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1 Istituto di Tecnologie
Biomediche Avanzate, Near-infrared spectroscopy (NIRS) could allow insights into
controversial issues related to blood lactate concentration
([La]b) increases at
submaximal workloads (
lactate threshold; near-infrared spectroscopy
THE QUESTION whether lactate accumulation in muscle and
blood at submaximal workloads is attributable to an imbalance between O2 supply and
O2 requirement in the working
muscles, that is, to muscle hypoxia, is controversial (6, 14, 17). The
issue is further complicated by the fact that lactate concentration in
blood ([La]b), as
usually determined in the exercise physiology laboratory, cannot be
considered a direct index of lactate production by muscles, because
muscles, as well as other tissues and organs, are also
consumers of lactate by oxidative metabolism for their energetic needs (6). In additon, lactate distribution throughout body
compartments appears to be regulated by complex mechanisms (14, 16).
Apart from its involvement in energy metabolism, other roles of lactate
have been recently suggested. For example, according to Stringer et al.
(35), lactic acidosis in muscle would facilitate
O2Hb dissociation and therefore
increase O2 extraction while
preserving the O2 pressure
gradient from capillary to mitochondria.
Some further insights into these issues could be obtained by the
utilization of near-infrared spectroscopy (NIRS), a noninvasive method
that allows the monitoring of muscle oxygenation on the principle that
the near-infrared light absorption characteristics of hemoglobin (Hb)
and myoglobin (Mb) depend on their
O2 saturation [see, for
instance, the recent reviews by Ferrari et al. (13) and by Mancini
(22)]. Some of the limits of NIRS measurements are discussed
below (see METHODS). In previous
NIRS studies conducted during incremental exercise (3, 5, 24, 25, 37),
[La]b values were not
determined. Other authors evaluated the relationship between
[La]b levels and
muscle resaturation kinetics at the end of exercise (8) and described
an association between muscle deoxygenation and
[La]b levels during
constant-load exercise (21) or between muscle deoxygenation and the
so-called ventilatory threshold. To our knowledge, no formal comparison
of NIRS-derived oxygenation indexes and
[La]b has been
performed during incremental exercise. The aim of this study was to
fill this gap. More specifically, we intended to evaluate whether,
during a standard incremental exercise conducted on a cycle ergometer,
indexes of muscle oxygenation obtained by NIRS were associated with the
onset of blood lactate accumulation or with some other parameters often
employed to determine the so-called lactate threshold (LT).
Subjects.
The experiments were carried out in Milan, Italy (altitude ~150 m) on
five men, who were well-trained mountain climbers {age, 32.8 ± 5.4 (SD) yr; height, 178 ± 11 cm; body weight, 73.3 ± 10.3 kg; blood Hb concentration ([Hb]), 14.7 ± 0.8 g/100 ml}, ~3 wk before they participated in a Himalayan
expedition to Mount Lhotse, Nepal (altitude 8,501 m). At the time of
the tests, the subjects were not acclimatized to altitude, as can be
deduced from their [Hb]. During the expedition, two of the
subjects reached the summit, whereas the other three reached an
altitude of ~8,000 m. All subjects did not utilize supplemental
O2 during the climb. The subjects gave their informed consent to participate in the study. All tests were
performed under the supervision of a cardiologist.
Measurements.
Measurements were carried out at rest and during an incremental
exercise (starting from 60 W, 30 W were added every 4 min up to
voluntary exhaustion) on an electrically braked cycle ergometer (Cardioline STS 3). No warm-up exercises were performed before the
incremental test.
ABSTRACT
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
). We combined, on five
well-trained subjects [mountain climbers; peak
O2 consumption
(
O2peak), 51.0 ± 4.2 (SD)
ml · kg
1 · min1]
performing incremental exercise on a cycle ergometer (30 W added every
4 min up to voluntary exhaustion), measurements of pulmonary gas
exchange and earlobe
[La]b with
determinations of concentration changes of oxygenated Hb
(
[O2Hb]) and
deoxygenated Hb ([HHb]) in the vastus
lateralis muscle, by continuous-wave NIRS. A "point of
inflection" of
[La]b vs.
was arbitrarily identified at the lowest
[La]b value which was
>0.5 mM lower than that obtained at the following .
Total Hb volume ([O2Hb + HHb]) in the muscle region of interest increased as a function of
up to 60-65% of
O2 peak, after which
it remained unchanged. The oxygenation index
([O2Hb 
HHb]) showed an
accelerated decrease from 60- 65% of
O2 peak. In the
presence of a constant total Hb volume, the observed
[O2Hb HHb]
decrease indicates muscle deoxygenation (i.e., mainly capillary-venular
Hb desaturation). The onset of muscle deoxygenation was significantly
correlated (r2 = 0.95;
P < 0.01) with the point of
inflection of [La]b
vs. , i.e., with the onset of blood lactate accumulation.
Previous studies showed relatively constant femoral venous
PO2 levels at higher
than ~60% of maximal O2
consumption. Thus muscle deoxygenation observed in the present study
from 60-65% of
O2 peak could be
attributed to capillary-venular Hb desaturation in the presence of
relatively constant capillary-venular
PO2 levels, as a consequence of a
rightward shift of the O2Hb
dissociation curve determined by the onset of lactic acidosis.
INTRODUCTION
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
METHODS
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
E, in
BTPS),
O2 uptake
(O2, in
STPD), and
CO2 output
(CO2, in
STPD) were assessed on a
breath-by-breath basis by a computerized system (Vmax 229, SensorMedics). E was calculated by
integration of the flow tracings recorded at the mouth of the subject
by a mass flow sensor. Volume calibration was performed before each
experiment, by means of a 3-liter syringe, at three different flow
rates. O2 and
CO2 were determined by
continuously monitoring PO2 and
PCO2 at the mouth of the subject
throughout the respiratory cycle and from established mass balance
equations. Calibration of the fast responding O2 (paramagnetic) and
CO2 (nondispersive infrared)
analyzers was performed before each experiment by utilizing gas
mixtures of known composition. Heart rate (HR) was determined from the
electrocardiogram, which was continuously monitored throughout the
tests. Arterial blood O2
saturation (SaO2) was monitored
continuously by pulse oximetry (Biox 3740 Pulse Oximeter, Ohmeda) at
the earlobe. Average values of E,
O2,
CO2, HR, and
SaO2 were calculated during the last
minute of rest and during the last 30-45 s of each workload. At
rest and during the last 30-45 s of each workload, 20 µl of arterialized capillary blood were taken from an earlobe, and capillary [La]b was determined
by an enzymatic method (ESAT 6661 Lactat, Eppendorf). No blood-gas
measurements were performed.
[HHb]) and oxygenated Hb concentration
([O2Hb]), although expressed in arbitrary
units (homologous across subjects), thereby providing a
semi-quantitative evaluation of muscle oxygenation. This instrument was
utilized for the present study. The probe unit, molded in elastic black
silicone rubber, has a silicon photodiode as a photodetector in the
center and two light-emitting diodes (peak wavelengths 760 and 840 nm)
on either side. The probe was firmly attached to the skin overlying the
lower one-third of muscle (~10-12 cm above the knee joint),
parallel to the major axis of the thigh, by a belt secured by Velcro
straps and biadhesive tape. The skin was carefully shaven previously.
Pen marks were made over the skin to indicate the margins of the belt
to check for any downward sliding of the probe during cycling. No
sliding was observed in any subject. Black cloths were put around the
probe and the skin to prevent contamination from ambient light. The probe was connected to a personal computer for data acquisition, analog-to-digital conversion, and subsequent analysis. The sampling frequency was set at 2 Hz. The distance between each light source and
the photodiode was 3 cm. Thus the penetration depth can be estimated to
be ~1.5 cm, as extensively discussed previously (10, 15). The
influence of subcutaneous adipose tissue on near-infrared light
propagation in leg muscle and on the sensitivity of NIRS instruments
has been recently investigated by ultrasound (15). Those
authors demonstrated that the near infrared light
penetrates shallow regions of muscle (~2-4
cm3 under the skin and
subcutaneous fat) even when the adipose tissue thickness is 1.5 cm.
Transmitted NIR light penetrates skin, subcutaneous fat, and underlying
muscle and is either absorbed or scattered within the tissues. Part of
the scattered light is detected by the photodetector. The absorption
characteristics of light at 760 and 840 nm depend on relative
oxygenation of Hb and Mb. Mb indeed has similar absorption spectra to
Hb. In human skeletal muscle, however, the ratio of [Hb] to
[Mb] is >5 (20, 22) so that the signals can be considered
as deriving mainly from Hb. This was also suggested by studies
conducted by simultaneous use of proton magnetic resonance spectroscopy
(which allows in vivo detection of deoxygenated Mb) and NIRS in
exercising humans (24). NIRS-obtained oxygenation values represent
volume-averaged values in the segment of tissue under consideration.
[O2Hb] and
[HHb], with respect to an initial value arbitrarily set
equal to zero, were calculated and expressed in arbitrary units (33).
The sum between the two variables
([O2Hb + HHb]) is
related to changes in the total Hb volume in the muscle region of
interest, whereas the difference between the two variables ([O2Hb HHb]) was taken as an oxygenation index (see also
RESULTS). Average
[HHb],
[O2Hb],
[O2Hb + HHb], and
[O2Hb HHb]
values were calculated at rest and during the last 30-45 s of each
workload to obtain steady-state values aligned in time with blood
sampling for [La]b determination.
Skinfold thickness at the site of application of the NIR probe was
determined at the end of the exercise protocol by a caliper (Holtain).
The obtained values were 5.3 ± 1.3 mm (range, 4.5-7.5 mm).
Statistical analysis. Data were expressed as means ± SD. Regression and correlation analyses were performed by the least squares method by utilizing a commercially available software package (InStat, GraphPad Software). The level of significance was set at P < 0.05.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Peak values obtained during the exhausting workload (288 ± 40 W)
for ventilatory, metabolic, and cardiovascular parameters were
E, 119.6 ± 14.5 l/min;
O2, 3.71 ± 0.40 l/min
(51.0 ± 4.2 ml · kg1 · min1);
CO2, 3.73 ± 0.54 l/min; SaO2, 94 ± 3%; HR, 182 ± 11 beats/min; and
[La]b, 8.5 ± 1.6 mM.
Individual SaO2 values are
shown in Fig. 1 as a function
of workload. Three of the subjects showed some arterial
desaturation at the exhausting workload.
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Individual values obtained by NIRS are shown in the
top and
middle panels of Figs.
2-6 as a function of workload. For each subject,
top panels show [HHb]
and [O2Hb] values,
whereas middle panels show
[O2Hb + HHb] and
[O2Hb HHb]
values. In all subjects [O2Hb + HHb]
underwent a slight linear increase as function of workload, up to
60-65% of the exhausting workload, after which the variable
remained substantially unchanged. The
[O2Hb + HHb] increase up to 60-65% of the exhausting workload was mainly
attributable to increased [HHb], because
[O2Hb] was
substantially constant in this workload range. In all subjects,
[O2Hb HHb]
decreased with increasing workload. According to visual inspection, the pattern of decrease appeared to be characterized by two linear functions with increasing slopes. The workload at which the change in
slope occurred was determined by iteratively fitting different combinations of two linear regressions to contiguous experimental points obtained during exercise and by evaluating which combination yielded the lowest sum of squared residuals. Resting values were not
utilized for this analysis because, as pointed out by Maehara et al.
(21), in resting subjects, the NIRS signal could be significantly contaminated by tissues other than skeletal muscle, such as the skin.
One subject (subject 1) showed a
leveling off in [O2Hb HHb] decrease at the highest workload. This value was not
utilized for the regression analysis. The combinations of linear
regressions with the lowest sum of squared residuals are shown in Figs.
2-6. A point of inflection of muscle deoxygenation was identified
at the workload at which the change in slope of
[O2Hb HHb]
occurred. These points of inflection are indicated by the arrows in the middle panels of Figs. 2-6. The
points of inflection corresponded also to the workload at which
[O2Hb] started to
decrease. It should be noted that
[O2Hb HHb]
can be considered a reliable oxygenation index only if
[O2Hb + HHb] is
constant. In the present study, muscle deoxygenation [as indicated by
the accelerated [O2Hb HHb] decrease that begins at 60-65% of peak
O2 consumption
(O2 peak)] was described in the presence of a constant
[O2Hb + HHb] (Figs. 2-6, middle panels), thereby
indicating a true deoxygenation. With a constant total Hb volume, the
increase in [HHb] and the decrease in
[O2Hb] (Figs.
2-6, top panels) suggest, indeed,
an imbalance between O2 delivery
and O2 demand in the region of
tissue under consideration. For workloads <60-65% of
O2 peak,
[O2Hb + HHb] showed
a slight linear increase (see Figs. 2-6,
middle panels). In this workload
range, the observed slight decrease in
[O2 Hb HHb] cannot be considered an indication of muscle deoxygenation, because the [O2Hb + HHb] increase was attributable to a [HHb] increase, whereas
[O2Hb] was
unchanged (Figs. 2-6, top
panels), thereby suggesting capillary-venular vasodilation.
Unfortunately, no mathematical methods that account for Hb volume
changes in the interpretation of deoxygenation indexes are available.
From the above discussion, however, it would seem that, in terms of muscle oxygenation, the change in slope at 60-65% of
O2 peak would be even
more pronounced than that observed for
[O2 Hb HHb]. The fact that onset of muscle deoxygenation occurred at about the same percentage of
O2 peak (60-65%)
at which [O2Hb + HHb] leveled off, after a steady increase at lower workloads, suggests that muscle deoxygenation occurred after the exercise-related vasodilatatory capacity within the muscle reached its maximum.
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Individual values of
[La]b vs. workload are
shown in the bottom panels of Figs.
2-6. In these panels, horizontal lines indicate the fixed values
of [La]b (2 and 4 mM)
that are conventionally used to determine the so-called lactate
threshold, or LT (1). [La]b showed the
classic curvilinear pattern of increase as a function of workload. In
recent years, several mathematical models were applied to describe this
pattern of increase (27) and to confirm or confute the existence of a
threshold. In the present study, we were simply interested in
identification of the workload at which lactate started to accumulate
significantly in blood. For descriptive purposes, without making any
inference on the mechanisms involved, we chose to identify a point of
inflection of [La]b
vs. workload as the lowest
[La]b value that was
>0.5 mM lower than the following one, i.e., according to an empirical method recently suggested by Zoladz et al. (38). These points of
inflection of [La]b
vs. workload are indicated by the arrows in Figs. 2-6,
bottom panels. In four of five
subjects, the point of inflection of
[La]b vs. workload was
the same as the point of inflection of muscle deoxygenation. In one
subject (subject 1), the point of
inflection of muscle deoxygenation was 30 W lower than the point of
inflection of [La]b
vs. workload. The highest workload corresponding to
[La]b values lower
than or equal to 2 or 4 mM was also determined. These workload values
were termed LT 
2 mM and LT 4 mM. The points of
inflection of [La]b
vs. workload, LT 2 mM and LT 4 mM were plotted for each subject as a function of the point of inflection of muscle deoxygenation (Fig.
7). The identity line between the variables
is also shown in the figure. A significant correlation
(r2 = 0.95;
P = 0.0045) was observed only between
the point of inflection of
[La]b vs. workload and
the point of inflection of muscle deoxygenation. Figure 7 shows that LT 4 mM clearly overestimated the point of inflection of muscle
deoxygenation. The point of inflection of muscle deoxygenation occurred
at 62 ± 7% of
O2 peak, the point of
inflection of [La]b
vs. workload was at 64 ± 4% of
O2 peak, LT 2 mM was
at 62 ± 5% of
O2 peak, and LT 4 mM
was at 80 ± 7% of
O2 peak.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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In recent years, NIRS has been used rather extensively to monitor
oxygenation changes in working muscles (3-5, 8, 21, 23, 24, 31,
37). This noninvasive method is based on the principle that the light
absorption characteristics of Hb and Mb in the NIR region change
depending on their O2 saturation
(7, 9, 13, 22). Some intrinsic limitations of this method were discussed above (see METHODS). NIR
light-absorption changes in muscle reflect changes in oxygenation at
the level of small blood vessels (small arterioles and venules),
capillaries, and intracellular sites of
O2 transport and uptake (23). As
mentioned above, NIRS cannot differentiate between absorption changes
due to Hb and Mb, because the absorption spectra of the two molecules
are the same. However, the ratio of [Hb] to
[Mb] in skeletal muscle is >5 (20, 22) so that most of
the absorption changes can be considered to be derived mainly from Hb,
as supported also by studies conducted by simultaneous use of proton
magnetic resonance spectroscopy (which allows in vivo detection of
deoxygenated Mb) and NIRS in exercising humans (24). During incremental
exercise, some endurance athletes show variable degrees of arterial
desaturation at maximal workload (11). This was the case also for the
present study, as shown in Fig. 1. On the basis of such premises, it
appears reasonable to assume that muscle desaturation observed in the present study, beginning at 60-65% of
O2 peak, indicated
mainly a Hb desaturation occurring at the capillary and venular level.
The main finding of the present study was that, during an incremental
exercise on a cycle ergometer, the onset of blood lactate accumulation
{arbitrarily defined as the lowest
[La]b value that was
>0.5 mM lower than the following one (see
RESULTS)} was significantly correlated with the onset of muscle (or, more precisely,
capillary-venular) deoxygenation, as assessed by NIRS. Muscle
deoxygenation could, in theory, be attributed to an accelerated fall of
capillary-venular PO2, occurring in
association with the appearance of lactate in blood. However, several
papers (30, 35) reported that, during incremental exercise, the
measured femoral venous PO2
(considered an index of end-capillary
PO2) or the calculated mean capillary
PO2 show, after an initial abrupt
decrease that occurs at low workloads, a tendency to level off (at a
femoral venous PO2 of ~17-20
Torr) at workloads >60% of
O2 max. Stringer et al.
(35), in particular, showed that the leveling off of femoral venous
PO2 occurred at workload just above
the so-called ventilatory threshold (2). Thus muscle deoxygenation
observed in the present study at workloads >60-65% of
O2 peak is likely
attributable to an accelerated capillary-venular Hb desaturation in the
presence of relatively constant capillary-venular
PO2 levels. This would imply a
rightward shift of the O2Hb
dissociation curve as a consequence of lactic acidosis. This is in
agreement with data obtained by Systrom et al. (36), who showed an
abrupt decrease of exercising calf muscle pH (determined by
31P-nuclear magnetic resonance spectroscopy) at ~65% of
O2 max. Such a pH
threshold occurred at a workload that was not significantly different
from that associated with the LT (determined by these authors by a
log-log plot of venous [La] vs.
O2). A rightward shift of the
O2Hb dissociation curve could also
derive from increased muscle temperature. According to Saltin and
Hermansen (32), however, muscle temperature is linearly related to
workload, so a temperature increase should not be responsible for
muscle deoxygenation that occurs abruptly at 60-65% of
O2 peak. As pointed out
by Stringer et al. (35), the rightward-shifted O2Hb
dissociation curve would allow an increased
O2 extraction, but at the same time it would prevent large falls in capillary
PO2, the driving force for peripheral
O2 diffusion. A well-preserved
peripheral O2 diffusion would be
compatible with data recently obtained by Richardson et al. (29),
according to which human muscle cytoplasmic PO2 (calculated on the basis of Mb
saturation, measured by proton magnetic resonance spectroscopy) is kept
constant at an average value of ~3 Torr during exercises from 50 to
100% of O2 max. These
authors did not observe a correlation between cytoplasmatic
PO2 and lactate efflux from the
exercising muscle. On the other hand, Duhaylongsod et al. (12) observed a negative linear relationship between the relative concentration of
oxidized cytochrome a,a3 (as determined by NIRS)
and lactate efflux from canine gracilis in vivo. In the present study,
our data showed only a significant correlation between the onset of muscle (capillary/venular) deoxygenation and the onset of blood lactate
accumulation and do not allow inferences on any cause-effect relationship between the two variables. A clearer picture
could be derived by future studies aimed at evaluation of relationships between the two variables during incremental exercises in acute hypoxia
and hyperoxia. The present data do not allow either inferences on the
issue of adequate vs. inadequate mitochondrial
O2 levels in the regulation of glycolysis.
Previous NIRS studies conducted during incremental exercise (3, 5, 24,
25, 37) did not assess blood lactate concentration. The study by Chance
et al. (8) evaluated the relationship between blood lactate levels and
the resaturation kinetics of Hb at the end of exercise. Belardinelli et
al. (3) and Bhambhani et al. (5) utilized NIRS during incremental
exercise and compared the observed pattern of deoxygenation with the
so-called ventilatory threshold (2). Although the patterns of
deoxygenation were different in the two studies, both groups claimed
that they were closely related to the ventilatory threshold. In both
studies, [La]b values were not
assessed. The pattern of deoxygenation observed in the present study
appears similar to that described by Belardinelli et al. (3) in a group
of trained and untrained subjects. Also these authors described an
accelerated muscle deoxygenation that occurred at ~50% of
O2 max, in
close correlation with the ventilatory threshold. Taken together, the
results of the present study and those of Belardinelli et al. suggest a
close relationship between NIRS-derived indexes of muscle oxygenation
and the ventilatory threshold or LT, when the latter is defined as the
lowest workload associated with a significant blood lactate
accumulation. Maehara et al. (21) observed a relationship between blood
lactate levels and NIRS-obtained muscle deoxygenation
during constant-load cycling exercise. These authors also described
(during constant-load cycling exercises above the LT) an increased
muscle deoxygenation and higher blood lactate levels when
O2 delivery to muscle was
presumably reduced, either by hypoxic breathing or by the inhalation of
low concentrations of carbon monoxide. Thus results from the present study and from that of Maehara et al. indicate that the association between NIRS-obtained muscle deoxygenation and blood lactate levels can
be described for different exercise protocols.
Although the onset of muscle deoxygenation correlated with the onset of
blood lactate accumulation, as defined by a >0.5 mM change in
[La]b, it did not
correlate with the LT defined by the 2 or 4 mM levels (1). Indeed, no
significant correlation could be found between the NIRS-derived index
of muscle oxygenation and the submaximal workloads associated with the
fixed [La]b values conventionally employed to determine the so-called LT, i.e., 2 or 4 mM
(1). In particular (see Fig. 7), the onset of muscle deoxygenation
occurred at workloads that were significantly lower than those
associated with [La]b
4 mM. Although more subjects of different training status would
probably be needed to confirm such a conclusion, the results of the
present study do not seem to provide a physiological basis (in terms of
muscle oxygenation) for the fixed
[La]b methods employed
to determine the LT. It might be hypothesized, however, that the
relationship observed between the 4 mM LT and sport performance levels
during endurance events (34) could be related to the subjects'
capacity to sustain a given level of muscle deoxygenation for
relatively prolonged periods of time.
As pointed out by Belardinelli et al. (4), one of the assumptions of the present study and other similar studies is that the portion of the vastus lateralis investigated by the NIRS technique is recruited in proportion to the relative work performed. This assumption seems reasonable, considering that 1) the placement of the probe should be over one of the motor points of the muscle (18), so that the region of the muscle should be recruited any time the muscle is activated; and 2) according to Miyashita et al. (26), the integrated electromyogram signal from the vastus lateralis increases almost linearly with work during cycling.
The subjects of the present study were a very homogeneous group of
elite altitude climbers. Although the subjects were
studied a few weeks before a Himalayan expedition, they were not
acclimatized to altitude at the time of the tests, as can be deduced
from their blood Hb levels (see
Subjects). Their
O2 peak values (see
RESULTS) are compatible with those
of well-trained subjects. The results of the present study, however,
will have to be confirmed in future investigations conducted with
subjects of different ages, training status, and gender.
Conclusions.
The onset of blood lactate accumulation during incremental exercise on
a cycle ergometer was highly correlated with the onset of muscle
(vastus lateralis) deoxygenation, as determined by NIRS. Both events
occurred at 60-65% of
O2 peak. Because
previous studies showed relatively constant femoral venous
PO2 levels at submaximal and maximal
workloads, muscle deoxygenation observed in the present study can be
attributed to capillary-venular Hb desaturation in the presence of
relatively constant capillary-venular PO2 levels, likely as a consequence
of a rightward shift of the O2Hb
dissociation curve, determined by the onset of lactic acidosis.
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ACKNOWLEDGEMENTS |
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We are grateful to the subjects who enthusiastically agreed to participate to the study, to Dr. Bruno Carù for clinical supervision of the subjects during the tests, and to Angelo Colombini and Marco Pellegrini for technical assistance. We are also grateful to Dr. L. Bruce Gladden for constructive criticism, and we thank OMRON of Kyoto, Japan, for the loan of the HEO-100 NIRS instrument.
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FOOTNOTES |
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The study was supported in part by the Ev-K2-CNR Strategic Project of the National Research Council of Italy, by EU Contract BMH4-CT96, 1658, and by North Atlantic Treaty Organization Collaborative Research Grant No. 972111.
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. §1734 solely to indicate this fact.
Address for reprint requests: B. Grassi, ITBA-CNR, Palazzo LITA, Via Fratelli Cervi 93, I-20090 Segrate (MI), Italy (E-mail: grassi{at}itba.mi.cnr.it).
Received 25 August 1998; accepted in final form 10 March 1999.
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REFERENCES |
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ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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