Human femoral artery diameter in relation to knee extensor muscle mass, peak blood flow, and oxygen uptake

G. Rdegran and B. Saltin

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American Journal of Physiology - Heart and Circulatory Physiology publishes original investigations on the physiology of the heart, blood vessels, and lymphatics, including experimental and theoretical studies of cardiovascular function at all levels of organization ranging from the intact animal to the cellular, subcellular, and molecular levels. It is published 12 times a year (monthly) by the American Physiological Society, 9650 Rockville Pike, Bethesda MD 20814-3991. Copyright 2000 the American Physiological Society. ISSN: 0363-6135, ESSN: 1522-1539. Visit our website at http://www.the-aps.org/.

Am. J. Physiol. Heart Circ. Physiol. 278: H162H167, 2000.

Human femoral artery diameter in relation to knee extensor muscle mass, peak blood ow, and oxygen uptake
G. RADEGRAN AND B. SALTIN Copenhagen Muscle Research Centre, Rigshospitalet, DK-2200 Copenhagen N, Denmark
Radegran, G., and B. Saltin. Human femoral artery diameter in relation to knee extensor muscle mass, peak blood ow, and oxygen uptake. Am. J. Physiol. Heart Circ. Physiol. 278: H162H167, 2000.It is not known whether the diameter of peripheral conduit arteries may impose a limitation on muscle blood ow 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 2.295.03) l/min during ergometer cycle exercise, performed one-legged dynamic knee extensor exercise up to peak effort at 68 7 W (range 55100 W). Peak values for knee extensor blood ow (thermodilution) and oxygen uptake of 6.06 0.74 (range 4.759.52) l/min and 874 124 (range 5901,521) ml/min, respectively, were achieved. Pulmonary oxygen uptake reached a peak of 1.72 0.19 (range 1.542.33) l/min. Diameters of common and profunda femoral arteries determined by ultrasound Doppler were 10.6 0.4 (range 8.212.7) and 6.0 0.4 (range 4.58.0) mm, respectively. Thigh and quadriceps muscle volume measured by computer tomography were 10.06 0.66 (range 6.1810.95) and 2.36 0.19 (range 1.313.27) 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 ow 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

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 specically utilized in their activity (79). 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 ow 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 ow and oxygen uptake, especially during one-legged knee extensor exercise.
METHODS

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EXTENSIVE STUDIES have been performed to elucidate the factors that limit skeletal muscle blood ow 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, 2022, 24). Peripheral factors such as local blood ow, oxygen diffusion and extraction, or mitochondria may then be

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Subjects. Eight healthy human subjects, seven men and one woman, with mean SE (range) age of 25.4 1.5 (2235) yr, height of 177.8 3.1 (158186) cm, and weight of 77.8 4.9 (4998) 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-01403/95). 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 510 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
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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 25 cm below the inguinal ligament. A thermistor (model 940302.5F, 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 ow measurements (2). A Harvard mechanical syringe pump (model 44, Harvard Apparatus) was used for constant infusion of saline solution at 0C. 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 ow measurements in the femoral vein (outow) 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 (VO2 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 ow (Qleg ) 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 57 min at a relative workload corresponding to 7580% 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 3040 min before performing an experimental ramp protocol starting at 2030 W for 3 min and increasing by 5 W every 30 s up to PPO. PPO was dened as the highest workload at which the subject could maintain the pace for at least 1 min. Measure ments of blood ow and VO2 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 VO2 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 xed perpendicular angle. The diameters of the common femoral artery (DCFA ) and its supercial (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 signicant (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 2125 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 signicant 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 signicant. A nonstatistically signicant comparison is indicated by P NS. The values given in the text are means SE.
RESULTS

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Femoral artery diameter. DCFA averaged 10.6 0.4 (range 8.212.7) mm (Fig. 1), which was 58 and 76% 0.002). larger than DSFA and DPFA, respectively (P

Fig. 1. Right (DRCFA ) and left (DLCFA ) common femoral artery diameters were the same [10.6 0.4 (range 8.212.7) mm and 10.5 0.4 (range 8.212.2) mm, respectively; P not signicant (NS)] but larger than their corresponding supercial and profunda branches (P 0.002). Right (DRSFA ) and left (DLSFA ) supercial femoral artery diameters were the same [6.7 0.3 (range 5.98.2) mm and 6.7 0.3 (range 5.57.9) mm, respectively; P NS] but slightly larger than right (DRPFA ) and left (DLPFA ) profunda femoral artery diameters (P 0.05). DRPFA and DLPFA were also the same [6.2 0.3 (range 5.37.9) mm and 5.8 0.4 (range 4.58.0) mm, respectively; P NS]. Values are means SE. Signicant differences (P 0.05): * from DCFA; from DSFA.

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DSFA averaged 6.7 0.3 (range 5.58.2) mm, which was 11% larger than DPFA, averaging 6.0 0.4 mm (range 4.58.0) (P 0.05). Knee extensor exercise. Table 1 shows the exercise induced increase (P 0.05) in heart rate, MAP, Qleg, VCleg, and leg oxygen uptake (VO2 leg ), as well as VO2 pulm. At peak effort, a load of 68 7 W (range 55100 W) was achieved. Muscle perfusion and VO2leg reached values at peak effort of 249 27 (range 149373) and 36 4 (range 2360) ml min l 100 g 1, respectively, based on the CT-determined muscle mass of 2.48 0.20 (range 1.373.43) kg. Thigh and quadriceps muscle volume measured by CT were 10.06 0.66 (range 6.1810.95) and 2.36 0.19 (range 1.313.27) liters, respectively. DCFA, but not DPFA, correlated with the quadriceps muscle mass (r 0.97, P 0.001) and thigh volume (r 0.88, P 0.004) (Fig. 2). However, DCFA and DPFA did not correlate with the absolute or muscle mass (knee extensor, KE)-related values at rest and at peak effort (QKE and VO2 KE ), or to the absolute and body mass-related values at rest and peak effort of VO2 pulm, or to PPO. Moreover, PPO did not correlate with quadriceps muscle mass or thigh volume. However, PPO correlated with peak QKE, peak VO2 KE, and peak O2 pulm V

Table 1. Effect of exercise on blood ow, heart rate, arterial pressure, vascular conductance, and oxygen uptake
Submaximal One-Legged Knee Extensor Exercise Peak One-Legged Knee Extensor Exercise

Rest

Qleg , l/min
HR, beats/min MAP, mmHg VCleg , ml min mmHg 1
1

0.24 0.02 (0.170.35) 69.4 2.1 (6680) 89.2 4.4 (79105) 2.6 0.3 (1.93.8) 19.1 2.9 (9.434.2) 342 27 (240460)

3.66 0.27* (2.695.01) 100.8 4.2* (92113) 98.1 3.2* (94117) 37.7 4.4* (2353) 443 26* (361564) 839 33* (7001,020)

6.06 0.74 (4.759.52) 135.4 8.1 (112171) 119.4 2.0 (114130) 52.6 7.3 (31.378.7) 874 124 (5901521) 1,720 190 (1,5402,330)

VO2 leg , ml/min VO2 pulm , ml/min

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Values are means SE of leg blood ow (Qleg ), heart rate (HR), mean arterial pressure (MAP), leg vascular conductance (VCleg ), and leg (VO2leg ) and pulmonary (VO2pulm ) oxygen uptake measurements in 8 subjects at rest and during 1-legged, dynamic, knee extensor exercise at a submaximal intensity of 30 W and at peak power output ( 68 7 W, range 55100 W). Signicant differences (P 0.05): * from rest; from rest and submaximal 1-legged, dynamic, knee extensor exercise.

peak QKE peak VO2 KE

and

0.094 PPO(W) 0.361 l/min (r 15.4 PPO(W) 174.8 ml/min (r 0.91, P 0.02) 0.94, P 0.006)

peak VO2 pulm

0.021 PPO(W) 0.291 l/min (r 0.92, P 0.01)

Ergometer cycle exercise. At PPO of 345 21 W (range 280420 W) a peak VO2 pulm of 3.90 0.31 (range 2.295.03) l/min was reached. This was signicantly higher (P 0.05) than during one-legged knee extensor exercise. DCFA (mean of right and left) correlated with peak VO2 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 VO2 pulm at rest. Moreover, DCFA did not correlate with PPO, although PPO correlated with peak VO2 pulm PPO

0.06 peak VO2 pulm(ml/min)

109.2 W (r 0.89, P 0.003)

DISCUSSION

This study demonstrates that the size of the vessels feeding the knee extensor muscle during exercise are of sufficient size not to compromise blood ow 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 specic muscle group. This is also in agreement with the nding that DCFA does not alter in size during this type of exercise (16). In contrast, the correlation

Fig. 2. Common femoral artery diameter (DCFA ) of knee extensorexercising leg was related to computer tomography-measured (CT) quadriceps muscle mass [Mqm CT, DCFA 2.244 Mqm CT (kg) 5.361 mm, r 0.97, P 0.001; A] and to total CT thigh volume [Vthigh CT, DCFA 0.605 Vthigh CT (kl) 4.559 mm, r 0.88, P 0.004; B]. No such correlation was evident for diameter of profunda branch (DPFA; not shown).

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Fig. 3. DCFA (mean of right and left) correlated with and was linearly related to peak pulmonary oxygen uptake (VO2 pulm ) during ordinary bicycle exercise [peak VO2 pulm 648.1 DCFA (mm) 2946.2 ml/min, r 0.91, P 0.002] but not to body mass-related peak value or absolute and body mass-related VO2 pulm at rest. DCFA did not correlate with and was not linearly related to peak power output (PPO) during ordinary bicycle exercise, whereas PPO correlated with and was linearly related to peak VO2 pulm, where PPO 0.06 peak VO2 pulm (ml/min) 109.2 W (r 0.89, P 0.003).

between DCFA and the tissue that it supplies and the close relationship between DCFA and peak VO2 pulm during ergometer cycle exercise suggest that the dimension of this artery could be a critical factor for limiting blood ow, 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 VO2 pulm, may reect the role of an anaerobic energy yield during an incremental exercise test. The correlation between PPO and peak QKE, peak VO2 KE, as well as peak VO2 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 dehydroge nase to have a limiting role for peak VO2 by the muscle, as previously suggested (4). Laminar or turbulent ow. Indications that the femoral arteries are not limiting can also be deduced from estimating the ow magnitude an artery can accommodate at various pressure gradients and whether the ow persists to be laminar. This ow (Q) can under different pressure gradients ( P) be estimated from Poiseuilles law Q [( r4)/(8 L)] P, where a Newtonian uid with viscosity ows 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, ows in the range of 22120 and 419 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. However, persistent turbulence could limit peak blood ow, by inducing energy losses with a drop in local pressure. This is not likely, though, because MAP is stable, with a minimal pressure gradient of 0.0331.0 mmHg/cm along the length of conduit arteries (13, 26). Moreover, the ow is traditionally said to shift to turbulent as the Reynolds (Re) number exceeds 2,000 3,000. Reynolds, however, stated that ow could remain undisturbed up to Re numbers of 12,000. Birkhoff (see Ref. 13) obtained values of 40,000. Thus, under steady-state conditions in a straight hollow tube, the breakpoint for turbulence to persist varies. Slight disturbances may even occur without interfering with the overall ow pattern. The Re number can be calculated assuming steady-state conditions for a Newtonian uid in a cylindrical tube with rigid walls: Re vD / (Q D / )/[6 104 (D/2)2] 5.623 Q/D, where v is the velocity of the uid, assuming a density ( ) of 1.06 kg/l and a viscosity ( ) of 4 10 3 kg m 1 s 1, with the blood ow (Q) in liters per minute and the diameter (D) in meters. Extrapolating to in vivo conditions, given that the inow of blood to the quadriceps muscle in the common femoral artery corresponds to the outow 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 ow persists even when Re numbers computed rise above the critical steady ow values (13). In fact, the pulsatile ow, 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 ow. The pulsatile ow is therefore protective and more stable than steadystate ow. Indeed, Attinger et al. (see Ref. 13) actually found pulsatile ow 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 inuence, the blood ow pattern is well dened, 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 ow requirements of the quadriceps muscle and thus not limiting for peak QKE. Ascending vasodilatation. Whether peak ow 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 microvas-

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cular 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 mark edly alter Q with the fourth power of the diameter change, according to: Q VC P [( r4)/(8 L)] P, where P is perfusion pressure gradient. However, in analogy with Ohms 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 ( 0.0331.0 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 ow 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 ow by 0.3%, i.e., by 0.018 l/min. Similarly, it would only contribute to 0.3% of the total blood ow increase during exercise at peak effort. An exercise-induced increase of DPFA could thus possibly only induce a slight redistribution of ow 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 ow increase ( 99%) as well as the drawing force for the redistribution of blood ow into the muscle of activity must be regulated on the microvascular level. Inuence 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 ber 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 VO2 but normal muscle ber sizes in the leg muscles (23). It is, however, not known whether the size of their conduit vessels adapts. Moreover, in light of the nding 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. We conclude that the diameters of the common and profunda femoral arteries are sufficiently dimensioned for the needs of the quadriceps muscle and therefore do not limit peak muscle blood ow, peak muscle oxygen uptake, or PPO during one-legged dynamic knee extensor exercise in humans. The common femoral artery diameter may, however, be a limiting factor during dynamic exercise with a larger muscle mass. The dimension and structure of the femoral arteries in healthy humans, furthermore, allow for a reasonably stable and nondisturbed ow pattern, minimizing the occurrence of persistent turbulence that could limit peak perfusion.
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The present work was nancially supported by a grant from the Danish National Research Foundation (50414). Address for reprint requests and other correspondence: G. Rade gran, Copenhagen Muscle Research Centre, Rigshospitalet, Section 7652, Tagensvej 20, Dk-2200 Copenhagen N, Denmark (E-mail: goranradengran@hotmail.com). Received 20 May 1999; accepted in nal form 16 August 1999. REFERENCES 1. Andersen, P., R. P. Adams, G. Sjgaard, A. Thorboe, and B. Saltin. Dynamic knee extension as model for study of isolated exercising muscle in humans. J. Appl. Physiol. 59: 16471653, 1985. 2. Andersen, P., and B. Saltin. Maximal perfusion of skeletal muscle in man. J. Physiol. (Lond.) 366: 233249, 1985. 3. Blomqvist, C. G., and B. Saltin. Cardiovascular adaptations to physical training. Annu. Rev. Physiol. 45: 169189, 1983. 4. Blomstrand, E., G. Radegran, and B. Saltin. Maximum rate of oxygen uptake by human skeletal muscle in relation to maximal activities of enzymes in the Krebs cycle. J. Physiol. (Lond.) 501: 455460, 1997. 5. Chapman, J. V. The technical aspects of Doppler ultrasound. In: The Noninvasive Evaluation of Hemodynamics in Congenital Heart Disease, edited by J. V. Chapman and G. R. Sutherland. London: Kluwer Academic, 1990, p. 134. 6. Gollnick, P. D., B. Armstrong, C. W. Saubert, K. Piehl, and B. Saltin. Enzyme activity and ber composition in skeletal muscle of untrained and trained men. J. Appl. Physiol. 33: 312319, 1972. 7. Huonker, M., M. Halle, and J. Keul. Structural and functional adaptations of the cardiovascular system by training. Int. J. Sports Med. 17: 164172, 1996. 8. Huonker, M., B. Simons, O. Schumacher, and J. Keul. Effect of dynamic versus static training on the dimensions and functions of the extremity arteries (Abstract). Eur. J. Appl. Physiol. 69: 40, 1994. 9. Keul, J., D. Konig, M. Huonker, M. Halle, B. Wohlfahrt, and A. Berg. Adaptation to training and performance in elite athletes. Res. Q. Exerc. Sport 67: 2936, 1996. 10. Kurjiaka, D. T., and S. S. Segal. Conducted vasodilation elevates ow in arteriole networks of hamster striated muscle. Am. J. Physiol. Heart Circ. Physiol. 269: H1723H1728, 1995. 11. Line, P. D., K. Kvernebo, J. Helgerud, and F. Ingjer. Aerobic endurance, anatomical factors and time properties of laser Doppler recorded skin postocclusive hyperaemia. Eur. J. Appl. Physiol. 64: 508512, 1992. 12. Milner, P., V. Ralevic, A. M. Hopwood, E. Feher, J. Lincoln, K. A. Kirkpatrick, and G. Burnstock. Ultrastructural localisation of substance P and choline acetyltransferase in endothelial cells of rat coronary artery and release of substance P and acetylcholine during hypoxia. Experientia 45: 121125, 1989. 13. Milnor, W. R. Hemodynamics. Baltimore, MD: Williams and Wilkins, 1982.

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