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1 Department of Physical Education, University of Las Palmas de Gran Canaria, 35017 Las Palmas de Gran Canaria, Canary Islands; 2 Instituto Nacional de Educación Física de Leon, University of Leon, 24071 Leon; and 3 Centro de Tecnificación de Ciclismo, Chiclana de la Frontera, 11130 Cádiz, Spain
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The aim of this study was to
evaluate the effects of severe acute hypoxia on exercise performance
and metabolism during 30-s Wingate tests. Five endurance- (E) and five
sprint- (S) trained track cyclists from the Spanish National Team
performed 30-s Wingate tests in normoxia and hypoxia (inspired
O2 fraction = 0.10). Oxygen deficit was estimated from
submaximal cycling economy tests by use of a nonlinear model. E
cyclists showed higher maximal O2 uptake than S (72 ± 1 and 62 ± 2 ml · kg
1 · min1,
P < 0.05). S cyclists achieved higher peak and mean
power output, and 33% larger oxygen deficit than E (P < 0.05). During the Wingate test in normoxia, S relied more on
anaerobic energy sources than E (P < 0.05); however, S
showed a larger fatigue index in both conditions (P < 0.05). Compared with normoxia, hypoxia lowered O2 uptake by
16% in E and S (P < 0.05). Peak power output, fatigue index, and exercise femoral vein blood lactate concentration were not
altered by hypoxia in any group. Endurance cyclists, unlike S,
maintained their mean power output in hypoxia by increasing their
anaerobic energy production, as shown by 7% greater oxygen deficit and
11% higher postexercise lactate concentration. In conclusion,
performance during 30-s Wingate tests in severe acute hypoxia is
maintained or barely reduced owing to the enhancement of the anaerobic
energy release. The effect of severe acute hypoxia on supramaximal
exercise performance depends on training background.
fatigue; anaerobic power; anaerobic capacity; lactate
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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THE IMPACT THAT ACUTE
SEVERE hypoxia has on aerobic and anaerobic energy yield during
the Wingate test remains unknown. Although moderate acute hypoxia
[inspired O2 fraction
(FIO2) = 0.13] has no effect on
either O2 uptake (
O2) or
performance during supramaximal exercise of a duration up to 30 s
(39), conflicting results have been reported about the
influence that higher levels of hypoxia might have on performance and
metabolism (22, 23). McLellan et al. (23)
observed unchanged mean power output (Pmean) and O2 during a 30-s Wingate test performed
with a FIO2 ~0.11. Prolonging the
Wingate test duration until 45 s consistently resulted in lower
O2 with hypoxia (22, 23)
whereas, compared with normoxia, Pmean during the 45-s Wingate test was
not affected by acute hypoxia in one study (23) and
slightly reduced (~3% less) in another investigation
(23). Small differences in the
FIO2 and time exposure to hypoxia before
the start of the Wingate tests could explain the apparently
contradictory results reported by McLellan et al. (22,
23). It was clearly shown, on the other hand, that during all-out exercise in acute hypoxia lasting 30 or 45 s, muscle
lactate accumulation is markedly increased, indicating a greater
anaerobic energy release with acute hypoxia (23).
Furthermore, some pieces of evidence suggest that during supramaximal
exercise producing exhaustion between 30 and 60 s the contribution
of the anaerobic energy sources is increased in acute moderate hypoxia
(22, 39). Whether a higher degree of hypoxia could enhance
anaerobic energy release during 30-s Wingate tests is not known.
It has been estimated that, in general, anaerobic energy sources
provide 70-80% of energy utilized throughout the Wingate test
(6, 28, 33, 40). However, compared with sprint
specialists, endurance-trained athletes have greater mean
O2 during the Wingate tests
(12) and obtain a higher fraction of the energy from
oxidative metabolism. In turn, sprint-trained athletes obtain a greater fraction of energy through the anaerobic pathways (6).
Thus it can be hypothesized that because endurance-trained athletes rely more on aerobic energy sources to perform all-out supramaximal exercise they will experience a relatively greater impairment of
performance than sprint-trained athletes with acute hypoxia, unless
they compensate for the reduction in O2
by enhancing the anaerobic energy release.
Therefore, the primary aim of this study was to find out whether the reduction in O2 supply elicited by severe acute hypoxia can be counteracted by enhancing anaerobic energy production during 30-s Wingate tests. Another purpose was to verify whether endurance-trained elite track cyclists would experience superior deterioration of performance than their sprint-trained counterparts during 30-s Wingate tests in acute hypoxia. To unravel more easily the effect of hypoxia, the FIO2 was reduced to 0.104, which is equivalent to an altitude of ~5,300 m. This level of hypoxia is close to the limit that a healthy nonacclimatized human can tolerate acutely during upright exercise (4, 32, 36).
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects
This study was approved by the ethics committee at the University of Las Palmas de Gran Canaria. The subjects were fully informed of the purpose and possible risks and benefits of their participation in the study before giving their written consent. Ten track cyclists from the Spanish National Team participated in this study. All them had qualified more than once among the first three finishers in the Spanish National Championship. The group included several National Champions and a silver medalist in the last World Championship, who was a sprint specialist. Five cyclists were sprint specialists, and the other five were endurance-trained cyclists. The mean ± SE ages, heights, weights, and percentages of body fat were 19.0 ± 0.7 vs. 18.8 ± 0.4 yr, 176 ± 2 vs. 179 ± 0.7 cm, 74.7 ± 3.1 vs. 65.8 ± 1.0 kg, and 13.2 ± 1.9 vs. 9.3 ± 0.5% in the sprint and endurance cyclists, respectively. Subjects were requested to follow similar diets and lessen physical activities during the 48 h before the experiments. They were also instructed to refrain from any food for at least 4 h before each test session.Experimental Protocol and Procedures
The percentage of body fat was estimated anthropometrically by using a population-specific equation, which was developed and validated in our laboratory by using dual X-ray absorptiometry as a gold standard (19). Subjects completed four test sessions in separate days. First, their maximalO2
(O2 max) and maximal power output
(Wmax) were assessed via an incremental exercise test to exhaustion (25 W/min, at 90 rpm). During the next 2 testing days, the relationship
between O2 and intensity (or cycling
economy) was determined. Then, during the last test session,
Wingate tests were carried out while the subjects were breathing either
room air (normoxia) or air from a Douglas bag containing 10.4%
O2 in N2 (hypoxia), equivalent to an altitude of ~5,300 m. This level of acute hypoxia was chosen because it reduces O2 max by nearly 50%
(10, 36), creating, therefore, a condition in which a
potential limitation to aerobic energy supply would be present during
the Wingate tests performed in severe hypoxia. Normoxic and hypoxic
Wingate tests were performed in random order and separated by a
recovery period of at least 1 h, which is enough to allow for a
complete recovery (6).
Cycling economy tests.
Cycling economy was determined by using 12 submaximal workloads at
intensities of between 60 and 90%
O2 max, at four different pedaling
rates: 60, 80, 100, and 120 rpm. Exercise intensities and pedaling
rates were administered in random order, separated by rest periods of
3-5 min. To reduce thermal stress and minimize water losses due to
sweating, subjects were fan cooled and ingested in total 600 ml of
water during the resting periods. Tests were performed at
18-24°C, 60-80% relative humidity, and 750-770 mmHg atmospheric pressure. The duration of each submaximal bout was set at 6 min. The mean O2 registered during the
last 2 min was taken as representative of each submaximal exercise
intensity. To relate O2 to power,
individual nonlinear regression equations were calculated by
least-square linear fit, applying the following nonlinear model:
O2 = a+b · W+c · rpm+d · rpm2,
which gave a standard error of estimate that was always lower than 100 ml/min of O2, where a, b,
c, and d are the constants to be determined by
the nonlinear regression equation; W is the exercise intensity; and rpm
is the pedaling rate.
Wingate tests.
To determine whole blood lactate concentration ([La]) in the femoral
vein, a 20-gauge catheter (Hydrocath, Ohmeda, Swindon, UK) was inserted
percutaneously by use of the Seldinger technique into the right femoral
vein under local anesthesia (2% lidocaine) as previously reported
(29). The catheter was inserted 2 cm below the inguinal
ligament and was advanced 12 cm toward the knee to avoid contamination
of the blood coming from the deep quadriceps muscle veins with
saphenous vein blood. Once in place, the catheter was sutured to the
skin to minimize the risk of movement or creasing, and the outlet of
the catheter was connected to a three-way stopcock. After a resting
period of ~5 min, subjects carried out a standardized warm-up
consisting of 10 min of continuous cycling at an intensity close
to 60% O2 max followed by
five maximal accelerations lasting for no more than 5-6 s. Then
the subjects rested for 10 min and were randomly assigned to a normoxic
or hyperoxic Wingate test. To minimize the risk of hypotension and
respiratory alkalosis during the hypoxic Wingate tests, the subjects
commenced to breathe from the hypoxic gas bag only 3 min before the
onset of the exercise (36). During the Wingate tests,
femoral vein blood samples were drawn continuously for periods of
5 s, given a total of six exercise samples. An hour later, the
Wingate test was repeated in the other condition. After both Wingate
tests, the subjects recovered in normoxia while lying on a bed, and
additional blood samples were withdrawn from the femoral vein 3, 5, 7, and 10 min after the start of the recovery period. Braking forces
equivalent to 0.11 kp per kg of body mass were used in all cyclists.
O2 and power output measured at
submaximal loads. Then the O2 deficit was computed as the
difference between the O2 demand and the O2
consumed during the supramaximal bouts (25, 39).
Respiratory variables.
Ventilatory and gas exchange variables were monitored breath-by-breath
by an open-circuit sampling system (CPX, Medical Graphics, St. Paul,
MN) and averaged every 15 s during the incremental exercise tests
and every 5 s during the Wingate tests. The metabolic cart was
calibrated with calibration gas mixtures of known O2 and
CO2 concentrations (accuracy 0.01%), which were provided
by the manufacturer (CPX, Medical Graphics). In our laboratory,
O2 and CO2 production during
submaximal cycling has been assessed with a coefficient of variation
lower than 5%, as well as with an intraclass reliability coefficient
higher than 0.98, as determined in six physical education students at
four different intensities on 4 different days. The highest
O2 value attained during the incremental
exercise tests was taken as the O2 max,
whereas the intensity attained just before exhaustion is referred to as
Wmax. The Wmax was adjusted by extrapolation depending on the duration
of the last step (18). To determine the kinetics of the
O2 on-response, breath-by-breath data
were averaged every 5 s and fit to a curve by using an exponential model, by means of the least-squares error approach. The curve-fitting procedure was iterated until any further changes in the parameters for
the model did not result in a reduction in the mean squared error
between the curve obtain from the model and the original data set. The
model used to fit the O2 on-data had a
constant, which corresponds to resting
O2, an amplitude term (b),
and a time constant (c) as follows
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O2(t) is the time-dependent
variation in O2.
Blood lactate. [La] was determined in whole blood by using a lactate analyzer (YSI 1500 Sport, Yellow Springs, CO) provided with hemolyzing agent (Triton X-100). With this instrument, we obtained a coefficient of variation for whole blood [La] assessment lower than 1%, for [La] between 1 and 26 mM. Recovery blood [La] curves were integrated over time and expressed as millimolar · seconds. Reported values correspond to the net area under curve, i.e., the area under the curve after accounting for the resting blood [La] immediately before the start of the Wingate tests.
Statistical Analysis
Descriptive statistics were performed on each variable to confirm the assumptions of normality and homocedasticity. The effect of O2 inspired fraction on femoral blood lactate during the Wingate tests was determined using a two-way repeated-measures analysis of variance with cyclists specialty as a two-level factor. In the case of a significant F value, planned comparisons were carried out by using a Student's paired or unpaired (as appropriate) t-test with Bonferroni correction to account for multiple comparisons. The significance level was set at P < 0.05. Data are expressed as means ± SE.| |
RESULTS |
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ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Differences Between Endurance- and Sprint-Trained Cyclists
Endurance cyclists showed higherO2 max than the sprint-trained cyclists
(72 ± 1 and 62 ± 2 ml · kg1 · min1,
P < 0.05). As depicted in Fig.
1A and Table
1, absolute and relative peak power
output (Pmax) and Pmean were greater in the sprint than in the
endurance cyclists. Accordingly, sprint cyclists reached greater
maximal and mean pedaling rates than endurance-trained cyclists (Fig.
1B). Sprint cyclists, however, fatigued faster than the
endurance cyclists, as indicated by the fatigue index during the
Wingate test, which was 0.46 ± 0.12 and 0.32 ± 0.12 W · s1 · kg1
body mass in the sprint and endurance cyclists, respectively (Fig.
2A; P < 0.05). In consequence, the sprint
cyclists' superiority in power output was reduced progressively during
the second half of the Wingate tests, developing in both groups almost
similar power output values per kilogram of body mass during the last 15 s (Fig. 1A). The sprint cyclists incurred a greater
O2 demand during the first 10-15 s of the Wingate test
(Fig. 1, C and D). Likely because of their
greater O2 max, the endurance cyclists
were able to consume 26% more O2 per kilogram of body mass
during the Wingate tests than the sprint cyclists (P < 0.05), because both groups utilized a similar percentage of their
O2 max during the Wingate tests in
normoxia (Fig. 2B). In fact, a close correlation was
observed between the mean O2 during the
Wingate test and O2 max (Fig.
2C; r = 0.86, P < 0.001).
With greater O2 demand and lower
O2, O2 deficit per kilogram
of body mass resulted 33% higher in the sprint than the endurance
cyclists (Fig. 1H). The difference between 26% superior
aerobic energy yield in the endurance cyclists and 33% greater
O2 deficit in the sprint cyclists leads to the ~8%
superior Pmean developed during the Wingate by the sprint specialists.
Despite these remarkable differences in anaerobic energy yield during
the Wingate tests, the rate of femoral vein blood [La] accumulation
during exercise was similar in the endurance and sprint cyclists. In
both groups, femoral blood [La] did not change during the first
15 s of exercise, but thereafter it augmented, describing a
parabola as exercise time passed (in all conditions, r = 0.99, P < 0.001; Fig. 1G). During the
first 10 min of the recovery period, the sprint cyclists accumulated
27% more lactate in the femoral vein than their endurance counterparts
(P < 0.05; Fig. 3).
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As depicted in Fig. 4 the anaerobic
energy contribution to the overall energy expended during the Wingate
test decreased following a parabolic pattern (r > 0.98, P < 0.01). The sprint cyclists obtained a
slightly greater proportion of energy through the anaerobic pathways
(Table 1). Extrapolation of the curves depicted in Fig. 3 to 0%
anaerobic energy contribution permits us to predict the duration that
an all-out test should have to enable a complete utilization of all
the anaerobic energy potential (Fig. 4). Because the sprint
cyclists had larger O2 deficit and obtained a greater fraction of energy through the anaerobic pathways, the rate of anaerobic energy release was much higher in the sprint than in the
endurance cyclists. Despite this fast recruitment of their anaerobic
capacity, the sprint cyclists needed 4-5 s more than the endurance
cyclists to fully express their anaerobic capacity.
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Effect of Severe Acute Hypoxia
The time course of power output, O2 demand,O2, O2 deficit, and blood
[La] during the normoxic and hypoxic Wingate tests are depicted in
Fig. 1. Although Pmax was not affected by hypoxia in any group, Pmean
and pedaling rate were reduced by 6-7% in the sprint cyclists
(P < 0.05). In the endurance cyclists, however, Pmean
and pedaling rate remained at same level as in normoxia. With a lower
Pmean, O2 demand was diminished in the sprint cyclists exercising in hypoxia (P < 0.05). In both groups,
hypoxia resulted in a 16% lower mean O2
(P < 0.01; Fig. 1E). The divergence between normoxic and hypoxic O2 during the
Wingate test began 10 s after the start of the test and became
more accentuated as the exercise progressed (P < 0.05).
Hypoxia had opposed effects on O2 deficit in sprint and endurance cyclists, inasmuch as, compared with normoxia, hypoxia resulted in a 5% lower O2 deficit in the sprint cyclists (P < 0.05), whereas it promoted a 7% greater value in the endurance cyclists (P < 0.05). This different effect was further sustained by a significant interaction effect in the ANOVA analysis. In agreement, the endurance cyclists achieved an 11% greater area under the blood [La] curve during the recovery period after the hypoxic Wingate tests (P < 0.05; Fig. 3), whereas recovery [La] was unaffected by hypoxia in the sprint cyclists. During the 30-s exercise period, however, the rate of blood lactate accumulation was similar in normoxia and hypoxia (Fig. 1G). Fatigue index was also similar in normoxia and hypoxia (Fig. 2A). The anaerobic contribution to the energy expenditure in hypoxia was greater than in normoxia. However, this effect was significant only in the endurance cyclists (P < 0.05).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The effect of severe acute hypoxia, equivalent to an altitude of
~5,300 m, on exercise metabolism and performance has been studied in
elite endurance and sprint-trained track cyclists. This study
demonstrates that severe acute hypoxia does not alter peak power output
and fatigue index during 30-s Wingate test. In contrast, Pmean is
reduced with acute severe hypoxia in sprint but not in
endurance-trained cyclists, despite the fact that in both groups mean
O2 was reduced by 16% during the
Wingate tests in hypoxia. In addition, it has been shown that, compared
with sprint, endurance-trained cyclists display superior maximal
aerobic power, attain lower Ppeak and Pmean, achieve a lower
O2 deficit, have a lower fatigue index, obtain a greater
fraction of the energy expended via oxidative pathways during a 30-s
Wingate test, and show a lower femoral venous blood [La] after the
Wingate test.
Effect of Severe Acute Hypoxia
In contrast to our hypothesis, Wingate test performance was only reduced with severe acute hypoxia in the elite sprint cyclists whereas it was maintained in the endurance cyclists. In both groups,O2 was lowered in the same proportion
(i.e., 16%), but because O2 per
kilogram of body mass was larger in the endurance cyclists, the
absolute reduction of O2 was slightly
greater in the endurance than the sprint cyclists. If we assume similar
cycling efficiencies in normoxia and acute hypoxia, the only possible
explanation for these findings is superior anaerobic energy release in
hypoxia (39). The fact that O2 deficit
increased with hypoxia in the endurance but not in the sprint cyclists
supports this concept. Several metabolic pathways are stimulated to
supplement energy production when aerobic metabolism is not capable of
matching aerobic ATP production to consumption, especially the
splitting of phosphocreatine and glycolysis. To our knowledge only
McLellan et al. (23) have investigated the effect of
moderate acute hypoxia on muscle metabolism during the Wingate test.
They reported that, compared with normoxia, muscle [La] doubles when
Wingate tests are performed in acute hypoxia. Because the glycolytic
branch of the anaerobic metabolism represents ~3/4 of the anaerobic
capacity (1, 3, 33), an increase in muscle lactate
accumulation of the magnitude reported by McLellan et al.
(23) would account for most of the reduction in aerobic
ATP generation with hypoxia in the present study.
It has been shown that during all-out bicycling lactate production commences almost at the onset of muscular contractions reaching concentrations up to ~7 (11), ~11 (16), and ~17-29 mM (3, 16, 23, 28) in 6, 10, and 30 s, respectively. Despite the superior muscle lactate accumulation with hypoxia, recovery blood [La] (measured in a forearm vein) was found to be slightly lower in hypoxia in one study (23) and similar to the normoxic conditions in another study from the same group (22). In a novel procedure, in the present study blood was sampled from the vicinity of the contracting muscle because systemic and local arm metabolism may interfere with forearm [La]. Moreover, by sampling blood every 5 s we have been able to measure for the first time the kinetics of femoral vein blood [La] accumulation during Wingate tests. Our data demonstrate that the kinetics of femoral venous blood lactate accumulation is independent of FIO2 during 30-s all-out exercise. In both conditions there was a 15-s lag between the onset of exercise and the beginning of blood lactate accumulation, indicating that most of the lactate produced at the onset of exercise is retained inside the muscle. No clue is given by the present study to explain why lactate is not released during the first 15 s of exercise. If the principal motor driving lactate net release is muscle pH (30), the fact that muscle pH is barely changed at the onset of exercise could facilitate muscle lactate accumulation, or perhaps the muscle lactate transporters must first be activated.
A number of studies have shown that the total anaerobic capacity cannot
be used up in 30 s (6, 7, 25, 26, 31, 33, 35).
Hypoxia appears to stimulate additional utilization of the anaerobic
capacity to compensate for the reduction in aerobic ATP production.
This effect was clear in the endurance cyclists, whereas the sprint
cyclists showed a small reduction in their O2 deficit,
which, combined with the lower O2, led
to decreased Pmean. The critical question is what limits performance
during the Wingate test? Our findings contrast with the prevailing
paradigm, which proposes that performance during the Wingate test is
limited by the rate of anaerobic energy release (2, 7),
which, in turn, depends on substrate availability and enzymatic control (7, 28, 35). It is well known that performance during the Wingate test is not limited by glycogen availability (16, 17, 23,
26). Our study novelly shows that neither the availability of
anaerobic energy nor the rate of anaerobic energy release limits performance during the Wingate test in the elite endurance cyclists. Our results point to the rate of ATP utilization as the
performance-limiting factor during the traditional Wingate test.
According to our results, the factors reducing the rate of ATP
hydrolysis should be common to the aerobic and anaerobic pathways. This
requirement is fulfilled by ADP and Pi, which accumulate
during all-out exercise and thus could set the upper limit of ATP
utilization throughout their inhibitory effects on muscle contraction
(9, 38). In contrast, according to our results,
performance in sprint cyclists appears to be substrate limited in
hypoxia, as reported in normoxia in nontrained (35) and
physically active subjects (7).
It should be highlighted that the level of hypoxia used in our study is very close to the limit that a human can tolerate acutely. During incremental exercise to exhaustion under these conditions, arterial PO2 values at exhaustion approached 30-35 mmHg (36). This level of hypoxia is very close to the limit that can be tolerated for a short time by an unacclimatized human and is similar to that reported in altitude-acclimatized subjects at the summit of Mt. Everest simulated in Operation Everest II (34). Severe hypoxemia, in turn, could have elicited central fatigue (27) or reduced peak leg blood flow (5). Although we cannot rule out a central component in fatigue appearance, in agreement with previous investigations performed with lower levels of hypoxia (22, 23), no effect of severe acute hypoxia on fatigue index or peak power output was found in this study. Furthermore, clinical signs of fatigue and the ventilatory response during the hypoxic Wingate tests (data not shown) were similar in both groups of cyclists. It does not seem, therefore, that differences in central fatigue mechanisms could explain the reduction of performance with hypoxia in the sprint cyclists.
Oxygen deficit, as measured in this study, is not a pure estimation of
the anaerobic energy utilized because the O2 consumed from
the O2 stores [especially O2 bound to
myoglobin, which has been estimated to be 2 mmol/kg wet wt
(14), and O2 bound to hemoglobin] at the
onset of the exercise is computed as the O2 deficit,
leading to an overestimation of the anaerobic energy production and,
conversely, an underestimation of the real
O2 (25). This intrinsic
error of the deficit method is, however, rather small because of the
comparatively low amount of O2 stored in the skeletal
muscle in relation to the magnitude of the O2 deficit. If
exercise bouts are performed in normoxia and hypoxia, the
O2 stores at the beginning of the exercise would be lower in the hypoxic condition, reducing the overestimation of the
O2 deficit. Resting myoglobin saturation, however, was
likely very similar in normoxia and hypoxia, owing to the especial
characteristics the O2 dissociation myoglobin curve, which
has an O2 pressure at which myoglobin saturation is 50%
that is close to 3 mmHg (30). With the level of
hypoxia used in this study, a resting arterial PO2 of 45-50 mmHg and saturation of
~80% have been reported (32). Consequently, the amount
of O2 stored as O2 bound to hemoglobin was
probably 20% lower at the onset of the hypoxic Wingate test. If this
was actually the case, the hypoxia-normoxia O2 deficit difference could have been even higher than the 7% calculated for the
endurance cyclists, and perhaps no reduction in O2 deficit with hypoxia would have been observed in the sprint cyclists. Assuming
that both groups had a similar reduction in their O2 stores
with hypoxia, our data demonstrate that endurance cyclists have a
greater capacity to enhance the anaerobic energy production in response
to hypoxia than the sprint cyclists. Perhaps the sprint cyclists are
already using their anaerobic energy at a rate close to the maximum in
normoxia, and, thus, they are not be able to compensate for a reduction
in aerobic ATP production with hypoxia via an enhancement of rate of
anaerobic energy release.
Differences Between Endurance and Sprint Specialists
One singularity of this study is the outstanding level of the cyclists examined, who were among the best in Spain with several very successful achievements in international competitions in both groups. In the case of the sprint cyclists, Ppeak and Pmean were among the highest reported in literature (8, 12, 22, 23, 40). It should be mentioned that the Pmax obtained in the Monark cycle ergometer was similar to and closely correlated with the Pmean measured during the first 30 s of a 500 m track sprint (measured in the 10 cyclists here studied with a SRM ergometer, data not shown; Ref. 8). The Pmean developed by these cyclists was far beyond the maximal aerobic power output; accordingly, O2 deficit was also higher than reported in previous studies for cyclists (8, 13, 40). As expected, sprint cyclists had lowerO2 max but much larger O2
deficit than the endurance specialists (8, 24). Assuming
that the sprint cyclists utilized 80-90% of their anaerobic
capacity in 30 s (6, 25, 31, 33), their actual
maximal accumulated O2 deficit can be estimated to lie in
between 75 and 85 ml/kg. In fact, it has been suggested that world
class sprint athletes may reach even higher O2 deficits (8, 25, 31). The superiority of sprint cyclists in
anaerobic power and capacity is probably the result of an increased
percentage of type II fibers, more appropriate enzymatic machinery to
produce ATP through anaerobic pathways, and enhanced buffer capacity
(8, 13, 20, 21). However, fatigue index was markedly
higher in the sprint than the endurance cyclists. Because sprint
cyclists have a higher proportion of type II fibers than the endurance cyclists (21), they should choose a faster pedaling rate,
because type II fibers are more efficient at a faster contraction speed (15). The drawback of this strategy is that type II fibers
are less resistant to fatigue (15). The election of high
pedaling frequencies may be advantageous for speed in track
competitions (37). In an interesting experiment using an
isokinetic cycle ergometer, Jones et al. (17) demonstrated
that the same Pmean is developed at 60 and 140 rpm, but peak power
output is considerably higher at 140 rpm, at the price, however, of an
increased fatigue index.
Withers et al. (40) reported that endurance-trained cyclists can utilize 94% of their anaerobic capacity in a 45-s all-out test. Using a different approach, we have estimated that the endurance cyclists might utilize the totality of their anaerobic capacity in 43 s whereas the sprint cyclists would need 47 s (see Fig. 3).
Limitations of the O2 Deficit as a Measure of the Anaerobic Energy Yield
Despite the limitations of O2 deficit as a method to estimate the anaerobic energy yield, we should emphasize that our estimations on the partitioning between aerobic and anaerobic energy sources during the Wingate test agree amazingly well with the ATP turnover rates reported by Parolin et al. (28). These authors measured the aerobic and anaerobic ATP turnover rate in muscle biopsies obtained at three different time points during an isokinetic Wingate test at 100 rpm. During the last 15 s of the Wingate test, the mean aerobic contribution to the energy expenditure was 54% in Parolin et al.'s work and 48% in our endurance cyclists. The small difference between our estimations and the biopsy data of Parolin et al. probably reflects the fact that lactate release from the muscle was not accounted for in Parolin et al.'s work. Thus they probably underestimated slightly the anaerobic contribution during the last 15 s of the Wingate test, a period in which we have shown an increase in femoral venous lactate.The real values of O2 deficit could be lower or higher than
reported here, but if we assume that mechanical efficiency during the
Wingate tests was similar in normoxia and acute hypoxia, as has been
demonstrated for submaximal exercise, then our conclusion that
anaerobic energy production is increased during 30-s all-out exercise
in hypoxia to account for the reduction in
O2 is irrefutable.
In summary, the effects of severe acute hypoxia, equivalent to an
altitude of ~5,300 m, on exercise metabolism and performance have
been studied in elite endurance- and sprint-trained track cyclists. We
have demonstrated that peak power output and fatigue index are not
altered by severe acute hypoxia, whereas mean
O2 is reduced by 16% in endurance- and
sprint-trained cyclists. Interestingly, despite this marked reduction
in O2, only endurance-trained cyclists
are able to maintain Pmean by increasing their anaerobic energy
production, which shows that neither anaerobic capacity nor the rate of
anaerobic energy release limits Wingate test performance in endurance
cyclists. Conversely, a small decrease, inferior to that expected from
the reduction in O2, of Pmean with
hypoxia is observed in the sprint-trained cyclists. Endurance-trained cyclists, on the other hand, possess superior maximal aerobic power and
obtain a greater fraction of the energy expended during a Wingate test
via oxidative pathways than sprint-trained cyclists. In turn,
sprint-trained cyclists display larger O2 deficit (+33%), rely more on anaerobic energy sources, and achieve higher peak and
Pmean during a Wingate tests. Sprint-trained cyclists, however, develop
fatigue at a faster rate than endurance-trained cyclists during
supramaximal all-out exercise. In contrast to the prevailing paradigm,
this study shows for the first time that performance during the
traditional Wingate test is not limited by anaerobic energy supply in
endurance cyclists.
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ACKNOWLEDGEMENTS |
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We would like to thank Jose Navarro de Tuero, Angel Vivas, and Mecánico Mei for excellent technical assistance.
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FOOTNOTES |
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This study was supported by a grant (08/UNI01/99) from Centro de Alto Rendimiento y de Investigación en Ciencias del Deporte, Consejo Superior de Deportes de España and by the University of Las Palmas de Gran Canaria (Proyectos de Infraestructura 2000).
Address for reprint requests and other correspondence: J. A. L. Calbet, Departamento de Educación Física, Universidad de Las Palmas de Gran Canaria, Campus Universitario de Tafira, 35017 Las Palmas de Gran Canaria, Canary Islands, Spain (E-mail: lopezcalbet{at}terra.es).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
First published October 4, 2002;10.1152/japplphysiol.00128.2002
Received 20 February 2002; accepted in final form 1 October 2002.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
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