© 1997 by European Society of Cardiology
Copyright © 1997, European Society of Cardiology
Time course of brachial artery diameter responses to rhythmic handgrip exercise in humans
Department of Kinesiology, University of Waterloo, 200 University Ave. W., Waterloo, Ont. N2L 3G1, Canada
* Corresponding author. Tel.: +1 (519) 888-4567, ext. 2516; Fax: +1 (519) 746-6776; e-mail: hughson@cgsa.uwaterloo.ca
Received 23 October 1996; accepted 11 March 1997
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Abstract |
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Objective: Whether the dimensions of conduit arteries contribute to the time course of change in blood flow during voluntary rhythmic exercise, and the mechanisms governing such a response in humans, are not known. Methods: The time course of change in the vascular and blood flow dynamics in the brachial artery during the transition between rest and 5 min of rhythmic handgrip exercise was assessed in humans using continuous measures of brachial artery mean blood velocity (MBV; pulsed Doppler), diameter (echo Doppler) and mean arterial pressure (Finapres). The exercise cadence was 1s/1s (Fast) and 1s/2s (Slow) work/rest schedules while supine with the arm positioned above or below the heart. Results: Brachial artery diameter of the active arm was reduced 5% at
10 s following the onset of exercise performed above the heart (P<0.05), irrespective of work rate, and returned to rest levels by 30 s with no concurrent changes in arterial pressure. By 2 min of the Fast contraction rate exercise, brachial artery diameter of the active arm was greater than rest (P<0.05) irrespective of arm position. Brachial artery dimensions in the contralateral inactive arm were not altered during exercise (P >0.05). Compared with rest, MBV and forearm blood flow at 5 s of exercise were increased in the active arm but were reduced transiently in the inactive limb (P<0.05). Conclusions: Conduit artery responses to exercise were dependent upon the work rate and arm position. The delayed dilation in the heavier exercise, independent of arm position, suggests that stimuli related to the metabolic activity of the distal active skeletal muscle may influence the dimensions of the conduit artery.
KEYWORDS Echo Doppler; Pulsed Doppler; Brachial artery; Forearm blood flow; Blood velocity; Vasoconstriction; Vasodilation
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1 Introduction |
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TopAbstract1 Introduction2 Methods3 Results4 DiscussionReferences |
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The changes in limb blood flow and vascular resistance with an increase in work rate are thought to reflect, primarily, microvascular and feed artery tone [1]. Local release of vasoactive metabolites [1, 2], endothelial relaxation factors [3, 4], and the basal level of sympathetic vasoconstrictor tone [5, 6]contribute to the regulation of these smaller vessels. The larger conduit arteries respond to increases or decreases in pressure [7], to passive alterations in flow [8–12], and to increases in sympathetic outflow [8]. These data have led to the hypothesis that conduit artery dilation with exercise facilitates flow conductance to the exercising muscle and reduces shear stress on the endothelial layer [13]. However, it is not known how conduit arteries respond during rhythmic dynamic exercise; the measured time course of change in conduit artery diameter, and the quantitative blood flow, during the transition from rest to rhythmic exercise in humans have not been reported.
We have used combined echo and pulsed Doppler techniques [14, 15]to follow changes in brachial artery diameter and blood flow velocity, respectively, during the transition from rest to dynamic handgrip exercise. Two different work rates were studied with the arm positioned below or above the heart to systematically alter the metabolic stresses and perfusion pressure of the exercise. To determine whether this small muscle mass exercise had any systemic effects, we observed the brachial artery diameter and mean blood velocity (MBV) in the inactive contralateral limb.
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2 Methods |
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TopAbstract1 Introduction2 Methods3 Results4 DiscussionReferences |
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2.1 Subjects
After providing signed consent to the test procedures, 7 young and healthy men volunteered for this study. All aspects of the study were approved by the Office of Human Research at the University. The average physical characteristics (±standard error of the mean) were 24.3±1.1 (range=21–28) years of age, 180±2 cm in height and 77.9±2.7 kg in weight.
The subjects came to the laboratory on 4 separate days. On the first 2 of these days, there was no formal data collection, but subjects completed a maximal voluntary contraction test, and they practised the rhythmic contractions while the experimenters determined optimal conditions for data collection.
2.2 Experimental design
Beat-to-beat measures of mean blood velocity, and frequent measures of diameter, were made from the brachial artery in the antecubital fossa region of the right elbow over 1 min of rest and 5 min of dynamic handgrip exercise. Exercise was performed in the supine position to reduce the contributions of changes in mean arterial pressure and cardiac filling pressure during exercise. Testing commenced after 20 min of supine rest. Both arms were placed, with elbows extended, on stable platforms. The platforms pivoted so that the position of the limbs could be manipulated. For the current study, the right arm was positioned at 50° above (Above) and below (Below) horizontal. The exercise, performed by the right hand, involved squeezing a hand lever which lifted and lowered a 4.4 kg weight (9.5% maximal voluntary isometric contraction) a distance of 5 cm over two different contraction rate protocols. In the first, the weight was lifted and lowered over 1 s with a 1 s relaxation period between contractions (Fast). In the second protocol, 2 s of rest were placed between each 1 s work phase (Slow). The order of arm position and contraction rate was counterbalanced across subjects. Three to 4 trials of this exercise were repeated in each experimental session with no less than 10 min rest between each trial. Care was taken to insure that MBV had returned to rest levels prior to the initiation of any trial. Arterial diameter measures were made during the first trial and MBV determinations during the subsequent 2–3 trials.
The left arm was positioned in two ways depending on the test protocol. When blood flow was being measured in the exercising right arm, an estimate of mean arterial blood pressure was obtained from the left hand by the finger cuff device (Finapres 2300, Ohmeda). Because we wanted to know the pressure at the flow measurement site, we positioned the left arm so that the finger cuff was at the same height as the Doppler probe for both Above and Below positions. In a second experimental protocol, the left arm was placed in the same 50° Above heart position as the exercising right arm. Subjects completed a Fast handgrip exercise protocol while MBV and diameter measurements were made in the inactive left arm. This test, performed at least 2 days following the measures for the active arm, was completed to see if the changes observed in the active arm were due to systemic or local effects.
All exercise tests were made with the subjects in a rested condition at least 2 h after their last meal. The subjects were asked to abstain from alcohol and caffeine for 24 h prior to a test. Tests were performed at a room temperature of 20–22°C.
2.3 Data acquisition and analysis
2.3.1 Diameter
The echo Doppler (Toshiba Model SSH-140A) image of the brachial artery was collected continuously and stored on video tape for analysis. For arterial imaging, we used a pulsed echo imaging system (B-mode) and an angle of approach at 90°. This angle is the most accurate of ultrasonic imaging methods [16]. The probe was positioned over the vessel near the junction of the biceps aponeurosis and muscle belly. The 7.5 MHz imaging probe was hand-held so that the probe could be manipulated to track the artery which, in some subjects, moved slightly in a predictable manner with each forearm contraction. To enhance the accuracy of these diameter measures, the experimenter and subject practised the exercise protocol prior to data collection.
An estimate of arterial diameter was made from the average of 3 measurements each at 20, 35 and 50 s during the initial minute of rest, and at 5, 10, 15, 20, 25, 30, 40, 50, 60 s and 1.5, 2, 3, 4, and 5 min time points of exercise. All diameter measurements were made when the forearm muscle was relaxed and during late diastole using an ECG trigger to update each arterial image at the same time point of the cardiac cycle.
2.3.2 Mean blood velocity
Beat-to-beat heart rate (Cambridge Model VS4 electrocardiograph) and MBV (pulsed Doppler velocimetry, Multigon Model 500V) were collected continuously, along with arterial blood pressure (BP), on a computer-based system at 100 Hz.
The collection and analysis of MBV by pulsed Doppler in our laboratory has been detailed in earlier reports [17–19]. Briefly, a 4.5 MHz pulsed wave Doppler probe was positioned over the brachial artery in the antecubital fossa to obtain MBV data. Instantaneous MBV values were averaged over each cardiac cycle using the QRS complex of the ECG tracing to signal the end of one heart beat and the beginning of the next. The beat-by-beat MBV and BP data from the repeated trials were time-aligned with the onset of exercise and ensemble averaged over 2 s time bins for the Fast, and 3 s time bins for the Slow, contraction rate protocols to include a contraction and relaxation phase in each value [15]. From these averaged data sets, MBV values were obtained at the same times used for the diameter estimations, indicated above. Limb blood flow at each time was calculated as BF=MBVx
r2. From the blood flow and blood pressure data, the mean forearm vascular conductance (VC) at rest was calculated as VC=FBF/BP (where FBF is forearm blood flow [ml/min]).
2.4 Statistics
For the active arm, the main effects of arm position, contraction rate, and time were analysed initially by a repeated measures three-way analysis of variance (ANOVA) (Statistical Analysis System, SAS) with MBV, arterial diameter and limb blood flow forming the dependent variables. Interaction analysis was performed by one- and two-way ANOVA procedures where appropriate. For the inactive arm, the effects of time were analysed by a repeated measures one-way ANOVA. The level of significance was set at P<0.05 and any significant differences were further analysed with Student-Newman-Keuls post hoc test. Data are presented as mean±standard error of the mean (s.e.m.).
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3 Results |
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TopAbstract1 Introduction2 Methods3 Results4 DiscussionReferences |
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During the Slow exercise protocol, BP was unchanged from rest. In the Fast tests, BP was elevated
10 mmHg by 5 min of exercise (Fig. 1). The average increase in BP on moving the arm from the Above to the Below heart position was 30 mmHg. The mean forearm vascular conductance at rest was 0.91±0.05 ml/mmHg/min in the Above position and 0.59±0.05 ml/min/mmHg Below the heart (P<0.05).
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3.1 Diameter
At rest, brachial artery diameter of the active and inactive arms (
4.2 mm) was not different between arm positions. At 10 s following the onset of Above exercise, the brachial artery diameter of the active limb was significantly reduced from rest levels during both the Fast and Slow work rates (P<0.05) (Fig. 2). By 30–60 s of exercise, this early reduction in diameter was reversed and the vessel dimensions returned to levels observed at rest. The early and transient changes in diameter were not observed with the arm in the Below position. After 2 min of Fast contraction rate exercise, brachial artery diameters were greater than rest (P<0.05) irrespective of arm position. In contrast, no brachial artery dilation was observed in the Slow tests performed in either arm position (Fig. 2).
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Significantly different from Slow work rate (1s/2s CR) (P<0.05). Arrow indicates the onset of exercise.3.2 Mean blood velocity and forearm blood flow
Forearm blood flow at rest was not different between the Above (65.6±5.4 ml/min) and Below (68.9±10.4 ml/min) positions. In the active arm, both MBV (Fig. 3) and forearm blood flow (Fig. 4) were significantly increased over rest by 5 s in all exercise conditions (P<0.05). For the active arm, both MBV (Fig. 3) and FBF (Fig. 4) were greater by 60 s of exercise in the Fast tests compared with the Slow (P<0.05).
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For the inactive arm, brachial artery diameters were unchanged between rest and exercise (Fig. 5). MBV and FBF in the inactive arm, measured in the Above, Fast condition, were significantly lower than rest at 5 s following the onset of exercise performed by the contralateral arm (P<0.05) but not at any other time points (Fig. 5). Note however, that although statistically significant the changes in inactive arm MBV following 5 s of exercise were within the previously determined variability of this measure [15].
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4 Discussion |
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TopAbstract1 Introduction2 Methods3 Results4 DiscussionReferences |
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With this study we have examined, for the first time, the time course of conduit artery diameter changes during rhythmic exercise in humans. These data extend our knowledge of conduit artery dynamics over previous studies which examined conduit artery responses in animals following contractions [9, 10, 20], and in humans following passively increased flows [11, 12]. In the current experiments, the brachial artery responded in a complex manner to dynamic exercise and more than one mechanism must have impacted on the dimensions of these vessels in ways which were dependent upon the prevailing arterial pressure, and muscle metabolism. At the onset of exercise a biphasic response was noted; an early, but brief, constriction at 10 s of exercise was followed by dilation which returned the diameter to resting levels by 30–60 s. This early reduction in diameter was quantitatively most apparent in the Above position. In the Fast, but not the Slow, tests the vasodilation continued progressively for exercise beyond 60 s. Submaximal rhythmic handgrip exercise did not appear to exert a systemic effect on vascular dimensions or blood flow as indicated by the responses of the inactive arm.
4.1 Critique of methods
In this study, the time course of conduit artery dynamics during the transition from rest to exercise was investigated. Acquisition of data pertaining to conduit artery control in humans requires methods which are non-invasive and which give high time resolution of the changes in mean blood velocity (MBV) and arterial diameter. Doppler ultrasound methods have provided beat-by-beat information on the dynamic responses of conduit artery MBV changes between rest and various forms of exercise [14, 21–23]. Echo Doppler ultrasound is capable of non-invasive and continuous investigations of conduit artery dimensions, but, to date, movement artefact during exercise has restricted the use of this methodology to rest conditions only [21–23]. In this and previous [14, 15]studies, we have demonstrated the use of echo Doppler techniques for measurements of arterial diameter changes during dynamic exercise. With a stable arm preparation and practice to track the predictable movements of the artery that occur with contractions, we have shown that the reproducibility of repeated diameter measures ranged from 2–4% both at rest and during contractions [15]. This value of reproducibility falls within the range of measurement error for the brachial artery because the measurement callipers of the Toshiba system move in increments of 0.1 mm. Thus, the 0.3 mm increase in diameter observed for the current tests is detectable using echo Doppler methods. A quantitatively more important source of variability in the Doppler blood flow is MBV. At rest, MBV may vary as much as 10–12% from one cardiac cycle to the next [15]likely due to rapid variations in blood pressure and stroke volume. The MBV variability is greater during contractions [15]. However, we have shown that averaging repeated trials over time bins which include both a contraction and relaxation phase of the exercise duty cycle maintains the variability during exercise at rest levels [15].
Our diameter measures of the brachial artery at rest are in close agreement with the estimated values of Safar et al. [7], but are somewhat larger than those reported by Sinoway et al. [11]and smaller than those of Anderson and Mark [8]. Although the volunteers recruited in each of these studies are reported to be young and healthy, brachial artery dimensions appear to be related to body mass which was not reported in the studies of Sinoway et al. [11]or Anderson and Mark [8].
4.2 Phase 1: early reduction in brachial artery diameter
To our knowledge, this is the first report of a transient reduction in the brachial artery diameter at the onset of exercise in humans. However, such an effect has been observed in surgically exposed femoral artery of dogs [10]and cats [20]. In isolated arterioles, the early constriction appears to be dependent upon both an increase in flow and the basal level of arteriolar tone [5, 6]. In the current study, increases in flow alone cannot explain the early constriction. The early reduction in diameter was most apparent in the Above trials and much less when the same work was performed below the heart despite similar increases in blood flow at 10–15 s of exercise. Indeed, calculations of the increase in shear rate above resting values (shear rate=8·MBV/Diameter) showed no difference between Above and Below arm positions. The increase in shear rate between rest and 10 s of exercise, when the reduction in diameter was greatest, was not different for the Above and Below arm positions during the Fast (123±16 and 166±41·s–1; Above and Below, respectively) and Slow (139±20 and 127±22·s–1; Above and Below, respectively) contraction rates.
The increase in blood velocity might alter vessel diameter by a mechanism independent of shear rate. Based on the principle of Bernoulli, conservation of energy in the circulation requires that, if blood velocity increases, then distending pressure must decrease [24]. However, this effect cannot explain the early decrease in diameter because even a 3-fold increase in velocity would result in a pressure decrease of less than 0.5 mmHg. It is unlikely that this amount of pressure change is sufficient to explain the observed effect.
The washout of a vasodilatory compound with increased flow cannot explain this response because the conduit artery is proximal to the active parenchymal tissue and is not in direct contact with muscle metabolites. The observation that the reduction in conduit artery diameter was most evident in the Above tests may support the speculation that the basal level of vessel tone determines the magnitude and direction of flow-induced changes to vessel diameter [5, 6]. Notably, forearm vascular conductance at rest was greater with the arm positioned above the heart.
Other factors which may affect conduit artery dimensions during exercise might include systemic sympathetic nervous system activation [8]and a reduction in arterial pressure [7]. It is unlikely that changes in sympathetic tone were involved because a constrictor response was not observed in the inactive contralateral arm. Also, the increase in muscle sympathetic nerve activity during mild-intensity rhythmic forearm contractions is delayed beyond 1–2 min [25]. In addition, blood pressure was unchanged between rest and the early moments of exercise in all tests of the current study. Importantly, brachial artery diameter was not different between arm positions even though blood pressure was changed by 30 mmHg. Thus, it does not appear that changes in blood pressure can account for the early reductions in diameter, although pressure changes within the active forearm are not known.
The early reduction in conduit artery diameter would have reduced blood flow by only 7% but may also have augmented the pressure drop across the downstream microvascular bed with the exercise hyperemia [26]. Consequently, blood flow through individual microvascular units serving the active tissue may have been altered. Therefore, the reversal of the early constriction towards resting levels by 30–60 s following the onset of exercise would facilitate more optimal tissue perfusion.
4.3 Phase 2: brachial artery dilation
Brachial artery diameters increased progressively as exercise continued in the Fast, but not the Slow, tests irrespective of arm position. In cats, Hilton et al. [20]concluded that such a dilation during contractions was due to a conducted vasodilatory signal originating from microvessels embedded within the active skeletal muscle. The time course of dilation observed in the current study agrees well with this concept and with previously determined time-dependent effects of vasoactive metabolites released from contracting skeletal muscle [27]. More recently, the upstream conduction of vasodilatory stimuli from parenchymal microvessels has been demonstrated [20]. In addition, the locus of control for vascular tone appears to shift from distal microvessels to more proximal feed and conduit arteries in conjunction with an increase in metabolic and hemodynamic stress [26, 28].
It is apparent, however, that conduit arteries of both dogs [9, 10]and humans [11]also dilate when blood flow is passively increased, without skeletal muscle contractions. Because forearm blood flow increased more in the Fast than the Slow tests, independent of arm position, it is possible that this delayed dilation was induced by the elevations in flow which were similar in both arm positions. However, several lines of evidence argue against such a mechanism. First, the dilation observed in the current study was delayed beyond the 20–45 s time course reported previously for flow-induced dilation [10, 11]. Second, it has been shown previously [10, 11]that flow-induced dilation of conduit arteries is graded with increases in flow, suggesting that if this mechanism was regulating the delayed dilation in the Fast tests, then it should also have been observed in the Slow tests, but to a lesser degree. However, the Slow tests resulted in a 3-fold increase in flow above rest with no dilation. Finally, the dilation did not develop until steady-state flows had been achieved.
The inability to temporally relate artery diameter with flow may indicate that flow-induced dilation is not an important mechanism for conduit artery responses during dynamic contractions, in contrast to observations made during passive increases in flow [8, 9, 11]. The observations that dilation develops with the heavier work rate exercise only, independent of arm position, does suggest that the conduit artery exerts some regulatory role over tissue perfusion in a manner that is related to the level of tissue metabolism. The dilation observed would provide a 6–7% increase in flow and oxygen transport during steady-state contractions. This, in conjunction with enhanced metabolite removal, and/or an enhanced flow for distribution into a larger vascular bed downstream with microvessel recruitment, may be an important determinant of muscle metabolism during the exercise.
4.4 Summary
In this study, beat-by-beat measures of both MBV and diameter of the brachial artery showed that these vessels are more than simple conduit pipes for blood transport. Rather, they respond in a complex dynamic manner during rhythmic exercise. The conduit artery responses to exercise varied according to the arm position and the resultant changes in arterial pressure, and the work rate. An early but transient reduction in diameter, under conditions of reduced hydrostatic pressure, was followed by further dilation above rest in heavier exercise. The delayed dilation in the heavier exercise, independent of arm position, suggests that stimuli related to the metabolic activity of the distal active skeletal muscle may influence the dimensions of the conduit artery. In turn, the conduit artery dilation may attenuate the pressure drop across the vascular bed, thereby facilitating flow distribution and capillary perfusion.
Time for primary review 28 days.
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Acknowledgements |
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This study was supported by the Natural Sciences and Engineering Research Council (NSERC) of Canada. Kevin Shoemaker and Maureen MacDonald were recipients of NSERC post-graduate scholarships.
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