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Copenhagen Muscle Research Centre, Rigshospitalet, DK-2200 Copenhagen N, Denmark
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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It is not known whether the diameter of peripheral conduit arteries may impose a limitation on muscle blood flow and oxygen uptake at peak effort in humans, and it is not clear whether these arteries are dimensioned in relation to the tissue volume they supply or, rather, to the type and intensity of muscular activity. In this study, eight humans, with a peak pulmonary oxygen uptake of 3.90 ± 0.31 (range 2.29-5.03) l/min during ergometer cycle exercise, performed one-legged dynamic knee extensor exercise up to peak effort at 68 ± 7 W (range 55-100 W). Peak values for knee extensor blood flow (thermodilution) and oxygen uptake of 6.06 ± 0.74 (range 4.75-9.52) l/min and 874 ± 124 (range 590-1,521) ml/min, respectively, were achieved. Pulmonary oxygen uptake reached a peak of 1.72 ± 0.19 (range 1.54-2.33) l/min. Diameters of common and profunda femoral arteries determined by ultrasound Doppler were 10.6 ± 0.4 (range 8.2-12.7) and 6.0 ± 0.4 (range 4.5-8.0) mm, respectively. Thigh and quadriceps muscle volume measured by computer tomography were 10.06 ± 0.66 (range 6.18-10.95) and 2.36 ± 0.19 (range 1.31-3.27) liters, respectively. The common femoral artery diameter, but not that of the profunda branch, correlated with the thigh volume and quadriceps muscle mass. There were no relationships between either of the diameters and the absolute or muscle mass-related resting and peak values of blood flow and oxygen uptake, peak pulmonary oxygen uptake, or peak power output during knee extensor exercise. However, common femoral artery diameter correlated to peak pulmonary oxygen uptake during ergometer cycle exercise. In conclusion, common and profunda femoral artery diameters are sufficient to ensure delivery to the quadriceps muscle. However, the common branch may impose a limitation during ergometer cycle exercise.
exercise; hyperemia; ultrasound Doppler
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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EXTENSIVE STUDIES have been performed to elucidate the factors that limit skeletal muscle blood flow and oxygen uptake at peak effort in humans. Although cardiac output may impose the limitation during whole body exercise, oxygen delivery is not thought to be limiting during exercise with a small muscle group (3, 20-22, 24). Peripheral factors such as local blood flow, oxygen diffusion and extraction, or mitochondria may then be of greater importance. Support for this notion is found in the markedly higher oxygen content in veins draining intensively contracting small muscle groups compared with ordinary bicycle exercise or running (2).
Diameter measurements of peripheral conduit arteries in humans indicate that large variations exist, even after normalization for body size. This appears to be related in part to training, because in some athletic groups adaptations have been found in the vessels that supply the muscles specifically utilized in their activity (7-9). Moreover, the common femoral artery diameter has been shown to correlate with peak pulmonary oxygen uptake (11). This suggests that the size of peripheral conduit vessels may be a limiting factor for the oxygen supply at peak effort.
It is not clear, however, whether the diameter of peripheral conduit arteries is sufficiently dimensioned in relation to the limb volume that they supply or whether the diameter may limit peak blood flow to and oxygen uptake in human skeletal muscle. Knowing that the common and profunda femoral artery supply the leg and the knee extensor muscle group, respectively, we investigated whether there was an association in humans between the diameter of these branches and knee extensor and thigh volume as well as peak muscle blood flow and oxygen uptake, especially during one-legged knee extensor exercise.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects. Eight healthy human subjects, seven men and one woman, with mean ± SE (range) age of 25.4 ± 1.5 (22-35) yr, height of 177.8 ± 3.1 (158-186) cm, and weight of 77.8 ± 4.9 (49-98) kg, volunteered to participate in this study. The subjects' engagement in exercise training varied from daily activities to regular endurance training. Before the experiments the subjects were informed about the experimental procedures, the potential risks and discomfort, and that they could withdraw at any time. They participated after signed informed consent. The experiments were carried out with the approval of the Ethical Committees of Copenhagen and Fredriksberg, Denmark (KF-01-403/95).
Experimental procedures. Before the experiments all subjects were familiarized with the one-legged dynamic knee extensor exercise model (1) by training at 60 rpm until they were comfortable and could fully relax the hamstring muscles, so that the work was done solely by the knee extensors (1, 19). Peak power output (PPO) was determined by an incremental test starting at 10 W and increasing by 5-10 W every third minute until the subjects could no longer keep the rhythm of 60 rpm.
The subjects reported to the laboratory in the morning of the experimental day. The femoral artery and vein of one leg were cannulated under local anesthesia (Lidokain, 20 mg/ml, Sygehus Apotekerne, Copenhagen, Denmark). The arterial (Ohmeda) and venous (Cook) catheters were inserted in the proximal direction ~2-5 cm below the inguinal ligament. A thermistor (model 94-030-2.5F, T. D. Probe, Edwards Edslab, Baxter, Irvine, CA) was inserted in the venous catheter and connected to a cardiac output computer (model 9520A, American Edwards Laboratories, Harvard Apparatus, Irvine, CA) for thermodilution blood flow measurements (2). A Harvard mechanical syringe pump (model 44, Harvard Apparatus) was used for constant infusion of saline solution at ~0°C. Arterial and venous blood samples were taken and analyzed for hemoglobin, oxygen saturation, PO2 (AVL 912 CO-Oxylite, AVL Medical instruments, Schaffhausen, Switzerland) and hematocrit. Limb oxygen uptake was calculated by multiplying the blood flow measurements in the femoral vein (outflow) by the arterial and venous difference in oxygen content (Ficks' principle). Heart rate (electrocardiogram) and intra-arterial blood pressure were recorded from a Kone Patient Data Monitor 565A (Medicoline, Valby, Denmark). The knee extensor force was measured with a strain gauge attached to the ergometer lever arm. All variables were recorded on a Gould recorder (model TA200, Gould) or on a personal computer (IBM compatible Pentium based). Pulmonary oxygen uptake (
O2 pulm)
was determined by a CPX Medical graphics instrument (Spiropharma A/S,
Klampenborg, Denmark). Leg vascular conductance
(VCleg) was calculated from the
formula leg blood flow
(
leg) = VCleg · 
P,
where P (pressure gradient) is assumed to be equal to mean arterial
pressure (MAP).
In the experiments, the subjects exercised for ~10 min at an absolute
workload of 30 W and then for 5-7 min at a relative workload
corresponding to ~75-80% of their individual PPO. The relative
workload was included as a comparison to PPO to ensure that each
subject reached his or her peak intensity. The subjects then rested for
~30-40 min before performing an experimental ramp protocol
starting at 20-30 W for 3 min and increasing by 5 W every 30 s up
to PPO. PPO was defined as the highest workload at which the subject
could maintain the pace for at least 1 min. Measurements of blood flow
and
O2 pulm
as well as sampling of blood were performed at rest and during
steady-state exercise as well as during the last minute at peak intensity.
On another experimental day, the peak
O2 pulm
of the subjects was determined during exercise on a Monark ergometer
cycle at 80 rpm. The subjects warmed up for 5 min at a light workload of 40 W. The load was thereafter raised by 40 W every 2.5 min until
near exhaustion and thereafter every 1 min to exhaustion.
Femoral artery diameter measurements.
The equipment and procedures of measurements were reported previously
(16). In brief, the instrument used was an ultrasound Doppler (model
CFM 800, Vingmed Sound, Horten, Norway) equipped with an annular phased
array transducer (APAT, Vingmed Sound) probe (11.5-mm diameter)
operating at an imaging frequency of 7.5 MHz. The femoral artery was
insonated (direction of ultrasound waves at site of measurement) distal
to the inguinal ligament at a fixed perpendicular angle. The diameters
of the common femoral artery
(DCFA) and its
superficial
(DSFA) and
profunda (DPFA)
branches were measured from longitudinal two-dimensional images stored (at a frame rate of 25 frames/s) in the ultrasound Doppler image buffer
and on optical disks. A time-averaged diameter
[D = D(systole1/3) + D(diastole2/3)]
based on the relative periods of the systolic (1/3) and diastolic (2/3)
blood pressure phases was assumed to be the most representative
diameter size (16). The diameters were determined along the central
axis of the ultrasound beam, where the best spatial resolution is
achieved. The best theoretical axial resolution corresponds to ~0.1
mm, i.e., one-half the spatial wavelength [
= c/(f), where
c is velocity of sound in soft tissue (1,540 m/s) and f is imaging frequency (7.5 MHz)] (5). This also
corresponds to the mean coefficient of variation within subjects of
~1% previously observed for the common femoral artery (16). Moreover, the diameter size during the day of the knee extensor exercise and during the day of the ergometer cycle were the same [P = not significant
(NS)].
Tissue volume measurements. A computer tomograph (CT; model Prospeed VX, General Electric CGR, Paris, France) was used to obtain precise estimates of muscle tissue volume and mass (17). A total of 21-25 serial segments, with a 10-mm thickness, were obtained every 20 mm along the thigh, starting distal from patella and going in the proximal direction toward the spina iliaca anterior superior. The volume of the quadriceps muscle was calculated from the mean area of two neighboring sections multiplied by the section distance, summed over the length of the muscle. The muscle mass of the CT measurements were calculated assuming a muscle tissue density of 1.049 kg/l (14).
Statistical analysis. Parametric statistics were used for data analysis. Analysis of variance for repeated measures was used when comparing more than two data groups and Tukey highly significant difference post hoc tests to distinguish where the differences were. Linear regression and Pearson correlation were employed. A P value < 0.05 was considered statistically significant. A nonstatistically significant comparison is indicated by P = NS. The values given in the text are means ± SE.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Femoral artery diameter.
DCFA averaged
10.6 ± 0.4 (range 8.2-12.7) mm (Fig.
1), which was ~58 and 76% larger than
DSFA and
DPFA,
respectively (P < 0.002).
DSFA averaged 6.7 ± 0.3 (range 5.5-8.2) mm, which was ~11% larger than
DPFA, averaging
6.0 ± 0.4 mm (range 4.5-8.0) (P < 0.05).
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Knee extensor exercise.
Table 1 shows the exercise- induced
increase (P < 0.05) in heart rate,
MAP, leg,
VCleg, and leg oxygen uptake
(O2 leg), as well as
O2 pulm.
At peak effort, a load of ~68 ± 7 W (range 55-100 W)
was achieved. Muscle perfusion and
O2leg
reached values at peak effort of ~249 ± 27 (range
149-373) and 36 ± 4 (range 23-60)
ml · min
l · 100 g1, respectively, based on
the CT-determined muscle mass of 2.48 ± 0.20 (range 1.37-3.43)
kg. Thigh and quadriceps muscle volume measured by CT were 10.06 ± 0.66 (range 6.18-10.95) and 2.36 ± 0.19 (range 1.31-3.27)
liters, respectively.
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KE and
O2 KE),
or to the absolute and body mass-related values at rest and peak effort
of
O2 pulm,
or to PPO. Moreover, PPO did not correlate with quadriceps muscle mass or thigh volume. However, PPO correlated with peak
KE, peak O2 KE,
and peak
O2 pulm
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Ergometer cycle exercise.
At PPO of 345 ± 21 W (range 280-420 W) a peak
O2 pulm
of 3.90 ± 0.31 (range 2.29-5.03) l/min was reached. This was
significantly higher (P < 0.05) than
during one-legged knee extensor exercise. DCFA (mean of
right and left) correlated with peak
O2 pulm
(r = 0.91, P < 0.002) (Fig.
3) but not with the body mass related-peak value or the absolute or body mass-related
O2 pulm
at rest. Moreover,
DCFA did not
correlate with PPO, although PPO correlated with peak
O2 pulm
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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This study demonstrates that the size of the vessels feeding the knee
extensor muscle during exercise are of sufficient size not to
compromise blood flow or impose a limitation even at peak intensities.
This is true for
DCFA as well as
for DPFA, the
diameter of the supplier of blood to this specific muscle group. This
is also in agreement with the finding that
DCFA does not
alter in size during this type of exercise (16). In contrast, the
correlation between
DCFA and the
tissue that it supplies and the close relationship between
DCFA and peak
O2 pulm
during ergometer cycle exercise suggest that the dimension of this
artery could be a critical factor for limiting blood flow, and thus
also oxygen delivery, to the whole limb during ergometer cycle exercise.
In addition, the lack of correlation between
DCFA and PPO
during ergometer cycle exercise, in contrast with the correlation of
PPO with peak
O2 pulm,
may reflect the role of an anaerobic energy yield during an incremental
exercise test. The correlation between PPO and peak
KE, peak
O2 KE,
as well as peak
O2 pulm during one-legged dynamic knee extensor exercise further supports the
notion that the quadriceps muscle is hyperperfused in this exercise
mode (2). Thus a situation is induced in which oxygen in the muscle is
available in excess also during intensive exercise. This allows the
oxidative enzyme oxogluturate dehydrogenase to have a limiting role for
peak O2 by the muscle, as
previously suggested (4).
Laminar or turbulent flow.
Indications that the femoral arteries are not limiting can also be
deduced from estimating the flow magnitude an artery can accommodate at
various pressure gradients and whether the flow persists to be laminar.
This flow () can under different pressure gradients
(P) be estimated from Poiseuille's law = [(
· r4)/(8 · 
· L)] · P,
where a Newtonian fluid with viscosity flows under laminar and
steady-state conditions in a cylindrical hollow tube, with rigid walls,
a length L, and a radius
r. If the full atmospheric pressure
"falls" over such a tube, flows in the range of ~22-120
and ~4-19 l/min could be achieved in tubes with dimensions
similar to the smallest (8.2 mm) and largest (12.7 mm)
DCFA and the
smallest (5.5 mm) and largest (8.0 mm)
DPFA, respectively. Extrapolation to in vivo conditions thus suggests that
the conduit artery diameters are overdimensioned to ensure regional delivery.
/ = ( · D · /)/[6 × 104(D/2)2] = 5.623 · /D,
where v is the velocity of the fluid,
assuming a density () of 1.06 kg/l and a viscosity () of 4 × 103
kg · m1 · s1,
with the blood flow () in liters per minute and the
diameter (D) in meters.
Extrapolating to in vivo conditions, given that the inflow of blood to
the quadriceps muscle in the common femoral artery corresponds to the
outflow of blood in the femoral vein (16), it is evident that such a
critical level could be reached. However, "The Re number is not a
reliable index of the factors that tend to produce turbulence in vivo
and nondisturbed flow persists even when Re numbers computed rise above
the critical steady flow values" (13). In fact, the pulsatile flow,
induced by the cardiac cycles as well as the contraction-relaxation
duty cycles (16, 18), interferes with the time required for vortexes to
develop and propagate, and it is not enough that a threshold level is
exceeded. Moreover, the Re number is a collective property of the whole
cross section and does not take into account the changing relative
velocities of different laminae in pulsating flow. The pulsatile flow
is therefore "protective" and more stable than steady-state flow.
Indeed, Attinger et al. (see Ref. 13) actually found pulsatile flow
that was laminar up to a mean Re number of at least 7,900.
In the present study we focused on young, healthy subjects in whom no
vascular irregularities were apparent. Also, even though the blood
velocity in the common femoral artery is markedly affected by the
intramuscular pressure variations during this type of exercise, with
the pulse pressure as a superimposed influence, the blood flow pattern
is well defined, stable, and of strong intensity (16, 18). Thus, in
light of the stable blood pressure and the small pressure drop on the
conduit arterial level (13), even though the Re number may reach the
critical range, the femoral branches seem overdimensioned for the flow
requirements of the quadriceps muscle and thus not limiting for peak
KE.
Ascending vasodilatation.
Whether peak flow in humans is further enhanced by an increase in
DPFA has not been
shown. An ascending vasodilatation has been suggested in animal models
to occur during exercise, spreading upstream electrogenically from the
microvascular level to the feeding arteries (10, 12, 15). A slight
change in the conduit artery diameter, under constant perfusion
pressure, has then been suggested to markedly alter
with the fourth power of the diameter change, according to:
= VC · P = [( · r4)/(8 · · L)] · P,
where P is perfusion pressure gradient. However, in analogy with
Ohm's law, the vascular system consists of the feeding conduit artery
in series with the microvasculature, each contributing with their
respective resistance (R) to the total resistance
(Rtotal)
(Rtotal = Rcond + Rmv, where
Rcond is resistance in conduit vessel and
Rmv is resistance
in microvasculature). Again, the local blood pressure gradient on the
level of the conduit arteries is very small (~0.033-1.0 mmHg/cm)
(13), compared with the blood pressure gradients of ~47 mmHg over
precapillary resistance vessels, ~13 mmHg over the capillary vessels,
and ~20 mmHg in the postcapillary resistance venules, before reaching
~5 mmHg in the large capacitance veins (26). Thus, if we calculate
Rtotal during
peak exercise from the formulas above and from our peak flow values,
accounting for the blood pressure gradients on the respective levels
and assuming that the conduit artery diameter is unchanged (16), and
relate it to
Rtotal if the
conduit artery diameter had dilated by 10%, it is found that such a
dilatation would only increase peak exercise blood flow by ~0.3%,
i.e., by 0.018 l/min. Similarly, it would only contribute to ~0.3%
of the total blood flow increase during exercise at peak effort. An
exercise-induced increase of
DPFA could thus
possibly only induce a slight redistribution of flow into the profunda
branch. However, in light of the proportionally larger cross-sectional
area of the microvasculature and its greater potency to vasodilatate,
in combination with the marked pressure gradient along its length, most
of the magnitude of blood flow increase (~99%) as well as the
"drawing" force for the redistribution of blood flow into the
muscle of activity must be regulated on the microvascular level.
Influence of training.
The present subjects' engagement in exercise varied from ordinary
daily life activities to regular endurance training, and there was a
substantial variation in vessel size. Whether similar relationships
between the conduit artery and tissue volume are also valid in
endurance-trained bicyclists and runners is not known. For instance,
bicyclists are characterized by profound adaptation of the thigh
muscles and not only by enlarged mitochondrial volume/capacity and
larger cross-sectional fiber size (6, 25) but also by a concomitant
enlargement of
DCFA (7, 9). What would be found in extreme endurance runners remains an open question. They are characterized by equally high muscle aerobic adaptation and
maximal O2 but normal muscle
fiber sizes in the leg muscles (23). It is, however, not known whether
the size of their conduit vessels adapts. Moreover, in light of the
finding that the peripheral arteries of weight lifters are
"underdimensioned" in relation to muscle and body mass (7, 9), it
is likely that it is the type, intensity, and duration of the training
and metabolic stress that are of greatest importance for any vascular
adaptations in conduit arteries rather than the actual tissue volume
per se (7, 9). For weight lifters it also seems more important to
preserve blood pressure than to increase the size of conduit artery diameters.
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ACKNOWLEDGEMENTS |
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The present work was financially supported by a grant from the Danish National Research Foundation (504-14).
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FOOTNOTES |
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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 and other correspondence: G. Rådegran, Copenhagen Muscle Research Centre, Rigshospitalet, Section 7652, Tagensvej 20, Dk-2200 Copenhagen N, Denmark (E-mail: goranradengran{at}hotmail.com).
Received 20 May 1999; accepted in final form 16 August 1999.
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
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 H. A. Silber, J. A.C. Lima, D. A. Bluemke, B. C. Astor, S. N. Gupta, T. K. Foo, and P. Ouyang Arterial Reactivity in Lower Extremities Is Progressively Reduced as Cardiovascular Risk Factors Increase: Comparison With Upper Extremities Using Magnetic Resonance Imaging J. Am. Coll. Cardiol., March 6, 2007; 49(9): 939 - 945. [Abstract] [Full Text] [PDF]
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D. W. Wray, A. Uberoi, L. Lawrenson, and R. S. Richardson Heterogeneous limb vascular responsiveness to shear stimuli during dynamic exercise in humans J Appl Physiol, July 1, 2005; 99(1): 81 - 86. [Abstract] [Full Text] [PDF]
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D. S. DeLorey, J. M. Kowalchuk, and D. H. Paterson Adaptation of pulmonary O2 uptake kinetics and muscle deoxygenation at the onset of heavy-intensity exercise in young and older adults J Appl Physiol, May 1, 2005; 98(5): 1697 - 1704. [Abstract] [Full Text] [PDF]
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H. A. Silber, P. Ouyang, D. A. Bluemke, S. N. Gupta, T. K. Foo, and J. A. C. Lima Why is flow-mediated dilation dependent on arterial size? Assessment of the shear stimulus using phase-contrast magnetic resonance imaging Am J Physiol Heart Circ Physiol, February 1, 2005; 288(2): H822 - H828. [Abstract] [Full Text] [PDF]
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P. Haouzi, B. Chenuel, and A. Huszczuk Sensing vascular distension in skeletal muscle by slow conducting afferent fibers: neurophysiological basis and implication for respiratory control J Appl Physiol, February 1, 2004; 96(2): 407 - 418. [Abstract] [Full Text] [PDF]
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 M. Louis, J. R. Poortmans, M. Francaux, J. Berre, N. Boisseau, E. Brassine, D. J. R. Cuthbertson, K. Smith, J. A. Babraj, T. Waddell, et al. No effect of creatine supplementation on human myofibrillar and sarcoplasmic protein synthesis after resistance exercise Am J Physiol Endocrinol Metab, November 1, 2003; 285(5): E1089 - E1094. [Abstract] [Full Text] [PDF]
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M. Miyachi, H. Tanaka, K. Yamamoto, A. Yoshioka, K. Takahashi, and S. Onodera Effects of one-legged endurance training on femoral arterial and venous size in healthy humans J Appl Physiol, June 1, 2001; 90(6): 2439 - 2444. [Abstract] [Full Text] [PDF]
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2946.2 ml/min, r = 0.91, P < 0.002] but not
to body mass-related peak value or absolute and body mass-related