| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Department of Kinesiology, University of Waterloo, Waterloo, Ontario, Canada N2L 3G1
 |
ABSTRACT |
|---|
 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
We tested the hypothesis that forearm blood flow (FBF) might be reduced during forearm exercise when a vasoconstrictor response was evoked by calf exercise during calf ischemia (CE + I). In nine healthy subjects, brachial artery FBF and finger-cuff mean arterial pressure (MAP) were measured beat by beat during rest and forearm exercise. CE + I initiated before 5 min of forearm exercise (condition A) increased MAP by 24% and reduced resting forearm vascular conductance (FVC) by 24% such that FBF remained at the same level as without CE + I (control, condition C). With the onset of forearm exercise, the difference in FVC between condition A and condition C was abolished; consequently, the FBF adaptation to exercise was greater after 3 min of exercise in condition A (247.0 ± 14.8 ml/min) than in condition C (197.1 ± 9.4 ml/min, P < 0.05) because of the elevated MAP. Gradual stimulation of the chemoreflex by the addition of CE + I at 3 min of a 9-min bout of forearm exercise (condition B) did not affect FVC such that progressive elevations in MAP resulted in proportional increases in FBF. We concluded that chemoreflex-mediated increases in systemic sympathetic nervous activity appear to affect resting FVC. Evidence from this study suggests that local factors responsible for initiating and maintaining vasodilation during moderate, small-muscle mass exercise can quickly override this vasoconstrictor influence such that FBF is elevated during exercise in direct proportion to the elevation in MAP.
vasoconstriction; blood pressure; exercise; sympathetic nervous system
| |
INTRODUCTION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
THE MUSCLE CHEMOREFLEX is a powerful mechanism for elevating systemic sympathetic nervous activity (SNA) (8, 26). Metabolic by-products of muscle contraction related primarily to anaerobic metabolism stimulate chemosensitive muscle afferent nerve fibers present in skeletal muscle (8), with the hydrogen ion appearing to be the predominant effector (37), although diprotonated phosphate has also been implicated (33). Stimulation of these afferents results in an elevated mean arterial pressure (MAP) achieved primarily via sympathetically mediated increases in systemic vasoconstriction, with elevations in heart rate (HR) playing a minor role (17). It is thought that the primary role of such a pressure-raising reflex is to correct a mismatch between blood flow and metabolism in ischemic exercising muscle (26). For this to be the case, the elevations in SNA to exercising muscle, which parallel those to resting muscle in both time course and magnitude, could not significantly affect the vascular bed of the exercising muscle mass. Evidence from dogs (20, 38) and humans (27) supports this view, with elevations in blood pressure restoring ~50% of the blood flow error in ischemic muscle. Such a result is consistent with the concept of a functional sympatholysis whereby local metabolic and flow-dependent vasodilatory factors attenuate the effect of elevated sympathetic activity on vascular conductance in the exercising muscle (14). However, in humans, Joyner (7) did not observe any restoration of blood flow in the exercising forearm made ischemic via 50 mmHg positive pressure, despite a progressive 20-mmHg increase in blood pressure. He postulated that this was caused by an increase in sympathetic activity to the exercising forearm muscles, resulting in a vasoconstriction. This is consistent with the concept of a sympathetic restraint whereby elevated sympathetic activity can reduce vascular conductance in an exercising muscle vascular bed (14).
The chemoreflex effect on vascular conductance in nonischemic exercising muscle has also been investigated. Mittelstadt et al. (18), in dogs running on a treadmill, found that terminal aortic occlusion severe enough to elicit an ~40-mmHg increase in blood pressure resulted in a forelimb vasoconstriction. However, the blood pressure elevation outweighed this constriction and forelimb blood flow was increased. Kagaya et al. (11) observed that the addition of exhausting handgrip exercise in humans performing moderate, rhythmic calf plantar flexion resulted in an ~20-mmHg increase in blood pressure within ~50 s and that exercising calf vasoconstriction contributed to this pressor response. In fact, the calf vasoconstriction outweighed the systemic blood pressure change such that exercising calf blood flow decreased. Both of these observations support the concept of a sympathetic restraint in nonischemic, exercising muscle.
At present, no evidence exists concerning the adaptation of blood flow in nonischemic muscle from rest to exercise under conditions of elevated SNA caused by stimulation of the chemoreflex in another muscle group. The response would depend on the relative effects of increases in blood pressure versus changes in muscle vascular conductance resulting from the competition between SNA and vasodilatory factors. Therefore, we used Doppler ultrasound to determine the forearm blood flow (FBF) response in the nonischemic, exercising forearm under two conditions: 1) a chemoreflex-mediated elevation in SNA established before the onset of forearm exercise, and 2) a progressive increase in chemoreflex-mediated SNA during steady-state exercise. We hypothesized that the elevated SNA would attenuate FBF adaptation from rest to exercise under the first condition and reduce the steady-state exercise FBF response in the exercising forearm under the second condition.
| |
METHODS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Subjects
Nine healthy young male subjects (20.4 ± 0.7 yr, mean ± SE) volunteered for this study and gave written consent, on a form approved by the Office of Human Research of the University, after receiving full written and verbal details of the experimental conditions and any potential risks involved. Each subject came to the laboratory on two occasions, once for familiarization and once to complete two trials in each of the three exercise protocols.Experimental Design
Forearm exercise and chemoreflex stimulation.
The subjects were supine with their right arms supported in an extended
position at an angle from the horizontal such that midforearm level was
~20 cm above heart level (Fig. 1).
Forearm exercise consisted of rhythmic, dynamic handgrip exercise at a contraction/relaxation duty cycle of 1 s/2 s performed in time with a
signal light. The load was equivalent to 20% of the subject's maximal
voluntary contraction (MVC) (9.43 ± 0.46 kg) determined from the
strongest of three attempts before the experiment. This work rate
resulted in an approximately fourfold increase in FBF from rest to
exercise, similar to the increase in calf blood flow response in the
experiment of Kagaya et al. (11).
|
Experimental protocol.
Figure 2 shows the three exercise
conditions. Before the experiments were initiated, the subjects were
supine for 30-40 min and the forearm was cooled with a fan. This
cooling was maintained throughout the experiments to minimize skin
blood flow contributions to resting and exercising FBF.
Condition A was used to evaluate the
effect of a background chemoreflex-mediated elevation in SNA on the
adaptation of FBF from rest to exercise. To accomplish this, CE + I was
performed for 4 min. This resulted in a progressive increase in blood
pressure. Pilot work had shown that this intervention could achieve a
20- to 25-mmHg increase in MAP before subjects had to cease calf
exercise because of discomfort. Therefore, in all experiments CE + I
was performed until MAP had stabilized at 20-25 mmHg above resting
levels, and thereafter the pressor response was maintained with
continued ischemia. After 1 min of rest during
ischemia, forearm exercise began and lasted for 5 min. At the
end of forearm exercise, the circulatory arrest cuffs were rapidly
deflated and the recovery of cardiovascular responses was followed for
5 min.
|
Data Acquisition
HR and MAP were measured beat by beat, with the latter at heart level, using a photoplethysmograph finger blood pressure cuff (Ohmeda 2300, Finapres, Lakewood, CO) on the middle finger of the left hand. Whereas this device measures finger arteriolar pressure and there is some change in the pressure waveform along the length of the arterial tree, Imholz and colleagues (6) have shown that there is only a 4- to 5-mmHg difference in the mean pressure at the finger versus the brachial artery.FBF was obtained beat by beat as the product of brachial artery mean blood velocity (MBV) and arterial cross-sectional area
![FBF (ml/min) = MBV (cm/s) ⋅ 60 (s/min)&pgr;[brachial artery diameter (cm)/2]<SUP>2</SUP>](/content/vol277/issue2/fulltext/H635/img001.gif)
|
Data Analysis
For each subject, the diameter data were fit with an exponential regression to reduce random measurement error and provide continuous diameter estimates for the beat-by-beat MBV, allowing beat-by-beat calculation of FBF. HR, MBV, and MAP data were saved continuously at 100 Hz on a dedicated computer via analog-to-digital conversion. For analysis, the beat-by-beat data were averaged into 3-s bins corresponding to the contraction/relaxation duty cycle and then averaged across all subject trials to determine the mean response profile. For condition C, data from rest and the first 3 min of exercise in condition B were also part of the averaged response, because this phase of condition B was identical to condition C. Mean values for HR, MAP, and FBF reported at rest are averages of the 60-s rest period. Mean values at different times during forearm exercise are averages of four contraction/relaxation duty cycles for each subject (12-s average).For estimates of forearm vascular conductance (FVC), the following procedure and rationale were applied. We and others (31, 36) (for review, see Ref. 13) have shown that the muscle pump can contribute to a change in blood flow through a vascular bed without a change in vascular conductance by expelling blood from the veins, thereby reducing the venous pressure and increasing the arterial-venous pressure gradient. Thus during dynamic exercise, dividing the exercising muscle blood flow by arterial pressure can only provide an estimate of what has been termed "virtual conductance" (31), representing both changes in resistance vessel caliber and the mechanical effect of muscle contraction. However, we have also shown that this mechanical effect of contraction does not occur when the exercising muscle mass is well above heart level (see Figs. 1 and 3 in Ref. 36) because the veins are virtually empty and little effective change in arterial-venous pressure gradient can be achieved by the mechanical effect of muscle contraction. Therefore, if one were to determine the flow for one cardiac cycle during relaxation (which is unaffected by the compressive effects of contraction) divided by the arterial pressure, this would be expected to provide the best estimate of true vascular conductance. For this reason the forearm was elevated 20 cm above heart level for all experiments. At rest, FVC was calculated as the average FBF/MAP over the 60-s rest period. At 20 s, 30 s, 40 s, 1 min, and every 30 s of exercise thereafter, FVC was calculated as the average of FBF measured over three separate beats during the relaxation phases between contractions divided by MAP of the corresponding beat.
Postexercise hyperemia was determined as the total FBF in excess of resting flow during the 5-min period of recovery after the cessation of forearm exercise.
Statistical Analysis
One-way repeated-measures ANOVA was used to determine the effects of exercise condition on HR, MAP, FBF, and FVC at rest and at different times during forearm exercise and on the postexercise hyperemia. The level of significance for ANOVA was set at P < 0.05, with significant differences further analyzed with Student-Newman-Keuls post hoc testing at the time points at which three conditions were being compared. All data are presented as means ± SE.| |
RESULTS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Adaptation From Rest to Exercise
CE + I before forearm exercise (condition A) elevated HR compared with control (condition C) (72.9 ± 5.8 vs. 59.7 ± 3.3 beats/min, respectively; P = 0.0028) and resulted in a 24% increase in MAP (122.5 ± 3.1 vs. 98.5 ± 2.7 mmHg, respectively; P < 0.0001). This indicated a strong activation of the muscle chemoreflex and suggested increased SNA (Fig. 3). This effect was maintained by ischemia when calf exercise ceased, as evidenced by the continued similar elevation of HR and MAP in condition A relative to condition C (Fig. 3). Resting FBF was not altered (P = 0.877) by the increase in MAP, because FVC was reduced by 24% (P = 0.0352); that is, the chemoreflex-mediated increases in SNA caused vasoconstriction of resistance vessels in the resting forearm muscles (see Figs. 3 and 4).
|
With the start of forearm exercise, FBF increased. This increase was
markedly greater in condition A than
in condition C because of the 5 min of
exercise in condition A (Fig. 3). The
difference in FVC in condition A
versus that in condition C was
abolished by 20 s of exercise (Fig. 4).
However, by 5 min of exercise, FVC in condition
A versus that in condition
C was decreased by 16% (P = 0.0018), although this did not
compensate completely for the 25% elevation in MAP at this time such
that FBF was still elevated in condition
A versus condition C
(247.9 ± 15.0 vs. 207.3 ± 9.4 ml/min, respectively;
P = 0.0197). In the control condition, only very minor changes in HR and MAP occurred during the course of
exercise, indicating that forearm exercise per se was of moderate intensity and that the forearm muscles were probably not ischemic.
|
Steady-State Exercise
FBF was relatively stable by 3 min of forearm exercise in the control condition. At this time in condition B, CE + I began. This resulted in an acute increase in HR but no immediate change in MAP (Fig. 3), suggesting that elevations in HR under these conditions did not significantly affect MAP. Progressive increases in MAP began after a delay of ~1 min and continued for the remaining 5 min of forearm exercise in condition B, eventually exceeding MAP in the control condition by 20% (128.6 ± 3.6 vs. 107.3 ± 3.7 mmHg, respectively; P = 0.0002) at the end of forearm exercise. Because FVC was not affected in condition B by the CE + I-induced progressive elevations in SNA (Fig. 4), the gradual elevation in MAP resulted in proportional changes in FBF (Fig. 3). HR, MAP, and FBF responses by the end of condition B were not different from those at the end of exercise in condition A (HR: 77.0 ± 4.5 vs. 76.9 ± 5.7 beats/min, respectively; P = 0.954; MAP: 128.6 ± 3.6 vs. 131.9 ± 4.1 mmHg, respectively; P = 0.138; FBF: 265.6 ± 12.8 vs. 247.9 ± 15.0 ml/min, respectively; P = 0.105), suggesting the achievement of a similar stimulation of the chemoreflex in both conditions.Postexercise Recovery
Figure 5 shows the time course of recovery of HR, MAP, and FBF after the end of exercise and the release of ischemia. In conditions A and B both HR and MAP displayed a large, rapid drop in the first 10-20 s of recovery, followed by a smaller progressive decrease toward baseline levels by 5 min. Little change was apparent in these variables after the cessation of forearm exercise in condition C. The total FBF postexercise hyperemia was markedly reduced in conditions A (121.4 ± 18.5 ml) and B (181.7 ± 26.9 ml) compared with that in condition C (309.1 ± 26.9 ml; P = 0.001). All three responses showed a similar, rapid decrease in flow over the first 10 s of recovery, at which time the reduction in flow in condition C became markedly slowed. By the end of the 5-min recovery period, FBF was similar between conditions.
|
| |
DISCUSSION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
The results of this study are in agreement with those of previous investigations that showed the muscle chemoreflex to cause vasoconstriction in resting human limbs (3, 8, 9, 37). The results did not support the working hypothesis that chemoreflex-mediated elevations in SNA would cause a vasoconstriction in the nonischemic, exercising forearm. Rather, the vasoconstrictor effect in the forearm muscle was abolished with exercise, resulting in a passive elevation in FBF during exercise because of elevations in MAP. This effect occurred both at the onset of a rest-to-exercise transition and when chemoreflex-mediated increases in SNA were progressively added during steady-state forearm exercise and demonstrates the existence of a functional sympatholysis under the conditions of this study. Observations of a markedly reduced postexercise hyperemia after the passive elevation in blood flow during elevated SNA suggest that this elevation in blood flow had a positive impact on skeletal muscle metabolism.
Use of CE + I to Elevate SNA
This study employed CE + I followed by maintained ischemia in an attempt to create and maintain elevations in forearm SNA. Because measurements of muscle SNA in the forearm were not possible in this study, there was no direct evidence confirming that CE + I evoked an elevation in forearm sympathetic vasoconstrictor activity and that this was maintained with calf muscle ischemia. However, numerous studies provide evidence that such a manipulation would consistently lead to elevated SNA in resting (3, 8, 37) and exercising (3, 18) muscle and that this would be maintained by ischemia (3, 8).It would be expected that CE + I would cause accumulation of both hydrogen ions (37) and diprotonated phosphate (33) as potential stimuli for the chemoreflex pressor response. Whereas this would be expected to elevate SNA considerably, resultant elevations in MAP would be sensed by arterial baroreceptors and the baroreflex might be expected to progressively oppose the vasoconstrictor component of the chemoreflex (6). This could explain the observation that the elevation in MAP tended to plateau at ~20-25 mmHg above control. Regardless, the magnitude by which MAP was elevated in this study was similar to that in other studies in which a significant effect on both resting and exercising muscle vascular conductance was observed (7, 10, 11). This, combined with the observation of a 24% reduction in FVC at rest, indicates that the CE + I intervention and maintained calf ischemia had a substantial effect on forearm SNA.
Functional Sympatholysis Versus Sympathetic Restraint
Original evidence for a functional sympatholysis stemmed from the observation that resistance changes in response to sympathetic stimulation in an in situ dog preparation were attenuated in exercise (12, 22). This evidence has been dismissed by some as a mathematical artifact (25) of the hyperbolic relationship of resistance and blood flow. The results of the current study in which FVC was reduced at rest, but not during exercise, is consistent with the concept of functional sympatholysis. Thus, during exercise, FBF increased in direct proportion to MAP.Numerous physiological mechanisms for a functional sympatholysis have
been clearly documented. Inorganic phosphate, ACh, adenosine, acidosis,
and potassium have all been demonstrated to inhibit sympathetic
neurotransmission (for review, see Ref. 30), as has nitric oxide (15).
There is evidence suggesting that sympatholysis affects predominantly
2-mediated constriction (1, 2,
34). It has been suggested (26) that control at this level of the arteriolar tree has minimal impact on vascular conductance. However, observations of an 2-mediated
sympatholytic effect with significant impact on limb vascular
conductance (2, 34) argue against this, suggesting instead that both
distribution of blood flow and total blood flow are affected by the
metabolic sensitivity of
2-mediated sympathetic
constriction. Given the rapidity of the observed sympatholytic effect
of exercise in this study, substances released early in exercise such
as adenosine, potassium, ACh, and nitric oxide might be involved.
Sympathetic restraint causes a reduction in skeletal muscle blood flow or vascular conductance relative to the metabolic demand. Some studies have demonstrated vasoconstriction in exercising muscle with elevations in sympathetic activity induced by recruitment of additional muscle (10, 11, 29). However, in other studies in which substantial increases in muscle norepinephrine spillover occurred in exercising muscle, either no change in vascular conductance was observed (23, 28) or it was reduced in proportion to the increase in MAP, suggesting that autoregulation might have been responsible (24).
Our results are qualitatively consistent with those of several studies (23, 28, 34) employing different experimental protocols but do not agree with the results of Kagaya et al. (10, 11). These investigators found a reduction in blood flow in the exercising calf muscles of supine subjects when exhaustive elbow flexion (10) or handgrip exercise (11) was added. It is possible that the magnitude of the sympathetic response was greater in their study compared with ours or that less SNA occurred in the calf muscle because of the high proportion of oxidative fibers in the human soleus muscle (34).
Passive Exercise Hyperemia: Speculation on Its Metabolic Impact
After both conditions A and B, in which FBF was elevated during exercise above the control condition, the postexercise hyperemia was reduced. This observation is consistent with a positive metabolic impact on the exercising forearm. Blood was not sampled from the forearm, but we observed previously that elevated blood flow at the onset of forearm exercise allowed for a more rapid adaptation of aerobic metabolism with lower blood lactate (5). It would also be expected that the supply of more oxygen, as shown by Haseler et al. (4) with inspiration of a hyperoxic gas mixture, would allow for partial resynthesis of phosphocreatine (PCr), resulting in a reduced postexercise oxygen consumption after moderate exercise (21).A reduced need for PCr resynthesis provides a plausible explanation for why blood flow returned to resting levels more rapidly after exercise under elevated flow conditions. However, it is not possible to identify the mechanism(s) responsible for how this was achieved, because this experiment was not designed to isolate such contributors. Therefore, we cannot exclude the possibility that the reduced postexercise hyperemia may not be directly related to muscle metabolism. For example, one contributor might be the baroreflex. Given that calf circulatory occlusion ceased immediately at the end of forearm exercise, calf vascular conductance would be near maximal at the onset of recovery. This might be expected to influence baroreflex control of blood pressure such that the more rapid vasoconstriction in the forearm during recovery in conditions A and B was part of a baroreflex regulation of systemic blood pressure. Obviously, for this to be possible, effective sympathetic constriction of the forearm would have to be reestablished shortly after exercise ceased. Another potential contributor to the more rapid flow recovery after exercise during elevated blood flow might be a reduced interstitial concentration of vasodilatory metabolites responsible for the postexercise hyperemia, in essence a "washout" effect of the elevated exercising forearm blood flow. However, such a reduction was also likely to have occurred during exercise yet had no apparent effect on exercising vascular conductance. Finally, it is not clear what role a myogenic response may have played, given that there was a sudden, rapid drop in systemic pressure at the end of forearm exercise when the calf occlusion cuffs were released.
In summary, the 24% increase in MAP was presumably a consequence of increased SNA caused by activation of the muscle chemoreflex pressor response by CE + I (8, 26). The elevation in MAP did not increase resting FBF because of a proportional reduction in FVC. However, when forearm exercise was initiated, the chemoreflex-mediated effect on FVC was abolished. Likewise, a gradual increase in SNA when CE + I was added during steady-state forearm exercise did not affect FVC. In both cases, FBF was elevated in proportion to MAP and the postexercise hyperemia was substantially reduced, suggesting a positive effect of this hyperemia on muscle metabolism.
There is clear evidence that exercising muscle is still under the influence of sympathetic vasoconstriction (19), and the rationale that this vasoconstrictor influence must limit the metabolic vasodilation when the capacity of the exercising muscle mass approaches that of cardiac output (25) is sound. However, there is equally clear evidence (2, 22, 34) supporting the existence of a functional sympatholysis in exercising muscle, and physiological mechanisms that could account for this phenomenon have been clearly documented (for review, see Ref. 30). The observations of this study are best explained by the existence of a rapidly acting functional sympatholysis in the exercising forearm, given the relative vasodilatory and SNA-mediated vasoconstrictor influences established by our exercise protocol. The rapidity of this sympatholysis suggests that sympatholytic affecters present early on in exercise (potassium, adenosine, ACh, nitric oxide) might be responsible for the initial effect. It remains to be determined exactly how sympathetic vasoconstriction, locally mediated vasodilation, and sympatholytic mechanisms in exercising muscle interact to determine whether a functional sympatholysis or a sympathetic restraint dominates the vascular response.
| |
ACKNOWLEDGEMENTS |
|---|
We thank echo Doppler ultrasound operators Heather Naylor and Michael Chambers for excellent technical help with data collection.
| |
FOOTNOTES |
|---|
This research was supported by the Natural Sciences and Engineering Research Council of Canada.
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: R. L. Hughson, Dept. of Kinesiology, Univ. of Waterloo, Waterloo, ON, Canada N2L 3G1 (E-mail: hughson{at}healthy.uwaterloo.ca).
Received 13 October 1998; accepted in final form 1 April 1999.
| |
REFERENCES |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
1.
Anderson, K. M.,
and
J. E. Faber.
Differential sensitivity of arteriolar 1- and 2-adrenoceptor constriction to metabolic inhibition during rat skeletal muscle contraction.
Circ. Res.
69:
174-184,
1991
2.
Buckwalter, J. B.,
and
P. S. Clifford.
Reduced vascular responsiveness to 2-adrenergic agonist during dynamic exercise (Abstract).
FASEB J.
12:
A691,
1998.
3.
Hansen, J.,
G. D. Thomas,
T. N. Jacobsen,
and
R. G. Victor.
Muscle metaboreflex triggers parallel sympathetic activation in exercising and resting human skeletal muscle.
Am. J. Physiol.
266 (Heart Circ. Physiol. 35):
H2508-H2514,
1994
4.
Haseler, L. J.,
R. S. Richardson,
and
M. C. Hogan.
Phosphocreatine hydrolysis during submaximal exercise: the effect of FIO2.
J. Appl. Physiol.
85:
1457-1463,
1998
5.
Hughson, R. L.,
J. K. Shoemaker,
M. E. Tschakovsky,
and
J. M. Kowalchuk.
Dependence of muscle 
O2 on blood flow dynamics at onset of forearm exercise.
J. Appl. Physiol.
81:
1619-1626,
1997
6.
Imholz, B. P. M.,
J. J. Settels,
A. H. van der Meiracker,
K. H. Wesseling,
and
W. Wieling.
Non-invasive continuous finger blood pressure measurement during orthostatic stress compared with intra-arterial pressure.
Cardiovasc. Res.
24:
214-221,
1990
7.
Joyner, M. J.
Does the pressor response to ischemic exercise improve blood flow to contracting muscles in humans?
J. Appl. Physiol.
71:
1496-1501,
1991
8.
Joyner, M. J.
Muscle chemoreflexes and exercise in humans.
Clin. Auton. Res.
2:
201-208,
1992[Medline].
9.
Joyner, M. J.,
and
W. Wieling.
Increased muscle perfusion reduces muscle sympathetic nerve activity during handgripping.
J. Appl. Physiol.
75:
2450-2455,
1993
10.
Kagaya, A.,
F. Ogita,
and
A. Koyama.
Vasoconstriction in active calf persists after discontinuation of combined exercise with high-intensity elbow flexion.
Acta Physiol. Scand.
157:
85-92,
1996[Medline].
11.
Kagaya, A.,
M. Saito,
F. Ogita,
and
M. Shinohara.
Exhausting handgrip exercise reduces the blood flow in the active calf muscle exercising at low intensity.
Eur. J. Appl. Physiol.
68:
252-257,
1994.
12.
Kjellmer, I.
On the competition between metabolic vasodilatation and neurogenic vasoconstriction in skeletal muscle.
Acta Physiol. Scand.
63:
450-459,
1965[Medline].
13.
Laughlin, M. H.
Skeletal muscle blood flow capacity: the role of the muscle pump in exercise hyperemia.
Am. J. Physiol.
253 (Heart Circ. Physiol. 22):
H296-H306,
1987.
14.
Laughlin, M. H.,
R. J. Korthuis,
D. J. Duncker,
and
R. J. Bache.
Control of blood flow to cardiac and skeletal muscle during exercise.
In: Handbook of Physiology. Exercise: Regulation and Integration of Multiple Systems. Bethesda, MD: Am. Physiol. Soc., 1996, sect. 12, chapt. 16, p. 705-769.
15.
Macedo, M.,
and
W. W. Lautt.
Shear-induced modulation by nitric oxide of sympathetic nerves in the superior mesenteric artery.
Can. J. Physiol. Pharmacol.
74:
692-700,
1996[Medline].
16.
Mancia, G.,
and
A. L. Mark.
Arterial baroreflexes in humans.
In: Handbook of Physiology. The Cardiovascular System. Peripheral Circulation and Organ Blood Flow. Bethesda, MD: Am. Physiol. Soc., 1983, sect. 2, vol. III, pt. 2, chapt. 20, p. 755-793.
17.
McCloskey, D. I.,
and
J. H. Mitchell.
Reflex cardiovascular and respiratory responses originating in exercising muscle.
J. Physiol. (Lond.)
224:
173-186,
1972
18.
Mittelstadt, S. W.,
L. B. Bell,
K. P. O'Hagan,
and
P. S. Clifford.
Muscle chemoreflex alters vascular conductance in nonischemic exercising skeletal muscle.
J. Appl. Physiol.
77:
2761-2766,
1994
19.
O'Leary, D. S.,
E. D. Robinson,
and
J. L. Butler.
Is active skeletal muscle functionally vasoconstricted during dynamic exercise in conscious dogs?
Am. J. Physiol.
272 (Regulatory Integrative Comp. Physiol. 41):
R386-R391,
1997
20.
O'Leary, D. S.,
and
D. D. Sheriff.
Is the muscle metaboreflex important in control of blood flow to ischemic active skeletal muscle in dogs?
Am. J. Physiol.
268 (Heart Circ. Physiol. 37):
H980-H986,
1995
21.
Radda, G. K.
Control of energy metabolism during muscle contraction.
Diabetes
45:
S88-S92,
1996.
22.
Remensnyder, J. P.,
J. H. Mitchell,
and
S. J. Sarnoff.
Functional sympatholysis during muscular activity.
Circ. Res.
11:
370-380,
1962
23.
Richardson, R. S.,
B. Kennedy,
D. R. Knight,
and
P. D. Wagner.
High muscle blood flows are not attenuated by recruitment of additional muscle mass.
Am. J. Physiol.
269 (Heart Circ. Physiol. 38):
H1545-H1552,
1995
24.
Richter, E. A.,
B. Kiens,
M. Hargreaves,
and
M. Kjaer.
Effect of arm-cranking on leg blood flow and noradrenaline spillover during leg exercise in man.
Acta Physiol. Scand.
144:
9-14,
1992[Medline].
25.
Rowell, L. B.
Human Cardiovascular Control. New York: Oxford Univ. Press, 1993.
26.
Rowell, L. B.
Neural control of muscle blood flow: importance during dynamic exercise.
Clin. Exp. Pharmacol. Physiol.
24:
117-125,
1997[Medline].
27.
Rowell, L. B.,
M. V. Savage,
J. Chambers,
and
J. R. Blackmon.
Cardiovascular responses to graded reductions in leg perfusion in exercising humans.
Am. J. Physiol.
261 (Heart Circ. Physiol. 30):
H1545-H1553,
1991
28.
Savard, G.,
E. A. Richter,
S. Strange,
B. Kiens,
N. J. Christensen,
and
B. Saltin.
Norepinephrine spillover from skeletal muscle during exercise in humans: role of muscle mass.
Am. J. Physiol.
257 (Heart Circ. Physiol. 26):
H1812-H1818,
1989
29.
Secher, N. H.,
J. P. Clausen,
I. Noer,
and
J. Trap-Jensen.
Central and regional circulatory effects of adding arm exercise to leg exercise.
Acta Physiol. Scand.
100:
288-297,
1977[Medline].
30.
Shepherd, J. T.,
and
P. M. Vanhoutte.
Local modulation of adrenergic neurotransmission.
Circulation
64:
655-666,
1981
31.
Sheriff, D. D.,
L. B. Rowell,
and
A. M. Scher.
Is rapid rise in vascular conductance at onset of dynamic exercise due to muscle pump?
Am. J. Physiol.
265 (Heart Circ. Physiol. 34):
H1227-H1234,
1993
32.
Shoemaker, J. K.,
Z. I. Pozeg,
and
R. L. Hughson.
Forearm blood flow by Doppler ultrasound during rest and exercise: tests of day-to-day repeatability.
Med. Sci. Sports Exerc.
28:
1144-1149,
1996[Medline].
33.
Sinoway, L. I.,
M. B. Smith,
B. Enders,
U. Leuenberger,
T. Dzwonczyk,
K. Gray,
S. Whistler,
and
R. L. Moore.
Role of diprotonated phosphate in evoking muscle reflex responses in cats and humans.
Am. J. Physiol.
267 (Heart Circ. Physiol. 36):
H770-H778,
1994
34.
Thomas, G. D.,
J. Hansen,
and
R. G. Victor.
Inhibition of 2-adrenergic vasoconstriction during contraction of glycolytic, not oxidative, rat hindlimb muscle.
Am. J. Physiol.
266 (Heart Circ. Physiol. 35):
H920-H929,
1994
35.
Tschakovsky, M. E.,
J. K. Shoemaker,
and
R. L. Hughson.
Beat-by-beat forearm blood flow with Doppler ultrasound and strain-gauge plethysmography.
J. Appl. Physiol.
79:
713-719,
1995
36.
Tschakovsky, M. E.,
J. K. Shoemaker,
and
R. L. Hughson.
Vasodilation and muscle pump contribution to immediate exercise hyperemia.
Am. J. Physiol.
271 (Heart Circ. Physiol. 40):
H1697-H1701,
1996
37.
Victor, R. G.,
L. A. Bertocci,
S. L. Pryor,
and
R. L. Nunnally.
Sympathetic nerve discharge is coupled to muscle cell pH during exercise in humans.
J. Clin. Invest.
82:
1301-1305,
1988.
38.
Wyss, C. R.,
J. L. Ardell,
A. M. Scher,
and
L. B. Rowell.
Cardiovascular responses to graded reductions in hindlimb perfusion in exercising dogs.
Am. J. Physiol.
245 (Heart Circ. Physiol. 14):
H481-H486,
1983
This article has been cited by other articles:
|
|
 |
|
  K. L. Walker, N. R. Saunders, D. Jensen, J. L. Kuk, S.-L. Wong, K. E. Pyke, E. M. Dwyer, and M. E. Tschakovsky Do vasoregulatory mechanisms in exercising human muscle compensate for changes in arterial perfusion pressure? Am J Physiol Heart Circ Physiol, November 1, 2007; 293(5): H2928 - H2936. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. A. L. Calbet, C. Lundby, M. Sander, P. Robach, B. Saltin, and R. Boushel Effects of ATP-induced leg vasodilation on VO2 peak and leg O2 extraction during maximal exercise in humans Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2006; 291(2): R447 - R453. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. S. Dyson, J. K. Shoemaker, and R. L. Hughson Effect of acute sympathetic nervous system activation on flow-mediated dilation of brachial artery Am J Physiol Heart Circ Physiol, April 1, 2006; 290(4): H1446 - H1453. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. E. Tschakovsky, K. Shoemaker, and M. A. Babcock Comment on Point:Counterpoint "The muscle metaboreflex does/does not restore blood flow to contracting muscles" J Appl Physiol, March 1, 2006; 100(3): 1084 - 1085. [Full Text] [PDF]
|
|
|
|
|
|
N. R. Saunders, K. E. Pyke, and M. E. Tschakovsky Dynamic response characteristics of local muscle blood flow regulatory mechanisms in human forearm exercise J Appl Physiol, April 1, 2005; 98(4): 1286 - 1296. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. E. Tschakovsky and R. L. Hughson Rapid blunting of sympathetic vasoconstriction in the human forearm at the onset of exercise J Appl Physiol, May 1, 2003; 94(5): 1785 - 1792. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Perrey, M. E. Tschakovsky, and R. L. Hughson Muscle chemoreflex elevates muscle blood flow and O2 uptake at exercise onset in nonischemic human forearm J Appl Physiol, November 1, 2001; 91(5): 2010 - 2016. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. R. Wright, D. I. McCloskey, and R. C. Fitzpatrick Effects of systemic arterial blood pressure on the contractile force of a human hand muscle J Appl Physiol, April 1, 2000; 88(4): 1390 - 1396. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
and
dotted line), gradual addition of chemoreflex-mediated elevations in
SNA starting at 3 min of forearm exercise (condition
B, 
and dashed line), and forearm exercise without
any chemoreflex-mediated elevations in SNA (condition
C, 
and continuous line). Forearm exercise began at
0 min for all conditions and ended at 5 min for
condition A and 9 min for
conditions B and
C. Condition
C between 
1 and 3 min represents average
response of trials in conditions B and
C over that time period, because
experimental conditions were identical during that time. Values at
selected times with error bars are means ± SE. * Significant
difference (P < 0.05) from control
(condition C) at corresponding
time.
