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Department of Medicine, University of California, San Diego, La Jolla, California 92093-0623
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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It remains uncertain whether the delayed onset of mitochondrial respiration on initiation of muscle contractions is related to O2 availability. The purpose of this research was to measure the kinetics of the fall in intracellular PO2 at the onset of a contractile work period in rested and previously worked single skeletal muscle fibers. Intact single skeletal muscle fibers (n = 11) from Xenopus laevis were dissected from the lumbrical muscle, injected with an O2-sensitive probe, mounted in a glass chamber, and perfused with Ringer solution (PO2 = 32 ± 4 Torr and pH = 7.0) at 20°C. Intracellular PO2 was measured in each fiber during a protocol consisting sequentially of 1-min rest; 3 min of tetanic contractions (1 contraction/2 s); 5-min rest; and, finally, a second 3-min contractile period identical to the first. Maximal force development and the fall in force (to 83 ± 2 vs. 86 ± 3% of maximal force development) in contractile periods 1 and 2, respectively, were not significantly different. The time delay (time before intracellular PO2 began to decrease after the onset of contractions) was significantly greater (P < 0.01) in the first contractile period (13 ± 3 s) compared with the second (5 ± 2 s), as was the time to reach 50% of the contractile steady-state intracellular PO2 (28 ± 5 vs. 18 ± 4 s, respectively). In Xenopus single skeletal muscle fibers, 1) the lengthy response time for the fall in intracellular PO2 at the onset of contractions suggests that intracellular factors other than O2 availability determine the on-kinetics of oxidative phosphorylation and 2) a prior contractile period results in more rapid on-kinetics.
oxygen uptake; exercise; oxidative phosphorylation; mitochondria; phosphorescence; cellular respiration
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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THERE HAS BEEN
CONSIDERABLE debate concerning the factors that determine the
time course of the increase in O2 uptake
(
O2 on-kinetics) with the initiation of
exercise or muscle contractions (for review see Ref. 28).
It remains uncertain whether the delivery of O2 to the
mitochondria is limiting at the onset of contractions, perhaps related
to adaptation of the cardiovascular and microcirculatory systems, or
whether mitochondrial O2 availability is adequate, and
therefore changes in other regulators of oxidative phosphorylation determine the mitochondrial response time. We recently demonstrated that convective O2 delivery to muscle and peripheral
O2 diffusion do not represent limiting factors for
the muscle O2 on-kinetics (10,
11) during transitions from rest to contractions corresponding to ~60% of the muscle peak O2 in
isolated muscle. These findings are in agreement with the hypothesis
that the limiting factors for O2
on-kinetics at these submaximal work intensities are not related to
insufficient O2 available for mitochondrial respiration but
likely reside within alternate regulatory pathways controlling skeletal
muscle oxidative metabolism (4, 5, 19, 32). However,
evidence obtained in exercising humans (8, 13) and in
contracting isolated muscle (12) has demonstrated that
O2 delivery to muscle may be one of the limiting factors
for O2 on-kinetics at higher exercise
intensities. In addition, other studies (9, 16) suggest
that muscle that has been previously exercised may exhibit faster
O2 on-kinetics, but it remains unclear
whether this is due to faster delivery of O2 to the
mitochondria or faster activation of key enzymatic processes within the
contracting cells that cause a more rapid activation of oxidative phosphorylation.
Therefore, the purpose of the present study was to use contracting
isolated single skeletal muscle fibers to test the hypotheses that
1) O2 supply to the mitochondria of these muscle
fibers is not limiting at the onset of steady-state contractions,
thereby suggesting that other intracellular regulators of oxidative
phosphorylation determine O2
on-kinetics, and 2) a prior period of muscle stimulation results in a more rapid activation of oxidative phosphorylation, which
also is a result of intracellular processes not related to
O2 availability. These hypotheses were tested by using a
novel technique (14) of measuring intracellular
PO2 in these single fibers so that
intracellular oxygenation could be monitored at the onset of contractions.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Experimental preparation. Adult female Xenopus laevis were doubly pithed and decapitated. Lumbrical muscles II-IV were removed, and single living muscle fibers (n = 11) were microdissected from the muscle. Dissections and experiments were performed in Ringer solution (in mM: 112 NaCl, 1.87 KCl, 0.82 CaCl2, 2.38 NaHCO3, 0.07 NaH2PO4, and 0.1 EGTA) at 20°C and 7.0 pH. After dissection, platinum clips were attached to the tendons and the fibers were mounted in a glass chamber. A solution of 10 mM fura 2 (Molecular Probes, Eugene, OR; for visual monitoring of the injection using excitation light at 390 nm) and 0.5 mM palladium-meso-tetra (4-carboxyphenyl) porphine bound to bovine serum albumin was injected into each single fiber by micropipette pressure injection. One tendon end was then attached to a force transducer system (model 400A, Aurora Scientific, Aurora, Ontario) for measurement of force development. The chamber was then placed on the stage of an inverted microscope configured for epi-illumination. The preparation was observed with a Nikon Fluor objective (×40, 0.70 numerical aperture) used dry. The fiber length was adjusted to achieve maximal force development (Po) for a single-twitch contraction.
Experimental protocol. Each fiber was continually perfused with Ringer solution that had been equilibrated with a gas mixture to produce a PO2 of ~30 Torr and a PCO2 of ~40 Torr. The value of PO2 was chosen as representative of a mean capillary PO2 that would surround working muscle fibers in vivo. Constant perfusion was maintained during each contractile period to maintain the experimental PO2 and to reduce the possible occurrence of unstirred layers surrounding the cell. After a 1-min rest period, tetanic contractions were induced by end-to-end stimulation (50 impulses/s of 1-ms duration at 9 V, with a train duration of 250 ms) using a Grass S48 stimulator (Quincy, MA). Each fiber was stimulated to contract at a frequency of one contraction every 2 s for a period of 3 min. After this first contraction period, each fiber was allowed to rest for 5 min. Immediately after the 5-min rest period, the fiber was again stimulated to contract at a frequency of one contraction every 2 s for 3 min. A Biopac Systems MP100WSW (Santa Barbara, CA) analog-to-digital converter was used to transform the analog force signal, and the digital data were collected and analyzed with AcqKnowledgeIII 3.5 software (Biopac Systems). Force was recorded in units of force per cross-sectional area (kPa). Individual peak force in a 3-min contraction period was compared with Po within that work run and reported as a relative percent. In some experiments, the PO2 of the Ringer solution in the chamber was monitored with a Clark-style electrode (model 733, Diamond General, Ann Arbor, MI) placed adjacent to the working fiber.
Intracellular PO2 measurement. A new technique (14), using a porphyrin O2 probe, was used to measure PO2 within these single skeletal muscle fibers. The phosphorescence quenching of the palladium-porphyrin O2 probe within each cell was measured through a system consisting of a flash lamp (Oxygen Enterprises, Philadelphia, PA), a 425-nm band-pass excitation filter, a 630-nm cut-on emission filter, and a photomultiplier tube for collection of the phosphorescence signal. To calculate phosphorescence lifetimes from the intracellular O2 probe, the phosphorescent decay curves from a series of 10 flashes (15 Hz) were averaged, and a monoexponential function was fit to the subsequent best-fit decay curve (analysis software from Medical Systems, Greenvale, NY). Phosphorescent-decay curves were recorded every 7 s from each cell throughout the experimental period. Previously determined values for the measured phosphorescence lifetime decay in a zero-O2 environment and the phophorescence quenching constant for the intracellular O2 probe were used to calculate intracellular PO2 (14).
The individual intracellular PO2 data points for each contractile period were fitted by a monoexponential function for subsequent comparison of the intracellular PO2 on-kinetics between the two contractile periods. The curve fitting was begun at the time point at which intracellular PO2 began to fall after initiation of contractions. In all cells, there was a time delay (TD) after the onset of contractions before intracellular PO2 began to fall. The TD was determined for each contractile period and added to the time at which the intracellular PO2 had fallen 50% from steady-state rest values to the new steady-state work value (obtained from the monoexponential curve fitting) to obtain the overall time required to achieve 50% response time (t50).Statistics. Repeated-measures analysis of variance was performed for the statistical analyses. In all analyses, the P < 0.05 level of significance was used. Results are reported as means ± SE.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Figure 1 illustrates the force
produced during the experimental protocol for one typical single
skeletal muscle fiber. The Po produced was not
significantly different between the first stimulation period and the
second in the 11 fibers used in the present study. In addition,
the mean fall in force development that occurred within a contraction
period (fatigue) was not significantly different between the two
stimulation periods for the 11 fibers, with the ratio of force
development at the end of the 3-min contractile period to the
Po for that contraction period being 83 ± 2 (SE) % in the first contractile period vs. 86 ± 3% in the second.
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A representative example of the fall in intracellular
PO2 at the onset of contractions for a single
fiber is illustrated in Fig. 2.
Intracellular PO2 was not significantly
different between the first and second contractile periods at either
the start of contractions (29 ± 2 vs. 35 ± 6 Torr) or the
steady-state value attained during the contractile period (6 ± 1 vs. 7 ± 2 Torr). In all contraction periods, the fall in
intracellular PO2 was well fit by a
monoexponential function, with all fibers showing a TD in the fall of
intracellular PO2 after the onset of
contractions. Figure 3 demonstrates the
difference in the TD between the first and second contractile periods,
with the TD in the first period (13 ± 3 s) being
significantly (P < 0.01) longer than in the second (5 ± 2 s). Finally, the time for the fall in intracellular
PO2 to reach t50 after
the onset of contractions, which includes the calculated TD, is
illustrated in Fig. 4. This was
significantly greater (P < 0.01) for the first
compared with the second contraction period, being 28 ± 5 and 18 ± 4 s, respectively.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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O2 uptake on-kinetics.
The cause(s) of the delayed onset of oxidative phosphorylation at the
onset of exercise or muscle contractions remains controversial (for
review see Ref. 28). Because of the difficulty in
determining intracellular oxygenation, it is uncertain whether
O2 availability at the mitochondria is adequate during this
transition period or whether other factors involved in the regulation
of mitochondrial respiration are rate limiting. In previous studies
utilizing an isolated in situ whole muscle model, it was demonstrated
that, during transitions from rest to contractions of low metabolic intensity (~60% of peak O2),
increasing convective O2 delivery or improving peripheral
O2 diffusion did not alter
O2 on-kinetics (10, 11).
However, we recently demonstrated in the same muscle model
(12) that an enhanced O2 delivery to
contracting muscle at high stimulation intensities may indeed result in
faster O2 on-kinetics, confirming
studies conducted in exercising humans (9, 16). Therefore,
for transitions to exercise (or contractions) of low metabolic
intensity, O2 availability to the mitochondria in whole
muscle appears adequate at the onset of contractions, and other
intracellular regulatory pathways represent the limiting factor(s) in
determining O2 on-kinetics. However, for
higher metabolic transitions, O2 availability to the
mitochondria together with the other intracellular constraints may
determine O2 on-kinetics.
Single fibers. Metabolic studies using human or whole muscle models can be difficult to interpret because of heterogeneity of blood flow and fiber recruitment patterns in the systems being examined. At the initiation of exercise, O2 availability at the microcirculatory level in vivo may be very heterogeneous, making the measurement of the actual O2 available to the mitochondria difficult to ascertain (6). To overcome these difficulties, the present study employed isolated single skeletal muscle fibers so that specific conditions could be accurately controlled by adjusting the extracellular environment. Therefore, O2 availability to the mitochondria was uniform around the fiber and determined solely by diffusive factors.
The amphibian muscle fibers used in the present study do not contain myoglobin; thus facilitated transport of O2 within the cell was not present. With a uniform PO2 around the cell and a constant diffusing capacity for O2 within the cell, an increase in O2 flux (O2) to the mitochondria can only be
attained by reducing the intracellular PO2.
Although it has not been demonstrated in this preparation (or any
other) whether the fall in intracellular PO2 is
directly correlated with a specific increase in
O2, we have noted that intracellular
PO2 falls in a manner proportional to
stimulation frequency (R. A. Howlett and M. C. Hogan, unpublished observations) in these single fibers, as would be expected if the fall
in intracellular PO2 were the primary means of
an increased O2. In addition,
the steady-state intracellular PO2 achieved during the two contractile periods was not different, which would be
expected for similar O2. Therefore, the
intracellular PO2 on-kinetics results found in
the present study were likely directly correlated with
O2 on-kinetics.
Intracellular PO2. A number of methods have been used to estimate or measure intracellular PO2 in skeletal muscle under various conditions (29), including O2 microelectrodes (31), myoglobin saturation as determined by cryomicrospectroscopy of frozen cell sections (8), and, more recently, spectroscopic relaxation determination of myoglobin saturation in whole muscle (20, 23). Each of these techniques has value under certain applications; however, none can provide a rapid, reliable measurement of intracellular PO2 in single skeletal muscle cells over extended periods of time under conditions of rest and increased metabolic rate. Recently, a new method (using the O2-dependent phosphorescence quenching of palladium-porphyrin compounds; Ref. 30) has been used successfully for measurements of microvascular PO2 (24, 27, 34) and has recently been adapted for measuring intracellular PO2 in single skeletal muscle fibers over extended periods of time (14).
Using this new method of measuring intracellular PO2 (14), the data from the present study demonstrated that there was substantial O2 available within the cell at the onset of contractions in these Xenopus single fibers. In fact, the PO2 within the fiber did not begin to fall until after a significant TD after the initiation of contractions (see Figs. 2 and 3). It should be noted that this measured TD was not influenced by a slow response of the measuring system, because changes in intracellular PO2 are immediate if the extracellular PO2 is altered (14). After the initial TD, there was a monoexponential fall in intracellular PO2 to a new steady-state value (see Fig. 2). The intracellular PO2 t50 value obtained in the present study was likely indicative of the 50% time required to achieve a steady state ofO2, because it has been demonstrated
previously that O2 steady state was
achieved in 1-1.5 min in these single skeletal muscle fibers
(7, 21). The results from the present study make it clear
that the time previously noted in these single isolated skeletal muscle
fibers for oxidative respiration to reach a steady-state value
(7, 21) was unrelated to O2 limitation. In
addition, the value of intracellular PO2
t50 calculated in the present study during the first contractile period was very similar to
O2 t50 values
obtained in both human and whole muscle exercise (2, 3, 5, 9, 10,
11, 13, 16, 32, 33).
Therefore, one of the significant findings of the present study was to
demonstrate that, because O2 was not the rate-limiting step
in the activation of oxidative phosphorylation at the onset of
contractions in these Xenopus single muscle fibers, other
factors related to the regulation of mitochondrial respiration were
likely rate limiting and thereby determined the
O2 response time. Whereas traditionally
the changes in intracellular [ADP] (where brackets denote
concentration) or the phosphorylation potential
([ATP]/[ADP][Pi]) have been regarded as important
regulators of cell respiration as metabolic demand increases, a number
of investigators (2, 17, 18) have demonstrated a strong
correlation between changes in phosphocreatine at the onset of exercise
and the rate of adaptation of O2. In
addition, it has been suggested that changes in cytosolic Ca2+ levels within the cell and particularly the
mitochondria may regulate oxidative phosphorylation (1,
25). Adaptive changes in any of these putative regulators of
mitochondrial respiration, or NADH availability, may require
substantial time at the onset of contractions, thereby resulting in the
O2 on-kinetic response. However, as we
(12) and others (9, 16) have demonstrated, at
very high metabolic rates, O2 availability to the
mitochondria may influence O2
on-kinetics, likely during the latter stages of mitochondrial
activation when O2 utilization becomes very high.
Finally, it should be noted that the O2 surrounding the
single fibers in the present study was uniform, unlike a single fiber in a whole muscle surrounded by a small number of capillaries. Under
such in vivo conditions, the supply of O2 to the
mitochondria is likely less adequate than in the single-fiber
preparation, so that it could be argued that O2 supply to a
working fiber in vivo may be more limiting than that seen in the
preparation used in the present study. However, the similar onset
t50 found in the present study compared with
t50 values found in humans, whole muscle, and
single fibers (2, 3, 5, 7, 9, 10, 11, 13, 16, 21, 32, 33)
provides compelling evidence that even in vivo O2
availability is adequate during the adjustment of
O2 at the onset of exercise. In fact,
with an abundant O2 supply around an isolated single fiber,
it would be expected that, if O2 availability were truly
rate limiting to mitochondrial respiration at the onset of
contractions, a steady state of
O2 would be achieved even
more quickly than in vivo, which is not the case (7, 21).
Prior activation of respiration.
A second important finding from the present study was that the second
contractile period, which followed the first contractile period by 5 min, had a significantly faster rate of fall in intracellular PO2 (see Figs. 3 and 4), again suggesting a
faster onset of O2. This phenomenon of
faster O2 on-kinetics after a prior
period of contractile activation has also been recently demonstrated in
exercising humans (9, 16). As in the first contractile period, during the second contractile period there remained a TD after
the initiation of contractions in which intracellular PO2 did not fall. Although this indicates that
O2 was abundant within the cell during the activation of
mitochondrial respiration in the second contractile period, the smaller
TD and calculated t50 in the second period
indicates that the increase in utilization of O2 occurred
at a faster rate as oxidative phosphorylation was likely activated more quickly.
O2 on-kinetics, it
has been shown that, when PDH is activated before exercise or
contractions, there is less subsequent perturbation of intracellular
homeostasis (15, 22, 26). The results from these prior
studies (15, 22, 26) suggest that oxidative respiration
was likely initiated more rapidly as a result of the PDH being in a
more active form, thereby decreasing the reliance on nonoxidative
metabolism (i.e., phosphocreatine hydrolysis and anaerobic glycolysis)
during the transition from the rest-to-work steady state.
Conclusion. The results of this study demonstrated that, in single Xenopus muscle fibers, O2 availability to the mitochondria was adequate during the adjustment of mitochondrial respiration to a step increase in ATP demand and that a prior activation of the single fiber resulted in a more rapid fall in intracellular PO2 during a subsequent contractile period. These results suggest that other regulators of mitochondrial respiration, rather than O2 availability, determine the rate at which oxidative phosphorylation is adjusted during the transition from rest to exercise and that prior activation of these regulators results in more rapid on-kinetics.
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ACKNOWLEDGEMENTS |
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The excellent technical assistance of Creed Stary is gratefully acknowledged.
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FOOTNOTES |
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This research was supported by the National Institute of Arthritis and Musculoskeletal Diseases Grant AR-40155.
Address for reprint requests and other correspondence: M. C. Hogan, Dept. of Medicine 0623, Univ. of California, San Diego, 9500 Gilman Dr., La Jolla, CA 92093-0623 (E-mail: mchogan{at}ucsd.edu).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 4 May 2000; accepted in final form 1 December 2000.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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 C. M. Stary, B. J. Walsh, A. E. Knapp, D. Brafman, and M. C. Hogan Elevation in heat shock protein 72 mRNA following contractions in isolated single skeletal muscle fibers Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2008; 295(2): R642 - R648. [Abstract] [Full Text] [PDF]
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 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]
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 L. M. K. Chin, R. J. Leigh, G. J. F. Heigenhauser, H. B. Rossiter, D. H. Paterson, and J. M. Kowalchuk Hyperventilation-induced hypocapnic alkalosis slows the adaptation of pulmonary O2 uptake during the transition to moderate-intensity exercise J. Physiol., August 15, 2007; 583(1): 351 - 364. [Abstract] [Full Text] [PDF]
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R. A. Howlett, C. A. Kindig, and M. C. Hogan Intracellular PO2 kinetics at different contraction frequencies in Xenopus single skeletal muscle fibers J Appl Physiol, April 1, 2007; 102(4): 1456 - 1461. [Abstract] [Full Text] [PDF]
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B. J. Gurd, S. J. Peters, G. J. F. Heigenhauser, P. J. LeBlanc, T. J. Doherty, D. H. Paterson, and J. M. Kowalchuk Prior heavy exercise elevates pyruvate dehydrogenase activity and speeds O2 uptake kinetics during subsequent moderate-intensity exercise in healthy young adults J. Physiol., December 15, 2006; 577(3): 985 - 996. [Abstract] [Full Text] [PDF]
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M. Burnley, J. H. Doust, and A. M. Jones Time required for the restoration of normal heavy exercise VO2 kinetics following prior heavy exercise J Appl Physiol, November 1, 2006; 101(5): 1320 - 1327. [Abstract] [Full Text] [PDF]
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A. M. Jones, N. J. A. Berger, D. P. Wilkerson, and C. L. Roberts Effects of "priming" exercise on pulmonary O2 uptake and muscle deoxygenation kinetics during heavy-intensity cycle exercise in the supine and upright positions J Appl Physiol, November 1, 2006; 101(5): 1432 - 1441. [Abstract] [Full Text] [PDF]
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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]
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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]
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 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]
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N. R. Saunders, K. E. Pyke, and M. E. Tschakovsky Dynamic response characteristics of local muscle blood flow regulatory mechanisms in human forearm exercise J Appl Physiol, April 1, 2005; 98(4): 1286 - 1296. [Abstract] [Full Text] [PDF]
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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]
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M. C. Hogan, C. M. Stary, R. S. Balaban, and C. A. Combs NAD(P)H fluorescence imaging of mitochondrial metabolism in contracting Xenopus skeletal muscle fibers: effect of oxygen availability J Appl Physiol, April 1, 2005; 98(4): 1420 - 1426. [Abstract] [Full Text] [PDF]
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Y. Chung, P. A. Mole, N. Sailasuta, T. K. Tran, R. Hurd, and T. Jue Control of respiration and bioenergetics during muscle contraction Am J Physiol Cell Physiol, March 1, 2005; 288(3): C730 - C738. [Abstract] [Full Text] [PDF]
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C. A. Kindig, R. A. Howlett, C. M. Stary, B. Walsh, and M. C. Hogan Effects of acute creatine kinase inhibition on metabolism and tension development in isolated single myocytes J Appl Physiol, February 1, 2005; 98(2): 541 - 549. [Abstract] [Full Text] [PDF]
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C. A. Kindig, C. M. Stary, and M. C. Hogan Effect of dissociating cytosolic calcium and metabolic rate on intracellular PO2 kinetics in single frog myocytes J. Physiol., January 15, 2005; 562(2): 527 - 534. [Abstract] [Full Text] [PDF]
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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]
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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]
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E. G. Mik, T. G. van Leeuwen, N. J. Raat, and C. Ince Quantitative determination of localized tissue oxygen concentration in vivo by two-photon excitation phosphorescence lifetime measurements J Appl Physiol, November 1, 2004; 97(5): 1962 - 1969. [Abstract] [Full Text] [PDF]
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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]
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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]
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D. S. DeLorey, J. M. Kowalchuk, and D. H. Paterson Relationship between pulmonary O2 uptake kinetics and muscle deoxygenation during moderate-intensity exercise J Appl Physiol, July 1, 2003; 95(1): 113 - 120. [Abstract] [Full Text] [PDF]
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N. Tordi, S. Perrey, A. Harvey, and R. L. Hughson Oxygen uptake kinetics during two bouts of heavy cycling separated by fatiguing sprint exercise in humans J Appl Physiol, February 1, 2003; 94(2): 533 - 541. [Abstract] [Full Text] [PDF]
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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]
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C. A. Kindig, K. M. Kelley, R. A. Howlett, C. M. Stary, and M. C. Hogan Assessment of O2 uptake dynamics in isolated single skeletal myocytes J Appl Physiol, January 1, 2003; 94(1): 353 - 357. [Abstract] [Full Text] [PDF]
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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]
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Z. Valic, J. S. Naik, S. B. Ruble, J. B. Buckwalter, and P. S. Clifford Elevation in resting blood flow attenuates exercise hyperemia J Appl Physiol, July 1, 2002; 93(1): 134 - 140. [Abstract] [Full Text] [PDF]
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H B Rossiter, S A Ward, J M Kowalchuk, F A Howe, J R Griffiths, and B J Whipp Dynamic asymmetry of phosphocreatine concentration and O2 uptake between the on- and off-transients of moderate- and high-intensity exercise in humans J. Physiol., June 15, 2002; 541(3): 991 - 1002. [Abstract] [Full Text] [PDF]
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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]
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C. A. Kindig, T. E. Richardson, and D. C. Poole Skeletal muscle capillary hemodynamics from rest to contractions: implications for oxygen transfer J Appl Physiol, June 1, 2002; 92(6): 2513 - 2520. [Abstract] [Full Text] [PDF]
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B. J Behnke, C. A Kindig, T. I Musch, W. L Sexton, and D. C Poole Effects of prior contractions on muscle microvascular oxygen pressure at onset of subsequent contractions J. Physiol., March 15, 2002; 539(3): 927 - 934. [Abstract] [Full Text] [PDF]
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R. A. Howlett and M. C. Hogan Intracellular PO2 decreases with increasing stimulation frequency in contracting single Xenopus muscle fibers J Appl Physiol, August 1, 2001; 91(2): 632 - 636. [Abstract] [Full Text] [PDF]
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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]
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B. J. Behnke, C. A. Kindig, T. I. Musch, W. L. Sexton, and D. C. Poole Effects of prior contractions on muscle microvascular oxygen pressure at onset of subsequent contractions J. Physiol., January 25, 2002; (2002) 200101316. [Abstract] [PDF]
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