ACSM 97: Hard Facts on High Intensity, High Heat, and High Altitude from the Mile-High City

Stephen Seiler, Institute of Health and Sport, Agder College, Kristiansand, Norway
Sportscience News
July-Aug 1997

Presentations reviewed: Skeletal Muscle and Lactate Exchange · High-Low and Other Altitude Training · Heat Acclimatization and Performance · Ergogenic Aids and Supplements · Amino Acids and Fatigue.

The 44th annual meeting of the American College of Sports Medicine attracted a record 5,000 attendees and over 1,700 scientific presentations. When you combine the massively parallel formal sessions, inquiries and haggling at the exhibit booths, and the accumulated hours of convention-hall and beer-hall discussions (where much of the really new information is shared), well, information overload was the phrase of the day, every day, for the four days of ACSM. Here are a few things I managed to distill from the deluge. Abstract numbers (#) refer to the May supplement of Medicine and Science in Sports and Exercise (MSSE).

My favorite lecture? Actually there were two. One was the elegant presentation on obesity research by Dr Claude Bouchard, the presenter of the prestigious Wolfe Memorial Lecture, which will be published in MSSE and is summarized in an accompanying report. Summarized below is my other favorite, a symposium on the role of skeletal muscle in lactate exchange during exercise. I'll then look at altitude training, heat acclimatization, ergogenic aids, and fatigue.
The symposium turned out to be a US-Canadian tag team affair. Bruce Gladden from Auburn University in the US kicked things off by remarking on the changing view of lactate in metabolism over the last 25 years. In 1970, Lehninger's Biochemistry text defined lactic acid as a metabolic end product which escapes from muscle cells as waste during conditions of oxygen deficiency. In 1996, the same text describes lactate as an intermediate produced in fully oxygenated tissue as a means of coordinating energy storage and utilization in different tissues.

Muscle as a lactate producer
Lawrence Spriet, from the University of Guelph in Ontario, presented data on lactate production in skeletal muscle and its enzymatic control. After laying out the maximal flux rates through each of the glycolytic enzymes and the flux rates at several exercise intensities, he reviewed the current state of thinking on the regulation of this pathway. While phosphorylase (grossly controlled by Ca++ and fine tuned by free AMP) , PFK (negative modulation by H+ is overridden by ADP, AMP and NH4+ until very low pH), and PDH (modulated by Ca++ but displaying fast and slow activation components) are still viewed as the major regulators, the interesting conclusion drawn by Spriet was that this control is loose. At an exercise intensity of 65% VO2max, PDH activity actually declines as a steady state is established, yet 30% of the pyruvate formed during glycolysis continues to be converted to lactate. Spriet argued that this is due to loose regulatory control, not hypoxia. It appears that glycolytic flux errs on the high side. Within the mitochondria, acetyl CoA and acetyl carnitine also climb in concentration gradually over 10 minutes of a 65% work bout, supporting the loose control hypothesis. After 1 min at 90% VO2max, LDH and PDH activity are roughly equal. At this high intensity some fibers are probably under-oxygenated, according to Spriet.

Skeletal muscle as lactate consumer
From Bruce Gladden I learned that skeletal muscle not only takes up lactate, but that it does so even at very high metabolic rates. This uptake seems to occur via a combination of diffusion and carrier processes. There is a progressive increase in lactate uptake with increasing plasma lactate concentration up to about 20-30 mM plasma concentrations. Peak lactate uptake rates in blood perfused skeletal muscle preparations are about 1 mmol/kg muscle/min.

What is the fate of lactate taken up by muscle during exercise?
Casey Donovan from the University of Southern California shared data from his perfused muscle preparations to address this issue. It appears that muscle begins to be a significant consumer of lactate at blood concentrations of about 2 mM. By 8 mM all fibers become lactate consumers, even at rest. What are the pathways for lactate removal once it is taken up by muscle? In type I fibers, the answer is oxidation and transamination. However, in IIb fibers glyconeogenesis is a major removal pathway. Yes folks, skeletal muscle CAN move lactate back up the glycolytic pathway to reform glycogen. We knew the liver could manage this, but skeletal muscle glycolysis was assumed to be a one-way path. Liver and skeletal muscle apparently use different pathways; the liver engages a detour involving the Krebs cycle, but skeletal muscle does not. Instead, against conventional wisdom, direct pyruvate kinase reversal occurs. This was another dogma dashed, as since 1959 we have been teaching students that this pathway was one-way in skeletal muscle due to the non-equilibrium kinetics of pyruvate kinase. Turns out this enzyme is at near-equilibrium after all, making the lactate story much more interesting.

Lactate Transport
Enter Arend Bonen from the University of Waterloo. The question Dr Bonen addressed was "how is lactate being moved across the muscle cell membrane?" Since the 80s, it has been reported that lactate traverses the sarcolemma via a transport mechanism and not merely via diffusion. It also appears that lactate transport is faster in oxidative fibers, and that transport capacity increases with training (~30% in a recent study from Copenhagen). The lactate transport plot has thickened lately. It seems that lactate transporters, like glucose transporters, come in more than one variety. The pieces to the puzzle are still accumulating, but it looks like some transporters are designed for exporting lactate out of the muscle, while others specialize in import. The likely possibility, based on the data and radio-immunomicrographs, is that lactate is pushed out of an active glycolytic fiber via "release transporters" only to be taken up by an immediately adjacent oxidative fiber with a high density of "uptake transporters."

George Brooks capped things off by saying that the lactate shuttle hypothesis he proposed in the 80s is alive and well. Indeed, it appears that lactate serves the body well as a vehicle for moving carbon around in the body.

Enzymatic control of glycolytic flux, even at moderate exercise intensities, results in excess production, which explains significant lactate production in the face of full oxygenation. The dogma of exquisite control of cellular metabolic flux took a hard knock. Working muscle is simultaneously producing and consuming lactate. The pathways for consumption include oxidation, transamination AND glyconeogenesis Endurance training seems to enhance the rate of lactate clearance more than it reduces the rate of appearance, at least in rats.
After looking at this year's buffet of altitude training research, I think it is fair to say that the published literature lags years behind the volumes of longitudinal data being collected and used by several national teams. Unfortunately, since they are more interested in winning medals then publishing papers, most of this data stay out of reach. And even if it were published, one of the critical findings that guides the national teams would not come through very well in the group statistics. That concept is "big individual differences." There were some interesting studies, nonetheless:


I am leaving a lot out of this section, mostly because we have seen it before.

Carbohydrate for endurance. A physiological puzzle that has emerged in the ergogenic aids and performance area surrounds the issue of the now repeated finding of an ergogenic effect of drinking carbohydrate solutions prior to and during intense steady state or intermittent exercise of less or equal to one hour duration. This finding received further corroboration, but nothing in the way of explanation. The ergogenic effect is not due to fluid ingestion, and occurs despite the fact that blood glucose levels are elevated above resting levels in both placebo and glucose consumers. Why does glucose ingestion improve performance under these conditions? Here are a few more pieces for the puzzle.

Creatine supplementation remains in focus, because rich supplement companies continue to pay for the research. The majority of the studies report significant improvements in anaerobic performance. The studies the supplement companies are not funding, related to possible side effects from long term creatine loading (lots of anecdotal evidence), are in the works, but the results are at least a year away. The one really interesting creatine study I saw showed that when you combine creatine loading with chronic ( 2 x 2.5 mg/kg per day) caffeine consumption, the benefit disappears ( # 1417).

Glycerol hyperhydration is now illegal, but is it ergogenic? Despite increasing fluid retention, glycerol administration in combination with fluid consumption did not improve sweat rate, alter temperature responses or prevent cardiovascular drift in a 106-min cycling ride performed at 24¡C. (#766). The environmental medicine folks at the US Army also tried glycerol hyperhydration during a low-intensity exercise session performed at 35¡C and 45% humidity. They found no thermoregulatory benefit of glycerol hyperhydration compared to water euhydration on any of the physiological responses.(#761). In another study, investigators found no advantage of glycerol hyperhydration over prehydration with 6% carbohydrate (#1419).

Ibuprofen reduces muscle soreness and inflammation. The pain and associated enzyme release 24 and 48 hours after a bout of eccentric exercise was significantly decreased when 400 mg Ibuprofen was taken every 8 hours for 48 hours after the exercise bout (#840).
This topic ties in with the central fatigue hypothesis championed by Eric Newsholme. The theory is that feeding branched-chain amino acids (BCAAs) during exercise will reduce central fatigue by reducing production of brain 5-hydroxy tryptophan (5HT, serotonin). When BCAA concentration goes down in the blood, 5HT production in the brain goes up because tryptophan competes with BCAAs for entry into the brain via the same carriers. Lower BCAA concentration after a long exercise bout means higher tryptophan concentration in the brain and higher 5HT production. There is evidence that tiredness and sleep are influenced by 5HT. Thus 5HT has been hypothesized as a cause of fatigue during very long endurance exercise. At least that is the theory.

Several authors presented data relevant to this theory. BCAA feedings during a 120-min treadmill run did indeed reduce brain 5HT concentration in running rats, but so did plain old glucose (#1096). Two studies of humans evaluated performance after Prozac or leucine supplementation to suppress brain 5HT concentration. There was no effect on anaerobic capacity or endurance at 90% VO2max (#1093, #1095).

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