Biochemical Strategies for Ultrarunning—Draft Version
Print E-mail
Written by Bruce R. Copeland, PhD   
Wednesday, 14 May 2008 15:49
Article Index
Biochemical Strategies for Ultrarunning—Draft
Page 2
Page 3
Appendix A: The Biochemistry of Muscle Contraction
Appendix B: The Biochemistry of Nerve Signaling
All Pages

In recent years, long distance runners have seen significant improvements in training techniques, general nutritional approaches, and gear—particularly footwear. Nevertheless in races (especially at distances of 50 miles or more) most ultrarunners continue to confront the same old challenges: muscle cramps, fatigue, stomach distress, and blisters. Indeed the idea persists—both in the general public and amongst ultrarunners—that ultrarunning is all about suffering. This article is an attempt to dispel that myth by explaining how ultrarunners can avoid or minimize these challenges through an understanding of some relevant biochemistry. Certain approaches advocated here are not entirely new—what is new is an attempt to help ultrarunners grasp why these approaches work and the biochemical/performance consequences of ignoring them.

Aerobic Exercise—It's All About the Mitochondria

Mitochondria are the intracellular powerhouses for most of our cells. They convert oxygen and fat or carbohydrate into ATP and specialized ion gradients. They play crucial roles in nerve and aerobic muscle cells, which continually require large amounts of ATP for function (see Appendix A: The Biochemistry of Muscle Contraction and Appendix B: The Biochemistry of Nerve Signaling.) In fact, an increase in the number and size of muscle mitochondria is one of the primary results of aerobic exercise training [McArdle WD, Katch FI and Katch VL (1996) Exercise Physiology: Energy, Nutrition and Performance (4th ed.). Philadelphia: Lea and Febiger; O'Toole ML and Douglas PS (1995) Applied physiology of triathlon. Sports Medicine 19:251-267, Tanaka H (1994) Effects of cross-training. Sports Medicine 18: 350-339]. The process of converting carbohydrate or fat and oxygen into ATP is a biochemical oxidation/reduction cycle that can be repeated reliably again and again as long as there are adequate supplies of everything needed for this process. It is fundamentally an oxidative process, so if something is not present in sufficient amount, the mitochondria may undergo oxidative damage, and any significant oxidative damage typically leads to mitochondrial destruction.

So what are the main things that mitochondria need for this process? Mitochondria can themselves produce or assemble most of the necessary proteins. They rely, however, on external sources of fat, carbohydrate, and certain electrolytes, as well as a pool of quinone molecules that mediate a critical step in the oxidation/reduction process. It follows that insufficient carbohydrate or carbohydrate and fat energy, insufficient electrolytes (for the mitochondria or their parent cells), or an inadequate quinone pool are the three things most likely to lead to mitochondrial oxidative damage and destruction.

You may at this point be thinking: "So what's the big deal if I kill off a few of my mitochondria? My body can make more." You are correct; your body will make more. The problem is that your event will be over before your body accomplishes that. Actually, you probably already know this if you have ever run a 50 or 100 mile race and developed muscle soreness during the race. Muscle soreness is one indication of mitochondrial destruction. Has that muscle soreness ever gone away before the end of the race? You spent weeks or months building up your mitochondria through training. Why destroy some of that halfway through an event?

In fact, there is an interplay between damage to mitochondria and damage to parent muscle and nerve cells. On the one hand, a lot of things can go wrong in muscle and nerve cells, and most of them can be repaired as long as the mitochondria in those cells are healthy. However, electrolyte imbalances make nerve and muscle cells inefficient, thereby stressing the capabilities of their mitochondria. As mitochondria begin to fail, they leak significant amounts of calcium into the cytoplasm, they no longer support the generation of proper action potentials in nerve and muscle cells, and they fail to protect their parent cells against oxidative damage. When enough mitochondria in a cell are damaged, the parent cell itself is programmed for destruction.

Mitochondrial destruction causes decreased performance. Directly or indirectly it leads to muscle cramps, and ultimately to mind-numbing fatigue. Conditions that produce mitochondrial destruction in muscle cells also cause mitochondrial destruction in the other cells of our body. So we don't just develop cramps and muscle fatigue, we also lose the ability to think clearly. It follows that one of the most important things we can do as endurance athletes is to avoid carbohydrate, electrolyte, and quinone depletion.


 
Comments (1) Comments are closed
Draft
1 Wednesday, 15 October 2008 15:17
Bruce Copeland
Due to popular demand, I have posted a draft version of this special topics article. References and figures remain to be completed, but the meat of the article is here for those of you who are desperate.

Bruce Copeland