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O2 max is unaffected by altering the temporal pattern of stimulation frequency in rat hindlimb in situ
1Faculty of Kinesiology and 2Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada T2N 1N4
Submitted 21 January 2003 ; accepted in final form 8 April 2003
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ABSTRACT |
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 TOP ABSTRACT METHODSRESULTSDISCUSSIONDISCLOSURESREFERENCES |
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O2 max) than beginning
immediately with an intense stimulation frequency because of a slower
progression of fatigue under the former conditions. In one group of animals,
the distal hindlimb muscles were electrically stimulated at a frequency of 60
tetani/min for 4 min (F60; n = 6 rats); in the other
group, the muscles were incrementally stimulated for 1 min at each of 7.5, 15,
30, and 60 tetani/min and for 2 min at 90 tetani/min (FInc;
n = 5 rats). Despite large differences in rate of fatigue [time to
60% of initial force was 47 ± 3 (SE) vs. 188 ± 1 s in
F60 and FInc, respectively] and the time at which
O2 max occurred (120
± 15 vs. 264 ± 6 s),
O2 max was not different
(419 ± 24 vs. 381 ± 44 µmol · min-1
· 100 g-1). Furthermore, time x tension integral at
O2 max (3.82 ±
0.41 vs. 4.07 ± 0.31 N · s) and peak lactate efflux (910
± 45 vs. 800 ± 98 µmol · min-1 · 100
g-1) were not different between groups. Thus our results show that
the more rapid progression of fatigue in F60 did not compromise the
aerobic metabolic response in electrically stimulated rat hindlimb muscles.
However, in both groups, O2 uptake and lactate efflux declined
after O2 max was attained
in similar proportion to a further fall in force, suggesting that ongoing
fatigue with intense contractions reduced ATP demand below that requiring
maximal aerobic and glycolytic metabolic responses once
O2 max was reached. maximal O2 uptake; aerobic metabolism; anaerobic metabolism; lactate
O2) on-kinetics], these
studies have not considered the influence of declining energy demand,
subsequent to fatigue, on the aerobic metabolic response. Skeletal muscle
recruitment in vivo at exercise onset involves a coordinated activation of
motor units (energy demand) in concert with increases in blood flow,
microvascular recruitment, and activation of intramyocyte metabolic pathways
(energy supply). As exercise intensity increases and/or fatigue occurs in
individual fibers, additional motor units may be recruited to provide the
required power output (for a review, see Ref.
13). As such, the consequences
of fatigue in individual fibers and/or motor units are not necessarily
manifest in a decline in externally measured power output (provided the power
required is submaximal). On the other hand, studies of contractile and
metabolic responses routinely made in preparations in situ, such as the
pump-perfused rat hindlimb (e.g., Refs.
15,
20), often utilize a
supramaximal electrical stimulation protocol that simultaneously recruits all
motor units via direct nerve stimulation. Intense muscle contractions, such as
these, yield a progressive fall in tension development (fatigue; particularly
at the higher stimulation frequencies, e.g., see Fig. 6 in Ref.
20), which occurs consequent
to a marked perturbation of the intramyocyte environment characterized by
elevations in lactate, Pi, and H+ concentrations and
ionic imbalances (for reviews, see Refs.
10,
29).
With regard to the potential influence that these metabolic perturbations
might have on aerobic metabolism, previous studies have shown that hypercapnic
acidosis reduces the maximal O2 uptake
(O2 max)
(14) and that elevations in
Pi and H+ concentrations directly inhibit mitochondrial
respiration at a given ADP concentration
(27). As such, it seems
logical that there may be circumstances where the metabolic disturbance caused
by intense contractions may not only lead to fatigue but also impair the
aerobic metabolic response. Such an effect could be mediated directly by the
afore-mentioned depression of mitochondrial respiration (e.g., by elevated
Pi and/or H+ concentration) or indirectly by a fall in
ATP demand (consequent to fatigue) below that obligating maximal aerobic
energy provision.
The purpose of this study was to determine whether slowing the development
of fatigue would have a favorable effect on aerobic metabolism and thus yield
a higher O2 max. To this
end, we employed a pump-perfused rat hindlimb preparation in which the distal
hindlimb muscles were activated by supramaximal electrical stimulation at a
frequency of 60 tetani/min for 4 min (F60) or for 1 min at each of
7.5, 15, 30, and 60 tetani/min and for 2 min at 90 tetani/min
(FInc). We hypothesized that the slower onset of fatigue and lactic
acidosis in FInc would yield a higher
O2 max than in
F60.
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METHODS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESREFERENCES |
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Bovine erythrocytes were collected each week from a local abattoir, by
using acid citrate dextrose as an anticoagulant. After collection, the
erythrocytes were washed in three changes of Krebs-Henseleit buffer by
centrifugation at 5,000 g, with aspiration of the supernatant and
buffy coat between washes. The washed erythrocytes were stored at 4°C in
Krebs-Henseleit buffer containing 5 mM glucose until used (within 3 days of
collection). On the day of experiments, the erythrocytes were washed a final
time and reconstituted in a Krebs-Henseleit buffer (pH = 7.4) containing 4.5%
albumin, 5 mM glucose, 100 µU/ml insulin, 1,000 µU/ml heparin, and 0.15
mM pyruvate. Hematocrit was 42 ± 1%, and hemoglobin concentration was
14.2 ± 0.2 g/dl. After the animal was anesthetized with 75 mg/kg
pentobarbital sodium (ip), the right iliac artery and vein were ligated and
the right gastrocnemius, plantaris, and soleus muscles were removed and
weighed. Catheters were inserted into the left iliac artery (22 gauge) and
vein (20 gauge) and were advanced into the respective femoral artery and vein
to initiate hindlimb perfusion. Ligatures were placed around the iliac artery
immediately inside the abdominal wall (proximal to the inguinal ligament) and
around the femoral vein to secure the arterial and venous catheters in place.
During experiments, the erythrocyte-containing perfusion medium (volume
400 ml) was recirculated after the first 50 ml of venous effluent were
discarded.
O2 and CO2 tension of the inflowing perfusate were controlled by using an oxygenator (4-liter flask containing 7 m of Silastic tubing) gassed by a high-O2 mixture (95% O2-5% CO2). The rate of perfusion was controlled by a peristaltic pump (Gilson Minipuls), with perfusion pressure monitored continuously via a pressure transducer (model PT300, Grass Instruments) placed at the same height as the rat hindlimb, in line with the arterial catheter. After catheterization, the animal was euthanized by a 25-mg intracardiac injection of pentobarbital sodium and the hindlimb secured to a metal baseplate. The Achilles tendon was cut from the foot and attached to a force transducer (model FT10, Grass Instruments) via noncompliant 2-0 silk string for measurement of isometric force development.
The sheath containing the articular, peroneal, and distal tibial nerve
branches was isolated, ligated, and cut proximally for electrical stimulation
after the inferior gluteal nerve was cut to prevent stimulation of the upper
hindlimb musculature (12). All
exposed tissues of the experimental hindlimb were wrapped in warm
saline-soaked gauze, Saran wrap, and aluminum foil (encompassing a thermistor
probe connected to a heat lamp) to prevent moisture and heat loss. Muscle and
perfusate temperatures were maintained at 37°C. After perfusion was
initiated, flow was incrementally increased (allowing pressure to stabilize
before further increasing flow) to elicit a flow-induced vasodilatory response
until the desired rate of perfusion was achieved (30 min). The perfusion
rate was then held constant for the remainder of each experiment (i.e., during
contractions).
Experimental protocol. Animals were divided into two groups. In
one group (F60; n = 6 rats) tetanic muscle contractions
(200-ms trains at 100 pulses/s, each 0.2-ms in duration) at a frequency of 60
tetani/min were evoked by electrical stimulation (Grass S48 electrical
stimulator) for 4 min, with muscle length and stimulation voltage (7 V)
adjusted to yield maximal tension. In the other group (FInc;
n = 5 rats), tetanic muscle contractions were elicited for 1 min at
7.5, 15, 30, and 60 tetani/min and for 2 min at 90 tetani/min. Blood samples,
drawn anaerobically from the arterial catheter immediately before contractions
and from venous effluent immediately before contractions and every 30 s during
muscle contractions (except for the first 2 contraction frequencies in the
incremental group, where samples were analyzed at the end of each minute),
were analyzed for hemoglobin concentration, O2 saturation
(So2), Po2, Pco2, glucose concentration,
lactate concentration, and pH by a blood-gas analyzer (Nova Biomedical Stat
Profile M). Blood O2 content was calculated by using the following
formula: O2 content = hemoglobin concentration x
So2 x 1.39 + 0.003 x Po2. Blood samples were
also drawn every 30 s for 4 min after contractions to monitor the decline in
lactate efflux in recovery.
O2 across the hindlimb
was calculated as the product of total hindlimb blood flow and the
arteriovenous O2 content difference, with the highest value taken
as the O2 max. Similarly,
lactate efflux was calculated as the product of total hindlimb blood flow and
the arteriovenous lactate concentration difference. To take account of the
differences in contractile demand between different frequencies of
contractions, the time x tension integral was calculated as the
integrated force (N) observed over each 30-s interval and is expressed over a
1-s interval (i.e., N x s). In calculating the time x tension
integral at O2 max, the
tension data were time aligned with
O2 by taking account of
the time required for venous blood leaving the contracting muscles to reach
the sampling port (20 s, calculated in each experiment on the basis of
the volume of blood in the circuit between the femoral vein and the venous
sampling port, and the rate of blood flow; R. T. Hepple, unpublished
observations).
Normalization procedures. Pilot experiments in our laboratory have
confirmed the findings of Gorski et al.
(12), who reported that the
total perfused mass in the hindlimb includes all of the muscles except the
gluteal muscles (C. C. Jackson and R. T. Hepple, unpublished observations). As
such, total perfused mass in the present experiments was estimated on the
basis of results showing that the distal hindlimb muscles stimulated in this
preparation (which include the gastrocnemius-plantaris-soleus muscle group,
tibialis anterior, and remaining tibial muscles; Ref.
12) comprise 29% of the total
perfused mass. Because most of the
O2 measured at rest is
contributed by these noncontracting tissues,
O2 during stimulation was
normalized to the mass of the contracting muscles after subtraction of the
O2 contributed by
noncontracting tissues (assumed to be 71% of values observed at rest).
Blood flow. Total hindlimb blood flow was verified by timed blood
collection at the end of each experiment. The difference in blood flow through
the arterial catheter vs. that collected from the venous catheter during
hindlimb perfusion experiments was 10%. After the contraction bout,
muscle blood flow distribution was determined via infusion of colored
microspheres. Briefly, 270,000 colored microspheres (15.5-µm diameter;
Dye Trak, Triton Technonology) suspended in Tween 20 were vortexed for 2 min
and slowly infused (pump output adjusted to maintain perfusion pressure) into
a side-arm port proximal to the arterial catheter, followed by slow infusion
of 2 ml of saline to flush remaining microspheres from the port (port volume =
0.4 ml). As described previously
(15), after the experiment the
left gastrocnemius, plantaris, and soleus muscles were excised and analyzed
for microsphere distribution by spectrophotometry (Biochrom Ultrospec 2100
Pro). Briefly, this involved digestion of individual muscles in test tubes
containing 4 M KOH in a heated water bath (60°C). The content of each test
tube was then filtered through 8-µm-pore membranes (Whatman Nucleopore) to
trap the microspheres. Each filter was placed in a microcentrifuge tube with
400 µl of N,N-dimethylformamide and vortexed to release the
colored contents from the microspheres. Absorbance was measured after 10 min
at a wave-length of 448 nm (yellow microspheres), and the number of
microspheres trapped in each muscle sample was calculated from the regression
equation provided by the manufacturer. The blood flow to the
gastroncemius-plantaris-soleus muscle group was determined as the product of
total hindlimb blood flow and the proportion of microspheres found in the
gastroncemius-plantaris-soleus muscle group. Similarly, muscle O2
delivery was calculated as the product of blood flow to the
gastroncemius-plantaris-soleus muscle group and the arterial O2
content. Because blood flow and convective O2 delivery in the
gastrocnemius-plantaris-soleus muscle group are representative of the total
contracting muscle mass (12,
24), O2 extraction
across the contracting muscles was estimated as the quotient of the
mass-specific O2 max and
blood flow for the gastrocnemius-plantaris-soleus muscle group.
Statistical analysis. Values are reported as means ± SE.
Differences between groups were assessed by a Student's t-test
(O2 max, convective
O2 delivery, and so forth) or two-way ANOVA with a Bonferoni post
hoc test (O2, lactate
efflux, tension development). The 
was set at 0.05.
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RESULTS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESREFERENCES |
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Contractile and metabolic responses. Resting
O2 and peak tension at
the onset of contractions were similar between groups
(Table 3). In contrast, the
rate of fatigue development was significantly slower in FInc, as
demonstrated by the significantly longer time required for tension to fall to
60% of the peak in this group (Table
3; Fig.
1A). Furthermore, whereas the time x tension
integral fell continuously in F60, it tended to increase in
FInc until a frequency of 90 tetani/min-1 was reached
(Fig. 1B). Similarly,
O2 increased more
gradually (Fig. 2), as did
lactate efflux (Fig. 3), in
FInc vs. F60. Despite this,
O2 max was not different
between groups, nor was the tension at
O2 max, time x
tension integral at O2
max, or peak lactate efflux (Table
3). Note that the values for
O2 max (21.2 ± 1.4
µmol/min) are very similar to those we have seen previously under similar
conditions of O2 delivery (21.7 ± 1.3 µmol/min; Ref.
15), and those seen by Hood et
al. in a very similar perfused rat hindlimb preparation (21 µmol/min;
Ref. 20). Furthermore, our
peak lactate efflux values at 30 tetani/min in FInc
(19–20 µmol/min) are similar to those reported by Spriet et al.
at 30 tetani/min (23 µmol/min; Ref.
26) after one takes into
account the 70% greater muscle mass recruited in their model.
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On average, O2 max was
reached by 2 min in F60 and between 4 min and 4 min 30 s in
FInc. Because there is a time delay of 20 s between the venous
effluent sampling line and the time at which the blood leaves the contracting
muscles (see METHODS),
O2 max was also
coincident with the metabolic responses incurred at 60 tetani/min in
FInc. In both groups, the time course for the
O2 and lactate efflux
profiles was remarkably similar, with both profiles demonstrating a
progressive increase to a maximal value followed by a decline as further
fatigue ensued. Further to this point, Fig.
4 demonstrates that there was a significant correlation between
the time that peak lactate efflux occurred and the time that
O2 max was reached. In 10
of 11 cases, O2 max was
reached in the 30 s before (n = 2) or coincident (n = 8)
with peak lactate efflux. In the one instance in which
O2 max occurred after
peak lactate efflux had been reached, lactate efflux was still at its highest
level when O2 max
occurred, after which both lactate efflux and
O2 fell from their peak
values.
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DISCUSSION |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESREFERENCES |
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O2 max was not different
between groups, suggesting that the fibers most affected by the early fatigue
were primarily low oxidative or that fatigue per se is unrelated to the
aerobic metabolic response. On the other hand, the time at which
O2 max occurred was
significantly correlated with the timing of peak lactate efflux, and, after
this point, O2 and
lactate efflux fell in similar proportion to a further reduction of force,
suggesting that this late fatigue affected fibers of both oxidative and
glycolytic character. Thus, although early fatigue in this model did not
adversely affect the maximal aerobic metabolic response, the subsequent falls
in O2 and lactate efflux
in similar proportion to a further fall in force are consistent with a reduced
energetic demand due to further fatigue after
O2 max was attained.
O2 and
fatigue as O2 max is
approached. The objective of our study was to determine whether a more
gradual increase in contraction frequency, and thus slower development of
fatigue, would benefit the aerobic metabolic response. Examination of the
contractile responses in each group shows that the FInc protocol
produced a more gradual fall in tension compared with the F60
protocol. The differences in temporal pattern of fatigue between groups are
even more apparent when one considers the time x tension integral. In
the FInc group, time x tension integral tended to increase
until contraction frequency was increased to 90 tetani/min and then exhibited
a consistent decline, whereas F60 was associated with a progressive
fall immediately from the beginning of contractions. Despite these differences
in development of fatigue, O2
max was not different between groups, nor was the time x tension
integral different at this point. The fact that the magnitude of
O2 max was not affected
by this markedly different development of fatigue demonstrates that the
fatigue observed in the F60 group while
O2 was still increasing
does not adversely affect aerobic metabolism. This could be explained if the
majority of fatigue observed during this period was occurring in muscle fibers
exhibiting low aerobic capacity and/or if the fall in force had not yet
reached a point where less than
O2 max was obligated to
meet the contractile demands. To address this latter possibility, one would
need to design a contraction scheme that induced fatigue rapidly enough to
cause contractile demand to fall below that obligating
O2 max before aerobic
metabolism was maximally activated. A complication to designing such an
experiment in situ is a compromise in blood flow and O2 delivery
because of the higher duty cycle (increasing the proportion of time the muscle
is not receiving blood flow because of microvascular compression during the
contraction phase; e.g., Ref.
1) that would be encountered at
higher contraction frequencies necessary to induce a more rapid rate of
fatigue.
Why should O2 fall
after O2 max is
attained? Note that although the time x tension integral was
increasing during most of the period in which
O2 was increasing in the
FInc group, taking account of the time delay between venous blood
leaving the contracting muscles and reaching the sampling site (20 s;
METHODS) showed that time x tension integral continuously
declined in all experiments after attainment of
O2 max, as was the case
in the F60 group. Thus it is striking that, in both contraction
schemes, O2 increased up
to a maximal level, which was not different between groups (despite a
considerably longer time to reach
O2 max in
FInc) and then gradually fell in similar proportion to a further
fall in time x tension integral. A similar phenomenon was observed by
Brechue et al. during isotonic tetanic contractions in a pump-perfused canine
gastrocnemius model whereby
O2 increased to a maximal
level within 3 min and then began to decline after 10 min in concert
with a further fall in power output (see Figs.
2 and
3, control series in Ref.
6). Considering what has been
established about the determinants of
O2 max, it is not clear
why O2 should fall after
O2 max is attained in our
model. Although it is well known that O2 supply is a primary
determinant of O2 max
(e.g., Refs. 4,
19,
21), a change in convective
O2 delivery cannot explain the fall in
O2 because convective
O2 delivery was held constant via pump perfusion and continuous
oxygenation of the circulating erythrocyte perfusate in our experiments.
Similarly, although some swelling within the myocytes (which would lengthen
O2 diffusion distances) is expected with pump perfusion (on the
basis of 17% increase in wet mass seen previously; Ref.
15), it seems unlikely that
the time course of this would be fast enough to account for the acute
reduction in O2 after
O2 max was attained. Thus
O2 must have decreased
after O2 max was attained
because either perturbation of the intramyocyte environment inhibited aerobic
metabolism or the continuing fall in force caused contractile energy demand to
fall below that obligating maximal aerobic metabolism. In considering the
first possibility, Harkema and Meyer
(14) previously found
hypercapnic acidosis caused a reduction in
O2 max in cat soleus
perfused in situ at 37°C, and Walsh et al.
(27) have recently shown that
elevated Pi and H+ concentrations directly reduce
mitochondrial respiration at a given ADP concentration in
saponin-permeabilized bundles of skeletal muscle fibers studied at 25°C.
These results suggest that acidosis per se has a direct effect on aerobic
metabolism and could have played a role in reducing
O2 after
O2 max was attained in
our experiments. The significant temporal correlation between
O2 max and peak lactate
efflux could be taken as support for this view. Indeed, one might also
conclude that these changes could help determine
O2 max by defining the
degree of intracellular perturbation that can be tolerated before
mitochondrial respiration becomes compromised.
On the other hand, there were no instances in which
O2 fell before force,
regardless of whether one considers the total force or the time x
tension integral. In addition, not only did
O2 fall after reaching a
maximal value but so, too, did lactate efflux. Note that the tendency for peak
lactate efflux to occur in the 30-s sampling period after
O2 max was attained could
be explained by a time delay necessary for facilitated diffusion of lactate
out of the myocytes. If the fall in
O2 were due to
compromised aerobic metabolism subsequent to acidosis, one might have expected
there to be a compensatory increase in glycolysis to meet the ATP demand,
which should have been reflected by a continued increase in lactate efflux. In
contrast, lactate efflux fell in concert with
O2, which suggests a
common cause to both phenomenon, and the fall in force (and thus contractile
energy demand) seems the most likely cause. Note also that lactate efflux fell
in a similar pattern after contractions stopped in both groups
(Fig. 3), demonstrating that
there was no difference in lactate transport out of the myocytes between
groups, and thus the lactate efflux measurements can be considered an
appropriate surrogate for lactate production.
One of the complicating factors in our investigation is the fact that the
distal hindlimb muscles of the rat exhibit a marked heterogeneity in metabolic
character. In our experiments, force is measured in the
gastrocnemius-plantaris-soleus muscle group, which is composed of muscles
containing primarily slow oxidative (soleus) and mixed fast-twitch (plantaris
and gastrocnemius) fibers (2).
Thus lack of knowledge about which fibers are fatiguing over the duration of
the contraction bout complicates the interpretation. Specifically, it is
difficult to know, except perhaps by inference (i.e.,
O2 max was not
compromised in the F60 group), whether the initial fall in fatigue
was evident exclusively in fibers of low oxidative capacity. We have attempted
to address this limitation by delicately separating the connective tissue
attachments between the soleus muscle and gastrocnemius-plantaris muscles and
making separate force measurements in the soleus and gastrocnemius/plantaris
muscle compartments in two experiments (D. J. Krause and R. T. Hepple,
unpublished observations). However, despite a similar temporal pattern of
fatigue in slow oxidative soleus muscle and the less oxidative
gastrocnemius-plantaris muscles (although to a smaller relative degree in
soleus muscle), the high specific tension measured in soleus (63 N/g)
relative to that measured in the gastrocnemius-plantaris muscle combined
(13 N/g) suggests that there was substantial "cross talk" in
force measurements between each muscle compartment (primarily affecting force
measured in the weaker soleus muscle), which prevents us from drawing
meaningful conclusions from these experiments at this time.
Fatigue and aerobic metabolic response. In considering how fatigue
might adversely affect aerobic metabolism, previous studies have shown that
phosphocreatine hydrolysis is proportional to
O2 across a broad range
of work rates in vivo (18,
25) and in vitro
(5,
17,
22,
23) and that the associated
liberation of Pi is linked to fatigue
(8,
9,
28). As suggested previously
(3), this may operate as a
self-limiting system. Specifically, at the same time as the increases in
NADH-to-NAD+ ratio, ADP-to-ATP ratio, creatine, and
Pi-activated mitochondrial respiration [for a review, see Connett
(7)], Pi also
diffuses into the sarcoplasmic reticulum, where recent evidence indicates
Pi precipitates with Ca2+ to reduce the amount of
Ca2+ released (8,
11,
28), leading to reduced
cross-bridge turnover and thus reduced force and ATP demand. In this paradigm,
once ATP demand falls below that provided by maximal aerobic respiration,
O2 would fall as a result
of a reduced drive on oxidative phosphorylation. This sequence of events is
consistent with the observations in the present study in that the initial fall
in tension was associated with an increase in
O2 and lactate efflux,
whereas O2 and lactate
efflux fell in similar proportion to the further fall in force after
O2 max was attained. As
noted above, because under no circumstances did
O2 or lactate efflux
decrease before force fell, it seems unlikely that reduced aerobic metabolism
caused a further fall in force but rather that a fall in force (and thus ATP
demand) likely caused a reduction in the requirement for aerobic and
glycolytic ATP production.
In summary, we found that slowing the progression of fatigue and lactic
acidosis had no effect on the
O2 max in contracting rat
hindlimb muscles. Specifically, despite a longer time to reach 60% of initial
tension and O2 max in
FInc, time x tension integral at
O2 max and peak lactate
efflux were remarkably similar in FInc and F60,
suggesting that the initial fatigue observed in this model does not compromise
the aerobic metabolic response or that insufficient fatigue had occurred to
reduce ATP demand below that obligating maximal aerobic metabolic activation.
In this latter respect,
O2 and lactate efflux
fell in similar proportion to a further fall in tension after
O2 max was reached in
both groups. On the basis of these latter observations, and the fact that
under no circumstances did
O2 or lactate efflux fall
before tension fell, we conclude that fatigue occurring subsequent to
attainment of O2 max
resulted in a fall in contractile energy demand below that obligating maximal
aerobic and glycolytic metabolic flux.
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DISCLOSURES |
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FOOTNOTES |
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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.
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REFERENCES |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESREFERENCES |
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O2 maximum during
repetitive tetanic contractions of dog muscle in situ. J Appl
Physiol 74:
1499-1503, 1993.This article has been cited by other articles:
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  V. Ljubicic and D. A. Hood Kinase-specific responsiveness to incremental contractile activity in skeletal muscle with low and high mitochondrial content Am J Physiol Endocrinol Metab, July 1, 2008; 295(1): E195 - E204. [Abstract] [Full Text] [PDF]
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 A. C. Betik, D. J. Baker, D. J. Krause, M. J. McConkey, and R. T. Hepple Exercise training in late middle-aged male Fischer 344 x Brown Norway F1-hybrid rats improves skeletal muscle aerobic function Exp Physiol, July 1, 2008; 93(7): 863 - 871. [Abstract] [Full Text] [PDF]
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D. J. Baker, D. J. Krause, R. A. Howlett, and R. T. Hepple Nitric oxide synthase inhibition reduces O2 cost of force development and spares high-energy phosphates following contractions in pump-perfused rat hindlimb muscles Exp Physiol, May 1, 2006; 91(3): 581 - 589. [Abstract] [Full Text] [PDF]
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D. J Krause, J. L Hagen, C. A Kindig, and R. T Hepple Nitric oxide synthase inhibition reduces the O2 cost of force development in rat hindlimb muscles pump perfused at matched convective O2 delivery Exp Physiol, November 1, 2005; 90(6): 889 - 900. [Abstract] [Full Text] [PDF]
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 J. L. Hagen, D. J. Krause, D. J. Baker, M. H. Fu, M. A. Tarnopolsky, and R. T. Hepple Skeletal Muscle Aging in F344BN F1-Hybrid Rats: I. Mitochondrial Dysfunction Contributes to the Age-Associated Reduction in VO2max J. Gerontol. A Biol. Sci. Med. Sci., November 1, 2004; 59(11): 1099 - 1110. [Abstract] [Full Text] [PDF]
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R. T. Hepple, J. L. Hagen, D. J. Krause, and D. J. Baker Skeletal Muscle Aging in F344BN F1-Hybrid Rats: II. Improved Contractile Economy in Senescence Helps Compensate for Reduced ATP-Generating Capacity J. Gerontol. A Biol. Sci. Med. Sci., November 1, 2004; 59(11): 1111 - 1119. [Abstract] [Full Text] [PDF]
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) and muscles were incrementally
stimulated for 1 min at each of 7.5, 15, 30, and 60 tetani/min and for 2 min
at 90 tetani/min (FInc; 
)]. Values are means ± SE;
n = 6 rats in the 60 tetani/min group and n = 5 rats in the
incremental group.
