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  http://www.sportsci.org/news/news9707/seiler.htm

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).

• The ACSM annual meeting is not a strictly American affair. It is undoubtedly the largest sport science related meeting in the world, and the world participates enthusiastically. About 25% of the scientific presentations are by non-American scientists, and the international flavor of the meeting is growing. Australia, Canada, The Netherlands, Germany, Scandinavia, and Japan struck me as being particularly well represented at the meeting.
• If ACSM abstracts are a reflection of program strength (debatable, yes), then here are some of the top sport science institutions in the US, based on number of abstracts published at ACSM in 1995 and 1996 (# 752): Ball State, U. of Florida, Indiana U., Oregon State, U. of Wisconsin-Madison, U. of Massachusetts, U. of Arizona, U. of Colorado, U. of Georgia, University of North Texas (Ft. Worth), University of Texas, Austin, Texas A&M;, U Texas-Southwestern (Dallas), Ohio State
• By my count, this year's hot topics were strength training for the elderly, and the obesity epidemic (yes its bad, getting worse, and no we aren't making a difference, but we will keep trying as long as there is grant money). On the other hand, research focusing on human sports performance and training was in relatively short supply. One regular attendee of the meeting who also edits a very popular sports magazine commented to me: "Ten years ago I could always come to this meeting and walk away with something to take straight to my readers that they could use in their training and racing. Now I can't find that." Maybe we have made a lot of progress in sport science, and the questions are getting more tricky. However, after chats with folks from around the globe, I also get the feeling that most of the really interesting training and performance data remain tucked away in the files of several national sports labs.
• For the first time, abstracts submitted with sponsorship by a fellow of ACSM were accepted without review. This move is not unprecedented in the scientific community and surely made the review process more manageable, as over half of the abstracts were sponsored. The down side was that overall quality of the research presentations seems to have suffered, according to word on the street and personal observation. Is the increase in accepted abstracts worth a drop in quality?

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.
 
SKELETAL MUSCLE AND LACTATE EXCHANGE
 
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.

Conclusions
 
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.
 
HIGH-LOW AND OTHER ALTITUDE TRAINING
 
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:

• Gender specificity in the altitude effect? Active but untrained males and females permanently residing at about 2000 m completed cycle ergometer tests at simulated altitudes of 0, 984, 1,640, and 2625 m in single blind fashion inside a hypobaric chamber. Females had significantly smaller decrement in VO2max throughout the range of hypoxic trials (10% vs 23% at 2625 m) (Robergs et al., # 777).
• On the other hand, it seems that lactate threshold is better maintained in males then females with increasing altitude. Comparing the same active, untrained altitude residers from above, increasing hypoxia detrimentally influenced lactate kinetics in females, but not males. This difference was independent of the reductions in VO2max (Robergs et al., # 774).
• James Stray-Gundersen reported on a study employing a modification of the sleep high-train low model. With an eye towards the impracticality of always coming down a mountain to train, they employed a 4-week period of sleeping high but training both high (steady-state work) AND low (interval training). The results were fewer trips down the mountain from the base height of 2000 m but equivalent acclimatization responses and the same improvement in sea level 5000-m performance (~15 seconds) observed in a previous study employing sleep high-train low (# 783). As a side note, in September Dr Stray-Gundersen will leave Dallas and spend a year in Norway giving EPO to athletes. Are the Norwegians cheating? No, they are trying to develop a test for EPO that is more sensitive than the indirect hemoglobin measurements being used now.
• Does altitude training have a unique impact on cardiac performance? The results of a 2-week sleep high (1950 m)-train low (sea level) German study on triathletes suggested improved systolic function without a change in diastolic function or diameters. A control group living and training at sea level had unchanged systolic function (#805)
• More evidence for a cardiac performance impact of altitude training was reported from the Karolinska Institute in Sweden. Seven elite male and female XC skiers lived and trained at 1900 m for one month. Roller-ski treadmill tests were performed before, during, and 5 and 11 days after the altitude sojourn. Besides a small increase in sea level VO2max (6 of 7 athletes, 3% average), the authors reported a significant increase in calculated left ventricular mass. Does the altitude-induced drop in heart rate at a given workload help overload the heart via increased stroke volume, despite lower blood volume? Does hypoxia have regulatory effects on the heart via increased cardiac sympathetic activation at rest? These questions were raised by the authors (# 810).
• Finally, I think I should report on what I believe to be the first ever double-blind altitude training study. Two groups of nine untrained subjects completed 5 weeks of endurance training (45 min., 3 times per week, 70% VO2max) in a hypobaric chamber regulated to simulate either sea level or 2590 m. The authors reported that hypobaria did not significantly enhance VO2max or time to exhaustion in a high intensity work bout, compared to sea level training. Note, though, that the increases were twice as large in the altitude group for both VO2max and endurance time.

 
HEAT ACCLIMATIZATION AND PERFORMANCE

• How Long Does Heat Adaptation Last? Not very long according to the guys at the Australian Institute of Sport. Heat-stress adaptations (decreased heart rate at submaximal workloads, reduced rectal temperature, increased plasma volume, increased sweat rate) observed in elite rowers during a 26-day training period at 32¡C were almost completely lost after 2-4 days at moderate temperatures. After the short break from the heat, only sweat rate remained elevated (#556 ).
• How Much Does Heat Hurt Performance? An increase in temperature from 23¡C to 32¡C (60% humidity) reduced average power during a 30-minute cycling time trial by 6.5% in national class cyclists despite similar core temperatures. Athletes seem to self-select a power output that allows them to remain below an upper body temperature limit (#558).
• How Should You Heat Adapt? Daily heat exposure (10 days straight) is superior to intermittent exposure (10 days over 3 weeks) for inducing acclimatization (# 563).
• Does Acclimatization Decrease Heat Storage? After heat acclimatization, athletes have lower final core temperatures after a standard exercise bout. Is this because of a reduction in the heat storage of the body? No, it appears to be due to small drop in resting core temperature. Heat-adapted athletes appear to be cooler at the end of hot humid exercise in large part because they start cooler (#560).
• What is the Fastest Way to Cool Down After Intense Exercise in the Heat? It turns out that passive cooling at room temperature beats out fan cooling, water spraying, or even fans plus water spraying. The fans and spraying may trigger rapid peripheral vasoconstriction, defeating the physiological shunting of heat from the core to the skin (# 564).
• Pre-cooling Improves Performance in the Heat. The folks at the Australian Institute of Sport worked hard to be ready for the heat and humidity of the Atlanta Olympics. Along the way they found that pre-cooling athletes with a cooling vest (10¡C skin temperature with vest compared to 33¡C without) improved performance. Triathletes had longer cycling time to exhaustion (3%) and higher peak power (3%) when they warmed up in the cooling vest compared to when they warmed up normally. Numerous Aussies used the vests during the Atlanta Olympics (#1501).

 
ERGOGENIC AIDS AND SUPPLEMENTS
 
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.

• Adding branched-chain amino acids to the glucose mix does not improve the ergogenic effect in males during high intensity running (# 720).
• A CHO-electrolyte drink improved proaction/reaction performance and reduced perceived effort in a soccer skills test administered to elite junior soccer players under hot, humid conditions after a 60-minute fatiguing run (#721).
• Females may not benefit in the same way as males (# 723).

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).
 
AMINO ACIDS AND FATIGUE
 
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).