I'm not fat, just fatish. I've bonked, then puked, then kept on riding. Not smart enough to stop.

 

Reason I ask (like you couldn't tell ) is that I have never bonked, that I know of anyway. I've been really tired before and have even had to stop riding because of severe leg/calf cramps but never to the point of complete exhaustion and that's what I imagine bonking is, complete exhaustion.
I've always been curious if it was because of my fat reserves or if I wasn't riding hard enough.

Thanks.
Lou.

Yes. I'm pretty fat for MTB racer and I bonk as everyone else
Fat is not used too much 'cos it's "slow" fuel. It gives you a lot of energy but it also requires a lot of energy to break down fat to glycogen.

 

Bonking is a large decrease in blood glucose levels due to glycogen depletion, a fat person doesn't store anymore glycogen than a skinny person.
Bonking isn't so much complete exhaustion. When it's happened to me, I get an increase sense of effort and an inability to go as fast as I was riding. Also, since brain cells run on glucose, when your bonk there are often mental signs such as dizziness, light-headedness, inability to think clearly, etc.

 

When you bonk you'll notice cause you can't go as fast, as Dwayne said. If you don't ride very fast to begin with, you probably won't notice. I have definitely noticed it during racing. In the last race I bonked and later on looking at the output from my heartrate monitor I noticed a 10bpm drop in average when I did. But that's riding at 100%, I don't notice it when I ride at trailriding pace.

 

having alot of fat and being able to efficiently break down fat for energy are two different things. Generally being in good endurance shape coincides with a more efficient fat metabolism. The the irony is that skinny guy/gal in great shape doesn't have as much fat to draw from and is more suseptible to bonking.

 

I bonked last Sunday.

But that was completely my fault.....only thing I ate was a Mars bar. That was dumb.

 

Hoping to...

I'm hoping to tonight but I'll have to ask my wife 1st...oh sorry, wrong topic.

P.S. I have no idea what you're talking about when you refer to "bonk..ing".

 

you would know when you bonk...

Anyone can bonk. I think I had read that even the skinniest marathon running has enough fat energy on their body to run 40 marathons.

The problem is you rarely use only fat and you would have to be going very sllloooowww to do it. The average person can make it about 3 hours with no food on a hard ride before bonking (running out of blood sugar).

I bonked on mile 30 of a century after getting no breakfast. It was awful, I remember my friends riding away from me and there was just no way to catch up. Next thing I know I had major tunnel vision. I finally stopped at a gas station when a 60-ish old lady with streamers passed me on her mountain bike and I watched her ride away from me.

I picked up fig newtons, coke, and a bunch of other stuff. I packed my pockets full, but even then the rest of the ride was a nightmare. My legs felt like they were breaking on the hills, I had no power to accelerate, and I was very slow.

The weird thing you will notice is that your liver will produce glycogen en route, but definitely not enough. I would feel great for 10 seconds and then it would all be gone again. The only way to recover from a bonk is to quit riding and hope you haven't set yourself back a week.

 

Anyone can bonk. I think I had read that even the skinniest marathon running has enough fat energy on their body to run 40 marathons.
QUOTE]

You may be right, let me retract that lower bodyfat % people are more susceptible to bonking till I find better proof/info. ( I still beleive its true for lower intensity endurance events ).

... the 40 marathons thing... considering a pound of fat yeilds ~ 3500 calories, I can see where that comes from... I'm not sure if it means its all expendable fat.

 

Thanks for the replies.
Pretty scary because I've experienced light-headedness a few times but I chalked it up as riding at too high a HR and not having O2 for my brain.
In everyone's experience, do those mental signs (light-headedness, etc.) come before the other physical signs?
Lou.

 

usually

In everyone's experience, do those mental signs (light-headedness, etc.) come before the other physical signs?
Lou.

I once read a study, I'm not sure who would have signed up for this (probably poor college students), where they had people ride until they bonked or complete failure. At that point they hooked up the electrostimulator to their muscles and they kept contracting for a long time.

I think the conclusion was that bonking starts in the brain, it's your brain telling you to stop and not necessarily you being completely out of gas, but getting close. It's amazing to think that just your brain uses 33% of your glycogen at any given time while out riding.

At any rate, you don't want to bonk... not only does it suck, but you will feel bad for a week afterwards and lose training time.

I heard an interesting analogy today about heart-rate training. Basically once you hit zone 4 it's like opening a valve at the bottom of your fuel tank and letting all the energy fly out. Lower intensities burn a mix of sugar and fat, once you get up to where you are breathing like crazy and hammering it's all blood sugar baby! And the by-product of glycogen synthesis (blood sugar burning) is our good old friend lactic acid, the feeling like your legs are breaking and locking up.

 

In everyone's experience, do those mental signs (light-headedness, etc.) come before the other physical signs?
Lou.

I usually notice the mental signs first. My wife can tell when I'm starting to bonk, because she'll ask me a question and there will be about a 2-3 second pause before I answer. Kind of funny...

bock

 

Thanks for the replies.
Pretty scary because I've experienced light-headedness a few times but I chalked it up as riding at too high a HR and not having O2 for my brain.
In everyone's experience, do those mental signs (light-headedness, etc.) come before the other physical signs?
Lou.

FWIW I'm diabetic, and based on my experience yes and no. Light-headedness is usually the first sign of low blood sugar (followed by shaking, then cold sweats), it's a good hint to eat some carbs, and if you do, after 10-20 minutes you can actually feel fine again (leg power restored), if low blood sugar was the only problem. When I've really bonked in the past I usually didn't have much warning until the legs shut down. True bonking as I understand it is fully depleted muscle glycogen, and is usually caused when exercise intensity is above the "fat burning" zone (3 or 4?) for around 2 hours or more, without enough (or any) carb intake. You may have noticed that even if you eat some carbs at that time (raising blood sugar) the bonked (dead muscles) effect could take some time to go away.

 

On a certain level you need to be in good enough shape to bonk. This is a generalization, but if you want to bonk, try not eating for five hours then go out and ride hard and don't drink water. Stay close to phones and streets and also carry several candy bars and some gatorade when you try this.

I have never bonked and I ride for two or more hours sometimes three times in a week. I always try to eat an hour before I leave (food in your stomach competes for the blood you need to pedal and move oxygen) and start drinking water several hours before. Then I carry some gatorade and some fruit to eat an hour or so into the ride.

I have felt light headed, but I immediately start eating and drinking if that happens, plus slow down or even stop for a bit.

 

Absolutely. In my experience it's mostly a matter of blood sugar levels dropping too low (I used to forget to eat for hours until I was shaking and weak - and once I hit that point I was done, no matter what I ate - I'd just be on a death march to get back to the truck). I've started eating half an energy gel pack every 30 minutes and haven't bonked since. I've been losing weight faster this way too, because it keeps my energy level and endurance up so I can ride harder and longer.

And yes, my mental signs (light-headedness) come before physical signs. I've found the more I stay ahead of it, the better I can ride.

 

Hers a pretty good article about bonking from ( http://www.medicdirectsport.com/athletictraining/default.asp?step=4&pid=59 )

Energy Sources In Prolonged Exercise
The term prolonged exercise is usually used to describe exercise intensities that can be sustained for between 30-180 minutes. Adenosine triphosphate (ATP) is the only source of energy that can be used to directly fuel muscle contraction. The body has three principal means of regenerating ATP:

Through breakdown of the limited muscle stores of phosphocreatine (PCr).

Through breakdown of muscle glycogen and the subsequent conversion of glucose-phosphate to lactate without the use of oxygen (glycolysis).
From the complete oxidation of carbohydrates and fat, with a small contribution from the oxidation of protein.
Both (1) and (2) occur without the use of oxygen and so are described as anaerobic processes, whereas (3) requires the use of oxygen and so is described as aerobic metabolism. Since the rate of ATP demand is relatively low in prolonged exercise compared with high intensity exercise PCr, carbohydrate and fat can all contribute to energy production.

The rates of PCr degradation and lactate production during the first few minutes of prolonged exercise are closely related to the intensity of exercise performed, and it is likely that energy production during this period would be compromised without this contribution from anaerobic metabolism. However, once a steady state has been reached, carbohydrate and fat oxidation become the principal means of resynthesising ATP.

Metabolism Of Carbohydrate And Fat
Muscle glycogen is the principal fuel during the first 30 minutes of exercise at 60-80% of the maximal oxygen uptake (VO2max). During the early stages of exercise, fat oxidation is limited by the delay in the mobilisation of free fatty acids (FFA) from adipose tissue.

At rest following an overnight fast the plasma FFA concentration is about 0.4 millimoles per litre (mmol/l). This is commonly observed to fall during the first hour of moderate intensity exercise, followed by a progressive increase corresponding with the breakdown of fat (lipolysis), which is stimulated by the actions of hormones including adrenaline, glucagon and cortisol. During very prolonged exercise, the plasma FFA concentration can reach 1.5-2.0 mmol/l and muscle uptake of blood-borne FFA is proportional to the plasma FFA concentration.

The glycerol released from adipose tissue cannot be used directly by muscle. However, glycerol (together with alanine and lactate) is taken up by the liver and used to form glucose in a process called gluconeogenesis. This helps to maintain liver glucose output as liver glycogen levels decline. The utilisation of blood glucose is greater at higher workrates, increases with exercise duration during prolonged submaximal exercise and peaks after about 90 minutes. The decline in blood glucose uptake after this time is attributable to the increasing availability of plasma FFA as fuel and the depletion of liver glycogen stores.

Hitting The Wall
At marathon running pace muscle carbohydrate stores alone could fuel about 80 minutes of exercise before becoming depleted. However, the simultaneous utilisation of body fat and liver carbohydrate stores enables ATP production to be maintained and exercise to continue. Ultimately though, ATP production is compromised due to muscle and hepatic carbohydrate stores becoming depleted and the inability of fat oxidation to increase sufficiently to offset this deficit. This is the point in the race that some athletes describe as "hitting the wall". The rate of ATP resynthesis from fat oxidation alone cannot meet the ATP requirement for exercise intensities higher than about 50-60% of the maximum oxygen uptake (VO2max). It is currently unknown which factor limits the maximal rate of fat oxidation during exercise (i.e. why it cannot increase to compensate for carbohydrate depletion), but it must precede acetyl-CoA formation as from this point fat and carbohydrate share the same fate. The limitation may reside in the rate of uptake of FFA into muscle from blood or the transport of FFA into the mitochondria rather than in the rate of oxidation of FFA in the mitochondria.

The glycogen store of human muscle is fairly insensitive to change in sedentary individuals. However, the combination of exercise and dietary manipulation can have dramatic effects on muscle glycogen storage. A clear positive relationship has been shown to exist between muscle glycogen content and subsequent endurance performance. Furthermore, the ingestion of carbohydrate during prolonged exercise has been shown to decrease fat mobilisation and oxidation, and to increase the rate of carbohydrate oxidation and endurance capacity. It is clear, therefore, that the contribution of orally ingested carbohydrate to total ATP production under these conditions must be greater than that normally derived from fat oxidation. The precise biochemical mechanism by which muscle glycogen depletion results in fatigue is presently unresolved. However, it is plausible that the inability of muscle to maintain the rate of ATP synthesis in the glycogen depleted state results in ADP and phosphate accumulation and consequently fatigue development.

Hypoglycaemia And Central Fatigue
Unlike skeletal muscle, starvation will rapidly deplete the liver of carbohydrate. The rate of glucose release from the liver in resting post-absorptive individuals is sufficient to match the carbohydrate demands of only the central nervous system. Approximately 70% of this release is derived from liver carbohydrate stores and the remainder from liver gluconeogenesis (synthesis of glucose from amino acids, glycerol and lactate). During exercise, the rate of liver glucose release is related to exercise intensity. Ninety per cent of this release is derived from liver carbohydrate stores, ultimately resulting in liver glycogen depletion. Thus, carbohydrate ingestion during exercise could also delay fatigue development by slowing the rate of liver glycogen depletion and helping to maintain the blood glucose concentration. Central fatigue is a possibility during prolonged exercise and undoubtedly the development of hypoglycaemia (low blood glucose concentration) could contribute to this.