will be covered in a future post…

      Insulin Resistance and type II diabetes

      It seems like an appropriate point to talk about what is different for people who have insulin resistance or type II diabetes.

      The previous explanation is how it works if you are metabolically healthy – if you don’t have insulin resistance / type II diabetes.  Here’s a graph:

      The normal person sees just a small spike of glucose and it quickly returns to normal, the pre-diabetic sees a spike and then a drop afterwards (this is likely not true for all pre-diabetics), and the type II diabetic starts with an elevated glucose level and a meal just spikes it way up.

      Part of what we are seeing is that the liver and muscles become less willing/able to absorb glucose out of the bloodstream, so it takes longer for the blood glucose to return to normal. When we get all the way to type II diabetes, there is something else going on. Earlier I talked about the process to deal with low blood glucose by converting liver glycogen to glucose. This normally only happens when blood glucose is low, but insulin resistance messes up the machinery that controls this, and the liver will release glucose even when glucose is normal or elevated. That is why the blood glucose is chronically high.

      The result is that those who are insulin resistant have chronically elevated levels of glucose and insulin, and since we know that elevated insulin reduces fat burning, they find it very hard to burn fat.

      Insulin resistance is not a binary thing, and it’s possible to be a little insulin resistant and not have it show up in standard tests. It is not confined to people who are overweight; it is possible to be insulin resistant and have a normal body weight.

      Summary

      Protein and fat digestion and storage are pretty simple, but because of the limited storage available for carbs, excess carbs just get stored as fat.

      Now that we’ve gotten that fat and glucose stored, in the next post we’re going to talk about how those are used by the muscles.

      Appendix

      This section contains some related information that isn’t necessary for the discussion but may be of interest…

      Protein and insulin

      I glossed over the relation of insulin to protein earlier in the post, but it comes up often enough I thought it was worth covering here.

      Insulin is a multipurpose storage hormone; not only does it signal the body to store glucose, it also signals it to store protein.

      But how can that work? Let’s perform a little thought experiment:

      We eat a high protein meal and the pancreas secretes insulin. That would cause the amino acids from the protein to be absorbed, but it would also tell the liver, muscle, and fat cells to pull glucose out of the bloodstream, and would therefore cause the blood glucose to plummet.

      Which would be bad.

      This is one of the simplifications that I made to keep things simpler. It turns out that the liver, muscle, and fat cells are not sensitive to the amount of insulin in the blood but rather to the ratio of insulin to glucagon in the bloodstream. Here’s a graph for what happens after a carbohydrate-rich meal:

      Image result for insulin glucagon protein meal

      Notice the inverse relationship between the insulin and glucagon values; this will move the insulin/glucagon ratio much higher so the glucose will be absorbed.

      Here’s what happens with a protein-rich meal:

      Image result for insulin glucagon protein meal

      There is a small insulin spike from the protein, but a large glucagon spike. That keeps the insulin/glucagon ratio low and blood glucose constant.


      Passport2Pain 2018

      This is my third attempt at the “Idiot Level” Passport2Pain course, and my third completion (2013, 2016, and 2018). In 2016 I left my GPS at home and apparently didn’t bother to write anything up, so any comparisons will be to 2013.

      My wife and I went over Friday afternoon to have dinner with and stay at the house of one of our ski instructor friends, who very conveniently lives 15 minutes from the starting line. I slept poorly as is my usual before big rides, but got up, skipped breakfast, and we headed over to the starting point.

      After the usual wait and ride introduction (“In thinking about fundraisers, we had an idea. It wasn’t a *good* idea, but it was an idea…”), we queued up to start. They start with 4-5 riders every 30 seconds or slow to spread the riders out. Contrary to the pre-ride description, they made no effort to actually send out the idiot (80 mile) route riders first; I knew to line up near the front but I would have been upset if I had to wait 40 minutes to start. Considering the difference between the two routes is well over two hours, they need to do better at this.

      We pedaled away from the start at Jensen Point, which is on this weird little spit. I started talking with a guy in a t shirt, jersey, and cutoffs; he had forgotten his clothes. He pulled ahead and took the first turn to exit the park area and immediately pancaked on this left side.

      It had, you see, rained the night before and it was 57 degrees and cloudy. So there was still a bit of moisture on the road, and likely a bit of oily film.

      He was fine and we rode off to start our quest, and I made a mental note not to ride too near to him – or any other riders – while the roads were wet.

      I generally describe P2P as riding all the way around Vashon island and taking every road that goes down to the beach.

      image

      That is hyperbole. There are, in fact, numerous hills that will will not ride down, but we will ride down a large number; overall, there are 25 climbs on the ride, most of which are in the 200-300’ range, plus a bunch of small hills and rollers. If you are doing a ride like RAMROD, there are really only 3 hills (Paradise, Backbone ride, and Cayuse), and that’s how you track your progress. On P2P they do have checkpoints where you get your passport stamped, but there are 18 of them.

      My approach is to just ride; I know what the parts are, and I know that I need to ride slow because the last set of hills is pretty bad.

      So, we head off, do a short climb, and then descend down to the first real climb, which is a weird down and up. And quickly run into our first issues.

      We roads and steep climbs do not mix. Going down you can just take it easy, and even with disc brakes I’m taking it easy on the still wet roads. The problem is when you start having to go up again. I can sit and ride up a 15% hill pretty easily and tough out a 20% hill, but it’s nice to be able to stand. Except if you do that, your rear wheel spins up. Which is bad. So, you just need to sit and suffer.

      The first 5 stops go by pretty fast; slow and careful on the descent, and then doing my best on the climbs to stay smooth and keep calm. This part of the ride is the warmup, though it’s a little nuts that the warmup has 8 main climbs and 2500’ of up over the first 25 miles. We then have 5 miles with a climb or two, and then turn off onto Burma Road.

      Burma is a mostly paved goatpath that rolls up down and around; they laid asphalt with doing as little grading as possible. Burma has one easy climb – say 13% or so – and then two hard climbs. They are aren’t very high, but they are well in excess of 20% (my GPS said 27 but I really don’t think they are quite that bad). The general way to attack Burma is to be able to ride slowly – say 3MPH – while standing, and if traffic permits, do a slight weave back and forth. It’s not categorically different than “The Widowmaker” in Sufferin’ Summits, and it’s quite a bit shorter, though it’s barely one lane wide.

      That is what I did on two previous rides, but Burma is fully shaded and quite wet this year. After spinning the rear up despite being really gentle, I just ride slowly and muscle my way up. Not fun at all and I’m stressing my legs much more than I hoped, but it’s either that or just fall over (I don’t think I could unclip and stop), so I ride up both pitches apprehensively and then get to meet the devil.

      Almost directly after, there’s another hill with a torn up descent at the bottom where you can barely stop and an ascent where you can’t stand, but that’s par for the course. Later this same hill has a solid 20% section, but luckily that pavement is dry and a real road so you can tack/paperboy back and forth and stand if you want to.

      There’s one more loop down to the water, a spin along the main highway, and we hit the lunch stop.

      I’ve been snacking a bit along the way; I have some nuts and I’m eating small amounts of carbs, and that’s working great except for 5 peanut M&Ms that give me a knot in the stomach.. At this point, I’m pretty tired and deciding whether to do the 55 mile or the 80. I eat the fillings of a very forgettable BLT and a bit of bread and then stop at the Thriftway for a Coke Zero but am stuck with a Diet Coke.

      I mean, seriously, what are they thinking?

      I text Kim to let her know where I am (she is doing a ride into the village for coffee) and tell her I’m 50/50 on which variant I will do and I’ll text her when I decide.

      I roll out. There’s a small and ugly climb on the next section, but this one is dry and I’m feeling decent until my right hamstring starts to cramp near the top of the hill. I stop, dig some electrolyte capsules out of my pack, and wash them down. Then it’s off to Evil Twin #1 and #2. They really aren’t that bad and I’m climbing a bit better after food and Diet Coke. The second stop has chips and guac, and I have a few, heavy on the Guac.

      And that’s all the hills on the 50 mile/6500’ route, so I need to make a decision. My toes and left shoulder hurt a little, but my legs are feeling okay, so I stop to text Kim and press on, onto Maury Island, and get ready to grit my teeth. Because as tough as the Burma Road section is, this section is a real bastard. It looks like it won’t be that bad – there are only 5 stops – but it’s a full 30 miles and over 3000’ of up.

      We work our way through 14, and then descend down to 15. This has the added pain that as I near the stop, I ride by our friend’s house and out in front my Outback is parked, with a perfect bike-shaped space in the back, beckoning to me. I manage to avoid the temptation, but man, the hill out is a major bitch, and I’m tacking back and forth for all I am worth. And it’s not like I’m getting passed much, since all the fast people are in front those near me are bound together in a brotherhood and sisterhood of suffering and pain.

      On the plus side, I’ve had no more cramping issues, so there is that.

      Then there’s an ugly descent, and we ride into Dockton. We have three stops left, so three hills, right? How bad could that be?

      I hate Dockton. We are down right at the water, but we climb 300’ up to the top of the island, and then we descend all the way to the water down yet another sketchy, wet, and slightly mossy road. For a measly stamp on our passports. Then we climb out that same damn hill, though the way from the water is worse.

      And then – and this is the wonderfully terrible part of this ride – we do it again. Climb 200’ up into the hills, all the way down to the water, collect our penultimate stamp, and then it’s another 250’ climb back to where we started.

      And the pain of Dockton is over. At this point I’m feeling pretty good; I *know* can finish the last hill, and then there are only a few rollers after that. I ride up a 150’ uncategorized hill – I mean really, it’s only a 7% and it feels very easy – in company with another rider, and I form a plan.

      There is only one hill left and my legs feel like they have a little something left. So, we come to the last hill – 330’ of fun or so – and I start climbing hard, which is somewhere between 230 and 280 watts as the hill steepens and eases (my earlier target was <200 watts if I could). My data shows that I’m 43 seconds faster than my 2013 ascent – a full 9% faster. I get to the top, have a little bit of popcorn, and spin out to finish the ride.

      The way back is about 4 miles with only a few rolling hills, so I push my speed up a bit. And then, finally, I finish, and get to have some well-earned barbecue with my spouse. It’s pretty good in the “Puget Sound Barbecue” category, but the brisket needed another couple hours in the smoker.

      Analysis

      Strava says I pulled 12 PRs on the route, and 9 of those were on hills. That makes me pretty happy, and I felt strong for most of the ride. It’s so much nicer and prettier than Sufferin’ summits.

      Stats:

      80.81 miles
      7:11:46 riding time
      9,949’ of up
      11.2 mi/hr average

      How does that compare to 2013? Well, in 2013 I rode 1.5 miles farther, which was probably due to more back-and-forth across the road, and finished in 7:13:27. My average speed then was 11.4 mil/hr, faster than this year, but my speed on descents was at least 25% slower than before because of the wetness.

      2013’s ride was done on my Trek Madone, a fine bike for making speed but it was pretty harsh on the crappy Vashon roads. This year I was on my Roubaix with disc brakes, a frame tuned to soak up vibration, shocks in the seat and steering head, and 28mm tires at 80 psi. It was gloriously better; the stuff that really would have beat me up last year was still annoying but not too bad.

      image


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