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Clinical ResearchCR
Noninvasive determination of exercise-induced
vasodilation during bicycle exercise using nearinfrared spectroscopy

Authors’ Contribution:
A Study Design
B Data Collection
C Statistical Analysis
D Data Interpretation
E Manuscript Preparation
F Literature Search
G Funds Collection

Ryotaro Kime1 ABCDEF, Joohee Im2 BD, Daniel Moser3 BD, Shoko Nioka2 AD,
Toshihito Katsumura1 DG, Britton Chance2 AD

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Received: 2008.02.21
Accepted: 2008.04.17
Published: 2009.03.01

Department of Sports Medicine for Health Promotion, Tokyo Medical University, Tokyo, Japan
Department of Biochemistry & Biophysics, University of Pennsylvania, Philadelphia, PA, U.S.A.
3
Graduate Hospital Human Performance & Sports Medicine Center, Wayne, PA, U.S.A.
2

Source of support: This study was supported in part by Grant-in-Aid for Young Scientists from the Japan Society
for Promotion of Science 18700536 to R. K

Summary

Background:

Material/Methods:

The purpose of this study was to examine the changes in total hemoglobin (Δ[tHb]) response during bicycle exercise at various constant workloads using near infrared continuous wave spectroscopy (NIRcws) in humans. We hypothesized that the Δ[tHb] during exercise may progressively increase as a result of a dilation of the vascular bed and/or capillary recruitment at lower constantwork rates.
Seven healthy subjects performed bicycle exercise at 20, 40, 60, 80, and 100% of maximal work
rates (Wmax) for 5 min. Muscle oxygenation change (Δ[Oxy]) and Δ[tHb] at the right vastus lateralis were monitored using a NIRcws device. Exercise-induced Δ[tHb] and Δ[Oxy] responses at
each constant workload were evaluated as functional Δ[tHb] change (f-Δ[tHb]) and functional
oxygenation change (f-Δ[Oxy]), respectively. Blood lactate concentration [La] was also evaluatedafter each exercise stage.

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© Med Sci Monit, 2009; 15(3): CR89-94
PMID: 19247245

Results:

Conclusions:key words:

At work rates 60%Wmax and below, after an initial decrease at the start of exercise, both Δ[tHb]and Δ[Oxy] showed progressive increases until the end of exercise. A signiﬁcant positive correlation was found between f-Δ[tHb] and f-Δ[Oxy] (p<0.01). In addition, there was a signiﬁcant negative relationship of [La] to f-Δ[tHb] during exercise (p<0.05).
These results provide evidence that increased muscle oxygenation during bicycle exercise up to
60%Wmax may be caused by increased O2 supply due to exercise-induced blood volume expansion. Subsequently, the cessation of increase in f-Δ[tHb] at higher intensity exercise may lead tolower muscle tissue oxygenation and higher lactate accumulation.

muscle oxygenation • muscle perfusion • oxygen uptake • lactate • bicycle exercise

Full-text PDF:

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Word count:
Tables:Figures:
References:

2728
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Author’s address:

Ryotaro Kime, Department of Sports Medicine for Health Promotion, Tokyo Medical University, 6-1-1 Shinjuku,
Shinjuku-ku, Tokyo 160-8402, Japan, e-mail: kime@tokyo-med.ac.jp

Current Contents/Clinical Medicine • IF(2007)=1.607 • Index Medicus/MEDLINE • EMBASE/Excerpta Medica • Chemical Abstracts • Index Copernicus

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Med Sci Monit, 2009; 15(3): CR89-94

Experimental protocol
Before the main experiment, all of the subjects performeda preliminary incremental bicycle exercise test (Monark
868, Sweden) to obtain their maximal workloads (Wmax).
The male subjects started at 100 watts (W), and the female
subjects started at 50 W. The workloads increased by 25 W
every 2 min until exhaustion.
On a separate day, the subjects performed 5 min of bicycle
exercise at 20, 40, 60, 80 and 100%Wmax. Each exercise stage
was performed in random order and 25–30 min of recovery
time intervened between trials. All of the bicycle tests were
performed in an upright position, and the pedal frequency
was maintained at 60 rpm during all exercise tests.

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Muscle perfusion increases linearly in relation to work intensity, and peak muscle perfusion was reported to reach
50 to 100-fold higher than resting [1]. The increased muscle perfusion is caused by the result of interactions of central vascular control mechanisms, locally mediated vasodilation of resistance vessels, and the mechanical effects ofmuscle contraction [1]. However, it is reported that the local vascular control systems within the myogenic factors
primarily cause exercise-induced functional hyperemia[2]. Metabolites from actively contracting muscle (i.e. adenosine, H+, lactic acid and CO2) diffuse into the interstitial space to the resistance arterioles and cause vasodilationand capillary recruitment. Functional hyperemia may coordinate blood ﬂow, red blood cell distribution, and decrease
perfusion heterogeneity in skeletal muscle during exercise[3,4]. Furthermore, the increased muscle perfusion raises
the O2 supply to a level compatible with O2 demand which
may lead to less O2 deﬁcit [5].

subjects were briefed about the experimental protocol, andwritten informed consent was obtained before the test. The
Institutional Review Board of the University of Pennsylvania
approved the research protocol.

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BACKGROUND

Although exercise-induced functional hyperemia is one of
the most important factors of O2 supply to myocytes [6],there are only a few studies that have monitored functional hyperemia in humans because of the difﬁculty in detecting it. Some studies have monitored muscle perfusion during exercise using functional magnetic resonance imaging(f-MRI) [7] and positron emission tomography (PET) [3,4].
However, the equipment is rather expensive and inconvenient for evaluation of muscle perfusion during dynamic
whole body exercise.
Near infrared continuous wave spectroscopy (NIRcws) has
been found to be a very useful technique for noninvasive
measurement of tissue oxygenation and total hemoglobin(tHb) change [8,9]. The use of NIRcws is becoming moreprevalent now in the ﬁeld of work and exercise physiology[8–11]. NIRcws has a great advantage over invasive forms andother more expensive noninvasive forms because the NIRcws
can monitor the changes in blood volume and oxygenation
within speciﬁc regions of muscle during static contraction[11,12] and various forms of dynamic contraction [13–16].
As the body of research using the NIRcws technique builds,
a better understanding of this technique’s reliability under
speciﬁc conditions will be understood [9]. Since NIRcws
can measure total hemoglobin change (Δ[tHb]) in muscle
tissue during dynamic exercise, this technique has the potential to determine exercise-induced blood volume expansion noninvasively. The purpose of this study was to examine this Δ[tHb] response during bicycle exercise at various
constant workloads using NIRcws in humans. We hypothesized that the Δ[tHb] during exercise may progressively increase as a result of dilation of the vascular bed and/or capillary recruitment at lower constant work rates.

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Clinical Research

MATERIAL AND METHODS
Subjects
Seven healthy volunteers (3 males, 4 females, age: 25.4
years, height: 170.7 cm, weight: 66.4±8.6 kg) participated in this study. All subjects were involved in various recreational activities, such as volleyball, soccer, jogging, andcycling, 2–3 times/wk, but none were trained athletes. All

Pulmonary VO2, HR and [La]Pulmonary O2 uptake (VO2, in STPD), and carbon dioxide production (VCO2, in STPD) were assessed using thebreath-by-breath method with an online metabolic system(SensorMedics 2900, Yorba Linda, CA). The O2 and CO2
analyzers were calibrated before each experiment by utilizing gas mixtures of known composition. Heart rate wasmonitored continuously during the experiment by a 3-lead
ECG (Biopack MP100 system, USA). Blood samples weretaken via ﬁngerstick for blood lactate concentration ([La])at 30 sec after each exercise stage, and analyzed by an enzymatic method (Accusport, Mannheim, Germany).
NIRcwsChanges in muscle oxygenation (Δ[Oxy]) and total Hb(Δ[tHb]) were measured by a two-wavelength (730 nm
and 850 nm) light-emitting diode NIRcws (cwNIRS; NIM,
Philadelphia, PA). The principle of the measurement andthe speciﬁcations of the NIRcws have been fully described[8,9]. The level of oxygenation of hemoglobin and/or myoglobin (Hb/Mb) alters the absorption of the light in muscle tissue. For example, as Hb/Mb is oxygenated, the absorbance at 730 nm decreases and the absorbance at 850 nm
increases, providing a different signal. The difference insignal (signal at 850 nm minus the signal at 730 nm) is deﬁned as Δ[Oxy], which should be sensitive to Hb/Mb O2
saturation and the sum signal to Δ[tHb] [9].
We used a NIRcws device developed to enable a high signal-to-noise ratio (S/N), such that the S/N of the present
NIRcws device was 6.3-fold greater than the Runman oxymeter [17]. Data acquisition sampling frequency was set at 2
Hz. We used one source and four photodetectors to cover a
4.23 cm square area to only monitor a single muscle in thisstudy. The source and detectors were installed in the centerand in the corners of a square shaped probe, respectively.
Each source-detector distance was 3.0 cm. The measurement
probe was placed at a point one-third (1/3) from the patella to the greater trochanter. For reliable probe position, thedistance was measured from the center of the patella andgreater trochanter to the probe on the vastus lateralis mus-

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Kime R et al – Monitoring of exercise-induced vasodilation

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100% Wmax

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cle. The probe was ﬁrmly attached to the skin and no sliding was observed in any subject. Δ[tHb] and Δ[Oxy] wereexpressed in ΔμM, and were corrected for fat layer thickness
effects by adapting the results of Monte Carlo simulation[18]. This calculation has its origin in our previous paperwith Niwayama et al. [19], in which we calculated quantitative measurement of muscle oxygenation using NIRcws withcorrection for the inﬂuence of fat layer thickness.
Statistics

The changes in recorded variables during the exercise experiments were analyzed by one-way ANOVA for repeatedmeasurements. Following a signiﬁcant F test, pair-wise differences were identiﬁed using Tukey’s honestly signiﬁcantdifference (HSD) post hoc procedure. When appropriate,signiﬁcant differences were also identiﬁed using Student’s
paired t-test. Regression and correlation analyses were performed by the least squared residuals method. The level ofsigniﬁcance was set at p<0.05.

RESULTS

Figure 2. Typical responses of Δ[tHb] and Δ[Oxy] to bicycle exercise.
The circle and triangle indicate Δ[tHb] and Δ[Oxy],
respectively. The area determined by dotted lines indicatesthe exercise period at 40%Wmax for 5 min. Δ[tHb] responseat each work rate was evaluated from the minimum values
occurring within 15 sec after the start of exercise to the
maximal values within 1 min before cessation of exercise asfunctional blood volume change (ƒ-Δ[tHb]). Also, Δ[Oxy]response at each work rate was also evaluated from theminimum value occurring within 1 min after the start ofexercise to the maximal value within 1 min before cessationof exercise as functional oxygenation change (ƒ-Δ[Oxy]).

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Figure 1. Changes in blood lactate concentration in relation to thepercentage of pulmonary VO2peak as a function of bicycle
workload.

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Med Sci Monit, 2009; 15(3): CR89-94[La] and Pulmonary VO2The [La] in relation to the percentage of pulmonary
VO2peak is displayed in Figure 1. [La] showed the classicalcurvilinear pattern of increase as a function of work rate.
Baseline [La] was 1.7±0.1 mM, and the [La] did not signiﬁcantly increase until 60%Wmax (3.0±0.2 mM), and increased more dramatically at higher work rates (80%Wmax;
5.3±0.4 mM, 100%Wmax; 8.2±1.0 mM).
Exercise- induced blood volume expansion
Typical responses of Δ[tHb] and Δ[Oxy] to bicycle exercise are illustrated in Figure 2. At the beginning of exercise, Δ[tHb] steeply decreased due to mechanical factors related to contraction. Following the steep decrease, Δ[tHb]reached minimum values within 15 sec after the start ofexercise. Thereafter, as the exercise continued there wasa progressive increase of Δ[tHb]. In this study, Δ[tHb] response at each work rate was evaluated from the minimum
values occurring within 15 sec after the start of exercise(Δ[tHb]initial) to the maximal values occurring within 1 min

before the cessation of exercise (Δ[tHb]end) as functional
blood volume change (f-Δ[tHb]). In addition, Δ[Oxy] also
decreased at the beginning of exercise due to the muscle
pump squeezing blood and increased muscle O2 consumption (muscle VO2). After Δ[Oxy] reached minimum values
within 1 min after the start of exercise, Δ[Oxy] also progressively increased as the exercise continued. Therefore, theΔ[Oxy] response at each work rate was evaluated from theminimum value occurring within 1 min after the start of exercise (Δ[Oxy]initial) to the maximal value occurring within
1 min before the cessation of exercise (Δ[Oxy]end) as functional oxygenation change (f-Δ[Oxy]), (Figure 2).
Relationship between f-Δ[tHb] and [La]Figure 3 shows the f-Δ[tHb] during exercise in relation
to the VO2peak. There were positive values of f-Δ[tHb] at
20, 40 and 60%Wmax, and the peak value of the f-Δ[tHb](29.7±4.0 μM) was obtained at 40%Wmax. The positive
value in the vertical axis indicates that Δ[tHb] increased as
the exercise continued. In contrast, f-Δ[tHb] at 80% and
100%Wmax only yielded a small change (10.1±5.0 μM) and anegative value (–13.6±5.0 μM), respectively. The f-Δ[tHb] at
80%Wmax was signiﬁcantly lower than 40% and 60%Wmax(p<0.05), and the f-Δ[tHb] at 100%Wmax was signiﬁcantly
lower than 20%, 40% and 60%Wmax (P<0.001).
The f-Δ[Oxy] in relation to%VO2peak is displayed in Figure 4.
As explained above, the positive value in the vertical axis indicates that the muscle tissue was oxygenating during exercise, not deoxygenating. There was a signiﬁcant increasein f-Δ[Oxy] at 20, 40 and 60%Wmax. f-Δ[Oxy] at 80% and
100%Wmax produced a small change (4.0±6.2 μM) and anegative value (–43.2±9.3 μM), respectively. Similar to the

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Med Sci Monit, 2009; 15(3): CR89-94

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Figure 5. Relationship between ƒ-Δ[tHb] and ƒ-Δ[Oxy] during
exercise. Each dotted line indicates zero point of ƒ-Δ[tHb]and ƒ-Δ[Oxy], respectively. The solid bold line represents
the linear regression line (r=0.975, p<0.01).

[La] (mM)

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Figure 3. ƒ-Δ[tHb] during exercise in relation to the VO2peak. The
dotted line indicates the zero point of ƒ-Δ[tHb] meaning
Δ[tHb] did not change between the start and end of
exercise. * P<0.05 and ** P<0.01 versus 20%Wmax;† P<0.05 and †† P<0.01 versus 40%Wmax, and ‡ P<0.05
and ‡‡ P<0.01 versus 60%Wmax.

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Figure 4. ƒ-Δ[Oxy] during exercise in relation to% VO2peak The dottedline indicates zero point of ƒ-Δ[Oxy] meaning Δ[Oxy] did
not change between the start and end of exercise. * P<0.05
and ** P<0.01 versus 20%Wmax; † P<0.05 and †† P<0.01
versus 40%Wmax, and ‡ P<0.05 and ‡‡ P<0.01 versus
60%Wmax.

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Clinical Researchf-Δ[tHb], the f-Δ[Oxy] was signiﬁcantly lower at 80%Wmax(p<0.05) and 100%Wmax (P<0.001) compared with 20, 40,
and 60%Wmax. The relationship between f-Δ[tHb] and fΔ[Oxy] was signiﬁcantly correlated as shown in Figure 5.
(p<0.01). In addition, there was a signiﬁcant negative correlation of f-Δ[tHb] to [La] as shown in Figure 6 (p<0.05).
Reproducibility of f-Δ [tHb] and f-Δ[Oxy]On a separate day, all of the subjects performed the same
exercise protocol at 20, 40 and 60%Wmax to determine thereproducibility of the f-Δ[tHb] and f-Δ[Oxy]. The variationof coefﬁcients for the f-Δ[tHb] and f-Δ[Oxy] were 6.3±2.4%
and 7.2±2.6%, respectively.

DISCUSSION
The main results of this study are that after an initial dropin Δ[tHb] during the ﬁrst minute of exercise, Δ[tHb] during exercise increased up to 60%Wmax, and this blood vol-Figure 6. Relationship between ƒ-Δ[tHb] and [La] during exercise.
The dotted line indicates zero point of ƒ-Δ[tHb]. The solidbold line represents the linear regression line (r=0.933,
p<0.05).
ume expansion was signiﬁcantly correlated with f-Δ[Oxy] and[La]. These results demonstrate that the increased muscle
oxygenation may be caused mainly by increased O2 supply
due to arteriolar vasodilation and capillary recruitment at
lower exercise intensities. Subsequently, no further increasein f-Δ[tHb] were seen at high exercise intensities, probably
because of increased intramuscular pressure, which in turn
may lead to lower muscle tissue oxygenation.
Validity of f-Δ [tHb]
As both Hb/Mb absorb light equally at the same wavelengths,
it is quite difﬁcult to separate the signal between Hb and Mb[9]. In this study, we used a NIRcws device which can measure concentration changes from the initial value at the beginning of the experiment. Total Mb concentration should
not change during each exercise test, unless Mb leaked due
to muscle damage. As the exercise type in the study was not
eccentric contraction at the vastus lateralis muscle, it is suggested that the agonist muscle had less muscle damage andMb leakage. In addition, all of the subjects completed theexercise tests within a day. This implies that Mb concentration in the skeletal muscle should not have changed during
the experimental period. In this study, therefore, we pre-

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Moreover, most of the Hb signal is thought to come fromsmall vessels because large arteries and veins have large Hbconcentrations that absorb all the light [9]. It is unlikely that
increased skin vasodilation affected the f-Δ[tHb] because
Mancini et al [20] suggested that the interaction of skinvasodilation during exercise could be ignored. Therefore,
the changes in NIRcws signals were mostly derived from theabsorption of light in small vessels such as arterioles, capillaries and venules.
Contamination of f-Δ [tHb] measurement from the smallvein

f-Δ[tHb] response

below, venous blood volume remained steady during bicycle
exercise after the initial drop of Δ[tHb] due to mechanicalfactors related to muscle contraction at the beginning of exercise. However, in our study, exercise at work rates higher
than 80%Wmax induced greater lactate accumulation, andincreased fast-twitch ﬁber recruitment. Subsequently, thegreater fast-twitch ﬁber recruitment may have led to higher blood return from capillaries and/or venules. Therefore,
we can not exclude the possibility that f-Δ[tHb] at 80% and
100%Wmax may have been inﬂuenced by the decreased
blood volume from capillaries and/or venules during thebicycle exercise. We suggested that the progressive expansion in Δ[tHb] during continuous exercise below LT should
be used for the purest evaluation of f-Δ[tHb], not the blunted response at higher work rates.

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Relationships of f-Δ[Oxy] and [La] to f-Δ[tHb]

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Upon the initiation of each exercise stage, Δ[tHb] andΔ[Oxy] decreased steeply due to blood redistribution suchthat this decreased Δ[tHb] may have been affected by themuscle pump squeezing blood through the capillaries andsmall vessels (Figure 2). Stick et al. [21] measured venous
pressure at the ankle during bicycle exercise at 50W andfound that when starting the exercise, venous pressure decreased within the ﬁrst minute to a level which remained
constant until the end of exercise. In this study, f-Δ[tHb] wasdeﬁned as changing values of Δ[tHb] from the minimum
values within 15 sec after the start of exercise to the peaklevel later in the exercise bout. Therefore, it is suggested
that after Δ[tHb] decreased as a result of mechanical factors related to muscle contractions at the start of exercise,venous blood volumes were constant during the bicycle exercise at 60%Wmax and below, the point at which [La] started to increase. In other words, any contamination effects
of venules to the measurement of f-Δ[tHb] is thought to be
negligible below the lactate threshold (LT). These results
suggest that the increasing Δ[tHb] caused by exercise continuation below LT may be derived from exercise-induced
functional hyperemia due to dilation of arterioles and/or
capillary recruitment.

Kime R et al – Monitoring of exercise-induced vasodilationSE

sumed that the Δ[tHb] signal came only from Hb and was
not contaminated by the Mb signal.

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Med Sci Monit, 2009; 15(3): CR89-94

It has been reported that exercise-induced increases in blood
ﬂow to skeletal muscle are primarily the result of local vascular control systems within the muscle tissue [2]. In addition, the primary determinant of sustained exercise hyperemia in skeletal muscle is metabolic vasodilation [2]. This
report suggests that metabolites from actively contracting
muscles diffuse into the interstitial space to the resistancearterioles and cause vasodilation and capillary recruitment
demonstrated as f-Δ[tHb]. Because higher exercise intensity
causes increased adenosine, phosphate, CO2 and potassium,and decreased blood PO2 and pH, arteriolar dilation may be
increased by continued exercise [2]. However, at higher exercise intensities, O2 supply to the muscle may be restrictedby mechanical effects due to increased intramuscular pressure [1,22,23]. This implies that at higher exercise intensities the mismatch of O2 supply with increased O2 demand
may lead to muscle tissue deoxygenation (Figure 5).
In this study, f-Δ[tHb] at 80% and 100%Wmax were below
the values at lower work rates. The lower f-Δ[tHb] at higher
work rates may be explained by increased intramuscular pressure. Stick et al. [21] found that at work rates 60%Wmax andWe found a strong negative relationship between f-Δ[tHb]
and [La] (Figure 6). Hogan and Welch [24] reported that
under hypoxic conditions, lactate production is increased
even if muscle O2 consumption is maintained. Recently, somestudies reported a strong positive correlation between blood
lactate level and epinephrine concentration which stimulated glycolysis via cAMP and relates to lactate production[24,25]. Richardson et al [26] suggested that lactate efﬂux
was not related to intracellular PO2, yet the lactate efﬂux was
higher in hypoxia than normoxia. Furthermore, a strong
relationship was found between net lactate efﬂux and arterial epinephrine concentration in hypoxia as well as normoxia. It is suggested that increased [La] during exercise
may be inﬂuenced by elevated sympathetic drive more soin hypoxia. The combination of previous studies with ourown present ﬁndings suggest that at higher exercise intensities, insufﬁcient O2 supply may cause muscle tissue deoxygenation, leading to increased sympathetic drive which may
result in an increase in [La].

CONCLUSIONSThe Δ[tHb] responses during various constant workloads
were measured as an indicator of exercise-induced functional
hyperemia using NIRcws in humans. The Δ[tHb] increased
during exercise below LT and this f-Δ[tHb] was signiﬁcantly correlated with f-Δ[Oxy] and [La]. These results suggestthat f-Δ[tHb] may be derived from dilation of vascular bed
and/or from capillary recruitment. The f-Δ[tHb] could be
used clinically to objectively evaluate changes in the functionof microcirculation from peripheral vascular disease [27]and also from chronic endurance exercise training.
Acknowledgements
The authors thank the subjects who participated in the study.
The authors are also grateful for revision of the manuscriptby Christa Colletti.

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