Written by justis berg
04 December 2010

Muscle Mutants I: Mega Glycogen & Nano Lactate

 

“I need a walker!” My gym buddy rarely complained, but two to four days after squats, he whimpered like a frightened puppy. “I feel like the lactate in my quads won’t leave me alone— like I’m being stalked!” he embellished. With that last statement my ears opened up, tuning into the “L” word and my long-standing love affair with it since grad school. “Sam, you’re a medical doctor. Have you ever heard of McArdle’s disease?” I asked. “Yeah… kind of… it’s a muscle disease,” he volleyed back, “but I don’t recall what the problem is.”

It was time for a “clinic” on muscle metabolism, and McArdle’s is such a fascinating disease for anyone into nutritional and exercise biochemistry— unless you have it. “Come on,” I said as we were walking (hobbling, for Dr. Sam) off the gym floor, “I’ll buy the protein/carb drinks.”

McArdle’s disease is a RARE one: if you have 100,000 friends on Facebook, chances are that no more than ONE would have it. It was first described almost 60 years ago.1 For the person with McArdle’s, they have ONE muscle feature that some athletes would gawk over: about TWICE the muscle glycogen content of a person without McArdle’s eating a medium carbohydrate content diet. Why? They are unable to break muscle glycogen down during muscle contractions. The other side of the sword is far sharper: with an inability to break down muscle glycogen (they CAN break down LIVER glycogen, that’s why they don’t die at a very early age…) their ability to perform intense exercise, or endurance exercise, is limited. QUITE LIMITED.

I shared this background with Dr. Sam, and I could see in his eyes that it was coming back to him. “The last time I heard this was in my Clinical Neurology rotation in medical school,” he said. “Sam— now here’s the very cool thing about being unable to break down muscle glycogen: a person with McArdle’s is essentially unable to form lactic acid/lactate during exercise. In fact, their muscle lactate and acidity actually can go DOWN during intense exercise…” I emphasized, “and yet DURING training they feel the burn and the pain just like you and I do.”

He was visibly perplexed as he harvested a question that had been brewing for a few minutes. “So they can still do some exercise, right, but really intense exercise, like how we trained chest and delts today, they couldn’t do that?” I nodded my head. “If you had McArdle’s,” I added in, “it would feel like this when you’re benching: 1 rep, 2, 3, 4, 5, 6 reps… if I was spotting you I would get in position and ever so lightly wrap my hands around the bar… 7 reps… put a fork in you— you’re DONE. No partial rep that I could help you on. You probably wouldn’t have any ‘warning’ that you couldn’t do one more rep, let alone even a partial or a negative. The metabolic light switch was flipped off, no gradual dimmer feature here. You would hit the wall and wouldn’t even know it until it hit you.”

“That says a lot about muscle glycogen, then, in terms of it being critical to support the energy demands of intense training,” he offered. “And to the first part of exercise, when you’re just beginning,” I added.

The doctor was now in the house: “Hold on. What about creatine/creatine phosphate, D-ribose, or even branched-chain amino acids— aren’t those muscle fuel sources during intense training?” A good question indeed, and then he added, “One would expect at least one of them to pick up the slack if glycogen couldn’t be broken down into glucose and burn through lactate to generate ATP. And all the buzz about branched chains being a critical fuel source for muscle during exercise, THEY should work!”

“Easy Doc,” I calmly stated. “ALL of those have been tried in McArdle’s— and all have essentially failed,2-4 although there is some OK evidence behind low-dose creatine5 but HIGH-dose creatine, in the amounts we usually ‘load’ with, makes it WORSE.4 This suggests something: if you can’t break down muscle glycogen, and supplementing with other ‘secondary’ fuels or fuel precursors doesn’t make a dramatic difference, then what role DO they have in muscle energetics DURING intense training if you CAN break down glycogen?”

He paused while his brain’s hard drive spooled up to a frenzied speed. “What about carbohydrate supplementation?” he blurted out. “Ah, Grasshopper, you have snatched the pebble from my hand,” I said smilingly. “You nailed it. If you can’t break down muscle carbs— glycogen— to deliver glucose to contracting muscle cells, and rapidly-available glucose burning as a fuel drives intense exercise and the start of exercise, then providing glucose from other sources SHOULD make a difference. Is that what you’re asking?” I offered. “EXACTLY! DOES IT?,” he said, almost as if he was trying to pick a fight with me.

“EXACTLY, IT DOES,” I replied, as the intensity from his face was replaced by a satisfactory smile. “Earlier studies had used intravenous glucose in McArdle’s and found a true increase in exercise capacity6,7, but delivering glucose to the blood via a needle produces a totally different hormonal response than from EATING carbs. Good ol’ sucrose— white sugar— was then tested and it, too, improved exercise capacity in McArdle’s.7

“Another study had a person with McArdle’s use a high-carb meal (pasta, rice and bread) an hour before running and over time, he was able to run for up to 60 minutes— but no more.8 Lastly, high-protein diets did not improve McArdle’s exercise capacity but high-carb diets did.9 McArdle’s shines a very different light on muscle metabolism and muscle fuel selection,” I concluded.

“So carbohydrate DOES appear to be the primary fuel we use when we train,” he conceded. “All of the guys in the gym complain about feeling no motivation before they train when they’re low-carbing, and they can’t train as hard and as long, either. And persons with McArdle’s don’t make lactate during exercise… ” He tried to continue, but I cut him off like a road rage-fueled driver trying to get to the first spot in line at the traffic light. “And like you— Dr. Cripple— they experience muscle soreness DAYS after exercise. Think it’s time to drop the lactate and soreness ‘stalker’ and get a REAL date,” I concluded.

 

References:

1. McArdle B Clin Sci, 1951;10:13-33.

2. MacLean DA, et al. Neurology, 1998;51:1456-9.

3. Vorgerd M, et al. Arch Neurol, 2002;59:97-101.

4. Steele IC, et al. J Neurol Sci, 1996;136:174-7.

5. Vorgerd M, et al. Arch Neurol, 2000;57:956-63.

6. Vissing J, et al. J Appl Physiol, 1992;72:1773-9.

7. Vissing J, et al. N Engl J Med, 2003;349:2503-9.

8. Pérez M, et al. Br J Sports Med, 2007;41:53-4.

9. Andersen ST and Vissing J. J Neurol Neurosurg Psychiatry, 2008;79;1359-63.