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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 |
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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.
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:
HEAT ACCLIMATIZATION AND
PERFORMANCE
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.
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).