Gabe Rinaldi
06-08-2006, 02:09 PM
Here are some comments from rowing coach Mike Caviston (from Randy Bickham):
I’ve copied your comment from another thread: “I, and I think others, would be interested in your thoughts on any implications of Brooks' work. See the NY Times thread under training.” Well, I can say that when I began my graduate work in Kinesiology, the textbook Exercise Physiology: Human Bioenergetics and Its Applications by George Brooks and Thomas Fahey had a tremendous influence on me and shaped my whole approach to the understanding of physiology and human performance. Since then I have read dozens of papers by Brooks and they tend to be clear and bring a different perspective to concepts that students of exercise science have been conditioned to accept without question, such as “oxygen debt”. For example, “Anaerobic Threshold: Review Of the Concept and Directions For Future Research” (Medicine & Science In Sports & Exercise, vol. 17, pp. 22-31, 1985) notes that “the [AT] hypothesis fails on the bases of theory and prediction”, and discusses lactate kinetics during exercise.
In 2004, a couple of researchers named Allen & Westerblad published a paper called “Lactic Acid – The Latest Performance-Enhancing Drug” (Science, vol. 305, pp. 1112-1113). It described how lactate can actually have ergogenic properties – at least for skinned, isolated animal fibers artificially stimulated in a laboratory setting. You would think scientists would know better than to make wholesale conclusions about the effects of lactate extrapolated to whole-body human beings during exercise, but the paper caused some ripples in the scientific literature. A couple of recent summaries regarding lactate & exercise are a point-counterpoint debate called “Lactic Acid Accumulation Is An Advantage/Disadvantage During Muscle Activity” (Journal of Applied Physiology, vol. 100, pp. 1410-1414, 2006) and “Lactic Acid and Exercise Performance: Culprit Or Friend?” by Cairns (Sports Medicine, vol. 36, pp. 279-291, 2006). So not only in the popular literature, but also in the scientific literature, has there been confusion about the effects of lactate on performance. (The whole “its bad – no, its good” thing reminds me of the Woody Allen movie “Sleepers” where the doctors of the future laugh at how it was once thought smoking was bad for you!)
In my experience, virtually everyone (scientists, coaches, athletes, laypeople, the media, etc.) has had a tendency to oversimplify muscular fatigue during exercise. For years past and probably for years to come, “Hard exercise causes lactic acid to form and that in turn causes fatigue/pain” is about as far as people take it. While it’s not completely clear exactly why muscles fatigue during short-term/high-intensity events like a 2K (as opposed to marathon-type events where glycogen depletion or dehydration are most likely to be the dominant factors), accumulation of various metabolites that interfere with the ability of muscle fibers to properly contract are probably the dominant factor (as opposed to effects on the central & peripheral nervous systems). Probably the biggest fatigue factor is the increase in intracellular Na+ and the increase in extracellular K+ that occurs with intense muscular contractions, altering the sarcolemma’s membrane potential and the fibers’ ability to respond to stimulation. (An excellent review is “Na+-K+ Pump Regulation and Skeletal Muscle Contractility”, by Clausen, Physiological Reviews, vol. 83, pp.1269-1324, 2003.) Other probable factors include Ca++ ions leaving the sarcoplasmic reticulum and entering the mitochondria and interfering with oxidative phosphorylation, and the toxic effects of ammonia that accumulates as the result of breakdown of amino acids as well as IMP (from AMP resulting from the myokinase reaction: ADP + ADP = AMP + ATP). And of course lactic acid, whose accumulation is associated with a decrease in pH (rise in acidity) of the muscle environment, which is known to inhibit enzymes that regulate the glycolytic process. I guess its no surprise that many researchers (and coaches, etc.) would focus on lactate since it is the easiest to measure. But it is one of only several factors that are involved in the fatigue process in what appears to be a complex and perhaps synergistic way. Clearly large accumulation of lactate is correlated with muscle fatigue in many (but not all) cases, though correlation is not causation. Also implicating lactate in the fatigue process is the fairly consistent research finding that artificial buffering (such as by consuming baking soda prior to exercise) can raise muscle pH and enhance performance. (Before anyone asks, I’m not eager to try this myself, since common side effects to bicarbonate loading include severe stomach cramps and diarrhea.)
The answer to the question of “Lactate – Friend or Foe?” is simple: it’s both. Brooks himself has noted that lactate “sits at a metabolic crossroads” and is a “two-edged sword”. Rapid glycolysis produces the necessary ATP that oxidative metabolism alone can’t provide, with lactate as a byproduct. This probably contributes to fatigue. You can’t make an omelet without breaking some eggs. But lactate is not simply a “waste product”; it’s a tremendously useful fuel and raw material for resynthesizing glycogen or amino acids. Some tissues thrive on lactate and are very efficient at oxidizing it for energy – tissues like the heart & Type I muscle fibers. (Modest amounts of lactate injected into the circulation would be and excellent ergogenic aid for marathon runners.) During exercise, lactate produced by glycolytic fibers can enter the bloodstream and circulate to oxidative fibers for consumption – an ideal means of efficiently distributing fuel to all working fibers while keeping tissue pH within tolerable limits. More energy production and reduced fatigue. Win, win. So, yes, lactate is a fuel – as has been known for decades. I can sympathize with Dr.Brooks’ frustration that some people can’t see the obvious (such as the proper way to pace a 2K…)
As I have been saying from the beginning, training for 2K racing needs to include the proper combination of high-intensity intervals and prolonged, low-moderate intensity workouts (“distance training”). Intense intervals maximize energy production, both aerobically and anaerobically (well-trained athletes produce more lactate than lesser trained counterparts). Distance work increases endurance and enhances the ability to resist fatigue; adaptations include increased lactate transporters in glycolytic fibers to help lactate enter the bloodstream, and increased mitochondria in oxidative fibers so they will be better able to utilize lactate as fuel. The whole lactate discussion illustrates why I subscribe to the “black box” approach to training & performance. Training goes in, and as long as the right performance comes out, we don’t really have to know what happens in-between. Some people feel compelled to assign causes without sufficient justification, which can actually cloud the issues and cause people to train inefficiently or incorrectly. (I could go off on a tangent about HR-based training, but I don’t have the energy.)
Mike Caviston
I’ve copied your comment from another thread: “I, and I think others, would be interested in your thoughts on any implications of Brooks' work. See the NY Times thread under training.” Well, I can say that when I began my graduate work in Kinesiology, the textbook Exercise Physiology: Human Bioenergetics and Its Applications by George Brooks and Thomas Fahey had a tremendous influence on me and shaped my whole approach to the understanding of physiology and human performance. Since then I have read dozens of papers by Brooks and they tend to be clear and bring a different perspective to concepts that students of exercise science have been conditioned to accept without question, such as “oxygen debt”. For example, “Anaerobic Threshold: Review Of the Concept and Directions For Future Research” (Medicine & Science In Sports & Exercise, vol. 17, pp. 22-31, 1985) notes that “the [AT] hypothesis fails on the bases of theory and prediction”, and discusses lactate kinetics during exercise.
In 2004, a couple of researchers named Allen & Westerblad published a paper called “Lactic Acid – The Latest Performance-Enhancing Drug” (Science, vol. 305, pp. 1112-1113). It described how lactate can actually have ergogenic properties – at least for skinned, isolated animal fibers artificially stimulated in a laboratory setting. You would think scientists would know better than to make wholesale conclusions about the effects of lactate extrapolated to whole-body human beings during exercise, but the paper caused some ripples in the scientific literature. A couple of recent summaries regarding lactate & exercise are a point-counterpoint debate called “Lactic Acid Accumulation Is An Advantage/Disadvantage During Muscle Activity” (Journal of Applied Physiology, vol. 100, pp. 1410-1414, 2006) and “Lactic Acid and Exercise Performance: Culprit Or Friend?” by Cairns (Sports Medicine, vol. 36, pp. 279-291, 2006). So not only in the popular literature, but also in the scientific literature, has there been confusion about the effects of lactate on performance. (The whole “its bad – no, its good” thing reminds me of the Woody Allen movie “Sleepers” where the doctors of the future laugh at how it was once thought smoking was bad for you!)
In my experience, virtually everyone (scientists, coaches, athletes, laypeople, the media, etc.) has had a tendency to oversimplify muscular fatigue during exercise. For years past and probably for years to come, “Hard exercise causes lactic acid to form and that in turn causes fatigue/pain” is about as far as people take it. While it’s not completely clear exactly why muscles fatigue during short-term/high-intensity events like a 2K (as opposed to marathon-type events where glycogen depletion or dehydration are most likely to be the dominant factors), accumulation of various metabolites that interfere with the ability of muscle fibers to properly contract are probably the dominant factor (as opposed to effects on the central & peripheral nervous systems). Probably the biggest fatigue factor is the increase in intracellular Na+ and the increase in extracellular K+ that occurs with intense muscular contractions, altering the sarcolemma’s membrane potential and the fibers’ ability to respond to stimulation. (An excellent review is “Na+-K+ Pump Regulation and Skeletal Muscle Contractility”, by Clausen, Physiological Reviews, vol. 83, pp.1269-1324, 2003.) Other probable factors include Ca++ ions leaving the sarcoplasmic reticulum and entering the mitochondria and interfering with oxidative phosphorylation, and the toxic effects of ammonia that accumulates as the result of breakdown of amino acids as well as IMP (from AMP resulting from the myokinase reaction: ADP + ADP = AMP + ATP). And of course lactic acid, whose accumulation is associated with a decrease in pH (rise in acidity) of the muscle environment, which is known to inhibit enzymes that regulate the glycolytic process. I guess its no surprise that many researchers (and coaches, etc.) would focus on lactate since it is the easiest to measure. But it is one of only several factors that are involved in the fatigue process in what appears to be a complex and perhaps synergistic way. Clearly large accumulation of lactate is correlated with muscle fatigue in many (but not all) cases, though correlation is not causation. Also implicating lactate in the fatigue process is the fairly consistent research finding that artificial buffering (such as by consuming baking soda prior to exercise) can raise muscle pH and enhance performance. (Before anyone asks, I’m not eager to try this myself, since common side effects to bicarbonate loading include severe stomach cramps and diarrhea.)
The answer to the question of “Lactate – Friend or Foe?” is simple: it’s both. Brooks himself has noted that lactate “sits at a metabolic crossroads” and is a “two-edged sword”. Rapid glycolysis produces the necessary ATP that oxidative metabolism alone can’t provide, with lactate as a byproduct. This probably contributes to fatigue. You can’t make an omelet without breaking some eggs. But lactate is not simply a “waste product”; it’s a tremendously useful fuel and raw material for resynthesizing glycogen or amino acids. Some tissues thrive on lactate and are very efficient at oxidizing it for energy – tissues like the heart & Type I muscle fibers. (Modest amounts of lactate injected into the circulation would be and excellent ergogenic aid for marathon runners.) During exercise, lactate produced by glycolytic fibers can enter the bloodstream and circulate to oxidative fibers for consumption – an ideal means of efficiently distributing fuel to all working fibers while keeping tissue pH within tolerable limits. More energy production and reduced fatigue. Win, win. So, yes, lactate is a fuel – as has been known for decades. I can sympathize with Dr.Brooks’ frustration that some people can’t see the obvious (such as the proper way to pace a 2K…)
As I have been saying from the beginning, training for 2K racing needs to include the proper combination of high-intensity intervals and prolonged, low-moderate intensity workouts (“distance training”). Intense intervals maximize energy production, both aerobically and anaerobically (well-trained athletes produce more lactate than lesser trained counterparts). Distance work increases endurance and enhances the ability to resist fatigue; adaptations include increased lactate transporters in glycolytic fibers to help lactate enter the bloodstream, and increased mitochondria in oxidative fibers so they will be better able to utilize lactate as fuel. The whole lactate discussion illustrates why I subscribe to the “black box” approach to training & performance. Training goes in, and as long as the right performance comes out, we don’t really have to know what happens in-between. Some people feel compelled to assign causes without sufficient justification, which can actually cloud the issues and cause people to train inefficiently or incorrectly. (I could go off on a tangent about HR-based training, but I don’t have the energy.)
Mike Caviston