Response Ability Update

The American Athletic Institute has asked Dr Thomas Balon, (a worldwide authority in muscle metabolism) and former editor of Exercise and Science in Sport, to overview our present studies with an explanation of the effects of alcohol at the metabolic level.  (see Dr Balon’s Bio below)

From:  Dr. Thomas Balon

John Underwood has solicited me to provide a rationale for explanation of the deleterious effects of acute alcohol consumption on athletic performance. In my answer, I have attempted to present a brief overview, which is hopefully comprehendible to the layperson yet comprehensive to those who want more than a superficial overview. For the convenience of the lay reader, I have provided the definition of some of the terms in parentheses.

First of all, one must consider the contribution of ethanol, the commonly ingested form of alcohol as a substrate (a metabolic fuel), its site of metabolism, and its effects on different organs.

Ethanol is not a carbohydrate, which can be used directly by skeletal muscle as a fuel for muscle contraction thus its value as an energy source is negligible. Furthermore, it is not a gluconeogenic precursor (a molecule, which can be converted into carbohydrate). But since its metabolic degradation (catabolism) occurs primarily in the liver, it will have an effect on multiple organs including skeletal muscle. The liver is the site of specific enzymes (proteins, which are biological catalysts), which include a) alcohol dehydrogenase, b) microsomal ethanol-oxidizing system (MEOS) and c) catalase which facilitate the catabolism of ethanol to acetaldehyde. However, upon the activation of these enzymes with the increase in ethanol consumption, a number of unwanted side effects occur.

When alcohol dehydrogenase is activated by the ingestion of ethanol, there is an increased conversion of nicotinamide adenine dinucleotide ( NAD+) to another form, NADH. When the ratio of NADH to NAD+ increases, there are multiple metabolic consequences, which include increased rate of glycolysis with a concomitant decrease in the rate of gluconeogenesis. Glycolysis, which is the breakdown of glucose in the absence of oxygen is metabolically inefficient as compared to the breakdown of glucose in the presence of oxygen. In addition, as a result of glycolysis, there is a net accumulation of lactate which results in a metabolic acidosis.

 With an impaired gluconeogenensis, (which is a series of reactions, which can catalyze the conversion of lactate to glucose, there is no mechanism either for removal of lactate or the replenishment of blood glucose thus hypoglycemia and cessation of muscle contraction occurs. Since ethanol must compete with a number of different compounds for MEOS, a compromised capacity to detoxify many other metabolites occurs thus compromising the individual.

Ethanol is a very small molecule. Because of its size and polarity (charge), it can readily enter (diffuse without the concomitant expenditure of energy in the form of ATP) through the cell membrane of skeletal muscle. In the process, ethanol can disrupt the molecular configuration of the fatty acyl groups of the phospholipids of the skeletal muscle. Ultimately, this could interfere with several processes including the entry of calcium ions into the nerve terminal or an increased binding of calcium to the sarcoplasmic reticulum of the muscle. Calcium is the cation (a positively charged ion) which is involved in the control of the rate of release of neurotransmitter into the synapse (the area between the nerve and the muscle) and plays the most important role in muscle contraction and relaxation.

Thus in summary, alcohol is not a fuel for muscle contraction and alters fuel metabolism to increase lactate production and decrease lactate degradation. Furthermore, disrupts the molecular configuration of skeletal muscle and compromises its ability to perform muscle contraction.

Dr. Thomas Balon, PhD

Dr. Thomas W. Balon Ph.D. is one of the preeminent muscle physiologists in the world, having examined the most intricate parameters of muscle metabolism for the past thirty years. He has served as an Associate Editor for journals such as Medicine and Science in Sports and Exercise and has authored over 45 full-length, refereed journal articles pertaining to diet, exercise, and performance. Dr. Balon was honored to write an Invited Perspective commemorating the 50th anniversary of the American College of Sports Medicine. He was an Associate Professor at the Beckman Research Institute at the City of Hope National Medical Center and is a former Group Manager of Molecular Pharmacology at Glaxo Smith Kline, the world’s second largest pharmaceutical company.

Dr. Balon has served on grant review panels and study sections for the National Institutes of Health, the National Cancer Institute and the American Diabetes Association. Dr. Balon recently stated, "The American Athletic Institute has set out to make sport better for future generations of athletes and I hope I can make some contribution to those efforts."