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1 Applied Physiology
Laboratory, ABSTRACT Koga, Shunsaku, Tomoyuki Shiojiri, Narihiko Kondo,
and Thomas J. Barstow. Effect of increased muscle temperature on oxygen uptake kinetics during exercise. J. Appl.
Physiol. 83(4): 1333-1338, 1997.
exercise transition; gas-exchange kinetics; oxygen transport; oxygen utilization; slow component of oxygen uptake
INTRODUCTION SEVERAL STUDIES have examined the effects of increased
temperature on muscle metabolism and exercise tolerance. Increased temperature elevates O2
consumption
( Elevated muscle temperature (Tm)
may speed It has also been speculated that the additional, slowly developing
The previous studies cited above focused on the effects of elevated
ambient temperature on exercise energetics and exercise tolerance
during prolonged protocols at heavy-intensity exercise. From these
studies it is unclear whether elevated
Tm per se, without concomitant
increases in core temperature and the resulting systemic responses,
would alter the initial energetic responses to moderate- or
heavy-intensity exercise. Therefore, the overall aim of the present
study was to evaluate the effects of increased
Tm on the energetics of short-term
(6 min) moderate-intensity (below LT) and heavy-intensity (above LT)
exercise under conditions where elevation in core temperature and the
resulting systemic responses were minimized.
METHODS
To test whether
increased muscle temperature (Tm) would improve
O2 uptake
(
O2) kinetics, seven men
performed transitions from rest to a moderate work rate [below
the estimated lactate threshold
(LTest)] and a heavy work
rate (O2 = 50% of the
difference between LTest and peak
O2) under conditions of normal Tm (N) and increased
Tm (H), produced by wearing hot
water-perfused pants before exercise. Quadriceps
Tm was significantly higher in H,
but rectal temperature was similar for the two conditions. There were
no significant differences in the amplitudes of the fast component of
O2 or in the time constants
of the on and off transients for moderate and heavy exercise between
the two conditions. The increment in
O2 between the 3rd and 6th
min of heavy exercise was slightly but significantly smaller for H than
for N. These data suggest that elevated
Tm before exercise onset, which
would have been expected to increase
O2 delivery and off-loading to the
muscle, had no appreciable effect on the fast exponential component of
O2 kinetics (invariant time
constant). These data further suggest that elevated
Tm does not contribute to the slow
component of O2 during
heavy exercise.
O2)
of isolated mitochondria by a Q10
effect and by decreasing the phosphorylation potential (ADP/O ratio)
(7, 36). An increase in blood temperature may facilitate unloading of
O2 from hemoglobin in the muscle
capillaries by a rightward shift of the oxyhemoglobin dissociation
curve. However, the net effect of elevated temperature on muscle and whole body metabolism in intact humans during exercise is
controversial. Pulmonary O2 uptake
(O2) has been reported to be
higher (24, 27), lower (14, 37), or unchanged (15, 32) in the heat compared with control ambient conditions. In addition to equivocal effects on steady-state O2,
it is unknown whether the kinetics of adjustment of muscle and
pulmonary O2 during the first
few minutes of moderate- or heavy-intensity exercise would be altered by increased temperature. The kinetics of muscle and pulmonary O2 are thought to be
primarily determined by intramuscular processes (19, 25, 26) and
modifiable by the kinetics of O2
delivery to the working muscles (21). The kinetics of
O2 can be slowed by
decreasing arterial O2 content
and/or delivery (13). However, there is no compelling evidence
that increased muscle O2 delivery can increase O2 kinetics in
healthy humans.
O2 kinetics in at
least two ways: 1) it may speed the
limiting reaction(s) associated with oxidative phosphorylation,
and/or 2) a rightward shift
of the oxyhemoglobin dissociation curve and any muscle vasodilation associated with increased temperature may facilitate
O2 delivery during the transition
to exercise. This expected improvement in O2 delivery could result in faster
O2 kinetics if the muscle O2 kinetics were
O2 delivery dependent in the
control condition. Current thinking suggests that this is more likely
to be true for exercise above than for exercise below the lactate
threshold (LT). We thus hypothesized that elevated
Tm would lead to faster O2 kinetics for exercise
above the LT, but not for exercise below the LT.
O2 (slow component) seen
during heavy exercise may be the result of the effect of rising
Tm on mitochondrial respiration and the phosphorylation potential mentioned above (36). A second hypothesis we tested was that the slow component of
O2 during heavy exercise
would be greater when Tm was
elevated before exercise onset.
O2 (the highest
O2 achieved during
exercise) in a thermoneutral environment (25°C, 50% relative
humidity). LT was estimated
(LTest) from gas-exchange criteria by finding the O2
above which the ventilatory equivalent for
O2 and the end-tidal
PO2 increased without an increase in
the ventilatory equivalent for CO2
or a decrease in end-tidal PCO2 (35).
O2 response (28). The final
exercise period was 6 min to determine the steady-state response. No
more than four transitions were completed by each subject on a single
day.
For the heavy-exercise tests, we chose a work rate that was estimated
to require a O2 equal to
50% of the difference (
) between the subject's
LTest and peak
O2, i.e.,
LTest + 0.50, based on the
initial O2/work rate
observed during the ramp exercise. Subjects performed one
rest-to-exercise transition of 6-min duration followed by a 5-min
recovery period under each Tm
condition.
Measurements.
Rectal temperature was continuously monitored by a thermistor probe
(model 401, Yellow Springs Instruments) inserted 10 cm beyond the anal
sphincter. Skin temperatures were measured by four thermistors placed
on the upper arm, chest, front of the thigh, and calf. The thigh and
calf values were averaged together, as were the upper arm and chest
values, for comparison between conditions.
Tm was measured 4 min before
exercise onset for at least one transition to each work rate by a
sterile 24-gauge needle thermistor (model 524, Yellow Springs
Instruments) that was inserted 3 cm into the vastus lateralis. In
addition, in separate experiments in four of the original subjects,
Tm was measured before the 6-min exercise transition to each work rate and within 30 s of the cessation of the exercise.
Subjects breathed through a low-resistance valve (Hans Rudolph)
connected to two pneumotachographs for measurement of inspiratory and
expiratory flows. This system was calibrated repeatedly by inputting
known volumes of room air at various mean flows and flow profiles.
Respired gases were analyzed by mass spectrometry (model MGA-1100,
Perkin-Elmer) from a sample drawn continuously from the mouthpiece.
Precision-analyzed gas mixtures were used for calibration. Gas-exchange
variables at the mouth were calculated breath by breath (5). HR was
continuously monitored via a three-lead electrocardiogram.
Analysis.
Individual responses during the rest-to-exercise transitions were time
interpolated to 1-s intervals. Responses to moderate exercise were
further averaged across all transitions for each subject and condition.
For the on and off transients, the response curves of
O2 and
CO2 output
(CO2) during
phase 2 (i.e., after the first
15-25 s up to 3 min of exercise) were fit by a single-exponential function that included an amplitude, a time constant, and a time delay,
using nonlinear least-squares regression techniques (8, 21, 22, 35).
The duration of phase 1 was determined
as the time from the onset of exercise to the inflection
points in the respiratory exchange ratio, end-tidal
PO2 and end-tidal PCO2 (35).
The initial 3 min of the response curves of
O2 and
CO2 during
phase 2 of the on and off transients
to heavy exercise were similarly fit by a single-exponential function
that included an amplitude of the fast component, a time constant, and
a time delay (2, 4, 28). Furthermore, the increment in
O2 between the 3rd and 6th
min of the transition was calculated as an index of the slow component
of the O2 kinetics (6, 18,
28).
Values are means ± SD. The data were analyzed by using a
repeated-measures analysis of variance design. Significant results were
further analyzed by Scheffé's post hoc test. Significance was
declared at P < 0.05.
RESULTS
Peak O2 averaged 44.5 ± 9.8 ml · kg
1 · min1,
and LTest averaged 23.2 ± 8.7 ml · kg1 · min1.
Mean skin temperature of the thigh and calf immediately before exercise
was significantly higher in condition H than in condition N: 39.4 ± 0.9 and 32.9 ± 0.7°C, respectively
(P < 0.01). Mean skin temperature of
the upper arm and chest was similar for the two conditions: 32.8 ± 0.7 and 32.4 ± 1.0°C for N and H, respectively. Rectal
temperature immediately before exercise was similar for the two
conditions: 37.3 ± 0.2 and 37.4 ± 0.2°C for N and H,
respectively. Tm before exercise
was significantly higher in condition H: 36.0 ± 1.0 and 38.0 ± 0.5°C in N and H, respectively
(P < 0.05). In separate experiments
(n = 4),
Tm immediately before and after the 6-min exercise bout was significantly higher in condition H than in
condition N (Fig. 1): for moderate
exercise, 35.3 ± 0.4 and 38.6 ± 0.3°C in N and H,
respectively, before exercise (P < 0.01) and 36.3 ± 0.9 and 39.2 ± 0.5°C in N and H,
respectively, after exercise (P < 0.01); for heavy exercise, 35.4 ± 0.4 and 38.9 ± 0.1°C in N
and H, respectively, before exercise
(P < 0.01) and 38.8 ± 0.4 and
40.3 ± 0.5°C in N and H, respectively, after exercise
(P < 0.05). Thus we were successful
in selectively warming the leg muscles before exercise and maintaining
this elevated Tm over the course
of exercise without causing significant elevations in core temperature.
,
dashed line) than in condition of normal muscle temperature (
, solid
line). Values are means ± SD; n = 4 subjects.
The response for O2 from rest
to exercise in a representative subject is shown for the two conditions
in Fig. 2. Selective warming of the legs
did not result in an increase in resting metabolic rate before exercise
(Table 1). There was no significant
difference in amplitude of the fast component of
O2 between the two
Tm conditions for moderate or
heavy exercise. Also, the gain for the difference in the fast component
between work rates was not significantly altered by elevated
Tm: 10.3 ± 1.7 and 10.1 ± 1.2 ml · min1 · W1
in N and H, respectively (Table 1). Furthermore, as shown in Table 1,
there was no significant effect of
Tm or exercise intensity on the
time constants for the on and off transients of
O2. The increment in
O2 between the 3rd and 6th
min of heavy exercise was significantly smaller for H than for N: 138 ± 66 and 205 ± 70 ml/min, respectively
(P < 0.05; Fig.
3).
O2) for transition from rest
to moderate (A) and heavy exercise
(B) in a representative subject
under conditions of normal muscle temperature (solid line) and
increased muscle temperature (dashed line). There were no significant
differences for amplitudes of fast component of
O2 or for time constants of
on and off transients for moderate and heavy exercise between normal
and increased muscle temperature.
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O2 between 3rd and 6th min of
heavy exercise under conditions of normal muscle temperature (,
solid line) and increased muscle temperature (, dashed line). Increment in O2 between 3rd
and 6th min of heavy exercise was slightly but significantly smaller
for increased than for normal muscle temperature.
There was no significant difference in amplitudes of
CO2 between the two
conditions for moderate or heavy exercise (Table 2). Furthermore, there was no significant
difference between the two conditions in the time constants for the on
and off transients of CO2 for
moderate or heavy exercise.
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The respiratory exchange ratio at the end of 6 min of exercise was similar for the two conditions: for moderate exercise, 0.89 ± 0.03 and 0.89 ± 0.05 in N and H, respectively; for heavy exercise, 1.09 ± 0.06 and 1.08 ± 0.04 in N and H, respectively.
HR was significantly higher in H than in N at rest (68 ± 6 and 79 ± 5 beats/min in N and H, respectively, P < 0.01) and at the end of 6 min of moderate exercise (95 ± 11 and 106 ± 8 beats/min in N and H, respectively, P < 0.05). HR at the end of 6 min of heavy exercise tended to be higher in H than in N: 163 ± 16 and 152 ± 15 beats/min, respectively (P = 0.07).
DISCUSSION
We had hypothesized that the kinetics of
O2 after the onset of heavy
exercise would be faster when Tm
was increased before exercise onset. However, we found no significant
reduction in the on and off time constants of
O2 for moderate or heavy
exercise as a consequence of elevated
Tm, contrary to our first
hypothesis. Furthermore, there was no significant difference between
the two conditions in the amplitudes of the fast component of
O2 during moderate or heavy
exercise. Whereas the amplitude of the primary exponential rise in
O2 has consistently been
found to increase linearly with work rate (2, 4, 13, 28), the time
constant has been found to remain unchanged (2, 4) or lengthen (13, 28)
for work rates above the LT compared with moderate exercise intensities.
Increased Tm during exercise could
have affected (speeded) the kinetics of the
O2 response to exercise by
1) speeding the rate-limiting
metabolic reaction(s) associated with oxidative phosphorylation,
and/or 2) speeding the
increase of O2 delivery to the
capillaries and mitochondria, if indeed the kinetics were O2-delivery dependent under the
test conditions. A rightward shift in the
O2-hemoglobin dissociation curve
may have occurred as a result of a possible increase in blood
temperature in the muscle tissues. Consequently,
O2 unloading from hemoglobin would
be enhanced during exercise in an increased
Tm condition. This would
facilitate (i.e., speed) muscle
O2
kinetics only if
O2
were O2-delivery or -diffusion
limited. We did not measure muscle blood flow in the present study.
However, if it is assumed that the fast component of
O2 kinetics reflects muscle
oxidative phosphorylation kinetics (1, 10, 19, 34), the finding of
unaltered time constants during phase
2 for below- and above-LT exercise suggests that the
factor(s) that determine muscle
O2
kinetics was not affected by increased
Tm.
One expectation was that increased
Tm would lead to an increase in
transient and steady-state muscle and pulmonary
O2 due to a
Q10 effect on muscle metabolism
and a decrease in the phosphorylation efficiency (ADP/O) in the muscle
(7, 36). However, this did not appear to occur, inasmuch as
O2 in H was not appreciably different from O2 in N. One
putative explanation for this finding is that oxidative phosphorylation
becomes uncoupled only above 40°C (7). Because
Tm in the present study was
40°C on average, even for the elevated temperature condition, the
phosphorylation efficiency presumably would not have been affected.
Conversely, an increased Tm may
have increased mechanical efficiency of working muscles and thus
reduced O2 because of the lowered viscous resistance in the muscle (11). Any temperature-related increase in O2 may thus have
been offset by increased mechanical efficiency (32), with the net
result being no measurable change in
O2.
In addition to possibly affecting aerobic metabolism, increased
Tm has been shown to cause a shift
to greater anaerobic metabolism, as evidenced by increased
intramuscular ATP utilization and creatine phosphate degradation, and
anaerobic glycolysis (12, 14, 15, 23, 37). In the present study, blood
lactate levels were not measured. However, we speculate that transient
lactate increase during short-term exercise (reflecting anaerobic
metabolism) was likely to have been similar in the two conditions,
since the respiratory exchange ratio and the kinetics of
CO2 were not significantly different.
The fast component of the O2
off-transient response is a reflection of the rate of readjustment of
oxidative phosphorylation during recovery and is not affected by
anaerobic metabolism (10). Therefore, the similarity of on- and
off-transient time constants of
O2 [symmetrical fast
component (3, 13, 33)] under the two
Tm conditions in the present study
suggests that muscle O2
utilization during recovery in the increased
Tm condition was not different
from that in the normal condition.
The increment in O2 between
the 3rd and 6th min of heavy exercise was slightly but significantly
smaller when Tm was elevated. A
number of factors have been postulated to contribute to the slow
component of O2 observed
during heavy exercise (1, 9, 16, 17, 33). These include the effects of
lactate, epinephrine, cardiac and ventilatory work, temperature,
less-efficient mitochondrial P-O coupling, reduced chemical-mechanical
coupling efficiency, and recruitment of lower-efficiency fast-twitch
motor units. Although the mechanism(s) underlying the phenomenon
remains speculative, the primary origin of the
O2 slow component appears to
be the working limbs (3, 6, 29, 33).
It has been postulated that the increase in
Tm during exercise may, via the
Q10 effect, contribute to the slow
component of O2 during heavy
exercise (20). Recently, Willis and Jackman (36) suggested that a
3°C rise in Tm could result in
an ~10% reduction in the efficiency of coupling of
O2 to ATP
production (ADP/O ratio) and thus contribute to the increase in the
slow component from the active limb during heavy exercise. However, in
vivo, neither increased Tm
[estimated from venous blood temperature (29)] nor elevated
core temperature (9, 30, 31) is associated with an increase in leg or
pulmonary O2, respectively,
in exercising humans. In the present study, increased
Tm was associated with a
significant reduction in the slow component of
O2 during heavy exercise.
These results are inconsistent with the hypothesis that an
exercise-induced increase in Tm is
the predominant mechanism of the slow component of
O2 during heavy exercise.
An alternative mechanism suggested for the
O2 slow component is the
recruitment of lower-efficiency, fast-twitch fibers that have a higher
O2 cost and a longer time constant
(1, 3, 17, 33). The small reduction in the
O2 slow component observed with increased Tm may indicate a
slight alteration in motor unit recruitment pattern, perhaps reflecting
activation of fewer fast-twitch fibers and/or more slow-twitch
motor units with a higher oxidative capacity. Conclusions regarding the
mechanisms of the reduced slow component of
O2 during heavy exercise
under the condition of increased
Tm require further analysis.
In conclusion, there were no significant differences for the amplitude
or the time constants of the fast component of the on and off
transients of O2 during
moderate and heavy exercise between control and elevated
Tm conditions. These data suggest that as work intensity or Tm
increased, O2 supply was not
limiting the initial, predominant muscle
O2
(and thus O2) kinetics. Furthermore, the increment in
O2 between the 3rd and 6th
min of heavy exercise was slightly but significantly smaller for
elevated Tm than for control.
These data contradict the hypothesis that an increase in
Tm contributes significantly to
the slow component of O2
during heavy exercise.
FOOTNOTES
Address for reprint requests: S. Koga, Applied Physiology Laboratory, Kobe Design University, 8-1-1 Gakuennishi-machi, Nishi-ku, Kobe, 651-21, Japan.
Received 20 February 1997; accepted in final form 11 June 1997.
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 T. Saitoh, L. F. Ferreira, T. J. Barstow, D. C. Poole, A. Ooue, N. Kondo, and S. Koga Effects of prior heavy exercise on heterogeneity of muscle deoxygenation kinetics during subsequent heavy exercise Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2009; 297(3): R615 - R621. [Abstract] [Full Text] [PDF]
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 A. M. Jones, J. Fulford, and D. P. Wilkerson Influence of prior exercise on muscle [phosphorylcreatine] and deoxygenation kinetics during high-intensity exercise in men Exp Physiol, April 1, 2008; 93(4): 468 - 478. [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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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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R. A. Ferguson, P. Krustrup, M. Kjaer, M. Mohr, D. Ball, and J. Bangsbo Effect of temperature on skeletal muscle energy turnover during dynamic knee-extensor exercise in humans J Appl Physiol, July 1, 2006; 101(1): 47 - 52. [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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 H.-Y. Ong, C. S. O'Dochartaigh, S. Lovell, V. H. Patterson, K. Wasserman, D. P. Nicholls, and M. S. Riley Gas Exchange Responses to Constant Work-Rate Exercise in Patients with Glycogenosis Type V and VII Am. J. Respir. Crit. Care Med., June 1, 2004; 169(11): 1238 - 1244. [Abstract] [Full Text] [PDF]
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J. S. M. Pringle, J. H. Doust, H. Carter, K. Tolfrey, and A. M. Jones Effect of pedal rate on primary and slow-component oxygen uptake responses during heavy-cycle exercise J Appl Physiol, April 1, 2003; 94(4): 1501 - 1507. [Abstract] [Full Text] [PDF]
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H. B. Rossiter, S. A. Ward, F. A. Howe, J. M. Kowalchuk, J. R. Griffiths, and B. J. Whipp Dynamics of intramuscular 31P-MRS Pi peak splitting and the slow components of PCr and O2 uptake during exercise J Appl Physiol, December 1, 2002; 93(6): 2059 - 2069. [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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 R. A. Ferguson, D. Ball, and A. J. Sargeant Effect of muscle temperature on rate of oxygen uptake during exercise in humans at different contraction frequencies J. Exp. Biol., April 1, 2002; 205(7): 981 - 987. [Abstract] [Full Text] [PDF]
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P. Krustrup, J. Gonzalez-Alonso, B. Quistorff, and J. Bangsbo Muscle heat production and anaerobic energy turnover during repeated intense dynamic exercise in humans J. Physiol., November 1, 2001; 536(3): 947 - 956. [Abstract] [Full Text] [PDF]
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R. A Ferguson, D. Ball, P. Krustrup, P. Aagaard, M. Kjaer, A. J Sargeant, Y. Hellsten, and J. Bangsbo Muscle oxygen uptake and energy turnover during dynamic exercise at different contraction frequencies in humans J. Physiol., October 1, 2001; 536(1): 261 - 271. [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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F Ozyener, H B Rossiter, S A Ward, and B J Whipp Influence of exercise intensity on the on- and off-transient kinetics of pulmonary oxygen uptake in humans J. Physiol., June 15, 2001; 533(3): 891 - 902. [Abstract] [Full Text] [PDF]
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F. Borrani, R. Candau, G. Y. Millet, S. Perrey, J. Fuchslocher, and J. D. Rouillon Is the {V}O2 slow component dependent on progressive recruitment of fast-twitch fibers in trained runners? J Appl Physiol, June 1, 2001; 90(6): 2212 - 2220. [Abstract] [Full Text] [PDF]
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L. Nybo, T. Jensen, B. Nielsen, and J. Gonzalez-Alonso Effects of marked hyperthermia with and without dehydration on {V}O2 kinetics during intense exercise J Appl Physiol, March 1, 2001; 90(3): 1057 - 1064. [Abstract] [Full Text] [PDF]
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B. W Scheuermann, B. D Hoelting, M L. Noble, and T. J Barstow The slow component of O2 uptake is not accompanied by changes in muscle EMG during repeated bouts of heavy exercise in humans J. Physiol., February 15, 2001; 531(1): 245 - 256. [Abstract] [Full Text] [PDF]
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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]
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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]
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C. A. Combs, A. H. Aletras, and R. S. Balaban Effect of muscle action and metabolic strain on oxidative metabolic responses in human skeletal muscle J Appl Physiol, November 1, 1999; 87(5): 1768 - 1775. [Abstract] [Full Text] [PDF]
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L. J. McCutcheon, R. J. Geor, and K. W. Hinchcliff Effects of prior exercise on muscle metabolism during sprint exercise in horses J Appl Physiol, November 1, 1999; 87(5): 1914 - 1922. [Abstract] [Full Text] [PDF]
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S. Koga, T. Shiojiri, M. Shibasaki, N. Kondo, Y. Fukuba, and T. J. Barstow Kinetics of oxygen uptake during supine and upright heavy exercise J Appl Physiol, July 1, 1999; 87(1): 253 - 260. [Abstract] [Full Text] [PDF]
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G. Ferretti ; and S. Koga Letters to the Editor J Appl Physiol, October 1, 1998; 85(4): 1593 - 1600. [Abstract] [Full Text] [PDF]
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