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Energetics of muscular exercise at work onset: The steady-state approach

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DOI: 10.1007/s00424-002-0991-x · Source: PubMed

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Pflugers Arch - Eur J Physiol (2003) 445:622–628
DOI 10.1007/s00424-002-0992-9

SKELETAL MUSCLE

M. P. Francescato · V. Cettolo · P. E. Prampero

Relationships between mechanical power, O2 consumption,

O2 deficit and high-energy phosphates during calf exercise in humans

Received: 20 March 2002 / Revised: 5 October 2002 / Accepted: 11 November 2002 / Published online: 19 December 2002

Springer-Verlag 2002

Abstract Whole-body O2 uptake (VO2), O2 deficit and Introduction

the concentration of high-energy phosphates (determined
by 31P spectroscopy) in human calf muscle were At the beginning of exercise, O2 uptake (VO2), as
measured during moderate aerobic square-wave exercise measured at the mouth, lags behind the energy require-
of increasing intensity in ten volunteers. Net VO2 (above ment for mechanical work performance, thus giving rise
resting) increased linearly with mechanical power, yield- to a “whole-body” or “gross” O2 deficit, which is repaid at
ing a delta efficiency of 13.1%. “Gross” O2 deficit the end of the exercise. A fraction of the oxygen deficit is
increased linearly with net VO2. The fraction of phos- covered by O2 released from blood and tissues stores. The
phocreatine (PC) split at steady state increased linearly remaining fraction, for exercise intensities below the
with the mechanical power and with the O2 deficit. If the anaerobic threshold, is covered by the splitting of high-
[PC] in resting muscle is known, the slope of the energy phosphates, mainly phosphocreatine (PC). These
regression between PC split and O2 deficit (in millimoles) relationships have been studied extensively in the
yields the P/O2 ratio. To calculate this, the O2 deficit was perfused dog gastrocnemius muscle in situ [13, 15, 20,
corrected for the amount of O2 derived from the body 30].
stores, as obtained from literature data. The value so More recently, the availability of phosphorus magnetic
obtained, for a resting [PC] of 30 mM was 5.9, consistent resonance spectroscopy (31P-MRS) has made it possible
with canonical textbook values. Furthermore, the ratio of to study the concentrations of muscle high-energy phos-
"true" O2 deficit to steady-state VO2 is a measure of the phates in detail and non-invasively also in exercising
time constant of VO2 kinetics at work onset at the muscle humans. Indeed, many studies have been devoted to
level: assuming a monoexponential time course without investigating the relationships between the concentration
time delays it amounted to about 17 s, close to the value of high-energy phosphates and exercise intensity in calf
that can be expected in mammalian muscle at 37 C. [2, 3, 5, 26, 39] or quadriceps [7, 31, 32, 33, 37, 40, 42]
muscles, both at steady state and during rest-to-work or
Keywords Calf exercise · High-energy-phosphates · work-to-rest transients. Whilst steady-state bag collec-
31
P-MR spectroscopy · Oxygen deficit · Body oxygen tions of expired air have demonstrated that the relative
stores [PC] is related to both VO2 and mechanical power [37],
Whipp and coworkers [31, 32, 33, 40] performed breath-
by-breath measurements of gas exchange by using a
modified mass spectrometer system, with the purpose of
comparing VO2 and PC breakdown kinetics.
Although simultaneous data on muscle concentrations
M. P. Francescato ()) · V. Cettolo · P. E. Prampero of high-energy phosphates and VO2 have been acquired in
Dipartimento di Scienze e Tecnologie Biomediche, humans, the relationships between O2 debt incurred at the
Universit degli Studi di Udine, onset or paid at the end of exercise, steady-state VO2,
P.le Kolbe 4, 33100 Udine, Italy concentration of high-energy phosphates in muscle and
e-mail: [email protected] mechanical work have not been investigated. The primary
Tel.: +39-0432-494336 purpose of this paper was thus to study in detail the
Fax: +39-0432-494301
relationships between these variables in the human calf
M. P. Francescato · V. Cettolo · P. E. Prampero muscles at the onset of moderate-intensity, square-wave
M.A.T.I. Centre of Excellence, exercise below the lactate threshold. The ratio between
Universit degli Studi di Udine, PC split and O2 deficit incurred at the onset of moderate
P.le Kolbe 4, 33100 Udine, Italy
 623

aerobic exercise mirrors the P/O2 ratio, since it is a Oxygen consumption measurements
measure of the amount of PC that needs to be split in
VO2 was determined by collecting consecutively the expired air in
order to “spare” a given amount of O2. Therefore, the four different Douglas bags at rest (5 min), during the “on”
second aim of this study was to assess quantitatively the transient (3 min), at steady state (3 min) and during the “off”
P/O2 ratio in exercising human muscles. To do this, transient (5 min). The volume and composition of the expired air
however, the O2 deficit incurred at the onset of exercise, were subsequently determined by means of a dry gas meter (MC-6,
SIM Brunt, Italy), a paramagnetic O2 meter (Oxynos 1-C analyser,
as measured, had to be corrected for the amount of O2 Leybold Heraeus, Switzerland) and an infrared CO2 meter (Binos 1
released from the body O2 stores, as obtained from the CO2 analyser, Leybold Heraeus). The gas analysers were calibrated
literature. frequently during the experiments using gas mixtures of known
composition. The mean VO2 and CO2 production (VCO2) during
each collection period were then calculated according to standard
open-circuit algorithms and the values expressed for standard
Materials and methods conditions (STPD).

Subjects
NMR imaging
Ten healthy adults (six men and four women, mean age
27.3€1.0 years) volunteered after having been thoroughly informed In a separate experimental session, leg muscle volumes were
about the aims and methods of the protocol. The mean height and determined using a standard body coil. Axial images of both legs
body mass of the subjects were 1.77€0.04 m and 72.8€4.4 kg, were obtained every 8.4 mm from the knee to the feet by using a
respectively. All subjects were healthy and moderately active, but multislice Spin Echo T1 weighted sequence (field of view 330 mm,
none was highly trained. The study was approved by the local 256256 pixel resolution). All images were exported to a work-
Ethics Committee. station for subsequent analysis. Two regions of interest (ROI), one
for each leg, encompassing the entire plantar flexor (PF) compart-
ment (including all muscles, connective tissue and vessels) were
Experimental setup drawn manually for each slice. For each leg, the PF volume was
calculated for each slice by multiplying the corresponding ROI area
The experiments were performed in a standard whole-body (i.e. PF cross-sectional area) by the proper slice thickness. Total leg
Magnetom SP 4000, 1.5 T scanner (Siemens, Erlangen, Germany) PF volume was calculated as the sum of individual slice volumes
located at the Radiology Unit of the School of Medicine of the from the tibial tuberosity to the ankle. All image processing was
University of Udine (Italy). Subjects lay in a supine position on a completed by the same investigator to eliminate interobserver bias.
variable-resistance calf ergometer built for in-magnet exercises, Total PF mass was calculated assuming a muscular density of
described in detail in [17]. Each experimental session consisted of 1.056 g/ml [41].
three trials of increasing intensity, separated by 5 min rest. Each
trial consisted of 5 min rest, 6 min exercise and 5 min recovery. The
interval between the end of one bout of exercise and the start of the Data treatment
next was thus 15 min. The exercises consisted of repeated
synchronous plantar flexions of both feet of about 30 at 0.83 Hz Spectroscopy data were analysed off-line using the magnetic
(imposed by a metronome), with the knee extended. In subsequent resonance user interface (MRUI) software [28, 29]. Signal inten-
trials, the exercise intensity was changed by changing the force sities and position of PC and inorganic phosphate (Pi) spectral
acting on the pedals (see [17]). Adjustable straps and belts peaks were calculated by means of the time-domain VARPRO/
maintained the subjects’ feet and body in the appropriate position minpack fitting program, using the appropriate starting values and
on the pedals and on the main frame, thus minimising unwanted without any prior knowledge. The first FID of each trial was
movements and muscle contractions. During all trials simultaneous discarded and no other correction for partial saturation was made,
measurements of mechanical power, VO2 and 31P spectroscopy assuming that the subsequent T1 relaxation of PC and Pi remained
were performed. Actual mechanical power was calculated from the constant throughout the exercise. PC signals were averaged over
outputs of the force and displacement transducers of the ergometer the 4 min rest to obtain the pre-exercise control value (PCr), while
(see [17] for details). the mean of the three steady-state values was considered as the
exercise value (PCs). Subsequently, the amount of PC split will be
expressed as a fraction of the resting value:
Magnetic resonance spectroscopy
PC r
PCs
DPC s =PC r ¼
31
P-MR spectra were acquired from the triceps surae by using a PCr
surface coil of 5 cm diameter positioned on the middle of the For each FID, intracellular pH was calculated from the equation [1,
medial belly of the gastrocnemius muscle of the right leg. The 38]:
magnetic field homogeneity was adjusted by manual global

shimming on the proton signal of tissue water until the peak was d
3:27
approximately Lorentzian in shape; the resulting mean peak width pH ¼ 6:75 þ log
5:69
d
at one-half maximum was 0.31€0.07 parts per million (ppm). After
switching to 31P, 16 spectra were acquired continuously throughout where d is the chemical shift of the Pi spectral peak relative to PC
the trials (5 at rest, 6 during exercise and 5 during recovery). A (in ppm).
sequence of radio-frequency impulses of 25.7 MHz were applied For each trial, the respiratory exchange ratio (RER) was
from the coil. 31P-MR free induction decay (FID) signals were calculated from VO2 and VCO2 and net VO2 (DVO2s) was
obtained in 2048 complex data points with a dwell time of 250 ms. determined as VO2 at steady state above resting. Moreover, the
Data were collected every 6 s and time-averaged over nine O2 deficit incurred at the onset of exercise was calculated as the
acquisitions obtaining a final time resolution of 1 min. The spectral difference between the amount of O2 consumed during the on-phase
signal-to-noise ratio was on average 11.5 dB, as calculated from the (of 3 min duration) and that consumed during an equal period at
estimated amplitudes and damping factors by the VARPRO steady state. Similarly, the O2 debt paid in recovery was calculated
software. from the difference between the amount of O2 consumed during the
off-phase (of 5 min duration) and that consumed during an equal
624
period of pre-exercise rest. The average of the two calculated
values was assumed to represent the whole-body oxygen deficit
incurred at the onset of exercise (O2def). This last was corrected for
the amount of O2 derived from the body stores, as obtained from
literature data, yielding the “net” O2 deficit (see the Appendix for
details).
Values are expressed as means€SEM; regressions were calcu-
lated by the least-squares method using a commercially available
statistics package (SPSS, Chicago, Ill., USA).

Results
The average overall VO2 at rest and at steady state during
the three exercise intensities was 0.25€0.01, 0.31€0.02, Fig. 1 Net oxygen consumption at steady state (DVO2s, ml/min/kg,
0.37€0.03 and 0.49€0.03 l/min respectively, the corre- left ordinate or W/kg, right ordinate) as a function of mechanical
sponding mechanical power of the three exercise levels power (Ws, W/kg); both parameters are expressed per unit of active
muscle mass. Regression refers to the left ordinate; 1 mlO2 was
being 1.69€0.20, 4.71€0.47 and 9.45€0.52 W respective- assumed to yield 20.4 J (respiratory quotient of 0.86)
ly. The mass of the plantar flexor (PF) muscles (sum of
both legs) was 2.48€0.19 kg. Mean mechanical power, net
VO2, RER and O2 deficit are reported in Table 1, together
with the fraction of PC split at steady state and the
intracellular muscle pH. Mechanical power, VO2 above
resting and O2 deficit are expressed per unit active muscle
mass. Intracellular pH was not affected by the exercise
within the investigated work range, nor did it change
during the first minutes of recovery.
Net steady-state VO2 (DVO2s, millilitres/minute/kilo-
gram), increased with the mechanical power (Ws, watt/kg)
as illustrated in Fig. 1. The relationship between the two
variables is described by the function DVO2s= 7.01+
22.52·Ws (n=30, r2=0.907). The reciprocal of the slope of
this regression represents the delta efficiency (Dh), which,
assuming an energy equivalent of 20.4 J/mlO2, was Fig. 2 The fraction of phosphocreatine split at the steady state of
13.1%. exercise (DPCs/PCr) increases linearly with the mechanical power
The fraction of PC split at steady-state exercise (DPCs/ (Ws, W/kg) expressed per unit active muscle mass
PCr) increased with the mechanical power per unit
active muscle mass, as illustrated in Fig. 2. The relation- grossO2 deficit, and O2def=5.55+0.282·DVO2s (n=30,
ship between PC split and power (Ws) is described by r2=0.745) for net O2 deficit (Fig. 3).
the relationship DPCs/PCr=0.0596+0.0625 Ws (n=30, Figure 4 shows the fraction of PC split as a function of
r2=0.741). Both the individual gross O2 deficit the net O2 deficit (i.e. gross O2 deficit corrected for the O2
(grossO2def, millilitres/kilogram, solid dots) and the net stores). If the O2 deficit is expressed in millimoles/
O2 deficit (O2def, millilitres/kilogram, open dots) were kilogram of active muscle, the corresponding relationship
related linearly to DVO2s according to the functions: is described by: DPCs/PCr=0.0113+0.194·O2def, (n=30,
grossO2def= 9.43+0.801·DVO2s (n=30, r2=0.904) for r2=0.848).

Table 1 Average mechanical power, net oxygen consumption three exercise intensities. When appropriate, data are normalized
(DVO2), respiratory exchange ratio (RER), O2 deficit, fraction of according to the active muscle mass. Means€SEM, n measure-
phosphocreatine split (DPCs/PCr, where the superscripts s and r ments. Range of mechanical power is also indicated
indicate steady state and rest respectively), pH at rest and for the
Rest Very low Low Medium
n 30 10 10 10
Mechanical power (W/kg) – 0.72€0.11 1.99€0.25 3.94€0.26
Power range (W/kg) – 0.47–1.62 1.30–3.60 2.59–5.61
Net VO2 (ml/min/kg) – 24.05€2.73 49.24€6.17 97.42€7.33
RER 0.94€0.05 0.84€0.04 0.85€0.04 0.89€0.03
Gross O2 deficit (ml/kg) – 27.96€2.94 50.41€6.42 86.71€6.69
DPCs/PCr – 0.09€0.01 0.18€0.02 0.32€0.02
pH 7.06€0.01 7.06€0.01 7.07€0.02 7.06€0.02
 625

change during the first minutes of recovery [22].

However, the work intensities were fairly high for this
type of muscle group. Indeed, the highest steady-state
(over 6 min) mechanical power for both limbs was
9.4€0.5 W, which is very close to the maximum power
sustainable without lactate production, the latter being
4.8 and 4.6 W (one leg only) under similar experi-
mental conditions [26, 35]. Additional evidence for the
intensity of exercise remaining within the aerobic
range was the observation that, even at the highest
work loads, [PC], after the initial 3 min, remained
stable until the end of the exercise.
Fig. 3 “Gross” O2 deficit (ml/kg, solid dots and upper regression)
and net O2 deficit (ml/kg, open dots and lower regression) incurred
at the onset of exercise as a function of the net O2 uptake at the Work efficiency
steady state of exercise (DVO2s, ml/min/kg); both parameters are
expressed per unit of active muscle mass The delta efficiency Dh of 13.1% calculated from the
present data, whilst being substantially lower than that
observed on the cycloergometer (about 20–22%, see
e.g. [18, 23]), is a fairly reasonable value for this type
of ergometer, with which a certain amount of negative
work is inevitably performed [17]. Indeed, calculation of
muscle O2 uptake from direct measures of calf blood flow
and arterio-venous O2 difference yields an efficiency of
13.6% [8], which is essentially equal to the present value.

PC splitting and work intensity

To the authors’ knowledge, only one group has reported

the percentage of resting PC split as a function of power
Fig. 4 The fraction of phosphocreatine split at the steady state of [5, 6]. Those data are, however, difficult to compare with
exercise (DPCs/PCr) increases linearly with the net O2 deficit the results of the present experiments, since the anthro-
expressed per unit active muscle mass. When the O2 deficit is
expressed in mmol/kg active muscle, the slopes of the regression pometrical characteristics of the subjects were not
lines have the meaning of the P/O2 ratio. The two dashed lines reported. Assuming that the mechanical power output
represent the theoretical iso-P/O2 lines corresponding to a P/O2 was equal for the two legs and that the average active
ratio of 5.9 for the indicated [PC] in resting muscle (see text for muscle mass was the same as in the present study (i.e.
details)
2.48 kg), the average value of all the individual slopes
reported in [6] is 6.25%/W per kg muscle (excluding the
highest two figures that yield an unreasonably high value
Discussion
of PC split/W). This is equal to the slope of the regression
Exercise intensity line between PC split and work rate obtained in the
present work (Fig. 2).
Our ergometer allows us to determine the mechanical
work and power with great accuracy [17]. We therefore
decided to spread the mechanical power data over the Relationship between O2 deficit and VO2
entire range of work intensities (see Fig. 1), rather than
having repetitions of a few intensities. Thus, no repeti- The slope of the regression between gross O2 deficit and
tions of the same workload were performed by the same DVO2s (Fig. 3, solid dots) is the so-called mean response
subject. time of the VO2 on-response, which, if it is assumed that
One of the purposes of the present study was to at the onset of exercise the time course of the O2 uptake,
describe in humans the relationships between mechanical as measured at the mouth, can be described by a
power, VO2 and O2 deficit at the onset of moderate, monoexponential function without time delay, is the time
square-wave exercise performed with the calf muscles at constant of O2 uptake kinetics at the mouth (tm; see
work rates below the lactate threshold. This goal was Appendix). This was 48.1 s, corresponding to a half-time
achieved, since the intracellular pH, as determined from of 33.3 s (t1/2=tmln 2), not dissimilar from that reported by
31 McCreary et al. [26], who, under similar experimental
P chemical shift during all three exercise intensities, did
conditions, obtained an average value of tm=41.9 s (when
not differ significantly from rest (Table 1) nor did it the highest value reported by those authors is discarded).
626
Table 2 The average, overall gross and net O2 deficits, together Relationship between PC split and O2 deficit
with the amounts of O2 released from pulmonary, venous blood and
Very low Low Medium The slope of regressions such as reported in Fig. 4
represents the relative change of PC brought about by the
n 10 10 10 contraction (or payment) of a given amount of O2 deficit/
Gross O2 deficit (ml) 69.3€9.5 125.4€18.8 211.7€19.3
Lung O2 stores (ml) 16.9€3.0 33.5€7.3 63.0€9.0 debt. If the latter is expressed in millimole/kilogram, the
Blood O2 stores (ml) 23.0€3.1 39.6€7.0 65.7€6.7 slope of the regression of DPCs/PCr on O2def, i.e.
O2 released from 0.3€0.0 0.7€0.1 1.5€0.2 0.194 mmol1, has the meaning of the traditional P/O2
myoglobin (ml) ratio if the O2 debt payment is considered, or of its mirror
Net O2 deficit (ml) 29.2€5.9 51.6€8.4 81.5€8.8
image if the O2 deficit is considered. Indeed, in this latter
case, a certain amount of O2 is “spared” because of the
splitting of a given amount of PC. However, to calculate
Depletion of O2 stores and O2 deficit the P/O2 ratio in absolute terms, the change of [PC] must
also be expressed in millimole/kilogram. This can be
At the onset of exercise, a certain fraction of the amount easily done by multiplying the obtained slope by [PCr],
of O2 utilized by the working muscles is derived from O2 i.e. by the [PC] in resting muscle. The [PCr] values
derived from lungs, blood and muscle O2 stores. Thus, reported in the literature vary widely, ranging from 17.8
since it can be safely assumed that in the present study no to 37.7 mmol/kg [2, 9, 16, 19, 21, 34, 39]. This great
lactic acid was produced, as shown by the absence of pH variability is probably due to the different methods by
changes, the whole-body O2 deficit, as calculated, is the which these values were determined. Generally, lower
sum of the amount derived from O2 stores changes and of values are found when [PC] is assessed from muscle
the “true” O2 deficit. In turn, the true O2 deficit is the O2 biopsies, since some artefactual PC breakdown between
equivalent of the amount of PC split at the onset of sampling and freezing is likely. Conversely, very high
exercise before a steady state is reached. It should be also values are obtained when [PC] is estimated from the area
pointed out that the true O2 deficit can not be repaid under the peak of PC as compared to the sum of the areas
during the exercise (for a review see [24]), a fact that is under the three peaks of ATP, in turn assumed to have a
also supported by the essential identity of the gross O2 predetermined concentration. Under these conditions, the
deficit incurred at work onset and of the gross O2 debt major sources of error are linked to the manual integration
paid at work offset (see Results). The amount of O2 of all the peaks and to the assumed [ATP]. The two
derived from the depletion of O2 stores during the rest to dashed lines in Fig. 4 represent the theoretical lines
work transient was calculated from data obtained in other corresponding to a P/O2 ratio of 5.9 when the PC
studies under similar experimental conditions (see Ap- concentration is assumed to be equal to the lowest
pendix) and is reported in Table 2 for the three work (17.8 mmol/kg) or to the greatest (37.7 mmol/kg) values
intensities. This table shows that the fraction of the reported above. A theoretical P/O2 ratio of 5.9 was chosen
whole-body O2 deficit covered by the O2 stores is since this value can be calculated from the average RER
relatively high, being on average 59.4€2.1%, the major value (i.e. 0.86) obtained in the present investigation,
contributions being derived from the pulmonary and assumed to be equal to the metabolic respiratory quotient
venous blood stores (43.9€2.1% and 55.0€2.1% of total, ([12], p. 169). The net O2 deficit data reported in Fig. 4
respectively). Even if the calculated O2 stores changes fall between the above two limits. If it is assumed that the
reported in Table 2 should be regarded with some caution, P/O2 ratio was indeed 5.9, the [PC] in resting muscle can
we consider them to represent a reasonable estimate of the be calculated to be 30.4 mmol/kg, a reasonable value,
amount of O2 released at work onset under the present indeed. In spite of the uncertainties introduced in the
experimental conditions. On this basis, therefore, the calculation by the indirect estimate of the changes in O2
overall gross O2 deficit was corrected to obtain the net O2 stores (use of mean values of the literature instead of
deficit, representing the O2 equivalent of PC splitting at individual measured parameters), the agreement with
work onset. This is reported in Fig. 3 (open dots) as a canonical textbook values seems worth emphasizing.
function of steady-state VO2 above resting (DVO2s). If it is In conclusion, the present experimental results and
assumed that the kinetics of VO2 at the muscle level at the calculations support the view that at the onset of square-
work onset can be described by a monoexponential wave aerobic exercise in humans, the O2 uptake at the
function, the slope of the regression between net O2 muscle level can be described by a monoexponential
deficit and DVO2s is the time constant of the O2 uptake function with a time constant of about 17 s. The resulting
kinetics at the muscle level. The value obtained, 16.9 s, is O2 deficit is covered by the splitting of PC with a P/O2
close to the 24 s determined in the perfused dog ratio close to 6.0.
gastrocnemius in situ [30].
Acknowledgements This research was supported by funds from
the Ministero dell’Universit e della Ricerca Scientifica (COFIN
1998, main investigator Prof. P.E. di Prampero).
 627
v
Appendix The changes in the venous blood stores (DO2S ) can be
estimated from the product of the venous blood volume
As a first approximation, during aerobic exercise of (VBV) and the change between the arterio- to mixed
moderate intensity, the O2 uptake (VO2) at the onset of venous blood oxygen difference at steady state:
exercise is a monoexponential function of time: [D(CaCv)s] and that prevailing at rest [D(CaCv)r], i.e.:
    
V O2 ðtÞ ¼ V Or2 þ D V Os2  1
e
t=tm DO2 Sv ¼ ½DðCa
Cv Þs
DðCa
Cv Þr   VBV
"  !  !#
where VO2r and DVO2s are the resting and the net steady- V Os2 V Or2
state VO2, respectively and tm is the time constant of the ¼ 
  VBV
process, as measured at the mouth. The O2 deficit Qs Qr
(grossO2def) incurred at the onset of exercise can thus be where Qs and Qr are the cardiac outputs at steady-state
calculated as: during exercise and at rest, respectively. VBV was
Z 1 assumed to be 65% of the total blood volume, in turn
 
def
grossO2 ¼ D V Os2  e
t=tm dt ¼ D V Os2  tm assumed to represent (in litres) 7% of body mass (in
0 kilograms) [36]. Q corresponding to the individual
Thus, the slope of the regression of DVO2s on O2 mechanical powers investigated in the present work was
deficit is the time constant of O2 uptake kinetics at the estimated from the data for calf exercises similar to the
mouth. In all subjects, the individual regressions between present ones [8]. This allowed us to determine the linear
grossO2def and DVO2s were characterized by r>0.980 relationship between Q (litres/minute) and mechanical
(n=3) and the average tm was 41.8 s (see Fig. 3, solid power (Ws, watt) as: Q=0.40Ws+5.84 (n=5, r2=0.945).
dots). At the onset of moderate aerobic exercise below the Thus, the individual DO2Sv values were obtained from the
anaerobic threshold, the grossO2def is covered by the net appropriate VO2 and Q values, the latter being derived
O2 deficit, i.e. the amount of energy in O2 equivalents from the corresponding mechanical power on the basis of
derived from PC splitting (O2def), plus the amount of O2 the above equation. They are reported in Table 2 for the
derived from the body stores (DO2S), i.e.: grossO2def= three exercise conditions.
O2def+DO2S. Thus, a prerequisite for the calculation of the The myoglobin desaturation for exercise intensities
net O2 deficit (O2def) is knowledge of DO2S. comparable to those of the present work was estimated
For all subjects and trials, we therefore estimated the from the data reported in [27]. These allowed us to
changes of whole-body O2 stores. These comprise mainly calculate the relationship between percentage deoxymyo-
the amounts of O2: i) contained in the lungs, ii) contained globin (%deoxyMb) and mechanical power (Ws):
in the venous blood and iii) bound to muscle myoglobin %deoxyMb=2.09Ws+14.2 (n=4, r2=0.968). Subsequently,
[11, 12, 14]. Thus, the corresponding changes during the knowing the individual mass of the plantar flexors (PF)
rest-to-work transients, or vice versa, yield the amount of and assuming a myoglobin concentration of 4.46 g/kg wet
O2 consumed by the muscles at work onset, but not “seen” muscle [25] and a binding capacity of 1.34 mlO2/g
at the mouth, or taken up at the mouth at work offset, but myoglobin, it was possible to estimate the extra amount of
not consumed by the muscle. oxygen released by myoglobin desaturation changes from
The changes in the pulmonary oxygen stores (DO2Sp) rest to exercise (DO2Sm) as: DO2Sm=(2.09·Ws/100)·4.46·
can be estimated from the difference between the time 1.34·(PF mass). The net or true oxygen deficit was finally
constant of VO2 measured at the mouth (tm) and that estimated for any given work load by subtracting the three
measured at the alveolar level (tp): changes in oxygen stores from the whole-body oxygen
 deficit: O2def=grossO2defDO2SpDO2SvDO2Sm. The in-
DO2 Sp ¼D V Os2  ðtm
tp Þ dividual DO2Sm and O2def values are also reported in
According to McCreary et al. [26] the time constant of Table 2 for the three exercise conditions.
the O2 consumption adjustment at the onset of calf
exercise, calculated at the alveolar level on a breath by
breath basis, is 41.9 s (ignoring the highest value reported References
by those authors). However, according to Cautero et al.
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