| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
O2 on-kinetics in isolated in
situ canine muscle
Department of Medicine, University of California, San Diego, La Jolla, California 92093-0623; Istituto di Tecnologie Biomediche Avanzate, Consiglio Nazionale delle Ricerche, I-20090 Segrate (MI); Department of Health and Human Performance, Auburn University, Auburn, Alabama 36849-5323; and Dipartimento di Scienze e Tecnologie Biomediche, Università di Milano, I-20090 Segrate (MI), Italy
 |
ABSTRACT |
|---|
Top
Abstract
Introduction
Methods
Results
Discussion
References
|
|---|
The mechanism(s)
limiting muscle O2 uptake
(
O2) kinetics was
investigated in isolated canine gastrocnemius muscles
(n = 7) during transitions from rest
to 3 min of electrically stimulated isometric tetanic contractions
(200-ms trains, 50 Hz; 1 contraction/2 s; 60-70% of peak
O2). Two conditions were
mainly compared: 1) spontaneous
adjustment of blood flow (
) [control, spontaneous (C Spont)]; and
2) pump-perfused
, adjusted ~15 s before contractions at a
constant level corresponding to the steady-state value during
contractions in C Spont [faster adjustment of
O2 delivery (Fast
O2 Delivery)]. During Fast
O2 Delivery, 1-2 ml/min of
10
2 M adenosine were
infused intra-arterially to prevent inordinate pressure increases with
the elevated . The purpose of the study was to
determine whether a faster adjustment of
O2 delivery would affect
O2 kinetics.
was measured continuously; arterial
(CaO2) and popliteal venous
(CvO2)
O2 contents were determined at
rest and at 5- to 7-s intervals during contractions;
O2 delivery was calculated as
· CaO2,
and O2 was calculated as
· arteriovenous O2 content difference. Times to
reach 63% of the difference between baseline and steady-state
O2 during contractions were
23.8 ± 2.0 (SE) s in C Spont and 21.8 ± 0.9 s in Fast
O2 Delivery (not significant). In
the present experimental model, elimination of any delay in
O2 delivery during the
rest-to-contraction transition did not affect muscle
O2 kinetics, which suggests
that this kinetics was mainly set by an intrinsic inertia of oxidative
metabolism.
gas exchange kinetics; muscle oxidative metabolism; submaximal exercise
| |
INTRODUCTION |
|---|
|
Top
Abstract
Introduction
Methods
Results
Discussion
References
|
|---|
IT HAS BEEN KNOWN FOR DECADES that on a step transition
from rest to exercise, or from a lower to a higher workload,
O2 uptake (O2) lags behind the power
output increase (12), following a time course usually termed
O2 on-kinetics. The
mechanism(s) determining this kinetics has been a matter of
considerable debate, mainly between those who consider it mainly
related to the rate of adjustment of
O2 delivery to the exercising
muscles (13-15) and those who support the concept that
O2 on-kinetics is mainly set
by an inertia of intramuscular oxidative metabolism (3, 32).
An experimental approach to discriminate between the two conflicting
hypotheses would be to increase the rate of adjustment of
O2 delivery to muscles and then
determine whether the O2 on-kinetics becomes faster or not. Unfortunately, previous studies conducted following this approach yielded conflicting results. Hughson
and co-workers (14), for example, described a significantly faster
O2 on-kinetics when their
subjects cycled in a supine position during the application of lower
body negative pressure, which presumably enhanced the rate of
O2 delivery to the exercising muscles (although the authors did not determine the kinetics of any
cardiovascular variable in this study) or performed forearm exercise
with the arm below (vs. above) heart level (15), i.e., in the presence
of a faster on-kinetics of the calculated forearm blood flow
(). On the other hand, Grassi et al. (10) recently described, in a group of heart-transplant recipients, an unchanged O2 on-kinetics in
the presence of a slightly faster cardiac output on-kinetics, obtained
by a preceding "warming-up" exercise, the purpose of which was to
establish more favorable conditions with regard to the adjustment of
O2 delivery to the increased metabolic demand. By utilizing an intense (above the lactate threshold) warm-up exercise, as opposed to the relatively lighter warm-up of
Grassi et al. (10), Gerbino et al. (8) observed a faster O2 on-kinetics during a
subsequent bout of high-intensity exercise. The same investigators
found that if the subsequent exercise bout was less intense (below the
lactate threshold), there was no effect of the warm-up on
O2 on-kinetics. It appears
difficult to reconcile these somehow conflicting results in a unifying
scenario. Some limitations of these studies were
1) in most cases, the on-kinetics of
O2 delivery to muscle could not be
directly determined, even though in some of the studies it was inferred
from other measurements; and 2) even
if present, changes in the on-kinetics of
O2 delivery were presumably
relatively small.
In the present study, utilizing the isolated canine gastrocnemius
muscle preparation (30), we were able to eliminate any delay in
O2 delivery to muscle during the
rest-to-contraction transition. The preparation, moreover, allowed a
direct determination of muscle O2
delivery and muscle O2
on-kinetics. In this preparation, arterial blood perfusing the muscle
can come from either the contralateral artery ("spontaneous"
flow) or from a pump controlled by the operator. It was then possible
to compare muscle O2
on-kinetics, during a rest-to-submaximal contractions transition, in a
condition of spontaneous adjustment of
O2 delivery (muscle self-perfused
through the contralateral artery), and in a condition in which any
delay in the adjustment of O2
delivery was eliminated by having the muscle pump perfused, from the
last 15-30 s of rest and throughout the contraction period, at a
constant , corresponding to the steady-state level
during contractions in the presence of spontaneous flow. We
hypothesized that, if muscle
O2 on-kinetics were indeed limited by the rate of adjustment of
O2 delivery, eliminating any delay
in the latter would allow faster
O2 on-kinetics to be
observed.
| |
METHODS |
|---|
|
Top
Abstract
Introduction
Methods
Results
Discussion
References
|
|---|
The study was conducted with the approval of the animal subjects committee of the University of California, San Diego, where the experiments were carried out.
Seven adult mongrel dogs of either sex were anesthetized with pentobarbital sodium (30 mg/kg), with maintenance doses given as required. The dogs were intubated with an endotracheal tube and ventilated with a respirator (model 613, Harvard). The esophageal temperature was maintained at ~37°C with a heating pad and a heating lamp. After the surgical preparation, the animals were treated with heparin (1,500 U/kg). Ventilation was maintained at a level that produced normal arterial PO2 and PCO2 values. PO2 and PCO2 values were continuously monitored in expired air and recorded on a strip-chart recorder.
Surgical preparation. The gastrocnemius-flexor digitorum superficialis muscle complex (for convenience referred to as "gastrocnemius") was isolated as described previously (30). Briefly, a medial incision was made through the skin of the left hindlimb from midthigh to the ankle. The sartorius, gracilis, semitendinosus, and semimembranosus muscles, which overlie the gastrocnemius, were doubly ligated and cut between the ties. To isolate the venous outflow from the gastrocnemius, all the vessels draining into the popliteal vein, except those from the gastrocnemius, were ligated. The popliteal vein was cannulated, and the venous outflow was returned to the animal via a jugular reservoir. The arterial circulation to the gastrocnemius was isolated by ligating all vessels from the femoral and popliteal artery that did not enter the gastrocnemius. The right femoral artery was catheterized for obtaining blood samples. This catheter was extended and placed into the left femoral artery so that the isolated muscle was perfused by blood from this contralateral artery. The arterial blood perfusing the muscle could then come directly from the contralateral artery (systemic pressure, self-perfused) or via a roller pump for controlled-flow perfusion.
The left sciatic nerve, which innervates the gastrocnemius, was doubly ligated and cut between the ties. All exposed tissues were covered with saline-soaked gauze and a plastic sheet to prevent cooling and drying. After the muscle was surgically isolated, the Achilles tendon was attached to an isometric myograph (Statham 1360 transducer) for monitoring tension development. The hindlimb was fixed at the knee and ankle and attached to the myograph with struts to minimize movement. Weights were used at the end of each experiment to calibrate the myograph.Experimental design.
Isometric tetanic muscle contractions were elicited by supramaximal
stimulation of the sciatic nerve with trains of stimuli (4-6 V of
0.2-ms duration at 50 Hz) lasting 200 ms, at a rate of 1 contraction/2
s for a 3-min period. Before each contraction period, the resting
muscle was passively stretched to the point at which the highest peak
tension was elicited on stimulation. Preliminary studies showed that
this stimulation pattern elicited 60-70% of the peak metabolic
rate (peak O2) for tetanic
contractions in this muscle. Contractions corresponding to 60-70%
of peak O2 were chosen to
avoid confounding factors deriving from significant fatiguing of
muscles. Tetanic contractions were chosen to allow a rapid attainment
of a steady state of developed force. A steady state of force was in
fact reached from the very first contraction cycle. For the purposes of
the study, it was indeed critical to obtain truly "rectangular"
increases in the forcing function, represented by the developed force.
Each isometric tetanic contraction lasted 200 ms and was separated from
the following contraction by 1.8 s, during which the muscle was
relaxing or relaxed. The contraction-relaxation cycles, therefore,
should not have interfered significantly with intramuscular
and O2
delivery.
[control condition,
spontaneous flow (C Spont)];
2) pump-perfused constant
, adjusted ~15-30 s before the start of
contractions at a level corresponding to the
steady-state value obtained during contractions in C Spont
["treatment" condition, characterized by a faster
adjustment of O2 delivery to the
gastrocnemius (Fast O2
Delivery)]; and 3) to control
for any effects of the pump-perfusion system per se, a second control
condition (C Pump), in which , controlled by the
pump, was manually regulated by an operator so as to maintain at rest
and during the contraction period a constant perfusion pressure of the
gastrocnemius corresponding to 120-140 mmHg. During preliminary
experiments it was shown that, in C Pump, the critical independent
variable for the present study, i.e., the kinetics of
O2 delivery to the gastrocnemius
during the rest-to-contraction transition, was similar to that observed in C Spont. A schematic representation of the experimental protocol is
shown in Fig. 1. The order of treatments
was randomized, except that C Spont was always performed before Fast
O2 Delivery because, as discussed
above, for the latter condition it was necessary to know the
spontaneous level at steady state during
contractions. When the blood supply to the gastrocnemius was switched
from self-perfused to pump perfused, or vice versa, enough time was
allowed for the hemodynamic parameters to stabilize.
|
, 1-2 ml/min of a
102 M adenosine solution
(in normal saline) were infused intra-arterially by a pump, beginning
from 20-30 s before the onset of contractions. The adenosine
infusion was then continued throughout the contraction period. This
dosage of the drug was previously shown to be effective in obtaining a
significant vasodilation at the muscle level (9, 17).
At the end of the experiment, the dogs were killed with an overdose of
pentobarbital sodium. The contralateral gastrocnemius was excised and
weighed, and the weight was utilized to normalize variables per unit of
muscle mass as appropriate.
Measurements.
to the gastrocnemius was continuously determined
in the popliteal vein by an ultrasonic flowmeter (T108, Transonic
Systems). The output of the flowmeter was set in the "pulsatile"
mode, and the filter cutoff frequency was set at 100 Hz. The flowmeter
probe (in-line type) was inserted in the vein as close as possible to the gastrocnemius. The flowmeter probe was calibrated before each experiment, and the calibration was checked against zero-flow and
against timed collection of blood in a graduated cylinder at different
flows. Values were sampled at 50 Hz by an analog-to-digital converter
and stored on disk via a computerized data-acquisition system
(AcqNowledge 3.0, Biopac Systems). Average values
were then calculated during discrete 3-s time intervals. Arterial
perfusion pressure of the gastrocnemius
(BPmus) was monitored
continuously via a catheter placed at the head of the muscle and
recorded on a strip-chart recorder. Vascular resistance was calculated
as BPmus/.
Systemic arterial blood pressure was monitored continuously via a
catheter placed in the carotid artery and recorded on a strip-chart
recorder.
.
Bubble-free blood samples were immediately stored in ice and analyzed
within 10-60 min of collection. Arterial and venous PO2,
PCO2, and pH were measured by a
blood-gas analyzer (IL 1306, Instrumentation Laboratories) at 37°C.
Arterial and venous hemoglobin concentration,
O2 saturation, and
O2 content (CaO2 and
CvO2, respectively) were measured
by a CO-oximeter (IL 282, Instrumentation Laboratories). These
instruments were calibrated before and during each experiment.
Dissolved O2 was accounted for in
calculating CaO2 and
CvO2. Plasma bicarbonate concentration was calculated from the measured pH and
PCO2 values by the
Henderson-Hasselbalch equation.
O2 of the gastrocnemius was
calculated from the Fick principle as
O2 = · arteriovenous O2 content difference
(CaO2 
CvO2).
O2 was calculated at
discrete time intervals corresponding to the timing of the blood
samples. Arterial and venous blood lactate concentrations
([La]a and
[La]v, respectively)
were determined in aliquots of the blood samples taken at rest and at
the end of the contraction period by utilizing a Yellow Springs
Instruments 23L blood-lactate analyzer. The blood samples, treated with
cetrimonium bromide to lyse blood cells and with sodium fluoride to
stop glycolysis, were stored on ice immediately after collection and
then kept at 4°C until analysis, which was performed within
4-6 h of collection.
Statistical analyses. Values were expressed as means ± SE. To check the statistical significance of differences between two means, a paired Student's t-test (2-tailed) was performed. To check the statistical significance of differences among more than two means, a repeated-measures analysis of variance was performed. Tukey's test was utilized to discriminate where significant differences occurred. The level of significance was set at P < 0.05. Statistical analyses were performed by utilizing a commercially available software package (InStat, GraphPad Software).
| |
RESULTS |
|---|
|
Top
Abstract
Introduction
Methods
Results
Discussion
References
|
|---|
The weight of the gastrocnemius muscles was 92 ± 14 g.
Resting values. Resting values of the main variables pertinent to O2 transport and utilization, acid-base status, and hemodynamics are shown in Table 1. For arterial hemoglobin concentration, PO2 (PaO2), PCO2 (PaCO2), CaO2, pH, and bicarbonate concentration, no significant differences were observed among the three conditions. This excludes any ordering effect on these variables deriving from the sequence of the experimental conditions, even though the latter could not be completely randomized (see METHODS).
|
and
O2 delivery
( · CaO2)
were higher in Fast O2 Delivery
compared with C Spont and C Pump.
O2 was not significantly
different among the three conditions, whereas
CaO2 CvO2 was lower and
CvO2 was slightly higher in Fast
O2 Delivery compared with C Spont
and C Pump. The fact that the observed difference (0.3-0.4
ml · 100 g1 · min1) in resting
O2 between Fast
O2 Delivery and C Spont and C Pump did not reach statistical significance could represent a type II
statistical error. Such difference could be attributed to imperfect timing in Fast O2 Delivery between
the determination of (which was adjusted by the
operator to the higher level ~15-30 s before contraction onset)
and blood sampling, because previous authors (see e.g., Ref. 30) showed
that, in this preparation, resting O2 is not elevated in the
presence of an elevated . In any case, a 0.4 ml · 100 g1 · min1
difference in baseline O2
cannot obviously influence the analysis of
O2 on-kinetics in the
presence of a O2 difference
between baseline and steady state during contractions which was higher than 10 ml · 100 g1 · min1.
[La]a and
[La]v were not
significantly different among the three conditions. In all conditions,
[La]v was not
significantly different from
[La]a. As a
consequence of the adenosine infusion, muscle vascular resistance
(BPmus/) was
lower in Fast O2 Delivery compared with C Spont and C Pump.
Steady-state values during contractions.
Steady-state values during contractions of the main variables pertinent
to O2 transport and utilization,
acid-base status, biomechanics, and hemodynamics are shown in Table
2 for the three experimental conditions.
For all variables no significant differences were observed among
the three conditions, with the exception of CaO2 CvO2 (lower in Fast
O2 Delivery than in C Spont) and
vascular resistance (lower in Fast
O2 Delivery than in C Pump).
Within each dog, O2 values at
steady state during contractions were slightly different (see also Fig.
4), and such difference was more pronounced in dog
2. Regression analysis showed that, on the average,
78% of the difference among steady-state
O2 values within each dog was
explained by differences in the imposed workload, which, with this
preparation, cannot be exactly reproduced in different trials. For
dog 2, differences in workload
accounted for 99% of the observed difference in steady-state
O2.
[La]a and
[La]v were not
significantly different among the three conditions. In all conditions,
[La]v was not
significantly different from [La]a.
[La]a and
[La]v were only
slightly elevated at steady state during contractions compared with
rest. Muscles did not show significant fatiguing during contractions.
|
Kinetics of , O2
delivery, and O2.
Average values (±SE) of ,
· CaO2,
CaO2 CvO2, and
O2 at rest and
during contractions are shown in Fig. 2 for
the three experimental conditions. The kinetics of
and
· CaO2
(i.e., the variables related to O2
delivery to muscle) were similar in C Spont and in C Pump, whereas in
Fast O2 Delivery the two variables were kept constant throughout the experiment at a level corresponding to the steady-state value observed during contractions in C Spont (Fig.
2A). Despite the marked differences
in the kinetics of and
· CaO2
between the control conditions and Fast
O2 Delivery, the kinetics of
CaO2 CvO2 and
O2 (i.e., the variables
related to O2 utilization by
muscle) appeared remarkably similar in all experimental conditions
(Fig. 2B). The similarity between the kinetics of the variables of O2
delivery and those of O2
utilization in C Spont and in C Pump, compared with their dissociation
in Fast O2 Delivery, can be better
appreciated in Fig. 3, in
which the same values in Fig. 2 were normalized so that resting values were set equal to 0 (or to 1 for and
· CaO2
in Fast O2 Delivery) and
steady-state values during contractions were set equal to 1. In Fig.
3B the abscissa was expanded to allow
better appreciation of the temporal responses of the variables during
the first minute of the contraction period. From this figure, it
appears that, also in C Spont and in C Pump, the variables of
O2 delivery increased more rapidly
during the first 15-20 s of contraction compared with the
variables of O2 utilization.
|
|
O2 on-kinetics in the three
experimental conditions, the values obtained for each experiment during
the contraction period were fitted by a monoexponential function of the
type
![<IT>y</IT>=<IT>a</IT>+<IT>b</IT>[1−<IT>e</IT><SUP>−(<IT>t</IT> − <IT>c</IT>)/<IT>d</IT></SUP>]](/content/vol85/issue4/fulltext/1394/img001.gif)
|
(1) |
|
O2 on-kinetics in
the three experimental conditions, Eq. 1 obtained with analysis
B was solved to calculate the time necessary to reach
50% (t50%,
corresponding to the half-time of the response) and 63%
[t63%,
corresponding to the time constant (
) of a monoexponential
response] of the differences between the resting baselines and
the steady-state values obtained during contractions. The time elapsed
during the first one to three
O2 points, neglected in
analysis B, were added to the times
obtained by solving the functions, so that the resulting times
corresponded to the points at which the
O2 response passed through 50 and 63% of the difference between the resting baseline and the steady
state during contractions (11). Both
t50% and
t63% were
calculated to allow an easier comparison with previous studies, which
utilized either half-time or to describe
O2 on-kinetics. The obtained
average values (±SE) of
t50% and
t63% for the
three experimental conditions are shown in Fig.
5. For both parameters, no significant differences were observed among the three conditions.
|
(for C Spont and C Pump), and the obtained
t50% values for this variable are shown in Table 3,
together with the
t50% for
O2. In both C Spont and in
C Pump, the t50%
for were significantly faster than the
t50% for
O2, confirming previous
observations by Piiper et al. (25) in a similar model.
|
| |
DISCUSSION |
|---|
|
Top
Abstract
Introduction
Methods
Results
Discussion
References
|
|---|
The main finding of the present study was that, in the isolated in situ
dog gastrocnemius preparation, a much faster on-kinetics of
O2 delivery to muscle did not
significantly affect muscle
O2 on-kinetics, indicating
that the latter, for transitions from rest to 60-70% of peak
O2, was mainly set by an
intrinsic inertia of muscle oxidative metabolism.
Background of the present study.
The dispute between those who consider
O2 on-kinetics mainly related
to the rate of adjustment of O2
delivery to the exercising muscles (13, 15) and those who support the
concept that O2 on-kinetics
is mainly set by an inertia of intramuscular oxidative metabolism (3,
32) is long lasting. Previous studies observed that the on-kinetics of
cardiac output (5, 6) and muscle (11, 25) followed
roughly a monoexponential pattern and were slightly faster than
pulmonary or muscle O2
on-kinetics. Other authors described very rapid muscle
increase and capillary recruitment at the onset of
muscle contractions (7). These results were usually interpreted as an
indication that O2 delivery on-kinetics was not the limiting factor for
O2 on-kinetics. On the other
hand, other authors described a slower pulmonary O2 on-kinetics in conditions
of reduced O2 availability to
muscles [e.g., in acute hypoxia (19)] or
slower cardiac output on-kinetics, obtained either by
administering 
-blockers (16) or by having the subjects cycle in a
supine position (4). The fact that reduced or slower
O2 delivery slows down
O2 on-kinetics, however, does
not demonstrate per se that the latter, in normal conditions, is
limited by O2 availability. The
ideal experimental approach to discriminate between the two conflicting
hypotheses mentioned above would be to increase the rate of adjustment
of O2 delivery to muscles and then
see whether O2 on-kinetics
becomes faster or not. Unfortunately, previous attempts to follow this
approach (8, 10, 14, 15) have yielded conflicting results. In most of
these studies, moreover, the on-kinetics of
O2 delivery to muscle could not be
directly measured and, even if present, the obtained changes in
kinetics parameters were likely rather small. From this background, the
present study was performed by utilizing an experimental model (an
isolated in situ dog gastrocnemius preparation) that allowed us to
directly determine O2 delivery on-kinetics and to completely abolish any delay in the convective adjustment of O2 delivery in the
rest-to-contraction transition.
Factors determining O2
on-kinetics in the present experimental model.
The observation of a statistically unchanged
O2 on-kinetics in the absence
of any delay in the adjustment of
O2 delivery in the
rest-to-contraction (60-70% of peak
O2) transition provides evidence in support of the hypothesis that the
O2 on-kinetics in the present
experimental model was not limited by bulk and O2 delivery to muscle but was
presumably determined by an intrinsic inertia of muscle oxidative
metabolism.
O2 on-kinetics could also be
influenced by intramuscular maldistribution of
/O2. It is
indeed well known that there are both spatial and temporal
heterogeneity of within active muscle (21, 26), and
at present it is not known whether this corresponds to
O2 heterogeneity. In the
present experimental model, however, all fibers of the muscle were
synchronously activated, so that the high in Fast
O2 Delivery, associated with
adenosine administration, must have reduced
/O2
maldistribution, if any were present. This, however, did not affect the
O2 on-kinetics. Other factors
possibly limiting O2
on-kinetics, which could not be evaluated in the present study, are
represented by the peripheral diffusion of
O2 from the red blood cells to the
mitochondria of muscle fibers and by intramuscular
O2 stores. For both of these factors, however, it is difficult to conceive differences among the
three experimental conditions that could have influenced the results of
the study.
The substantial monoexponential increase in muscle
O2 (after an initial delay;
see the discussion below) observed in the present study confirms
previous observation by others in canine (1, 7, 25) muscle. The
t50% values
obtained in the present study (~18 s) in C Spont are very close to
the values obtained by Piiper et al. (25) in a similar preparation. In the present study, however, the monoexponential muscle
O2 increase during the
on-transition was, for the first time to our knowledge, clearly
dissociated from O2 delivery
on-kinetics, which itself follows, after an initial abrupt increase, a
monoexponential pattern in normal conditions, as shown in the present
study. The observation that muscle
O2 on-kinetics followed a
monoexponential pattern, even in the presence of a constantly elevated
O2 delivery, appears to be in
agreement with some metabolic models of muscle respiratory control
during contraction (2, 20, 23), according to which a single reaction
with first-order kinetics controls muscle
O2. This reaction can be
identified with ATP resynthesis, the rate of which is directly
proportional to creatine concentration, i.e., to one of the products of
phosphocreatine splitting.
A monoexponential curve, however, did not satisfactorily fit the first
one to three O2 values
(corresponding to the first 5-10 s) of the contraction period.
Indeed, during the initial phase of contractions,
O2 increase was in most cases
less pronounced compared with the ensuing phase of monoexponential
increase, confirming previous observations in canine muscle (1, 7). The
sluggish O2 increase during
the initial phase of contractions observed in the present study can be
attributable, at least in part, to a transit- delay phenomenon from the
sites of gas exchange in the muscle and the site where venous blood
samples were taken. In other words, gas exchange occurring in the
muscle would manifest its effects on venous blood composition only
after a dead-space volume of venous blood is washed out. In the present
study, such delay was reduced to the minumum allowed by the
experimental model by having the venous blood samples taken as close as
possible to the gastrocnemius and by accounting for, in the calculation of O2, the measured
dead-space volume of blood from the site of venous blood sampling and
the site where the vein leaves the gastrocnemius. However, it was
obviously impossible to account for the dead-space volume of blood from
the site where the vein leaves the muscle and the sites of
intramuscular gas exchange. In any case, venous blood volume inside a
muscle such as the canine gastrocnemius can be estimated to be ~2 ml
(27), so that, in presence of , such as those
measured in the present study, the time necessary to wash out such a
volume of blood would be only ~1-3 s. Thus, on the basis of the
results of the present study, the transit-delay phenomenon does not
seem to completely account for the sluggish
O2 increase during the
initial 5-10 s of contractions. It might then be hypothesized
that, intramuscularly as well, the O2 increase does not follow a
monoexponential pattern from the very beginning of work. Such a
finding, if confirmed by future studies specifically aimed at
evaluating the initial phase of the transition, could bring some
influence to bear on the various models of control of oxidative
metabolism during muscular contraction.
Methodological limitations of the experimental model.
In the present experimental model, the muscle is acutely denervated and
is perfused by blood from the contralateral (right) femoral artery. In
this respect, we cannot exclude with certainity that intramuscular
patterns could be somewhat different from those
obtained in animals in vivo. This appears unlikely, however, considering that all hypothesized "metabolic regulators" of
intramuscular [e.g., see the review by
Laughlin and Armstrong (18)] are unaffected by the preparation.
As far as bulk to muscle is concerned, the pattern
observed in the present study is similar to those observed in studies
in which the left femoral artery was used (e.g., see Ref. 25).
and O2 delivery, i.e., with the
critical issue of the study. The contraction pattern could also have
caused more intramuscular blood pooling compared with physiological
contraction patterns. The synchronous contraction of the muscle every 2 s, however, presumably determined a near-complete extrusion of blood
from the muscle, thereby canceling any effect of blood pooling. In any
case, the contraction pattern was the same in the three conditions, so
that in this respect also the results of the study would not be
affected.
The metabolic transition considered in the present study was from rest
to submaximal (60-70% of peak
O2) contractions.
The obtained results, therefore, might apply only to rest-to-submaximal contractions transitions and not to transitions from contractions of
lower to higher metabolic intensities, or to transitions involving contractions of metabolic intensities closer to the muscle's peak O2.
The question could be raised if the adenosine infusion had some
metabolic effects at the muscle level. Although theoretically possible
(24), significant metabolic effects appear unlikely, considering that
resting O2, as well
as the developed force, muscle fatigue,
O2, and other metabolic
variables at steady state during contractions, were not significantly
different in Fast O2 Delivery
compared with control conditions. Moreover, it has previously been
shown that, with the same preparation and the same adenosine dosage as
in the present study, the drug does not significantly affect maximal
O2 (17).
Extrapolation of the present data to humans.
The results of the present study cannot be directly extrapolated to
exercising humans. The main reasons for this can be summarized as
follows. 1) The contraction pattern
was obviously unphysiological (see above).
2) Fiber type composition of dog
gastrocnemius muscle [predominantly constituted by type I and
type IIa fibers (22)] is different compared with that of human
muscle {although the difference is small if endurance athletes
are considered [e.g., see the review by Saltin and Gollnick
(28)]}. 3) Resting
to muscle, in control conditions, was 6- to 10-fold
higher than those observed in humans (e.g., see Ref. 27). This can be
attributable to a "scaling" effect among mammals of different
body sizes (31), as well as to the high percentage of oxidative fibers
in dog muscle (see also above) and to the surgical procedures utilized
in isolating the muscle (18). It must be noted, however, that the
patterns of and
O2 increase at contraction
onset appear remarkably similar in canine [as shown by the
present and by previous studies (25)] and in human muscles (11,
15), the only difference being faster kinetics in dogs, presumably as a
consequence of the higher percentage of oxidative fibers.
Conclusions.
In the isolated in situ dog gastrocnemius preparation, the abolishment
of any delay in the adjustment of convective
O2 delivery to muscle in the
rest-to-contraction (60-70% of peak
O2) transition does not
significantly affect muscle
O2 on-kinetics, indicating that the latter was mainly set by an intrinsic inertia of muscle oxidative metabolism.
| |
ACKNOWLEDGEMENTS |
|---|
The authors are grateful to Drs. Paolo Cerretelli and Peter D. Wagner for constructive criticism and to Nick Busan and Jeffrey Struthers for skillful technical assistance.
| |
FOOTNOTES |
|---|
This study was supported by National Institutes of Health Grants HL-17731, AR-40155, and 1RO1AR-40342; by the American Heart Association, Kentucky Affiliate Grant; and by North Atlantic Treaty Organization Collaborative Research Grant 950173.
Address for reprint requests: B. Grassi, ITBA, CNR, Palazzo LITA, Via Fratelli Cervi 93, I-20090 Segrate (MI), Italy (E-mail: <grassi{at}itba.mi.cnr.it>).
Received 4 September 1997; accepted in final form 1 June 1998.
| |
REFERENCES |
|---|
|
Top
Abstract
Introduction
Methods
Results
Discussion
References
|
|---|
1.
Barbee, R. W.,
W. N. Stainsby,
and
S. J. Chirtel.
Dynamics of O2, CO2, lactate and acid exchange during contractions and recovery.
J. Appl. Physiol.
54:
1687-1692,
1983
2.
Binzoni, T.,
and
P. Cerretelli.
Bioenergetic approach to transfer function of human skeletal muscle.
J. Appl. Physiol.
77:
1784-1789,
1994
3.
Cerretelli, P.,
D. W. Rennie,
and
D. R. Pendergast.
Kinetics of metabolic transients during exercise.
In: Exercise Bioenergetics and Gas Exchange, edited by P. Cerretelli,
and B. J. Whipp. Amsterdam, The Netherlands: Elsevier, 1980, p. 187-209.
4.
Cerretelli, P.,
D. Shindell,
D. R. Pendergast,
P. E. di Prampero,
and
D. W. Rennie.
Oxygen uptake transients at the onset and offset of arm and leg work.
Respir. Physiol.
30:
81-97,
1977[Medline].
5.
Cerretelli, P.,
R. Sikand,
and
L. E. Farhi.
Readjustments in cardiac output and gas exchange during onset of exercise and recovery.
J. Appl. Physiol.
21:
1345-1350,
1966
6.
De Cort, S. C.,
J. A. Innes,
T. J. Barstow,
and
A. Guz.
Cardiac output, oxygen consumption and arteriovenous oxygen difference following a sudden rise in exercise levels in humans.
J. Physiol. (Lond.)
441:
501-512,
1991
7.
Gayeski, T. E. J.,
R. J. Connett,
and
C. R. Honig.
Oxygen transport in rest-work transition illustrates new functions for myoglobin.
Am. J. Physiol.
248 (Heart Circ. Physiol. 17):
H914-H921,
1985
8.
Gerbino, A.,
S. A. Ward,
and
B. J. Whipp.
Effects of prior exercise on pulmonary gas-exchange kinetics during high-intensity exercise in humans.
J. Appl. Physiol.
80:
99-107,
1996
9.
Gorman, M. W.,
J. K. Barclay,
and
H. V. Sparks.
Effects of ischemia on O2 tension, and vascular resistance in contracting canine skeletal muscle.
J. Appl. Physiol.
65:
1075-1081,
1988
10.
Grassi, B.,
C. Marconi,
M. Meyer,
M. Rieu,
and
P. Cerretelli.
Gas exchange and cardiovascular kinetics with different exercise protocols in heart transplant recipients.
J. Appl. Physiol.
82:
1952-1962,
1997
11.
Grassi, B.,
D. C. Poole,
R. S. Richardson,
D. R. Knight,
B. K. Erickson,
and
P. D. Wagner.
Muscle O2 uptake kinetics in humans: implications for metabolic control.
J. Appl. Physiol.
80:
988-998,
1996
12.
Hill, A. V.,
and
H. Lupton.
Muscular exercise, lactic acid, and the supply and utilization of oxygen.
QJM
16:
135-171,
1923.
13.
Hughson, R. L.
Exploring cardiorespiratory control mechanisms through gas exchange dynamics.
Med. Sci. Sports Exerc.
22:
72-79,
1990[Medline].
14.
Hughson, R. L.,
J. E. Cochrane,
and
G. C. Butler.
Faster O2 uptake kinetics at onset of supine exercise with than without lower body negative pressure.
J. Appl. Physiol.
75:
1962-1967,
1993
15.
Hughson, R. L.,
J. K. Shoemaker,
M. E. Tschakovsky,
and
J. M. Kowalchuck.
Dependence of muscle O2 on blood flow dynamics at onset of forearm exercise.
J. Appl. Physiol.
81:
1619-1626,
1996
16.
Hughson, R. L.,
and
G. A. Smyth.
Slower adaptation of O2 to steady state of submaximal exercise with -blockade.
Eur. J. Appl. Physiol.
52:
107-110,
1983.
17.
Kurdak, S. S.,
M. C. Hogan,
and
P. D. Wagner.
Adenosine infusion does not improve maximal O2 uptake in isolated working dog muscle.
J. Appl. Physiol.
76:
2820-2824,
1994
18.
Laughlin, M. H.,
and
R. B. Armstrong.
Muscle blood flow during locomotory exercise.
In: Exercise and Sport Sciences Reviews, edited by R. L. Terjung. New York: Macmillan, 1985, vol. 13, p. 95-136.
19.
Linnarsson, D.,
J. Karlsson,
L. Fagreus,
and
B. Saltin.
Muscle metabolites and oxygen deficit with exercise in hypoxia and hyperoxia.
J. Appl. Physiol.
36:
399-402,
1974
20.
Mahler, M.
First-order kinetics of muscle oxygen consumption, and equivalent proportionality between O2 and phosphocreatine level. Implications for control of respiration.
J. Gen. Physiol.
86:
135-165,
1985
21.
Marconi, C.,
N. Heisler,
M. Meyer,
H. Weitz,
P. Cerretelli,
and
J. Piiper.
Blood flow distribution and its temporal variability in stimulated dog gastrocnemius muscle.
Respir. Physiol.
74:
1-14,
1988[Medline].
22.
Maxwell, L. C.,
J. K. Barclay,
D. E. Mohrman,
and
J. A. Faulkner.
Physiological characteristics of skeletal muscles of dogs and cats.
Am. J. Physiol.
233 (Cell Physiol. 2):
C14-C18,
1977
23.
Meyer, R. A.
A linear model of muscle respiration explains monoexponential phosphocreatine changes.
Am. J. Physiol.
254 (Cell Physiol. 23):
C548-C553,
1988
24.
Newby, A. C.,
Y. Worku,
P. Meghji,
M. Nakazawa,
and
A. C. Skladanowski.
Adenosine: a retaliatory metabolite or not?
News Physiol. Sci.
5:
67-70,
1990.
25.
Piiper, J.,
P. E. di Prampero,
and
P. Cerretelli.
Oxygen debt and high-energy phosphates in gastrocnemius muscle of the dog.
Am. J. Physiol.
215:
523-531,
1968.
26.
Piiper, J.,
D. R. Pendergast,
C. Marconi,
M. Meyer,
N. Heisler,
and
P. Cerretelli.
Blood flow distribution in dog gastrocnemius muscle at rest and during exercise.
J. Appl. Physiol.
58:
2068-2074,
1985
27.
Rowell, L. B.
Human Circulation Regulation During Physical Stress. New York: Oxford Univ. Press, 1986.
28.
Saltin, B.,
and
P. D. Gollnick.
Skeletal muscle adaptability: significance for metabolism and performance.
In: Handbook of Physiology. Skeletal Muscle. Bethesda, MD: Am. Physiol. Soc., 1983, sect. 10, chapt. 19, p. 555-631.
29.
Stainsby, W. N.,
and
A. B. Otis.
Blood flow, blood oxygen tension, oxygen uptake and oxygen transport in skeletal muscle.
Am. J. Physiol.
206:
858-866,
1964.
30.
Stainsby, W. N.,
and
H. G. Welch.
Lactate metabolism of contracting dog skeletal muscle in situ.
Am. J. Physiol.
211:
177-183,
1966.
31.
Weibel, E. R.
The Pathway for Oxygen. Structure and Function in the Mammalian Respiratory System. Cambridge, MA: Harvard Univ. Press, 1984.
32.
Whipp, B. J.,
and
S. A. Ward.
Physiological determinants of pulmonary gas exchange kinetics during exercise.
Med. Sci. Sports Exerc.
22:
62-71,
1990[Medline].
This article has been cited by other articles:
|
|
 |
|
  P. A. Sperandio, A. Borghi-Silva, A. Barroco, L. E. Nery, D. R. Almeida, and J. A. Neder Microvascular oxygen delivery-to-utilization mismatch at the onset of heavy-intensity exercise in optimally treated patients with CHF Am J Physiol Heart Circ Physiol, November 1, 2009; 297(5): H1720 - H1728. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. Vogiatzis, D. Athanasopoulos, H. Habazettl, W. M. Kuebler, H. Wagner, C. Roussos, P. D. Wagner, and S. Zakynthinos Intercostal muscle blood flow limitation in athletes during maximal exercise J. Physiol., July 15, 2009; 587(14): 3665 - 3677. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. M. Jones, R. C. Davies, L. F. Ferreira, T. J. Barstow, S. Koga, and D. C. Poole Reply to Quaresima and Ferrari J Appl Physiol, July 1, 2009; 107(1): 372 - 373. [Full Text] [PDF]
|
|
|
|
|
|
R. C. Davies, R. G. Eston, D. C. Poole, A. V. Rowlands, F. DiMenna, D. P. Wilkerson, C. Twist, and A. M. Jones Effect of eccentric exercise-induced muscle damage on the dynamics of muscle oxygenation and pulmonary oxygen uptake J Appl Physiol, November 1, 2008; 105(5): 1413 - 1421. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. J. Harper, L. F. Ferreira, B. J. Lutjemeier, D. K. Townsend, and T. J. Barstow Matching of blood flow to metabolic rate during recovery from moderate exercise in humans Exp Physiol, October 1, 2008; 93(10): 1118 - 1125. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. A. Zoladz, L. B. Gladden, M. C. Hogan, Z. Nieckarz, and B. Grassi Progressive recruitment of muscle fibers is not necessary for the slow component of VO2 kinetics J Appl Physiol, August 1, 2008; 105(2): 575 - 580. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. R. Chiappa, A. Borghi-Silva, L. F. Ferreira, C. Carrascosa, C. C. Oliveira, J. Maia, A. C. Gimenes, F. Queiroga Jr, D. Berton, E. M. V. Ferreira, et al. Kinetics of muscle deoxygenation are accelerated at the onset of heavy-intensity exercise in patients with COPD: relationship to central cardiovascular dynamics J Appl Physiol, May 1, 2008; 104(5): 1341 - 1350. [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]
|
|
|
|
|
|
N. Lai, G. M. Saidel, B. Grassi, L. B. Gladden, and M. E. Cabrera Model of oxygen transport and metabolism predicts effect of hyperoxia on canine muscle oxygen uptake dynamics J Appl Physiol, October 1, 2007; 103(4): 1366 - 1378. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. B. Stephens, D. Constantin-Teodosiu, and P. L. Greenhaff New insights concerning the role of carnitine in the regulation of fuel metabolism in skeletal muscle J. Physiol., June 1, 2007; 581(2): 431 - 444. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. J. Harper, L. F. Ferreira, B. J. Lutjemeier, D. K. Townsend, and T. J. Barstow Human femoral artery and estimated muscle capillary blood flow kinetics following the onset of exercise Exp Physiol, July 1, 2006; 91(4): 661 - 671. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Burnley, C. L. Roberts, R. Thatcher, J. H. Doust, and A. M. Jones Influence of blood donation on O2 uptake on-kinetics, peak O2 uptake and time to exhaustion during severe-intensity cycle exercise in humans Exp Physiol, May 1, 2006; 91(3): 499 - 509. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Lador, M. Azabji Kenfack, C. Moia, M. Cautero, D. R. Morel, C. Capelli, and G. Ferretti Simultaneous determination of the kinetics of cardiac output, systemic O2 delivery, and lung O2 uptake at exercise onset in men Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2006; 290(4): R1071 - R1079. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. L. MacPhee, J. K. Shoemaker, D. H. Paterson, and J. M. Kowalchuk Kinetics of O2 uptake, leg blood flow, and muscle deoxygenation are slowed in the upper compared with lower region of the moderate-intensity exercise domain J Appl Physiol, November 1, 2005; 99(5): 1822 - 1834. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. Grassi, M. C Hogan, K. M Kelley, R. A Howlett, and L. B. Gladden Effects of nitric oxide synthase inhibition by L-NAME on oxygen uptake kinetics in isolated canine muscle in situ J. Physiol., November 1, 2005; 568(3): 1021 - 1033. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. P Wilkerson, J. Rittweger, N. J. A Berger, P. F Naish, and A. M Jones Influence of recombinant human erythropoietin treatment on pulmonary O2 uptake kinetics during exercise in humans J. Physiol., October 15, 2005; 568(2): 639 - 652. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. D. Paterson, J. M. Kowalchuk, and D. H. Paterson Effects of prior heavy-intensity exercise during single-leg knee extension on vO2 kinetics and limb blood flow J Appl Physiol, October 1, 2005; 99(4): 1462 - 1470. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. D. Paterson, J. M. Kowalchuk, and D. H. Paterson Kinetics of V.02 and femoral artery blood flow during heavy-intensity, knee-extension exercise J Appl Physiol, August 1, 2005; 99(2): 683 - 690. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. M. Stary and M. C. Hogan Intracellular pH during sequential, fatiguing contractile periods in isolated single Xenopus skeletal muscle fibers J Appl Physiol, July 1, 2005; 99(1): 308 - 312. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. A. Kindig, R. A. Howlett, and M. C. Hogan Effect of contractile duration on intracellular PO2 kinetics in Xenopus single skeletal myocytes J Appl Physiol, May 1, 2005; 98(5): 1639 - 1645. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. F. Ferreira, D. K. Townsend, B. J. Lutjemeier, and T. J. Barstow Muscle capillary blood flow kinetics estimated from pulmonary O2 uptake and near-infrared spectroscopy J Appl Physiol, May 1, 2005; 98(5): 1820 - 1828. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. F. Ferreira, B. J. Lutjemeier, D. K. Townsend, and T. J. Barstow Dynamics of skeletal muscle oxygenation during sequential bouts of moderate exercise Exp Physiol, May 1, 2005; 90(3): 393 - 401. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. J. Gurd, B. W. Scheuermann, D. H. Paterson, and J. M. Kowalchuk Prior heavy-intensity exercise speeds V{middle dot}O2 kinetics during moderate-intensity exercise in young adults J Appl Physiol, April 1, 2005; 98(4): 1371 - 1378. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. A. Zoladz, Z. Szkutnik, K. Duda, J. Majerczak, and B. Korzeniewski Preexercise metabolic alkalosis induced via bicarbonate ingestion accelerates V{middle dot}2 kinetics at the onset of a high-power-output exercise in humans J Appl Physiol, March 1, 2005; 98(3): 895 - 904. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. A. Roberts, S. J. G. Loxham, S. M. Poucher, D. Constantin-Teodosiu, and P. L. Greenhaff Acetyl-CoA provision and the acetyl group deficit at the onset of contraction in ischemic canine skeletal muscle Am J Physiol Endocrinol Metab, February 1, 2005; 288(2): E327 - E334. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Stellingwerff, L. Glazier, M. J. Watt, P. J. LeBlanc, G. J. F. Heigenhauser, and L. L. Spriet Effects of hyperoxia on skeletal muscle carbohydrate metabolism during transient and steady-state exercise J Appl Physiol, January 1, 2005; 98(1): 250 - 256. [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]
|
|
|
|
|
|
J. A Timmons, D. Constantin-Teodosiu, S. M Poucher, and P. L Greenhaff Acetyl group availability influences phosphocreatine degradation even during intense muscle contraction J. Physiol., December 15, 2004; 561(3): 851 - 859. [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]
|
|
|
|
|
|
P. Krustrup, Y. Hellsten, and J. Bangsbo Intense interval training enhances human skeletal muscle oxygen uptake in the initial phase of dynamic exercise at high but not at low intensities J. Physiol., August 15, 2004; 559(1): 335 - 345. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. J. Haseler, C. A. Kindig, R. S. Richardson, and M. C. Hogan The role of oxygen in determining phosphocreatine onset kinetics in exercising humans J. Physiol., August 1, 2004; 558(3): 985 - 992. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Fukuba, Y. Ohe, A. Miura, A. Kitano, M. Endo, H. Sato, M. Miyachi, S. Koga, and O. Fukuda Dissociation between the time courses of femoral artery blood flow and pulmonary VO2 during repeated bouts of heavy knee extension exercise in humans Exp Physiol, May 1, 2004; 89(3): 243 - 253. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. M. Jones, D. P. Wilkerson, S. Wilmshurst, and I. T. Campbell Influence of L-NAME on pulmonary O2 uptake kinetics during heavy-intensity cycle exercise J Appl Physiol, March 1, 2004; 96(3): 1033 - 1038. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. L. Olive, J. M. Slade, C. S. Bickel, G. A. Dudley, and K. K. McCully Increasing blood flow before exercise in spinal cord-injured individuals does not alter muscle fatigue J Appl Physiol, February 1, 2004; 96(2): 477 - 482. [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]
|
|
|
|
|
|
M. Endo, S. Tauchi, N. Hayashi, S. Koga, H. B. Rossiter, and Y. Fukuba Facial cooling-induced bradycardia does not slow pulmonary V.O2 kinetics at the onset of high-intensity exercise J Appl Physiol, October 1, 2003; 95(4): 1623 - 1631. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. M Jones, D. P Wilkerson, K. Koppo, S. Wilmshurst, and I. T Campbell Inhibition of Nitric Oxide Synthase by L-NAME Speeds Phase II Pulmonary VO2 Kinetics in the Transition to Moderate-Intensity Exercise in Man J. Physiol., October 1, 2003; 552(1): 265 - 272. [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]
|
|
|
|
|
|
M. C. Hogan, B. Grassi, M. Samaja, C. M. Stary, and L. B. Gladden Effect of contraction frequency on the contractile and noncontractile phases of muscle venous blood flow J Appl Physiol, September 1, 2003; 95(3): 1139 - 1144. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. Grassi, S. Pogliaghi, S. Rampichini, V. Quaresima, M. Ferrari, C. Marconi, and P. Cerretelli Muscle oxygenation and pulmonary gas exchange kinetics during cycling exercise on-transitions in humans J Appl Physiol, July 1, 2003; 95(1): 149 - 158. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. A. Howlett and M. C. Hogan Dichloroacetate accelerates the fall in intracellular PO2 at onset of contractions in Xenopus single muscle fibers Am J Physiol Regulatory Integrative Comp Physiol, February 1, 2003; 284(2): R481 - R485. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Burnley, J. H. Doust, D. Ball, and A. M. Jones Effects of prior heavy exercise on VO2 kinetics during heavy exercise are related to changes in muscle activity J Appl Physiol, July 1, 2002; 93(1): 167 - 174. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Fukuba, N. Hayashi, S. Koga, and T. Yoshida VO2 kinetics in heavy exercise is not altered by prior exercise with a different muscle group J Appl Physiol, June 1, 2002; 92(6): 2467 - 2474. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Somfay, J. Porszasz, S.-M. Lee, and R. Casaburi Effect of Hyperoxia on Gas Exchange and Lactate Kinetics Following Exercise Onset in Nonhypoxemic COPD Patients Chest, February 1, 2002; 121(2): 393 - 400. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. P Campbell-O'Sullivan, D. Constantin-Teodosiu, N. Peirce, and P. L Greenhaff Low intensity exercise in humans accelerates mitochondrial ATP production and pulmonary oxygen kinetics during subsequent more intense exercise J. Physiol., February 1, 2002; 538(3): 931 - 939. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Bangsbo, M. J. Gibala, P. Krustrup, J. Gonzalez-Alonso, and B. Saltin Enhanced pyruvate dehydrogenase activity does not affect muscle O2 uptake at onset of intense exercise in humans Am J Physiol Regulatory Integrative Comp Physiol, January 1, 2002; 282(1): R273 - R280. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. K. Evans, I. Savasi, G. J. F. Heigenhauser, and L. L. Spriet Effects of acetate infusion and hyperoxia on muscle substrate phosphorylation after onset of moderate exercise Am J Physiol Endocrinol Metab, December 1, 2001; 281(6): E1144 - E1150. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H B Rossiter, S A Ward, J M Kowalchuk, F A Howe, J R Griffiths, and B J Whipp Effects of prior exercise on oxygen uptake and phosphocreatine kinetics during high-intensity knee-extension exercise in humans J. Physiol., November 15, 2001; 537(1): 291 - 303. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Perrey, M. E. Tschakovsky, and R. L. Hughson Muscle chemoreflex elevates muscle blood flow and O2 uptake at exercise onset in nonischemic human forearm J Appl Physiol, November 1, 2001; 91(5): 2010 - 2016. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. A. Kindig, P. McDonough, H. H. Erickson, and D. C. Poole Effect of L-NAME on oxygen uptake kinetics during heavy-intensity exercise in the horse J Appl Physiol, August 1, 2001; 91(2): 891 - 896. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. C. Hogan Fall in intracellular PO2 at the onset of contractions in Xenopus single skeletal muscle fibers J Appl Physiol, May 1, 2001; 90(5): 1871 - 1876. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Koga, T. J. Barstow, T. Shiojiri, T. Takaishi, Y. Fukuba, N. Kondo, M. Shibasaki, and D. C. Poole Effect of muscle mass on {V}O2 kinetics at the onset of work J Appl Physiol, February 1, 2001; 90(2): 461 - 468. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. B. Gladden Lactic acid: New roles in a new millennium PNAS, January 16, 2001; 98(2): 395 - 397. [Full Text] [PDF]
|
|
|
|
|
|
B. Grassi, M. C. Hogan, K. M. Kelley, W. G. Aschenbach, J. J. Hamann, R. K. Evans, R. E. Patillo, and L. B. Gladden Role of convective O2 delivery in determining VO2 on-kinetics in canine muscle contracting at peak VO2 J Appl Physiol, October 1, 2000; 89(4): 1293 - 1301. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Burnley, A. M. Jones, H. Carter, and J. H. Doust Effects of prior heavy exercise on phase II pulmonary oxygen uptake kinetics during heavy exercise J Appl Physiol, October 1, 2000; 89(4): 1387 - 1396. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Bangsbo, P. Krustrup, J. Gonzalez-Alonso, R. Boushel, and B. Saltin Muscle oxygen kinetics at onset of intense dynamic exercise in humans Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2000; 279(3): R899 - R906. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. L. Parolin, L. L. Spriet, E. Hultman, M. G. Hollidge-Horvat, N. L. Jones, and G. J. F. Heigenhauser Regulation of glycogen phosphorylase and PDH during exercise in human skeletal muscle during hypoxia Am J Physiol Endocrinol Metab, March 1, 2000; 278(3): E522 - E534. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. A. Howlett, G. J. F. Heigenhauser, and L. L. Spriet Skeletal muscle metabolism during high-intensity sprint exercise is unaffected by dichloroacetate or acetate infusion J Appl Physiol, November 1, 1999; 87(5): 1747 - 1751. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Hayashi, M. Ishihara, A. Tanaka, and T. Yoshida Impeding O2 unloading in muscle delays oxygen uptake response to exercise onset in humans Am J Physiol Regulatory Integrative Comp Physiol, November 1, 1999; 277(5): R1274 - R1281. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H B Rossiter, S A Ward, V L Doyle, F A Howe, J R Griffiths, and B J Whipp Inferences from pulmonary O2 uptake with respect to intramuscular [phosphocreatine] kinetics during moderate exercise in humans J. Physiol., August 1, 1999; 518(3): 921 - 932. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. E. Tschakovsky and R. L. Hughson Interaction of factors determining oxygen uptake at the onset of exercise J Appl Physiol, April 1, 1999; 86(4): 1101 - 1113. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
) at
rest and during contractions in 3 experimental conditions.
A: dogs
1-4, left to
right, respectively.
B: dogs
5-7, left to
right, respectively. Monoexponential
functions (solid lines) that yielded lowest average values of squared
residuals (analysis B) are also
shown. Vertical dashed lines indicate contraction onset. See text for
further details.
