| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1 Department of Exercise and Sport Science, Manchester Metropolitan University, Alsager ST7 2HL; 2 School of Sport, Exercise and Leisure, University of Surrey Roehampton, London SW15 3SN; and 3 University Department of Anaesthesia, Withington Hospital, Manchester M20 2LR, United Kingdom
 |
ABSTRACT |
|---|
 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
The purpose of this study was to test
the effect of oral creatine (Cr) supplementation on pulmonary oxygen
uptake (
O2) kinetics during moderate
[below ventilatory threshold (VT)] and heavy (above VT) submaximal
cycle exercise. Nine subjects (7 men; means ± SD: age
28 ± 3 yr, body mass 73.2 ± 5.6 kg, maximal
O2 46.4 ± 8.0 ml · kg
1 · min1)
volunteered to participate in this study. Subjects performed transitions of 6-min duration from unloaded cycling to moderate (80%
VT; 8-12 repeats) and heavy exercise (50% change; i.e., halfway between VT and maximal O2; 4-6
repeats), both in the control condition and after Cr loading, in a
crossover design. The Cr loading regimen involved oral consumption of
20 g/day of Cr monohydrate for 5 days, followed by a maintenance dose
of 5 g/day thereafter. O2 was measured
breath by breath and modeled by using two (moderate) or three (heavy)
exponential terms. For moderate exercise, there were no differences in
the parameters of the O2 kinetic
response between control and Cr-loaded conditions. For heavy exercise, the time-based parameters of the O2
response were unchanged, but the amplitude of the primary component was
significantly reduced with Cr loading (means ± SE: control
2.00 ± 0.12 l/min; Cr loaded 1.92 ± 0.10 l/min;
P < 0.05) as was the end-exercise
O2 (control 2.19 ± 0.13 l/min; Cr
loaded 2.12 ± 0.14 l/min; P < 0.05). The magnitude of the reduction in submaximal
O2 with Cr loading was significantly
correlated with the percentage of type II fibers in the vastus
lateralis (r = 0.87; P < 0.01;
n = 7), indicating that the effect might be related to
changes in motor unit recruitment patterns or the volume of muscle activated.
economy; steady state; fiber type
| |
INTRODUCTION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
MANY ATHLETES SUPPLEMENT
THEIR diet with creatine (Cr) monohydrate to increase
intramuscular phosphocreatine (PCr) concentration ([PCr]) and Cr
concentration ([Cr]) and to improve performance in multiple-sprint
activities (8, 12, 18). Relatively few studies have
examined the influence of Cr supplementation on oxygen uptake
(O2) during exercise, and the results of
these studies have been inconclusive. In one study, a reduction
in whole body O2 was observed during
repeated, maximal sprint exercise after Cr loading (1). In
contrast, Rico-Sanz and Marco (30) reported a significant
increase in O2 during high-intensity
submaximal exercise at ~90% of the power output at maximal
O2
(O2 max). Two other studies have
reported no effect of Cr loading on O2 during submaximal incremental exercise (37) or continuous
submaximal and supramaximal exercise (2). Most of these
studies measured the O2 response on just
one occasion, and the measurement tended to be discontinuous (e.g., one
measurement every 30 s) (1, 2, 37). Accurate
determination of exercise O2 requires consideration of the measurement error, and confidence in the data may
require several repeat transitions to sufficiently enhance the
signal-to-noise ratio (24).
No previous studies have examined the kinetics of the
O2 adaptation from rest to either
moderate [below the lactate threshold (LT)] or heavy (above the LT)
submaximal exercise after Cr loading. In the transition from rest to
exercise, the rate at which O2 adjusts
to meet the anticipated steady-state requirement is reciprocally related to the splitting of PCr (31), but it is presently
unknown what effect, if any, Cr loading has on the rate of adaptation of O2 at the onset of exercise. The
purpose of this study, therefore, was to examine the effect of Cr
loading on O2 kinetics, including the
"steady-state" O2, during moderate
and heavy exercise. We hypothesized that Cr loading would increase
O2 during heavy (30) but
not moderate exercise but have no effect on the time constant of the
primary O2 response.
| |
METHODS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Subjects.
Nine healthy subjects (7 men) volunteered to participate in this study,
which was approved by Manchester Metropolitan University Ethics
Committee. The subjects were (means ± SD) 28 ± 3 yr of age,
their body mass was 73.2 ± 5.6 kg, and their
O2 max was 46.4 ± 8.0 ml · kg1 · min1. The
subjects were recreationally active but not highly trained. The
subjects were all fully familiar with laboratory exercise testing
procedures. None of the subjects had ingested Cr as a supplement within
18 mo of the start of the study.
Methods.
The subjects first performed a ramp exercise test (30 W/min) to the
limit of tolerance on an electrically braked cycle ergometer (Ergoline,
Jaeger, Germany) for the determination of the ventilatory threshold
(VT) and the O2 max. All tests were
performed at a cadence of 75 revolutions/min. The breath-by-breath data were collected and displayed at 10-s intervals. The VT was determined visually as an increase in CO2 production relative to
O2. The O2 max was accepted as the highest 10-s
value recorded before volitional exhaustion.
O2 at the VT (moderate exercise) and
50% of the difference between the O2 at
VT and O2 max (heavy exercise). To
determine precisely the kinetic features of the
O2 response with and without Cr loading,
the subjects performed 8-12 bouts of moderate exercise and
4-6 bouts of heavy exercise in each condition (i.e., control and
Cr loaded). Each square-wave exercise bout included a baseline of 3 min
of unloaded cycling, 6 min of either moderate or heavy exercise, and 6 min of unloaded cycling in recovery. In any one test session, subjects
performed a maximum of two transitions to moderate exercise and one
transition to heavy exercise. The moderate exercise bouts always
preceded the heavy exercise bouts. No more than two test sessions were
performed on any day, and, where this occurred, test sessions were
separated by at least 1 h. Pulmonary gas exchange was measured
breath by breath during all square-wave tests (see below), and heart
rate was measured every 5 s with a telemetric heart rate monitor
(Polar Sports Tester, Kempele, Finland). A fingertip capillary blood
sample was collected immediately before and immediately after two bouts
of moderate exercise and two bouts of heavy exercise in each condition
to determine change (
) in blood lactate concentration ([lactate]) (YSI 1500, Yellow Springs Instruments).
The subjects performed repeated bouts of moderate and heavy exercise,
both in the control condition and after Cr loading. The Cr loading
regimen involved the consumption of 20 g of Cr monohydrate
(Highfive, Leicester, UK) per day for 5 days. The subjects dissolved
the Cr in 250 ml of warm orange squash and consumed the Cr in four
equally spaced doses of 5 g. It is known that this loading regimen
results in a significant increase in intramuscular [Cr] and [PCr]
(19, 21). The subjects then consumed a maintenance dose of
5 g Cr per day until they had completed all of the exercise bouts
required in the Cr-loaded condition. The conditions were presented in a
crossover design. Five subjects performed the control condition
exercise bouts first before loading with Cr and performing the exercise
bouts in the Cr-loaded condition. The other four subjects first loaded
with Cr and were tested in this condition; these subjects were then
tested in the control condition 35-50 days later to allow for Cr
washout, it having been demonstrated that the time required for total
muscle Cr to return to basal levels is ~4 wk (16, 25).
Body mass was recorded before each exercise test session by using
balance scales.
Pulmonary gas exchange was measured breath by breath during all
exercise tests. Subjects breathed through a low-resistance turbine
volume transducer (Jaeger Triple V), which had a dead space of 90 ml.
Gas was continuously drawn down a capillary line into rapid response
gas analyzers (Jaeger Oxycon Alpha, Hoechberg, Germany).
O2, CO2 production, and
minute ventilation were calculated and displayed breath by breath once
the delay between the volume and concentration signals had been
accounted for. The volume transducer was calibrated before each test
with a 3-liter calibration syringe (Hans Rudolph), and the analyzers
were calibrated with certified standard gases.
The breath-by-breath data were linearly interpolated to provide
second-by-second values. For each subject, the data from the repeated
exercise bouts were time aligned and averaged to provide one set of
second-by-second data for each variation of the protocol (i.e., control
moderate, control heavy, Cr moderate, and Cr heavy). The time course of
the O2 response after the onset of
exercise was described in terms of a two-component (moderate exercise) or three-component (heavy exercise) exponential function, by using iterative nonlinear regression techniques in which minimizing the sum
of squared error was the criterion for convergence. Each exponential
curve was used to describe one phase of the response. The first phase
began at the onset of exercise, whereas the other terms began after
independent time delays (4)
|
|
![+A<SUB>p</SUB> ∗ [1−<IT>e</IT><SUP>−(t−TD<SUB>1</SUB>)/&tgr;<SUB>p</SUB></SUP>] phase II (primary component)](/content/vol92/issue6/fulltext/2571/img003.gif)
|
![+A<SUB>s</SUB> ∗ [1−<IT>e</IT><SUP>−(t−TD<SUB>2</SUB>)/&tgr;<SUB>s</SUB></SUP>] phase III (slow component)](/content/vol92/issue6/fulltext/2571/img004.gif)
|
O2(b)
is the baseline O2 measured in the 3 min
preceding the onset of exercise; Ac,
Ap, and As are the amplitudes of the exponential curves fitting the cardiodynamic, primary, and slow components, respectively; 
c,
p, and s are the respective time
constants; and TD1 and TD2 are the time delays. The cardiodynamic component was terminated at TD1 and given
the value for that time. The amplitude of the primary response
(A'P) was defined as the increase in
O2 from baseline to the asymptote of the
primary component. The absolute amplitude of the primary O2 response was calculated as the sum of
baseline O2 and
A'P. The amplitude of the
O2 slow component was determined as the increase in O2 from TD2 to
the end of exercise, rather than from the asymptotic value
(As), which may project beyond the value at 6 min (end exercise). In addition to the kinetic analysis, the absolute
O2 values around 2 and 6 min were
checked, but these did not differ from the parameters derived from the model.
Muscle biopsies. Seven of the subjects had undergone a muscle biopsy of the vastus lateralis within 12 wk of their participation in the present study as part of another experiment in our laboratory (28). Briefly, ~200 mg of muscle were obtained from the lateral portion of the right vastus lateralis muscle with a conchotome biopsy procedure under local anesthetic (1% lignocaine hydrochloride). Standard histochemical procedures were used for the determination of myofibrillar ATPase activity, and muscle fibers were subsequently classified as either type I or type II, according to their pH lability. Muscle fiber type was expressed as a percentage of the number of fibers of each type counted relative to the total number of fibers counted.
Statistical analysis.
The results were analyzed by using two-tailed paired t-tests
with significance accepted when P < 0.05. The
relationship between muscle fiber type and changes in
O2 with Cr loading was explored by using
Pearson's product-moment correlation coefficient. The results are
presented as means ± SE.
| |
RESULTS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
The Cr loading regimen caused a significant increase in body mass (from 73.2 ± 1.9 to 74.2 ± 1.8 kg; P < 0.05), whereas there was no change in the control condition (from 73.2 ± 1.9 to 73.3 ± 2.0 kg).
The results for moderate exercise are shown in Table
1. There were no significant differences
in the parameters of the O2 kinetic
response between the control and Cr-loaded conditions.
|
The results for heavy exercise are shown in Table
2. There were no significant differences
in the temporal features of the O2
response (i.e., time constants and time delays) between the two
conditions. However, both the amplitude of the primary
O2 response and the end-exercise
O2 were significantly reduced in the
Cr-loaded condition (P < 0.05; Fig.
1). The reduction in O2 with Cr loading was significantly
correlated with the percentage of type II muscle fibers in the vastus
lateralis (r = 0.87; P < 0.01;
n = 7; Fig. 2). Blood
lactate accumulation was also significantly reduced after Cr loading
(P < 0.05; Table 2).
|
|
|
In the control condition, the time constant of the primary component
was significantly longer (i.e., the kinetics were slower) for heavy
exercise (27.1 ± 2.2 s) compared with moderate exercise (17.3 ± 1.7 s; P < 0.05). Furthermore, the
gain of the primary component (A'P/power
output) was significantly lower in heavy exercise (9.9 ± 0.6 ml · min1 · W1) than in
moderate exercise (10.8 ± 0.5 ml · min1 · W1;
P < 0.05).
| |
DISCUSSION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
The primary original finding of this study is that Cr loading
leads to a significant reduction in O2
during heavy, but not moderate, submaximal exercise, with no change in
the time constant of the primary component.
It is perhaps not surprising that Cr loading had no effect on the time
constant of the fundamental O2 response.
It could be considered that a significantly greater contribution of PCr hydrolysis to the ATP turnover after Cr loading might spare
O2 demand and slow the O2
on-kinetics. Alternatively, because the fundamental increase in
O2 at the onset of exercise is
temporally linked to the splitting of PCr (31), additional
PCr hydrolysis per unit time after Cr loading might be expected to
speed the O2 kinetics. The Cr loading
regimen that we used would be expected to increase total muscle Cr by
15-20% with 25-40% of this being stored as PCr (12,
21). However, there is presently no evidence that Cr loading
increases the magnitude of PCr hydrolysis in a single rest-to-exercise
transition (12, 35). For example, in the study of Snow et
al. (35), the reduction in intramuscular [PCr] (from
86.1 mmol/kg dry mass at rest to 38.9 mmol/kg dry mass after 20 s
of maximal cycle sprinting) after Cr loading was similar to the
reduction in the control condition (from 83.8 mmol/kg dry mass at rest
to 34.7 mmol/kg dry mass).
Our finding of an ~4% reduction in O2
during heavy exercise after Cr loading was in contrast to our
hypothesis and is intriguing. Our subjects performed multiple repeats
from unloaded cycling to moderate (8-12 transitions) and heavy
exercise (4-6 transitions) in a crossover design, and we are,
therefore, confident that this effect is real and is not the result of
experimental error or noise in the data. A reduction in
O2 during heavy exercise after Cr
loading was evident in all nine subjects, although the effect was small
in some subjects. On average, there was no difference between the
response of the group that performed the control tests first and the
group that performed the Cr-loaded tests first, indicating that
35-50 days were sufficient to allow muscle [Cr] to return to
normal in the latter group (16, 25).
Only a limited number of previous studies have measured
O2 during exercise with and without Cr
loading (1, 2, 30, 37). Balsom et al. (1)
reported a reduction in O2 after the
seventh bout of repeated supramaximal cycling exercise with the use of
Douglas bag collections of expired air. However, Balsom et al.
(2) could detect no change in
O2 during continuous running at ~120%
O2 max after Cr loading, and Stroud et
al. (37) reported no difference in
O2 during submaximal incremental
treadmill exercise. In both of these studies,
O2 was not analyzed breath by breath but
was averaged over 30-s periods, and the exercise bouts were only
performed once. It is possible that, with only one measurement, noise
in the data (24) obscured any difference in
O2 between the conditions. Also, in
running, an increase in body mass resulting from the Cr loading will
increase the energy cost of running at a particular submaximal speed,
and it is possible that this could counteract any reduction in
O2 that might otherwise have been
evident. Recently, Rico-Sanz and Marco (30) reported that
the total volume of oxygen consumed by trained cyclists during 3-min
periods of cycling at 90% of the power output at
O2 max was greater after Cr loading. However, in that study, the order of testing in the experimental group
was not randomized; i.e., subjects were always tested in the control
condition first. In addition, there was a trend for total
O2 to also be higher at the same
exercise intensity in the group who consumed a placebo, and it is not
clear whether this effect was accounted for in the statistical analysis.
It has been demonstrated that the addition of Cr to skeletal or cardiac
muscle cell cultures increases the rate of oxidative phosphorylation
(7, 34, 41). It has been proposed that a Cr-PCr shuttle
exists in which Cr is transported to the mitochondria and PCr is
delivered to the sites at which energy is required (7).
The activity of Cr kinase in the mitochondrial intermembrane space is
coupled with the rate of aerobic respiration (32), and it
has been suggested that the increased rate of oxidative phosphorylation
after the addition of Cr to cultures of cardiomyocytes results from an
increased sensitivity of respiration to ADP (33). The
PCr-to-Cr ratio, which dictates the free ADP concentration, is reduced
with Cr loading, and this should, in theory, stimulate mitochondrial
respiration. ADP appears to be restricted to the outer mitochondrial
membrane in cardiac and type I muscle fibers (32), and
this restriction might explain the influence of Cr on the rate of
respiration in these fibers (33). Differences in the
regulation of respiration between type I and type II skeletal muscle
fibers have been reported previously, and this appears to result from
differences in mitochondrial function (13, 43). The
addition of Cr to cultures of type II muscle fibers has not been shown
to cause an increased respiratory rate (23). On the other
hand, a positive correlation has been reported between the proportion
of type I fibers and the increase in the rate of aerobic respiration
when Cr was added to a culture of human skeletal muscle fibers
(39). These observations might help to explain the
discrepancy between the present study, in which
O2 was reduced during heavy, submaximal
exercise after Cr loading, and the study of Rico-Sanz and Marco
(30), in which O2 appeared
to be increased after Cr loading at a similar exercise intensity. The
subjects in the study of Rico-Sanz and Marco were highly trained
long-distance cyclists (O2 max ~64
ml · kg1 · min1), whereas
our subjects were recreationally active in a number of sports but not
well trained (O2 max ~46
ml · kg1 · min1). It is
quite possible, therefore, that there were differences in the
proportion of type I fibers in the active muscles between the subject
groups. Seven of our subjects had undergone a muscle biopsy of the
vastus lateralis within 12 wk of their participation in the present
study as part of another experiment in our laboratory (28). There was a significant correlation between the
percentage of type II fibers in the vastus lateralis and the reduction
in A'P (i.e., the
O2 at the end of the primary adaptive
phase) during heavy exercise (Fig. 2). In other words, subjects with a
higher proportion of type II muscle fibers evidenced a larger reduction
in O2 during heavy exercise after Cr loading.
It is unlikely that the energy turnover would have been reduced for the
same power output after Cr loading. Therefore, it has to be considered
that Cr loading alters muscle efficiency (i.e., it increases oxidative
coupling efficiency, P/O) in some way. It has previously been
demonstrated that subjects with a high proportion of type II fibers
have a lower gain of the primary component (and a larger contribution
of the O2 slow component to the
end-exercise O2) than subjects with a
low proportion of type II fibers (4). Pringle et al.
(28) have also shown that the proportion of type II fibers
is negatively related to the gain of the
O2 primary component during heavy and
severe, but not moderate, exercise. It is possible, therefore, that Cr loading affects the pattern of motor unit recruitment during heavy exercise. Evidence for this includes the following: 1)
muscle fiber type is only related to the amplitude of the
O2 primary component during exercise
above the LT, where type II muscle fibers are likely to be recruited
(4, 28), and Cr loading lowered O2 during heavy but not moderate
exercise (Fig. 1); and 2) the effect of Cr loading was
greater in subjects with a high proportion of type II fibers (Fig. 2).
It is presently unclear why a predominance of type II muscle fibers is
related to improved efficiency (i.e., lower
O2 for the same power output) during
both constant-load (4, 28) and incremental
(5) exercise in humans when, in vitro, type II fibers
produce greater heat and consume more oxygen for the same tension
development (13, 17).
Whereas a greater recruitment of type II fibers during heavy exercise
after Cr loading is one explanation for our results, an alternative
explanation is that Cr loading causes a reduction in the total amount
of muscle mass recruited. It is unclear whether the increase in
fat-free mass seen with Cr loading (15) is the result of
increased protein synthesis or is due simply to water retention.
However, there is evidence that Cr loading reduces EMG activity during
submaximal exercise (36). It has been suggested that the
increase in muscle PCr availability resulting from Cr loading might
reduce the rate of muscle fatigue by reducing the rate of anaerobic
glycolysis and, therefore, the degree of intramuscular acidosis
(29, 42). It has been estimated that a relatively high
proportion of the energy cost of muscle contraction (30-50%) can
be attributed to processes independent of the actomyosin-ATPase, such
as the activities of the sarcoplasmic reticulum Ca2+-ATPase
and the sarcolemmal Na+-K+-ATPase
(38). If fewer muscle fibers are recruited to meet
the ATP requirement of performing the external work after Cr loading, the ATP cost of the "support processes" involved in maintaining intracellular homeostasis may be reduced. This, in turn, could explain
a reduction in whole body O2. Additional
studies are needed to clarify the mechanism by which
O2 during heavy exercise is reduced
after Cr loading.
There was no significant change in the respiratory exchange ratio
during either moderate (~0.94) or heavy (~1.05) exercise after Cr
loading. Therefore, the reduced O2
during heavy exercise cannot be explained by a shift in substrate
utilization toward additional carbohydrate oxidation. Indeed, the
accumulation of blood lactate over the 6-min bout of heavy exercise was
significantly reduced after Cr loading. Assuming that a 1.0 mM increase
in blood lactate above resting values is equivalent to the consumption of ~3.0 ml O2/kg body mass (14) and that the
increase in blood [lactate] reflects muscle lactate production to a
similar extent in the two conditions, it can be estimated that Cr
loading spared O2 demand by an additional ~132 ml. It is
interesting to speculate on whether the small reduction in the energy
cost of heavy exercise after Cr loading (evidenced by significant
reductions in both pulmonary O2 and
blood [lactate]) might enhance exercise performance. In running,
it is possible that any advantage from the Cr loading might be negated
by the concurrent increase in body mass, which would tend to increase
the energy cost of exercise. In cycling, where body mass is less
important to performance, at least on the flat, it is feasible that Cr
loading could enhance endurance exercise performance. To date,
relatively few studies have examined this possibility. However, in the
study of Rico-Sanz and Marco (30), subjects' time to
exhaustion during alternating cycling at 30 and 90% of the power
output at O2 max was significantly increased from ~30 to ~37 min after Cr loading, with no significant change in the placebo group. Additional studies are needed to examine
the influence of Cr feeding on performance in non-weight-bearing endurance activities.
An important issue in the study of O2
kinetics is whether the time constant of the primary component is
increased (i.e., the kinetics are slowed) during heavy compared with
moderate exercise. The literature is equivocal on this issue, with some
studies demonstrating slower primary O2
kinetics during heavy exercise (e.g., Ref. 27) and others
demonstrating no change (e.g., Ref. 6). Studies demonstrating slower kinetics have been interpreted as evidence that
the primary kinetics are limited by O2 availability during heavy exercise (40). It has been suggested that previous
studies that have addressed this issue have used an insufficient number of transitions and/or subjects to allow confidence in the data (20). Given that we used a large number of transitions in
the present study, it may be pertinent to comment on differences in the
kinetic features of the O2 response to
moderate and heavy exercise in the control condition. In the present
study, the time constant of the primary component was significantly
longer for heavy exercise (27.1 ± 2.2 s) than for moderate
exercise (17.3 ± 1.7 s). It is unclear why these results
differ from our laboratory's previous observations of no difference in
the primary time constant between moderate and heavy cycle exercise
(9, 10). It was also of interest that the gain of the
primary component (calculated as the increase in
O2 in this phase per unit increase in
power output) was significantly lower for heavy exercise (9.9 ± 0.2 ml · min1 · W1) than for
moderate exercise (10.8 ± 0.2 ml · min1 · W1).
Whereas it has previously been considered that the gain of the
primary component remains constant throughout the continuum of
submaximal exercise (6, 27), trends for a lower gain with increasing exercise intensity have been noted previously in running (11) and cycling (3, 10, 26). This pattern of
a longer primary time constant and a reduced gain of the primary
component during heavy exercise is consistent with there being a
greater recruitment of type II muscle fibers and, therefore, a greater contribution of the characteristics of
O2 in type II fibers to the overall
pulmonary O2 signal during heavy
exercise. The time constant of O2 at the
onset of contraction is longer in isolated (rodent) muscles with a
predominance of type II fibers (22), and the time constant
of the primary component during heavy exercise is longer in subjects
with a high proportion of type II fibers in the vastus lateralis
(28). Furthermore,
O2/power output is lower in
subjects with a high proportion of type II muscle fibers during both
ramp exercise (5) and constant-load exercise above the LT
(4, 28).
In conclusion, this study has shown that Cr loading causes a small but
significant reduction in O2 during
heavy, but not moderate, submaximal exercise, with no change in the
primary time constant. The reduction in
O2 was present at the end of the primary
component and persisted throughout the exercise bout. It is possible
that Cr loading influences motor unit recruitment patterns or the
volume of muscle mass recruited during heavy submaximal exercise, but
additional studies are needed to clarify the mechanism responsible for
this effect.
| |
FOOTNOTES |
|---|
Address for reprint requests and other correspondence: A. M. Jones, Dept. of Exercise and Sport Science, Manchester Metropolitan Univ., Hassall Road, Alsager ST7 2HL, UK (E-mail: a.m.jones{at}mmu.ac.uk).
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 February 1, 2002;10.1152/japplphysiol.01065.2001
Received 23 October 2001; accepted in final form 25 January 2002.
| |
REFERENCES |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
1.
Balsom, PD,
Ekblom B,
Soderlund K,
Sjodin B,
and
Hultman E.
Creatine supplementation and dynamic high-intensity intermittent exercise.
Scand J Med Sci Sports
3:
143-149,
1993.
2.
Balsom, PD,
Harridge SDR,
Soderlund K,
Sjodin B,
and
Ekblom B.
Creatine supplementation per se does not enhance endurance exercise performance.
Acta Physiol Scand
149:
521-523,
1993[Web of Science][Medline].
3.
Barstow, TJ,
Casaburi R,
and
Wasserman K.
O2 uptake kinetics and the O2 deficit as related to exercise intensity and blood lactate.
J Appl Physiol
75:
755-762,
1993
4.
Barstow, TJ,
Jones AM,
Nguyen PH,
and
Casaburi R.
Influence of muscle fiber type and pedal frequency on oxygen uptake kinetics of heavy exercise.
J Appl Physiol
81:
1642-1650,
1996
5.
Barstow, TJ,
Jones AM,
Nguyen PH,
and
Casaburi R.
Influence of muscle fibre type and fitness on the oxygen uptake/power output slope during incremental exercise in humans.
Exp Physiol
85:
109-116,
2000[Abstract].
6.
Barstow, TJ,
and
Mole PA.
Linear and nonlinear characteristics of oxygen uptake kinetics during heavy exercise.
J Appl Physiol
71:
2099-2106,
1991
7.
Bessman, SP,
and
Geiger PJ.
Transport of energy in muscle: the phosphorylcreatine shuttle.
Science
211:
448-452,
1981
8.
Birch, R,
Noble D,
and
Greenhaff PL.
The influence of dietary creatine supplementation on performance during repeated bouts of maximal isokinetic cycling in man.
Eur J Appl Physiol
69:
268-270,
1994[Web of Science].
9.
Burnley, M,
Jones AM,
Carter H,
and
Doust JH.
Effects of prior heavy exercise on phase II pulmonary oxygen uptake kinetics during heavy exercise.
J Appl Physiol
89:
1387-1396,
2000
10.
Carter, H,
Jones AM,
Barstow TJ,
Burnley M,
Williams CA,
and
Doust JH.
A comparison of oxygen uptake kinetics during treadmill running and cycling ergometry.
J Appl Physiol
89:
899-907,
2000
11.
Carter, H,
Pringle JSM,
Jones AM,
and
Doust JH.
Oxygen uptake kinetics during treadmill running across exercise intensity domains.
Eur J Appl Physiol
86:
347-354,
2002[Web of Science][Medline].
12.
Casey, A,
Constantin-Teodosiu D,
Howell S,
Hultman E,
and
Greenhaff PL.
Creatine ingestion favorably affects performance and muscle metabolism during maximal exercise in humans.
Am J Physiol Endocrinol Metab
271:
E31-E37,
1996
13.
Crow, MT,
and
Kushmerick MJ.
Chemical energetics of slow- and fast-twitch muscles of the mouse.
J Gen Physiol
79:
147-166,
1982
14.
Di Prampero, PE.
Energetics of muscular exercise.
Rev Physiol Biochem Pharmacol
89:
143-222,
1981[Medline].
15.
Earnest, CP,
Snell PG,
Rodriguez R,
Almada AL,
and
Mitchell TL.
The effect of creatine monohydrate ingestion on anaerobic power indices, muscular strength and body composition.
Acta Physiol Scand
153:
207-209,
1995[Web of Science][Medline].
16.
Febbraio, MA,
Flanagan TR,
Snow RJ,
Zhao S,
and
Carey MF.
Effect of creatine supplementation on intramuscular TCr, metabolism and performance during intermittent, supramaximal exercise in humans.
Acta Physiol Scand
155:
387-395,
1995[Web of Science][Medline].
17.
Gibbs, CL,
and
Gibson WR.
Energy production of the rat soleus muscle.
Am J Physiol
223:
864-871,
1972.
18.
Greenhaff, PL,
Casey A,
Short AH,
Harris R,
Soderlund K,
and
Hultman E.
Influence of oral creatine supplementation on muscle torque during repeated bouts of maximal voluntary exercise in man.
Clin Sci (Lond)
84:
565-571,
1993[Medline].
19.
Harris, R,
Soderlund K,
and
Hultman E.
Elevation of creatine in resting and exercising muscles of normal subjects by creatine supplementation.
Clin Sci (Lond)
83:
367-374,
1992[Medline].
20.
Hughson, RL,
Tschakovsky ME,
and
Houston ME.
Regulation of oxygen consumption at the onset of exercise.
Exerc Sport Sci Rev
29:
129-133,
2001[Medline].
21.
Hultman, E,
Soderlund K,
Timmons JA,
Cederblad G,
and
Greenhaff PL.
Muscle creatine loading in men.
J Appl Physiol
81:
232-237,
1996
22.
Kushmerick, M,
Meyer RA,
and
Brown TR.
Regulation of oxygen consumption in fast- and slow-twitch muscle.
Am J Physiol Cell Physiol
263:
C598-C606,
1992
23.
Kuznetsov, AV,
Tiivel T,
Sikk P,
Kaambre T,
Kay L,
Danahsrad Z,
Rossi A,
Kadaja L,
Peet N,
and
Saaks VA.
Striking differences between the kinetics of regulation of respiration by ADP in slow-twitch and fast-twitch muscles in vivo.
Eur J Biochem
241:
909-915,
1996[Web of Science][Medline].
24.
Lamarra, N,
Whipp BJ,
Ward SA,
and
Wasserman K.
Effect of interbreath fluctuations on characterizing exercise gas exchange kinetics.
J Appl Physiol
62:
2003-2012,
1987
25.
Odland, LM,
MacDougall JD,
Tarnopolsky MA,
Elorriaga A,
and
Borgmann A.
Effect of oral creatine supplementation on muscle [PCr] and short-term maximum power output.
Med Sci Sports Exerc
29:
216-219,
1997[Web of Science][Medline].
26.
Ozyener, F,
Rossiter HB,
Ward SA,
and
Whipp BJ.
Influence of exercise intensity on the on and off transient kinetics of pulmonary oxygen uptake kinetics in humans.
J Physiol
533:
891-902,
2001
27.
Paterson, DH,
and
Whipp BJ.
Asymmetries of oxygen uptake transients at the on- and offset of heavy exercise in humans.
J Physiol
443:
575-586,
1991
28.
Pringle, JSM,
Doust JH,
Carter H,
Campbell IG,
Tolfrey K,
and
Jones AM.
Influence of muscle fibre type on oxygen uptake kinetics during moderate, heavy and severe intensity cycle exercise (Abstract).
J Physiol
539:
55-56,
2002.
29.
Rico-Sanz, J.
Creatine reduces human muscle PCr and pH decrements and Pi accumulation during low-intensity exercise.
J Appl Physiol
88:
1181-1191,
2000
30.
Rico-Sanz, J,
and
Marco MTM
Creatine enhances oxygen uptake and performance during alternating intensity exercise.
Med Sci Sports Exerc
32:
379-385,
2000[Web of Science][Medline].
31.
Rossiter, HB,
Ward SA,
Doyle VL,
Howe FA,
Griffiths JR,
and
Whipp BJ.
Inferences from pulmonary O2 uptake with respect to intramuscular [phosphocreatine] kinetics during moderate exercise in humans.
J Physiol
518:
921-932,
1999
32.
Saks, VA,
Rosenshtraukh LV,
Smirnov VN,
and
Chazov EI.
Role of creatine phosphokinase in cellular function and metabolism.
Can J Physiol Pharmacol
56:
691-705,
1978[Web of Science][Medline].
33.
Schneider, C,
Stull GA,
and
Apple FS.
Kinetic characterisation of human heart and skeletal muscle CK isoenzymes.
Enzyme
39:
220-226,
1988[Web of Science][Medline].
34.
Seraydarian, MW,
Artaza L,
and
Abbott BC.
Creatine and the control of energy metabolism in cardiac and skeletal muscle cells in culture.
J Mol Cell Cardiol
6:
405-413,
1974[Web of Science][Medline].
35.
Snow, RJ,
McKenna MJ,
Selig SE,
Kemp J,
Stathis CG,
and
Zhao S.
Effect of creatine supplementation on sprint exercise performance and muscle metabolism.
J Appl Physiol
84:
1667-1673,
1998
36.
Stout, J,
Eckerson J,
Ebersole K,
Moore G,
Perry S,
Housh T,
Bull A,
Cramer J,
and
Batheja A.
Effect of creatine loading on neuromuscular fatigue threshold.
J Appl Physiol
88:
109-112,
2000
37.
Stroud, MA,
Holliman D,
Bell D,
Green AL,
MacDonald IA,
and
Greenhaff PL.
Effect of oral creatine supplementation on respiratory gas exchange and blood lactate accumulation during incremental treadmill exercise and recovery in man.
Clin Sci (Lond)
87:
707-710,
1994[Medline].
38.
Szentesi, P,
Zaremba R,
van Mechelen W,
and
Stienen GJM
ATP ulilisation for calcium uptake and force production in different types of human skeletal muscle fibres.
J Physiol
531:
393-403,
2001
39.
Tonkonogi, M,
Harris B,
and
Sahlin K.
Mitochondrial oxidative function in human saponin-skinned fibers: effects of prolonged exercise.
J Physiol
510:
270-286,
1998.
40.
Tscakovsky, ME,
and
Hughson RL.
Interaction of factors determining oxygen uptake at the onset of exercise.
J Appl Physiol
86:
1101-1113,
1999
41.
Veksler, VK,
Kuznetsov AV,
Anflous K,
Mateo P,
van Deursen J,
Wieringa B,
and
Ventura-Clapier R.
Muscle creatine kinase-deficient mice. II. Cardiac and skeletal muscles exhibit tissue-specific adaptation of the mitochondrial function.
J Biol Chem
270:
19921-19929,
1995
42.
Volek, JS,
and
Kraemer WJ.
Creatine supplementation: its effect on human muscular performance and body composition.
J Strength Cond Res
10:
200-210,
1996.
43.
Willis, WT,
and
Jackman MR.
Mitochondrial function during heavy exercise.
Med Sci Sports Exerc
26:
1347-1353,
1994[Web of Science][Medline].
This article has been cited by other articles:
|
|
 |
|
  A. M. Jones, D. P. Wilkerson, and J. Fulford Influence of dietary creatine supplementation on muscle phosphocreatine kinetics during knee-extensor exercise in humans Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2009; 296(4): R1078 - R1087. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Glancy, T. Barstow, and W. T. Willis Linear relation between time constant of oxygen uptake kinetics, total creatine, and mitochondrial content in vitro Am J Physiol Cell Physiol, January 1, 2008; 294(1): C79 - C87. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Y. Endo, M. Kobayakawa, R. Kinugasa, S. Kuno, H. Akima, H. B. Rossiter, A. Miura, and Y. Fukuba Thigh muscle activation distribution and pulmonary VO2 kinetics during moderate, heavy, and very heavy intensity cycling exercise in humans Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2007; 293(2): R812 - R820. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Koga, D. C. Poole, T. Shiojiri, N. Kondo, Y. Fukuba, A. Miura, and T. J. Barstow Comparison of oxygen uptake kinetics during knee extension and cycle exercise Am J Physiol Regulatory Integrative Comp Physiol, January 1, 2005; 288(1): R212 - R220. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. P Wilkerson, I. T Campbell, and A. M Jones Influence of nitric oxide synthase inhibition on pulmonary O2 uptake kinetics during supra-maximal exercise in humans J. Physiol., December 1, 2004; 561(2): 623 - 635. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. P. Wilkerson, K. Koppo, T. J. Barstow, and A. M. Jones Effect of prior multiple-sprint exercise on pulmonary O2 uptake kinetics following the onset of perimaximal exercise J Appl Physiol, October 1, 2004; 97(4): 1227 - 1236. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. W. Scheuermann and T. J. Barstow O2 uptake kinetics during exercise at peak O2 uptake J Appl Physiol, November 1, 2003; 95(5): 2014 - 2022. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. B. Rossiter, S. A. Ward, F. A. Howe, D. M. Wood, J. M. Kowalchuk, J. R. Griffiths, and B. J. Whipp Effects of dichloroacetate on VO2 and intramuscular 31P metabolite kinetics during high-intensity exercise in humans J Appl Physiol, September 1, 2003; 95(3): 1105 - 1115. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. S. M. Pringle, J. H. Doust, H. Carter, K. Tolfrey, and A. M. Jones Effect of pedal rate on primary and slow-component oxygen uptake responses during heavy-cycle exercise J Appl Physiol, April 1, 2003; 94(4): 1501 - 1507. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
