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,1 School of Exercise and Sport Science, The University of Sydney, Lidcombe, 1825; 2 School of Human Movement, Recreation and Performance, and 3 Exercise Metabolism Unit, School of Life Science and Technology, Centre for Rehabilitation, Exercise, and Sport Science, Victoria University of Technology, Footscray, 8011; and 4 School of Health Sciences, Deakin University, Burwood, 3125, Australia
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The effects of sprint
training on muscle metabolism and ion regulation during intense
exercise remain controversial. We employed a rigorous methodological
approach, contrasting these responses during exercise to exhaustion and
during identical work before and after training. Seven untrained men
undertook 7 wk of sprint training. Subjects cycled to exhaustion at
130% pretraining peak oxygen uptake before (PreExh) and after training
(PostExh), as well as performing another posttraining test identical to
PreExh (PostMatch). Biopsies were taken at rest and immediately
postexercise. After training in PostMatch, muscle and plasma lactate
(Lac
) and H+ concentrations, anaerobic ATP
production rate, glycogen and ATP degradation, IMP accumulation, and
peak plasma K+ and norepinephrine concentrations were
reduced (P < 0.05). In PostExh, time to exhaustion was
21% greater than PreExh (P < 0.001); however, muscle
Lac accumulation was unchanged; muscle H+
concentration, ATP degradation, IMP accumulation, and anaerobic ATP
production rate were reduced; and plasma Lac,
norepinephrine, and H+ concentrations were higher
(P < 0.05). Sprint training resulted in reduced
anaerobic ATP generation during intense exercise, suggesting that
aerobic metabolism was enhanced, which may allow increased time to fatigue.
anaerobic ATP production; lactate; oxidative metabolism; hydrogen ion; potassium
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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INTENSE EXERCISE RESULTS in a marked elevation in ATP utilization, provokes considerable metabolic and ionic perturbation in contracting skeletal muscle, and is characterized by a rapid onset and pronounced degree of muscular fatigue that is evidenced by a decline in power output (8, 16, 23, 25, 27, 30, 34, 35, 37). Sprint training typically enhances performance during single or repeated bouts of brief intense exercise (3, 4, 19, 26, 30, 35, 39). However, the fundamental metabolic and ionic mechanisms enabling this adaptation remain controversial.
Augmented muscle glycolysis during intense exercise after sprint
training is suggested by findings of higher phosphofructokinase (PFK)
activity (14, 17, 19, 35) and higher accumulation of
muscle lactate (4, 17, 30, 35) and glycolytic
intermediates (30) after fatiguing maximal exercise.
Conversely, a lack of change after sprint training has also been
reported for PFK (32) and glycogen phosphorylase
activities (19, 35). Similarly, after sprint training, no
change was evident during exhaustive exercise in glycogen degradation
(30), glucose-6-phosphate accumulation (17),
muscle lactate (Lac) accumulation (39), or
the arteriovenous blood Lac concentration difference
across the exercising leg (26, 32). Thus the effects of
sprint training on glycolysis during exercise are unclear. A similar
controversy exists for the effects of sprint training on aerobic
metabolism during intense exercise. Although muscle oxidative
enzyme activities are higher after sprint training (14, 19,
32), oxygen uptake (
O2) during
brief, intense exercise was unchanged in one study (30)
and tended to be higher after training in another (26).
Consequences of intense exercise include muscle adenine nucleotide
degradation and muscle K+ loss. The effects of sprint
training on each of these remain unresolved. For example, adenine
nucleotide degradation was reduced after training in one study
(39) but unchanged in two others (4, 30).
Although sprint training increased muscle sodium-potassium ATPase
(Na+-K+-ATPase) content (27) and
increased net Na+ and K+ uptake by contracting
muscle during intense exercise (25), the expected training
effect of reduced exercise-induced hyperkalemia was not evident after
sprint training (25, 27).
Thus, despite extensive investigation into the effects of sprint training on muscle metabolism and, to a lesser extent, ionic regulation, many important issues remain unresolved. Interpretation of the findings in every study cited above is compromised by the methodological approach taken, in that subjects in these studies have been examined while performing greater work after training. Furthermore, very few studies (25, 26, 30) have adopted the more appropriate integrative approach whereby each of the respiratory, metabolic, and ionic adaptations to sprint training has been examined. We speculate that the application of a more rigorous methodological approach will resolve these inconsistencies in the sprint training literature. Such an approach demands analysis of training-induced adaptations under conditions of identical work before and after training, in addition to the commonly employed exhaustive performance test.
This study investigated the effects of sprint training on respiratory,
metabolic, and ionic perturbations during intense exercise conducted at
an identical power output in two separate tests: one test matched for
duration in pre- and posttraining trials and the other continued until
exhaustion. We hypothesized first that aerobic metabolism would be
enhanced during identical exercise conditions after sprint training,
which would therefore result in reductions in muscle Lac
and H+ contents, anaerobic ATP production, ATP degradation,
IMP accumulation, and plasma K+ concentration
([K+]). Secondly, we hypothesized that, as a consequence
of these changes, the exercise time to exhaustion would be extended in a separate posttraining test at the same power output, thus allowing similar metabolic and ionic perturbations to be evidenced during exercise as occurred before training.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects
Seven healthy, recreationally active male subjects gave informed consent to participate in this study, which was approved by The University of Sydney Human Ethics Committee. Each subject abstained from caffeine and alcohol consumption and refrained from strenuous exercise for 24 h before each exercise test. Subjects presented at the laboratory 2-3 h postprandial. Subject characteristics (means ± SD) were as follows: age, 22.0 ± 3.0 yr; height, 180.0 ± 5.1 cm; and body mass, 76.1 ± 2.5 kg.Exercise Tests
Each exercise test was conducted in the same order pre- and posttraining, with the exception of the 30-s all-out tests, which were conducted in the first and last training sessions (Fig. 1).
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Incremental test.
Before training (2 days after an identical familiarization trial),
subjects cycled on an electronically braked ergometer (Ergoline 800s,
Mijnhardt, Netherlands) for 4 min at 60, 90, 120, and 150 W to obtain
steady-state O2, followed immediately by
a 25 W/min incremental test to volitional fatigue to obtain peak oxygen
consumption (O2 peak).
O2 peak was defined as the highest oxygen consumption (O2) measured during
a 30-s period. Heart rate and rhythm was monitored via
electrocardiogram. Expired volume was determined using a
pneumotach (Hans Rudolph), and expired gas fractions were
determined by oxygen and carbon dioxide analyzers (Ametek, Thermox
Instruments, Pittsburgh, PA). A computer displayed, measured,
and derived variables every 10 s. A linear regression was
applied to steady-state O2 and
power output data, and, in conjunction with the
O2 peak, was used to determine a power
output equivalent to 130% O2 peak
for the subsequent sprint tests. One to two days after the final
training session, peak and submaximal O2
were reassessed using an identical protocol.
Constant load sprint tests.
respiratory test.
Before training, a sprint test (PreResp) was conducted to exhaustion on
the electronically braked cycle ergometer for measurement of
ventilation and gas exchange. After a 3-min warm-up at 20 W, subjects
pedaled at 130% O2 peak, at 110 rpm.
Exhaustion was defined as the inability to maintain a cadence 
80 rpm
despite strong verbal encouragement. This test was conducted separately from the invasive sprint test (see below), both for practical reasons
and to minimize the stressful effects of complex testing procedures on
subjects. Posttraining, the respiratory sprint test to exhaustion
(PostResp) was repeated using an identical protocol. Two data sets were
generated from this respiratory test. The PostResp data was contrasted
at the same time as exhaustion had occurred in the PreResp test (i.e.,
providing a posttraining matched comparison for PreResp) and
at posttraining exhaustion. Peak cardiorespiratory values were
calculated as the two highest consecutive 10-s readings during
exercise. The accumulated and mean O2
and oxygen deficit were calculated according to Medbø et al.
(28).
All-out sprint test. In addition, after familiarization on a separate day, a 30-s "all-out" sprint was conducted on an air-braked cycle ergometer (Repco, Melbourne, Australia) as the first bout in the first and final training sessions. The ergometer was instrumented with an Exertech work-monitor unit (Repco) to allow determination of total work and peak power output. The operating principles of the air-braked cycle ergometer have been described and validated elsewhere (22) with test procedures as previously described (27).
Training
Subjects undertook a supervised, progressive high-intensity cycling training program 3 times per week, for 7 consecutive weeks (27). Briefly, each session was comprised of four (week 1) to ten (weeks 6 and 7), 30-s all-out sprints on a mechanically braked cycle ergometer (Monark 668, Varberg, Sweden), with each sprint being separated by 3-4 min of passive rest.Muscle Sampling and Analyses
Two muscle samples were obtained during each invasive test. The first sample was taken during supine rest and the second immediately at the cessation of exercise, while the subject was supported on the cycle ergometer. The skin and the fascia overlying the vastus lateralis muscle were anesthetized using 2% Xylocaine (without epinephrine), and a percutaneous biopsy was performed with suction applied. Muscle samples were immediately immersed in liquid nitrogen. The mean time from cessation of pedaling until freezing the muscle sample was 15.8 ± 0.9 s. Owing to technical difficulties in obtaining the muscle sample after exercise in two subjects in PostExh, muscle biopsy data are reported for five subjects in PostExh vs. PreExh comparisons. Frozen muscle was weighed, freeze-dried, and reweighed to obtain the wet-to-dry weight ratio, which was higher after exercise than at rest (P < 0.05) but did not differ between test day (P = 0.90); ratios averaged 4.09 ± 0.05 in PreExh, 4.12 ± 0.07 in PostMatch, and 4.08 ± 0.05 in PostExh. Dried muscle was dissected free from visible blood and connective tissue, powdered, extracted, and analyzed for the adenine nucleotides (ATP, ADP, AMP) and IMP by HPLC (41), and for ATP, phosphocreatine (PCr), creatine, Lac, and glycogen
by standard enzymatic, fluorimetric methods (18). Muscle
metabolites (except glycogen and Lac) in pre- and
posttraining samples were corrected to the respective, individual peak
total creatine (TCr) content obtained before and after training and
expressed as millimoles per kilogram dry mass (dm). To integrate the
muscle metabolite data, the total anaerobic ATP production was
calculated as the sum of dry weight muscle anaerobic ATP production
(36) and the ATP equivalent from blood Lac
(see below). Total active wet weight muscle mass, assumed to be 8.6 kg
(34), was converted to dry weight by dividing by the individual wet-to-dry weight ratio. To attempt to account for the
Lac that escaped the muscle during the exercise period,
the amount of Lac present in whole blood at rest was
determined from resting blood Lac concentration
([Lac]) and a value (4.883 liters) for resting blood
volume (BV), reported for a similar group of subjects in whom BV was
found to be unchanged after a training program identical to that of the
present study (12). The amount of Lac
present in the blood immediately after exercise was determined from the
BV adjusted for exercise-induced changes and the blood [Lac] immediately at the cessation of exercise. The
difference between the amount of Lac after exercise and
the amount in blood at rest was taken to represent the amount of
accumulated Lac and was then multiplied by 1.5 to convert
to an ATP equivalent and added to the muscle anaerobic ATP production.
Muscle pH was determined on freeze-dried muscle (20) using
techniques described elsewhere (38). The ratio of the rise in muscle H+ concentration ([H+]) relative to
the work performed during exercise (
[H+]/work) was
calculated. In vitro buffering capacity (
in
vitro) was determined as described elsewhere
(20), whereas in vivo buffering capacity
(in vivo) was calculated from the rise in muscle Lac during exercise divided by the decline in
muscle pH (35).
Blood Sampling and Analyses
Arterialized venous blood was sampled via a 22-gauge catheter inserted in a dorsal hand vein. Arterialization was achieved by placing the subject's hand in a perspex box with a heating fan attached. Blood was sampled into two syringes at rest (while the subject was seated on the cycle) immediately after exercise and then at 1, 2, 5, 10, and 20 min of recovery. Because of the intense nature of the exercise, the muscle biopsy, and the passive recovery, the 5- to 20-min recovery blood samples were obtained with the subject supine. Due to technical problems, the number of samples for exercise and 1-min recovery was reduced by one to three. Specific numbers are detailed in the text accompanying the tables and figures.The first blood sample at each sampling time (except 20-min recovery)
was used to determine catecholamine concentrations. The blood was
placed in ice-chilled heparinized tubes containing 14 µl sodium
metabisulfite (5 g/dl), gently mixed, and kept on ice (<30 min) until
centrifuged. The plasma was stored at 
80°C until analysis by HPLC
with electrochemical detection. Briefly, 0.5 ml plasma was adsorbed
onto activated alumina in 0.5 ml Tris buffer (0.5 M), pH 8.6, containing 1% sodium EDTA. After addition of 25 µl 3,4 dihydroxybenzylamine (200 nM) and 25 µl sodium
metabisulfite (0.5 mg/ml), the solution was mixed for 10 min.
The catecholamines were eluted with 125 µl of 0.1 M perchloric acid
containing 400 µM metabisulfite, after washing with two 1-ml aliquots
of chilled MilliQ water. Aliquots (100 µl) of the eluted solution
were injected onto a 15-cm Novapak column (Waters, Millipore). The
mobile phase consisted of 23.4 g NaH2PO4,
2 H2O, 0.5 g Na2EDTA, 1.171 g Na octylsulfonic acid, 1 ml orthophosphoric acid, and 45 ml of methanol per liter of MilliQ water.
The second blood sample was withdrawn into a syringe coated with
lithium heparin and used to determine hematocrit, hemoglobin concentration ([Hb]), whole blood [Lac], and plasma
electrolytes. The syringe was then tightly capped and placed on ice
until determination of pH, PO2, and
PCO2 (BMS3 MK2 blood gas analyzer, Radiometer).
Hematocrit was measured in duplicate and [Hb] in triplicate using the
cyanomethemoglobin method, and the percentage change in plasma (PV)
and blood volumes (BV) was calculated (11). Whole blood
and plasma [Lac] were determined using standard
enzymatic, spectrophotometric techniques. Plasma [K+] and
Na+ concentration ([Na+]) analyses were
performed in triplicate using a flame photometer (IL 943, Instrumentation Laboratory). The increase in plasma [K+]
from rest to the end of exercise was calculated
([K+]).
Statistics
Comparisons between the sprint trials for muscle data were made using repeated-measures, two-by-two (sampling time, i.e., rest vs. exercise; training status) ANOVA (40). A significant interaction effect in this analysis indicates a difference between the respective pre- and posttraining delta values (rest minus exercise or vice versa) and hence a difference in metabolite degradation or accumulation. One-way repeated-measures ANOVA was used to determine whether test order influenced resting muscle metabolite values in PreExh, PostMatch, or PostExh and to compare respiratory data in the 130%O2 peak tests. Blood data were
analyzed using two-way (time, training status) ANOVA for repeated
measures, with Newman-Keuls tests used when a significant F
ratio was found for a main effect and t-tests used when an
interaction effect was found. Two-tailed, paired t-tests
were used to compare subject characteristics and other single pre- and
posttraining values. Significance was accepted at P < 0.05. Results are reported as the means ± SE unless otherwise indicated.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Performance
Maximal 30-s sprint peak power (9.4%, 1,158 ± 57 vs. 1,267 ± 38 W; pre- vs. posttraining, respectively) and total work (10.6%, 25.1 ± 1.1 vs. 27.8 ± 0.5 kJ; pre- vs. posttraining) were increased after training (P < 0.05).Time to exhaustion (21%) and work (21%, Fig.
2) at 130% pretraining
O2 peak were increased in
PostExh compared with PreExh (P < 0.001). The
PostMatch exercise duration (82.6 ± 10.9 s), and thus work
output (Fig. 2), did not differ from PreExh. Time to exhaustion in the
pretraining respiratory test (PreResp, 77.9 ± 10.8 s) tended
to be less than during the pretraining invasive test (PreExh, 82.9 ± 10.5 s; P = 0.051). The total work was greater in PreExh than PreResp (P < 0.05; Fig. 2). In the
posttraining tests, time to exhaustion was very similar in the
respiratory (PostResp, 100.4 ± 12.0 s) and the invasive test
(PostExh, 100.0 ± 12.1 s), and thus work did not differ
(Fig. 2).
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Respiratory Measures
The incremental exerciseO2 peak
(7%, 3.79 ± 0.16 vs. 4.05 ± 0.15 l/min, pre- vs.
posttraining, respectively; P = 0.07) and maximum power
(7.5%, 332 ± 13 vs. 357 ± 9 W, pre- vs. posttraining,
respectively; P < 0.05) were higher after sprint training. Hence the power output (441 ± 25 W) that elicited 130% O2 peak before training was estimated
at 122 ± 0.04% of O2 peak
posttraining (P = 0.06). Similarly, the 130% O2 peak power output was slightly lower
after training when expressed as a percentage of the peak power
attained in the maximal 30-s sprints (38.6 ± 2.9 vs. 35.0 ± 2.3%; P < 0.05).
In exercise to exhaustion after training (PostResp), peak minute
ventilation (E; P < 0.05; Table
1) and the accumulated oxygen uptake
(35%, P < 0.01) and deficit (19%, P < 0.05) were higher than in the PreResp test (Table 2), partially
reflecting the 29% longer test duration.
In PostResp, mean
E was higher (P < 0.05; Table 2), mean O2 tended to be
higher (6%, P = 0.12), and the mean oxygen deficit
tended to be lower (8%, P = 0.13) than in the PreResp
test. The PostResp matched comparison revealed lower peak values for
HR, E, carbon dioxide production
(CO2), respiratory exchange ratio,
and E-O2 ratio than
in the PreResp test; however, the O2 did
not differ (Table 1). Similarly, the mean HR, E, and
CO2 in PostResp "matched" were lower
after training compared with PreResp (Table 2). However, neither the accumulated O2 nor the accumulated
oxygen deficit differed between PreResp and the matched PostResp
comparison. Furthermore, the absolute rates of change of
E, CO2,
O2, and HR in the first 50 s of
exercise (common to all subjects) were not altered after training (data
not shown).
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Muscle
Resting muscle metabolite concentrations. No effect of test order was found for any resting metabolites (data not shown), except the ATP and total adenine nucleotide (TAN) contents, which were lower in the second invasive posttraining sprint test than pretraining (P < 0.05). However, there were no differences between the two posttraining tests. The posttraining reduction in TAN content was not due to a loss of TCr, because TCr did not differ with training (P = 0.74).
High-energy phosphates and degradation products.
In PostMatch, compared with PreExh, the degradation of PCr was
unaltered; however, the fall in ATP (P < 0.01) and TAN
(P < 0.05) during exercise were reduced, resulting in
an attenuated rise in IMP (P = 0.001; Table
3). Exhaustive exercise also resulted in
less TAN (P = 0.057) and ATP degradation and a smaller
rise in IMP after training (P < 0.05) but similar PCr degradation
(Table 4).
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Glycogen, lactate, [H+], and
[H+]/work.
In PostMatch, reductions were found in each of muscle glycogen
degradation (P < 0.01; Table 3), muscle
Lac and H+ accumulation (P < 0.05; Table 3; pH at exhaustion in PreExh 6.58 ± 0.05, PostMatch
6.76 ± 0.07; P < 0.05; n = 6),
and [H+]/work (41%, P < 0.05;
n = 6; Fig. 3), compared
with PreExh. In PostExh, greater work was performed, yet muscle
glycogen and Lac at exhaustion were similar before and
after training (Table 4). Despite this, the rise in muscle
[H+] with exhaustive exercise was diminished by 34%
(P = 0.05; n = 4; Table 4) and
[H+]/work by 45% (P < 0.07;
n = 4; Fig. 3) in PostExh compared with PreExh.
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Estimated anaerobic ATP production.
The estimated total anaerobic ATP production was 520.8 ± 25.4 mmol in PreExh and was reduced by 19% to 421.0 ± 48.4 mmol in PostMatch (P < 0.05), with a consequent 24% lower
anaerobic ATP production rate (P = 0.058; Fig.
4). In PostExh, the estimated total
anaerobic ATP production did not differ from PreExh (516.0 ± 35.3 vs. 467.3 ± 38.1 mmol, PreExh vs. PostExh, respectively), and,
accordingly, the rate of anaerobic ATP production was 25% lower
(P = 0.056; n = 5; Fig. 4).
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Buffering capacity.
in vitro did not differ between the pretraining and the
first and second posttraining tests, when expressed either per gram dry
weight (P = 0.85; 156.6 ± 3.0, 157.0 ± 2.1, and 155.6 ± 3.4 µmol HCl · g1
dm · pH1) or per gram wet weight
(P = 0.17; 39.3 ± 1.2, 38.5 ± 1.2, and 38.2 ± 0.8 µmol HCl · g1 wet
wt · pH1). in vivo was also
unaltered by training, either in PreExh vs. PostMatch (171.1 ± 3.4 vs. 185.5 ± 20.2 µmol
Lac · g1
dm · pH1, respectively; P = 0.51; n = 6) or in PreExh vs. PostExh (172.9 ± 5.1 vs. 192.9 ± 13.0 µmol
Lac · g1
dm · pH1, respectively; P = 0.23;
n = 4).
Blood
PV.
In PreExh, plasma volume fell during and for 5 min after exercise, then
returned to a level 8.1 ± 1.6% lower than rest by 20 min
(P < 0.001). In PostMatch, the PV recovered more
rapidly to be only 2.7 ± 1.5% below rest by 20 min
(P < 0.001; Fig. 5). The
PV did not differ between PreExh and PostExh tests (Table 5).
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Plasma potassium.
Plasma [K+] was elevated at the end of exercise and then
fell to remain below resting values at 5 to 20 min recovery.
During PostMatch, plasma [K+] (mean ± SE
difference; 0.11 ± 0.05 mmol/l P < 0.05), peak
plasma [K+] (11%) (P < 0.001; Fig.
6A), and [K+]
(31%, 1.49 ± 0.17 vs. 1.02 ± 0.16 mmol/l, PreExh vs.
PostMatch, respectively; P < 0.05; n = 6) were all reduced compared with PreExh. In contrast, during PostExh,
peak plasma [K+] (Fig. 6B), and hence
[K+] (1.40 ± 0.18 vs. 1.55 ± 0.31 mmol/l,
PreExh vs. PostExh, respectively; n = 5), were not
different to PreExh.
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Plasma catecholamines.
Plasma norepinephrine concentration ([NEpi]) was lower in PostMatch
than PreExh at 1 and 10 min of recovery (P < 0.05;
Fig. 7A), whereas plasma
epinephrine concentration ([Epi]) was not different (Table
6). Both plasma [NEpi] and [Epi] were
higher after training in PostExh (P < 0.05; Table 5);
however, post hoc t-tests determined only [NEpi] to be
higher at 5 min recovery in PostExh (P < 0.05).
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Plasma lactate and [H+].
In PostMatch, plasma [Lac] was 40% less during
exercise, reached a lower peak, and was lower from 5 min postexercise
than in PreExh (P < 0.01, Fig. 7B). Plasma
[H+] was less in PostMatch at all times compared with
PreExh (P < 0.01; Fig. 7C). In contrast,
during PostExh, both plasma [Lac] and
[H+] were higher than in PreExh (means ± SE
difference, 1.4 ± 0.4 mmol/l and 1.5 ± 0.8 nmol/l,
respectively, P < 0.05; Table 5).
Oxygen and carbon dioxide tensions. Mean arterialized venous PO2 was slightly higher (P < 0.05) in the PreExh and PostExh tests (both 73 ± 3 mmHg) than in the PostMatch test (67 ± 3 mmHg). Arterialized venous PCO2 was 37.9 ± 0.8, 34.8 ± 1.5, and 36.7 ± 1.1 mmHg at rest in PreExh, PostExh, and PostMatch, respectively. PCO2 was not different in the tests to exhaustion; however, the rise in PCO2 immediately after exercise was lower in PostMatch than in PreExh (P < 0.05).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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This study employed a unique methodological approach to
investigate the effects of sprint training on respiratory, metabolic, and ionic variables during exercise in humans, which allowed us to
resolve many of the controversies in the literature. Values for these
variables, obtained during exercise continued until exhaustion, were
contrasted against those obtained during exercise at the same absolute
work rate and duration, before and after training. For the
first time, we unequivocally demonstrated that sprint training
reduces the metabolic and ionic perturbations in exercised muscle
and blood during intense exercise matched for power output and work
production. Our matched-work exercise comparison reveals that the major
adaptation to sprint training is not anaerobic, with reductions in
muscle glycogenolysis, Lac content, and
[H+] all evident after training. In contrast, the
respiratory, metabolic, and ionic responses during exhaustive exercise
were similar before and after training. The indexes of anaerobic
metabolism were not augmented during exhaustive exercise after
training, despite the increased exercise duration, suggesting the
importance of aerobic adaptations to performance after sprint training.
Attenuated Glycogenolysis and Glycolysis During Maximal Exercise After Sprint Training
The lower glycogen degradation, coupled with lower muscle and plasma Lac accumulation, indicate attenuated
glycogenolysis and glycolysis during intense matched exercise after
sprint training. Thus our conclusions differ sharply from other studies
that conducted only a posttraining test to exhaustion (4, 14, 17,
19, 30, 35). Reduced glycogenolysis may be caused by the
attenuated net ATP degradation, resulting in lower free AMP, reduced
phosphorylase activation, and the release of PFK inhibition. In
exercise to exhaustion, glycogen degradation, Lac
accumulation, and the total anaerobic ATP production were all unchanged
after training, despite a 21% longer exercise duration. Consequently,
the anaerobic ATP production rate was 25% lower than in PreExh. This
demonstrates that the relative contribution of anaerobic ATP generation
may be reduced, concomitant with improved performance during intense,
exhaustive exercise. Unchanged muscle Lac accumulation
and anaerobic ATP production, but higher plasma [Lac],
with exhaustive exercise suggests that sprint training may enhance
blood flow and/or Lac transport, with the latter shown
recently (33). If so, this suggests that we may have
underestimated muscle anaerobic ATP production after training. Even so,
the potential increase in muscle Lac transport after
sprint training (33) is less than half the calculated 25%
reduction in muscle anaerobic ATP production, so our conclusions are
not significantly affected by this consideration.
Reduced anaerobic metabolism during intense exercise after sprint
training in the present study is consistent with findings of unchanged
(39) or lower muscle Lac accumulation
(32), attenuated ATP degradation (39), and an unchanged arteriovenous Lac difference (26,
32) when greater work was performed during an exhaustive
exercise bout after sprint training. However, the duration of rest
intervals separating sprint bouts during training may be another
differential factor. Studies reporting increased blood or muscle
Lac after sprint training (14, 30) employed
10- to 15-min rest periods between 30-s sprints, whereas the present
and previous study (26) used only 3- to 4-min rest
periods. Extended recovery intervals should facilitate metabolic
recovery, thus allowing each sprint to be performed more anaerobically
(34). Both studies that employed longer rest periods also
included numerous 6- or 15-s sprints, which demand extremely high rates
of PCr breakdown and glycolytic flux (36) and hence may
more selectively "train" these pathways. A further explanatory
factor may be the different tests used, because incremental exercise to
exhaustion (35) presents a markedly different metabolic
challenge than an all-out 30-s sprint (e.g., 26, 39) and a sprint to
exhaustion at a constant power output. Although the matched
work test represented a slightly lower relative intensity (130% vs.
122% O2 peak), at such high work rates
this small difference cannot account for the marked changes observed in
glycogenolysis after training.
Increased Oxidative Metabolism During Maximal Exercise After Sprint Training
We provide strong metabolic evidence suggesting enhanced muscle oxidative metabolism after sprint training. The reduced glycogen degradation, Lac accumulation, anaerobic ATP production
rate, and improved energy balance (indicated by attenuated ATP
degradation and IMP accumulation during intense matched-work exercise
after training) are all consistent with improved muscle oxidative
metabolism. The most likely sources of ATP previously derived from a
higher glycolytic rate are via greater pyruvate and/or intramuscular
triglyceride oxidation. Others have found increased
-hydroxyacyl-CoA-dehydrogenase (32), citrate synthase,
and succinate dehydrogenase activities (14, 19) after
high-intensity training, suggesting increased mitochondrial density,
which may also concomitantly increase total pyruvate dehydrogenase
(PDH; PDHt). Because brief, intense exercise results in
complete conversion of PDHt to the active form PDHa (34), increased PDHt may result in greater PDHa during exercise. Even if PDHa
was unchanged, a slower rate of pyruvate presentation would probably
permit a greater proportion to be oxidized, thus constituting a
considerable energetic advantage after training. Others have suggested
significant intramuscular triglyceride oxidation during intense
exercise (5, 23), but no one has investigated the effects
of sprint training.
Although the metabolite data strongly indicate increased aerobic ATP
production in the contracting muscle, both
O2 and the oxygen deficit during matched
work were unchanged after training. The reduction in muscle anaerobic
ATP generation during exercise in the PostMatch test equated to a
theoretical increase in O2 of 0.33 ± 0.14 l/min. It is possible that such an increase in O2 after training escaped our detection
limits, although this seems unlikely given the near significance of the
0.26 l/min increase in O2 peak
posttraining. An interesting alternate possibility, based on the
lower peak and mean E during matched work, is that sprint training may reduce the respiratory muscle work and
O2 (1, 10), thus allowing
increased exercising leg muscle O2 without any change in the whole body O2.
In the absence of blood flow measurements and arteriovenous differences
for oxygen content, we cannot partition the whole body
O2 into leg and respiratory muscle
components. However, in support of our interpretation, respiratory
muscle unloading, which decreased respiratory muscle O2, allowed an increased leg blood flow
and O2 during maximal exercise
(9). Our data are also consistent with the possibility that mechanical efficiency was increased after training. Efficiency is
higher as intense exercise is continued and is higher in subsequent bouts when intense intermittent exercise is performed (2); however, the effect of high-intensity training is unknown. The onset
rates of E, O2,
CO2, and HR were unaltered after
training. However, these are influenced by all body tissues and
therefore do not preclude the possibility that training may result in
tighter metabolic coupling within contracting muscle, with more rapid increments in aerobic metabolism, and attenuated metabolic
perturbations. Such a change may be related to enhanced sensitivity of
mitochondrial respiration to the phosphorylation potential, as
suggested for endurance training (6).
Reduced Resting ATP but Less ATP Imbalance in Intense Exercise After Sprint Training
A marked attenuation in net ATP breakdown and IMP accumulation during exhaustive exercise was seen after training, despite increased performance, in close agreement with a previous report (39). An even more striking effect was evident in the matched-work test, with ATP degradation reduced from 33 to 10% and IMP accumulation reduced by 74% after training. Increased oxidative ATP generation may play an important role in facilitating an improved ATP synthesis/degradation balance.Our findings of reduced resting ATP and attenuated net ATP degradation contrast with other reports (4, 30). Because improved ATP balance was found in both the matched-work and exhaustive posttraining sprint tests, the explanation may lie in the differing training programs. The present and two earlier studies (13, 39) used brief recovery intervals (50 s to 4 min) between exhaustive sprint bouts during training, whereas, in the opposing studies (4, 30), one used considerably longer recovery intervals (30), and no interval was specified in the other (4). The irreversible loss of adenine nucleotides may be greater with brief rest intervals (13), perhaps explaining the reduction in resting ATP. In addition, because frequently repeated sprints necessitate progressively greater oxidative ATP generation (34), the resultant training effect may contribute to an attenuated ATP degradation during intense exercise.
Enhanced H+ Regulation During Intense Exercise After Sprint Training
This study is the first to demonstrate reduced muscle H+ accumulation during intense exercise after sprint training, which may be due to reduced H+ production and/or enhanced H+ removal. The lower Lac and
H+ accumulation in muscle and blood in PostMatch provides
strong evidence for a reduction in Lac and H+
production after training. However, muscle [H+] was also
lower in PostExh than in PreExh, despite a similar Lac
accumulation and performance of more work, suggesting that training may
have enhanced H+ clearance. Muscle in vitro
was unchanged, consistent with other studies (21, 30, 33),
and thus cannot explain the lower exercise muscle [H+]
after training. Muscle in vivo was unchanged
after training, in contrast to another sprint training study
(34). However, the small sample size in this and another
study (30) suggests the possibility of a Type II error.
The Na+/H+ exchange capacity was increased
after high-intensity training in rats (15) and may
contribute to enhanced muscle [H+] regulation in human
muscle after sprint training. Finally, muscle intracellular
[H+] depends on the concentrations of the intracellular
strong ions, principally Na+, K+,
Lac, and Cl, as well as
PCO2 and the concentration of weak acids (16). Greater muscle Na+ and K+ uptake during maximal
exercise was found after sprint training (25), suggesting
less reduction in the muscle strong ion difference and thus lower
[H+] accumulation. However, the effects of sprint
training on muscle strong ion difference remain to be clarified.
Reduced Exercise-Induced Hyperkalemia
We demonstrated, for the first time, reduced hyperkalemia during intense exercise after sprint training, when work was matched. In contrast, the peak plasma [K+] during exhaustive exercise was unchanged after training, despite greater work being performed. These findings demonstrate enhanced K+ regulation after training and explain previous observations of unchanged peak exercise plasma [K+] after sprint training, because work output was greater after training in these studies (25, 27). The mechanisms accounting for improved K+ regulation during intense exercise after training remain poorly understood (24) but may include reduced K+ release from contracting muscle into plasma and/or enhanced K+ clearance from plasma. This may result from an increased Na+-K+-ATPase content (27) and/or increased Na+-K+-ATPase activation in active and/or inactive muscles after training (24). It is also likely that sprint training increased muscle blood flow (26, 29), consistent with reduced [NEpi] after training in PostMatch. Although reduced vasoconstrictive outflow may permit higher blood flow to contracting muscles, and hence increase K+ washout, it may contemporaneously increase flow to inactive areas and thus improve K+ clearance (7). Because disturbances in muscle K+ and Na+ have been implicated in muscle fatigue (31), enhanced K+ regulation is consistent with augmented muscular performance after training.In summary, the present comprehensive investigation into the effects of
sprint training contrasted the metabolic, ionic, and respiratory
responses to intense exercise, when work was precisely matched, and
with exercise to exhaustion after sprint training. This approach
allowed novel findings, during matched-work exercise, of reductions in
the anaerobic ATP production rate, adenine nucleotide degradation,
muscle and plasma [H+] and [Lac], plasma
[K+], and ventilation after sprint training. Furthermore,
during exercise continued until exhaustion, greater work was
performed after training, and muscle metabolic disturbances were
similar or attenuated compared with before training. The anaerobic ATP production rate was lower, suggesting that sprint training may enhance
muscle oxidative metabolism, which may allow an increased time before fatigue.
| |
ACKNOWLEDGEMENTS |
|---|
The knowledge, professionalism, skill, and humor of our friend and esteemed colleague the late Prof. John R. Sutton were highly valued, and he remains greatly missed.
| |
FOOTNOTES |
|---|
Deceased 7 February 1996.
We are appreciative of the dedication of our subjects during testing and training. We thank Dr. Roger Adams for statistical advice, Justine Naylor for constructive comments, Greg Castle for assistance in data collection, and the Renal Laboratory staff, Royal Prince Alfred Hospital, Sydney, who kindly provided the method for catecholamine analysis.
This work was supported by a grant to M. J. McKenna from the University of Sydney.
Address for reprint requests and other correspondence: M. J. McKenna, Dept. of Human Movement, Recreation and Performance (F022), Victoria Univ. of Technology, P.O. Box 14428, MCMC, Melbourne, Victoria, 8001, Australia (E-mail address: michael.mckenna{at}vu.edu.au).
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.
Received 9 December 1999; accepted in final form 1 June 2000.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
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, Incremental peak O2
consumption (
, respiratory sprint test, 130% pretraining
, invasive
sprint test, 130% pretraining
