Athletic
Performance at the 2001 ACSM Meeting Will
G Hopkins Department
of Physiology and School of Physical Education, University of Otago, Dunedin
9001, New Zealand. Email. Sportscience
5(2), sportsci.org/jour/0102/wgh.htm, 2001 (3919 words) Reviewed by Stephen Seiler, Institute of
Sport, Agder University College, Kristiansand, Norway Anthropometry: skinfolds are still OK. Mechanisms: sites of
fatigue, and non-lactic acidosis. Muscle Damage: benefits of vitamin C,
anti-inflammatories, proteases, L-carnitine, and massage. Nutrition:
ribose seems to enhance repeated sprints.
Overtraining: it's hard to monitor. Performance Genes:
we're still waiting. Tests,
Technology: something for everyone. Training,
Performance: simulated altitude, optimum altitude, better warm-ups,
oxygenized water, effective strength training, and tight jumping shorts. Reviewer's Comment: advances in EPO detection, and
reflections on a fatigue symposium. Reprint pdf · Reprint doc KEYWORDS:
altitude, anthropometry, elite athletes, ergogenic aids, nutrition,
overtraining, performance enhancement, tests, training |
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The
annual meeting of the American College of Sports Medicine, this year in
Baltimore May 30-June 2, was the venue for a total of nearly 2000
presentations of original research, case reports, and review-type lectures in
exercise and sports medicine and science.
Inevitable clashes in timetabling meant I had to miss many of the
talks I was interested in. I even
missed key posters, because there were so many and because the poster hall
was so far from the talks. By Friday I was suffering from conference shock
and nearly took the day off to visit the Smithsonian Institutes in Washington
DC. I'm glad I didn't, because Friday
turned out to be the best day for me.
The other three days were also winners. This
article is a summary of presentations relevant to athlete assessment and
sport performance. Mostly I've only
summarized the abstracts. My apologies
to the authors of good abstracts I've missed on my way through. My apologies also to the experts who gave
lectures. Unfortunately the abstracts
for these lectures are unusable, either because they are written in the
results-will-be-presented manner, or because the presentations for up to five
speakers are shoe-horned into one normal-length abstract, or because there is
simply no abstract for some types of session.
Hence a plea to the ACSM program committee: upgrade and extend the abstracts of these
valuable talks by publishing one information-rich
full-length abstract for each speaker, regardless of the
session. Sure, we can buy the tapes,
but who has the time, or--if you live outside the US--the money? In my
opinion, many abstracts had serious flaws.
Here's my advice on how to improve them in future… • Show the magnitude
of an effect,
even when the effect is not statistically significant. Our core business is estimating magnitudes
of effects, not testing for null effects. • Show the precision
of your estimate as likely or confidence limits, which represent the range within which the
real (population) value is 95% likely to fall. If instead you use a P value or statistical
non/significance, you will mystify most readers and probably misinterpret
your own findings. • Interpret the
magnitude of the effect and its likely limits in plain language. Is the observed effect trivial,
small, moderate or large? How big or
small is it likely to be in reality? • Conclude "no
effect" only when both confidence limits are trivial.
Lack of statistical significance by itself is not a sufficient reason
to conclude little or no effect. To put it another way, failure to reject the
null hypothesis is not a sufficient reason to accept the null hypothesis.
Generations have misunderstood this point. • Show standard
deviations. These convey the useful impression of
variation within groups. The reader
can also gauge magnitude of a difference or change in the mean as a fraction
or multiple of the within-group standard deviation(s). • Do not show standard
errors of the mean. These convey the less useful impression of
statistical significance, and only in the special case of non-repeated
measures with equal-sized groups. Standard errors do NOT convey statistical
significance in controlled trials. • For athletes, show
performance effects as percent changes or differences, because the smallest effects
that matter to athletes are best expressed as percents (~0.5-2%, depending on
the sport and measure of performance). • Avoid abbreviations for everything except units of
measurement. Abbreviations almost
always make anything hard to read. A keystroke, word, or space limit is no
excuse. • Don't submit two
abstracts when one is appropriate. This advice is ACSM policy. The meeting would benefit from fewer
abstracts. In what
follows, the # sign indicates the number of the Abstract in Medicine and
Science in Sports and Exercise, Volume 31, Supplement 5. You may have trouble tracking down the
supplement, which this year was distributed only to conference attendees. At
the time of writing, you can still view most abstracts at the FASEB-ACSM
site. Hydration
status of adult males and females
substantially affected percent fat
determined by bioelectric impedance and by near-infrared interactance
but not by skinfolds (#86). A Tanita bioelectric impedance device trailed the
field, but there was nothing to choose between hydrostatic
weighing, skinfolds, and
dual X-ray absorptiometry (DXA) for
assessment of percent fat in collegiate athletes,
relative to the criterion multi-compartment method (#1365). There
were many other anthropometric methods
papers. See #77-88 and #1349-1370. A team
from Cape Town headed by Tim Noakes gave a mini-symposium on fatigue entitled "the ATP paradox, or why muscles do
not develop rigor during exercise" (#537). Their idea is that depletion of energy
(adenosine triphosphate, ATP) in muscle fibers during hard exercise would
produce something akin to rigor mortis. Noakes didn't say why that would be
bad, but I guess that having even a few stiff fibers scattered through a
muscle would compromise muscle function and/or cause muscle damage during
contraction. It follows that fatigue
could be a protective mechanism to stop us pushing muscle fibers to the point
of stiffness. The speakers made a case for the central nervous system as the
site of this fatigue: they claimed that we can't voluntarily recruit all
fibers in a muscle, even in all-out exercise.
They also claimed that metabolic changes in active muscle modify
recruitment of fibers via the central nervous system but do not produce performance-limiting
fatigue in the muscle itself. These claims are debatable, depending on the
type of exercise. In any case, there must also be a stiffness-limiting
protective fatigue mechanism within muscle fibers, because "no previous
study has demonstrated… [that] muscle rigor occurs in human subjects… even
when their muscles are stimulated electrically" (cited from the
abstract, italics mine). The nature and relative importance of
central-fatigue and muscle-fatigue mechanisms in various forms of exercise
will be important future presentations from the Cape Town team. Most subjects (#260) and most healthy, young, active subjects (#262) showed a plateau in maximum oxygen consumption, which
is consistent with the idea that oxygen transport to the active muscles is
the limiting factor in endurance for such subjects. The effect of caffeine on performance of
isometric contractions to fatigue appears to be mediated via cortical
excitability in male subjects
(#934). That's evidence for fatigue in
the central nervous system. Speed skaters fatigue faster than
comparable cyclists, probably because
the crouched position in speed skating reduces blood flow to active muscles
(#1342). Changes
in pH in a test tube (#1565) appear to support the view that lactic acid does
not contribute directly to the increase in acidity
in muscle cells during intense exercise. Do the hydrogen ions come from breakdown of
ATP or are they released early on in the pathway of the breakdown of glucose
to lactate? Whatever, we don't produce lactic acid--we produce hydrogen ions
and lactate ions! So, should we refer
to metabolic acidosis rather than to lactic acidosis? Probably. For details,
see the article in this issue of Sportscience by Rob
Robergs. Megadosing
(3 g/d) with vitamin C before
eccentric arm exercise in untrained subjects
reduced the perception of soreness by an unstated amount and tended to reduce
serum concentration of muscle creatine kinase, a marker for muscle damage
(#694). Similarly, 9 d of 800 mg/d of
vitamin C nearly halved serum myoglobin (another marker of muscle damage)
after unaccustomed downhill running in physically
active males, but claims for less loss of muscle function were not
backed up with data (#695). The
anti-inflammatories (pain killers) Ibuprofen
and Bromelain had "no
effect" on pain or function following unaccustomed eccentric elbow
flexion in an apparently high-powered study of untrained (?) subjects (20 males, 20 females), but the
design (crossover?) and effects were not stated, and the analysis (MANOVA)
was underpowered (#696). Vicoprofen
may have done a bit better than Ibuprofen
for several measures of damage and function in the first 2 d following
eccentric exercise in healthy men (#1110; not enough data in the abstract). Celecoxib was a bit better than Ibuprofen and placebo for physician-assessed
recovery of sprained ankles over 11 d in a cross-sectional study of 443 adults (#1109). The same researchers found similar effects for
Celecoxib and Naproxen on ankle sprain (#1121). Supplementation
with pancreatic proteases four
times a day over 4 d before and after downhill running reduced pain and loss
of function in leg muscles of males
(#697). The abstract featured detail
of methods but no magnitudes of effects. L-carnitine
supplementation for 3 wk before "intense hypoxic exercise" (a
series of squats) reduced pain after exercise by a worthwhile notch on a pain
scale, and it reduced plasma myoglobin by an unstated amount compared with
placebo in a 1-wk washout crossover study of healthy active men (#698). Possible mechanism:
reduction in oxidative stress (#1233). Massage 2
h after eccentric exercise of the hamstrings probably reduced the perception
of soreness and may have affected muscle function of subjects, but without data in the abstract
it's hard to say (#699). In a similar study of mostly athletes and active adults, massage increased
range of motion moderately (effect size ~0.8); there was probably also a
modest effect on strength (no data) and "muscle tissue energy
absorption" (?), but not pain (#1103). There was
a trend towards a small sparing of muscle-protein breakdown in endurance runners on a high-protein vs moderate-protein diet
(#919). There
weren't enough data for me to adequately assess an apparent trend towards
less acute exercise-induced muscle damage in male
subjects supplementing with cracked
pine pollen (#923). Compared
with placebo, caffeine enhanced
performance lasting several hours on a cycle ergometer when the competitive cyclists took it as pills before
the test, as pills during the test, and as Coca-Cola during the test (#249).
The effect, obscured partly by abbreviations, was ~3% for mean power in a
30-min time trial following a 2-h pre-load. On the other hand, caffeine
apparently (no data) had no effect on performance of sprints or on overall
time in a 100-km performance test with elite
cyclists (#944). Supplementation
for 11 d with ribose (the 5-carbon
sugar that forms part of ATP and all other nucleic acids) may enhance
performance of multiple sprints repeated over several days by as much as 5%
(#251) in healthy subjects, but it's
very expensive stuff. Possible
mechanism: it partially reduced the fall in intramuscular adenine nucleotide
concentration that occurred over 5 d of hard training (#943). Relative to
placebo, ribose also produced a 22% increase in reps in 10 sets to failure
following 4 wk of supplementation combined with heavy resistance training in body builders (#938); data on changes in body
composition by DEXA were not reported, because--you guessed it--they weren't
statistically significant. It's
reasonably clear that a high-fat diet
followed by carbohydrate loading is
better than a high-carbohydrate diet
for ultra-endurance. In a crossover study (#291), seven competitive cyclists had either 6 d of high
fat and 1 d of high carbohydrate or 7 d of high carbohydrate. On fat with carbo-loading they went 5%
further (equivalent to an 11% increase in mean power) in a 1-h time trial on a
cycle ergometer after 4 h at moderate intensity. The conditions (breakfast,
supplements, exercise intensities) were more realistic than in previous
studies, and a P value of 0.11 for the effect is equivalent to chances of
94.5% that the true effect was positive. The mechanism? Probably glycogen sparing resulting from
fat adaptation, coupled with the extra glycogen from the day of
carbo-loading, because oxidation of fat during the performance test was still
high after fat with carbo-loading (#292). The herbal-based
supplement Cordymax increased fat
oxidation in endurance athletes but
apparently (no data!) had no clear-cut effect on maximum oxygen consumption
(#928). Supplementation
with sodium phosphate (4 g/d for 4
d) apparently had "no effect" on a Wingate sprint or maximum oxygen
consumption in a crossover with 12 trained male
cyclists, but without data in the abstracts…? (#929, 936). Amino-acid
supplementation appeared to reduce effects of short-term resistance
overloading on testosterone and hemoglobin indices in resistance-trained men (#1905, no data). Highlights
of a zillion abstracts (#1142-1166) on the short-term effects of creatine supplementation on
performance: almost twice the effect
in females as in males (#1152), and worthwhile effects in soccer (#1149) and
squash (#1151) players. There were no studies of effects of chronic
supplementation on performance. I've ignored the substantial number of
abstracts that did not include sufficient data. In an
abstract made virtually impenetrable with abbreviations, 60 d of
supplementing with bovine colostrum
vs a whey-protein control during upper-limb resistance training in unspecified subjects produced some
hypertrophy, but it was in skin or other non-contractile tissue (#1913). Sleeping heart rate seemed to have little relationship to training load, but whether the
four runners got near to overtraining
is not clear (#750). Serum prolactin, catecholamine
excretion, and nightly and morning heart
rate monitored 4 weeks before, 4 weeks during, and 8 weeks after a
training camp aimed at overtraining 11 cyclists
and triathletes did not give a consistent picture of the increased
workload (#1621, 1623). But again, was anyone overtrained? It's hard
to make generalizations about the relationships between blood tests, training
loads, and performance
in 12 highly trained swimmers
(#1920). It looks like you have to get
to know your individual athletes when you monitor for overtraining. The gene
for angiotensin converting enzyme--the ACE
gene--has been a candidate for a performance gene, but now it's
pretty-much down the gurgler. There
were weak (?) associations of ACE-gene forms with muscularity in a comparison
of elite body builders with controls
(#1809, no usable data), and an apparent (weak?) association with endurance in Japanese athletes was different
from that in other studies (#1810, no data).
One of my students didn't find any obvious association between ACE
genotype and response to altitude exposure in a small sample of runners (#11). A session
on genetic aspects of performance didn't include any breakthroughs
(#1294-1298). There wasn't a
consistent effect of the two forms of the gene
for ciliary neurotrophic factor on strength
training in arms and legs of healthy adult males (#1560). Forms of the gene for the most
abundant mitochondrial protein were
associated (weakly?) with maximum oxygen
consumption in blacks but
not whites (#1813, no data). A mutant form of the gene for creatine kinase was associated (weakly?) with
lower maximum oxygen consumption
training response in blacks, but the
response in whites was, if anything,
the opposite: reduced oxygen consumption at a submaximal workload following
training (#1814, no data). Conclusion:
no performance gene yet. If your cycle ergometer has a flywheel, its inertia
substantially attenuates peak power in Wingate tests (#1856). You can correct
for it. Profiling
is a bit passé, but if you want to know how people are using or refining tests on athletes, see #133 (cycling),
#883-904 (cycling, softball, soccer, tennis, football, swimming), #1372-1394
(volleyball, basketball, rugby, ice hockey, surfing, rowing, soccer,
trathlon, running, football, rock climbing, BMX, cheerleading!), #1921-1927
(motor racing, cycling, canoeing, hockey, surfing, soccer). See the
poster session on validity and reliability
for potentially useful stuff on sit-and-reach (#1686), pulmonary diffusion
capacity (#1688), using a 3-L syringe to calibrate metabolic carts (#1689),
cardiac output (#1690), the Cosmed portable metabolic system (#1691), jumps
vs shuttle runs (#1692), 1RM vs 3RM (#1693), a lumbar extension dynamometer
(#1694), knee-extension test (#1696), swimming lactate threshold (#1698), a
shuttle test (#1700), and an aerobic dance test (#1702). There was
no room to put it in the abstract, so here's the main point I made in my part
of the mini-symposium on reliability: the typical (standard) error of measurement
has to be similar in magnitude to the smallest clinically or practically
important change in the measurement, if you want to track such changes in
individuals or in studies with modest sample sizes (#983; download
my PowerPoint presentation). Other
points from the session: Andy Jackson
talked about averaging several trials to improve reliability, and Greg
Atkinson told us to watch out for differences in reliability between
subjects. The
typical variation in performance time
of elite cyclists from race to race
is ~0.5% in the 1-km sprint and ~1.3% in road time trials of 46-75 km
(#964). Divide these by ~2 to get the
smallest worthwhile performance effect, then multiply by ~2 to convert time
to mean power. So, you're chasing changes of 0.5-1.5% in mean power when you
test top cyclists. Eleven runners sleeping and resting in an altitude tent for an average of 8-11 h/d for
4 wk experienced on average an enhancement of performance in a ~5-min run to
exhaustion that was the equivalent of ~1.5% in a time trial (#11). The effect wasn't exactly clear-cut,
though. In an
unusual semi-crossover controlled study (#1634), 19 cyclists slept for 8-10 hours a night in an altitude house for 5, 10 or 15 d before
performing a 4-min supramaximal cycling test at low altitude. Enhancement was similar for the three
durations of exposure and averaged 2.3% in mean power relative to when cyclists in each group did their control
training. (The 2.3%
is probably contaminated partly by a practice effect.) There was also a whopping 13% relative
increase in maximum accumulated oxygen deficit in the test, suggesting the
performance enhancement was mediated primarily by a change in anaerobic
capacity. So only 5
d in an altitude house or tent is enough?
Or is it all just a placebo effect? In a
study of the effect of different altitudes
on sea-level performance, 48 runners
living high for 4 wk at 1780, 2085, 2454 or 2805 m while training high-low at
1250-3000 m experienced gains of 1.1, 2.8, 2.7, and 1.4% in 3000-m
running time (#1642). Gains in maximum
oxygen consumption were somewhat correlated. Conclusion: optimum altitude for
live-high train-low is 2000-2500 m. Four out
of five male high jumpers who were
undertwisted at the peak of the jump apparently needed to increase their
"catting" (#572), whereas four out of five undertwisted females
apparently needed a more vertical position at the takeoff. This practical application of kinematics needs following up with an
intervention. One set
of reps per session in a 10-wk strength-training
program with previously untrained
subjects produced a 22% increase in 1RM strength, whereas three
sets produced a 31% increase. The
authors misinterpreted statistical non-significance as equal effectiveness
(#435). In subjects with up to 2 y weight-training experience, there was
"no significant difference" in the effects of three sets of two
reps at 90% 1RM vs a traditional 8-rep program of three sets at 65, 70 and
75% 1RM, but without data… (#1827). Two bouts
of high-speed running (apparently
between 1500-m and 3000-m pace for a few minutes) on a treadmill twice a week
for 4 wk improved 3000-m time-trial time by about 3% in highly trained runners. We don't know what happened in a control
group or in a group who ran at the same intensity for slightly longer,
because these groups had "no significant improvement" (#748). And there was no comparison of groups. In collegiate footballers, a 10-wk program of single sets of high-intensity resistance training
(unstated weekly frequency) produced a greater increase in time to exhaustion
in upper- and lower-body isokinetic exercise than a traditional multi-set
program (#756). There weren't enough
data in the abstract for me to estimate the difference meaningfully. Active recovery between high-intensity bouts had such a positive effect on
performance of total work in a Wingate test that the difference (~7%)
relative to the usual passive recovery was clear cut with the sample of only
three ice-hockey players (#780). The
optimum rest interval for gains in
bench-press strength in recreational weight
trainers appears to be 4-6 min (#1828, 1829). Doubling
the usual duration of the morning warm-up slowed
time-trial time of age-group competitive
swimmers by 1.9%, whereas cutting the
afternoon warm-up to one-third of normal had little effect (#893). Replacing
the last 5 min of the usual aerobic warm-up with
high-intensity sprints resulted in 4.6% higher peak power and 2.0% higher
mean power in a 2-min kayak ergometer sprint test with experienced male paddlers (#1916). Spectacular! High-load
low-rep maximal-effort strength training made
an improvement in running economy in soccer
players that should amount to a 4-5% enhancement in endurance performance
(#1529). Wow! This paper is consistent with other recent publications on the
benefits of high-intensity resistance training for endurance athletes. Here's an
unusual potential measure for talent
identification:
concentration of various intramuscular phosphates, as determined by
magnetic resonance spectroscopy. In junior ice speed
skaters, it predicted capacity for sprint performance 6 y later
(#837). The
longer the running distance, the
bigger the difference in world-record performance between males and females: 7% for the 100 m through
19% for 200 km (#902). Reviewer's note: these competitive performance data
certainly do not support theories and limited laboratory tests suggesting
greater fatigue resistance in females. Does
drinking oxygenized water (water
saturated with oxygen gas) really enhance endurance performance (#945)? You
can't get nearly enough oxygen into water to account directly for the higher
arterial saturation (91% vs 87%) the authors observed at the end of the
constant-load test to exhaustion on a cycle ergometer in this double-blind
crossover study of 20 male and female regular
exercisers. There was even
a significant effect on performance in an incremental test for the fitter
subjects (2.6% for performance time, which would convert to less for peak
power), although that kind of post-hocery needs following up with another
study. Again, the dissolved oxygen can't account directly for the
effect. The findings mystified the
authors. And
finally, tight neoprene-butyl rubber
shorts enhanced jump performance in 10 female and 10 male varsity sprinters
and jumpers (#1340; no data). Energy storage during the
counter-movement phase of the jump? I was
also in Baltimore for the ACSM meeting.
A recurring theme during lectures and lively, lunch-time
discussions--complete with laptop presentations of data!--was the increasing
sophistication and effectiveness of erythropoietin
(EPO) testing. International cooperation is paving the way. By the
2002 Winter Olympics, multi-factorial blood-profile testing will be in
place. If you are using EPO, they will
get you. More importantly, if you were
using EPO, they'll still get you!
New banned substances will continue to appear, but in many cases, a
test will be developed even before they hit the market. Nice work, guys! It was
standing room only for the mini-symposium on fatigue
(the ATP Paradox…) by Tim Noakes, Zig Gibson and Vicky Lambert (#537). The
talks were entertaining and at times thought provoking. Questions raised about how the CNS
determines and carries out accurate pacing strategies at the start of
exercise were quite captivating.
However, the apparent attempt to force a paradigm shift from
peripheral contractile fatigue mechanisms to central mechanisms was weak. A lot more research needs to be done before
we reinterpret a great deal of existing work supporting the importance of
peripheral fatigue mechanisms. --Stephen Seiler
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