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1Division of Cardiology, Pennsylvania State University College of Medicine, Milton S. Hershey Medical Center, Hershey, Pennsylvania 17033; and 2Lebanon Veterans Affairs Medical Center, Lebanon, Pennsylvania 17042
Submitted 10 March 2003 ; accepted in final form 7 May 2003
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ABSTRACT |
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 TOP ABSTRACT METHODSRESULTSDISCUSSIONDISCLOSURESREFERENCES |
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physiology; vasoconstriction; central command; sympathetic nervous system
Two neural processes contribute to this complex process of sympathetic activation and flow redistribution. The first, central command, is a central process that evokes parallel activation of motor and sympathetic systems (10, 36, 39). The second is a theory that suggests the SNS is engaged when mechanically and metabolically sensitive afferents within contracting skeletal muscle increase their discharge rates (9, 16, 20, 25, 32–34, 40).
Studies in human subjects, beginning with the classic report of Mark et al.
(20), have used recordings of
sympathetic nerve traffic to examine these control systems including how the
systems regulate the SNS during exercise. The following general concepts have
emerged from prior reports: 1) during static exercise,
metabolite-sensitive afferents contribute importantly to an increase in muscle
sympathetic nerve activity (MSNA) with an onset latency >60 s
(9,
20,
33,
34,
40); 2) central
command increases MSNA with an onset latency of 
3 s, which is an effect
seen at handgrip maximal voluntary contraction (MVC) levels >50%
(38); and 3)
mechanoreflex augments MSNA with an onset latency of 6 s
(12), a response that is
"sensitized" by muscle contraction
(2) and limb congestion
(23).
A number of animal reports suggest that the muscle mechanoreflex engagement is the primary cause for the renal vasoconstrictor that is seen with muscle contraction (11, 13, 14, 37). Middlekauff et al. (24) examined renal vasoconstrictor responses in humans by using positron emission tomography (PET) scanning techniques. The authors noted that renal vascular resistance (RVR) increased during the first 2 min of a 2.5-min handgrip period at 10% MVC. Surprisingly, the magnitude of the increase in RVR "early" during the 10% MVC paradigm was quite similar to the values observed during the last 2 min of a 3.5-min bout of 30% MVC as well as the value seen during the posthandgrip circulatory arrest (PHG-CA) that followed 30% MVC. Clearly, the limited time resolution of the PET technique and the need to study different groups of subjects for different paradigms made interpretation of these observations difficult.
In this article, we report on our efforts to apply Doppler ultrasound
methods to the study of renal flow during muscle contraction paradigms. This
method provides excellent time resolution and allows multiple paradigms to be
performed on the same subjects. Using this method, we found that muscle
contraction evokes renal vasoconstriction with an onset latency of 6–10
s and an MVC threshold of 50% for handgrip exercise and 30% for biceps
contraction. This increase in RVR during biceps contraction was not due to
central command. Finally, during fatiguing handgrip exercise, metaboreceptors
contribute 40% of the increase in RVR that is seen at the end of
exercise. These findings suggest that in humans, muscle mechanoreflex
engagement is the primary determinant of RVR during muscle contraction.
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METHODS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESREFERENCES |
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Recent advances in duplex ultrasonography provide the opportunity to visualize and simultaneously assess blood flow dynamics within intra-abdominal blood vessels such as the renal artery (4, 18). Accordingly, duplex ultrasound (HDI 5000, ATL Ultrasound; Bothell, WA) was used to examine renal hemodynamics as subjects performed four arm and forearm exercise paradigms.
Subjects were studied in the postabsorptive state and were supine as the
renal artery was scanned (via an anterior abdominal approach). A curved-array
C5-2 Doppler probe with a 2.5-MHz pulsed Doppler frequency was used. The focal
zone was at the depth of the renal arteries. The probe insonation angle to the
skin was 60°. To obtain the highest quality Doppler tracings
possible, the Doppler transducer had to be maintained in a constant position
on the subject's abdominal wall. During our pilot experiments, we noted that
the renal artery moved with respect to the abdominal wall during the various
phases of respiration, and thus we could not maintain high-quality velocity
tracings during both phases of the respiratory cycle. Nevertheless, for each
subject, we obtained velocity data during the same phase of the respiratory
cycle for all portions of the respective paradigms. Accordingly, for each
person, the data were obtained in the same phase of the respiratory cycle. No
subjects performed the Valsalva maneuver during the protocols.
Cardiac cycle Doppler signals were analyzed to determine the mean blood flow velocity (MBV). Each velocity measurement was normalized with a time constant of 1 s for the RVR calculations. For each data point, we averaged two or three cardiac cycles. Data smoothing was not used to obtain mean velocity data. Software developed for the HDI 5000 was used to analyze Doppler signals. In each cardiac cycle, the peak-velocity envelope was traced manually to determine the MBV. The RVR represents the quotient of mean arterial pressure (MAP) and the respective MBV value. RVR is expressed in arbitrary units (au).
HR (obtained by electrocardiogram), BP (measured with Finapres, Ohmeda; Madison, WI), and beat-by-beat renal artery blood flow velocity (RBV) measurements were obtained continuously throughout all protocols. Resting BP was determined using an automated sphygmomanometer (Dinamap, Critikon; Tampa, FL). A force transducer was used to measure the force of muscle contractions.
Study Protocols
Fatiguing static handgrip exercise followed by PHG-CA. In this protocol, the time course of renal vasoconstriction during sustained, fatiguing static handgrip was characterized. A second goal was to determine the role played by metabolite-sensitive muscle afferents in evoking renal vasoconstriction. This was done by examining RVR during PHG-CA (20).
Baseline HR, MAP, and RBV measurements were collected for 5 min. Static handgrip exercise at 40% of MVC was then performed until the subjects (n = 9) were unable to maintain the prescribed tension. At the end of contraction, all subjects graded their perceived level of effort as 20 on the Borg scale (3). Immediately before the handgrip exercise was ended, PHG-CA was initiated by inflating a previously placed arm cuff to 250 mmHg.
Graded intensity of static handgrip exercise. The aim of this protocol was to examine RVR within the first few seconds of handgrip exercise. A second aim was to determine the temporal relationship between renal vasoconstriction and BP. A final goal was to examine the effects of MVC (by percent) on RVR.
After baseline data were collected, subjects (n = 9) performed
15-s bouts of static handgrip at 10, 30, 50, and 70% of MVC using the
nondominant forearm. This sequence was the same for all subjects. Subjects
rested for 1 min between each handgrip exercise bout.
Graded intensity of biceps contraction. The biceps MVC level was determined in each subject at the beginning of the protocol. In determining the MVC values, care was taken to ensure that subjects (n = 6) used only the biceps muscle. After baseline data were collected, the subjects performed voluntary biceps contractions at 7, 15, 30, and 60% of MVC.
Voluntary versus involuntary biceps contractions. The aim of this protocol was to determine whether involuntary biceps contraction evokes renal vasoconstriction. Involuntary contraction eliminates central command (20, 23).
In each subject (n = 6), involuntary biceps contraction was
induced by percutaneous electrical stimulation. Electrical pads (5 x
5cm2) were placed 3 cm apart. The biceps muscle was then
electrically stimulated (200 V; phase duration, 0.3 ms; phase interval, 0.1
ms). Electrical biceps contraction evoked 15–30% of MVC without
causing pain. Once tension reached a steady state, it could be sustained for
5–7 s. The subjects then performed 15 s of voluntary biceps
contractions at the same tension that had been generated during involuntary
contraction.
Data Analysis and Statistics
Beat-by-beat sequential analyses of HR, MAP, RBV, and RVR were performed for all subjects in each protocol.
In the fatiguing static handgrip protocol, the time to fatigue for each subject was noted, and the HR, BP, flow velocity, and RVR values at 10, 20, 40, 60, 80, and 100% were determined (35). To ensure that RVR measurements obtained during PHG-CA represented steady-state values, data from the last 30-s time period are presented and used in the statistical analysis. PHG-CA values were compared with baseline data using a paired t-test.
In the graded static tension paradigms, data were analyzed in 5-s time periods. Statistical analyses were performed separately on each 5-s period (i.e., 0–5, 6–10, and 11–15 s, respectively). For the involuntary contraction paradigm, data obtained during the first 5 s after steady-state involuntary tension were compared with the same tension that had been generated by voluntary contraction and to baseline values. The voluntary contraction data used in these analyses were the 11- to 15-s data.
Data are presented as means ± SE. Repeated-measures one-way ANOVA and Dunnett's test were applied to compare variables to baseline data. The level of significance was set at P < 0.05.
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RESULTS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESREFERENCES |
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The time to fatigue at 40% MVC was 112 ± 14 s. At 10% of the time to
fatigue, HR and BP values were higher than the baseline measurements. Renal
flow was 7% lower and RVR was 16% higher than baseline values
(Fig. 1). RVR at 100% of the
time to fatigue was 76% greater than the baseline value. Of note, the
reduction in RBV paralleled the increase in BP
(Table 1).
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During PHG-CA, RVR was greater than the baseline measurement (2.1 ± 0.2 vs. 2.8 ± 0.2 au; P < 0.017; n = 8). However, the RVR value during PHG-CA represented only 40% of the RVR value seen at end grip. PHG-CA values for the other measured variables are shown in Table 2.
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Graded Handgrip Contraction Protocol
The data for HR, MAP, RVR, and RBV are shown in Fig. 2 and Table 3. No increase in vascular resistance was found in the 0- to 5-s time frame (i.e., the P value for 0- to 5-s RVR was not significant). Vascular resistance measurements for the 6- to 10-s (P < 0.016) and 11- to 15-s (P < 0.026) time periods were higher than baseline values. Post hoc analyses demonstrated that vascular resistance values during handgrip exercise were different from baseline measurements at 50 and 70% MVC for the 6- to 10- and 11- to 15-s time periods.
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Biceps Contraction Protocol
Static biceps contraction increased RVR early (one-way ANOVA main effect, P < 0.042; Fig. 3). Post hoc analyses demonstrated a trend toward a significant effect at the 7% and 30% workloads (comparisons to baseline, P < 0.092 at 7% and P < 0.073 at 30%; Fig. 3). The effects of biceps contractions were more pronounced at the 6- to 10- and 11- to 15-s time periods. Comparisons to baseline values demonstrated that the 30% workload (6–10 s and 11–15 s) and the 60% workload values were different from baseline measurements. Notably, BP did not increase during biceps contraction (Table 4).
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Involuntary Contraction Paradigm
Involuntary biceps contraction led to renal vasoconstriction (one-way ANOVA; P < 0.037), whereas voluntary contraction at the same workload did not evoke renal vasoconstriction (Fig. 4). The increase in RVR was 9% with voluntary contraction and 29% with involuntary contraction.
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DISCUSSION |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESREFERENCES |
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Study Findings
Fatiguing static handgrip exercise led to a progressive increase in RVR
measurements. This effect was seen at the 10% endurance time (11 s). Thus
this effect was not due to metaboreflex engagement, because the onset latency
for this response in humans is 1 min for static handgrip
(20). Of note, the increase in
RVR was also associated with a rise in MAP. This elevation in RVR could either
have been due to mechanoreflex-mediated sympathetic vasoconstriction or renal
myogenic vasoconstriction of the renal artery. Myogenic constriction occurs
when transmural pressure increases within a blood vessel
(7). Thus the increase in BP
alone conceivably could have evoked renal vasoconstriction. Prior work
suggests that myogenic constriction can be seen in the renal vasculature
(29).
Although RVR values were greater than baseline measurements, during PHG-CA,
this value was only 40% of the end-grip level. This is different from the
response observed in skeletal muscle, where end-grip MSNA values are similar
to those observed during PHG-CA. This finding has been widely interpreted to
suggest that muscle metaboreceptor engagement is almost entirely responsible
for the increase in MSNA that is seen at end grip
(9,
20,
27,
31,
33,
34,
40). Because the renal effect
was observed early (i.e., at the 10% fatigue time), and the PHG-CA response
represented less than one-half of the end-grip RVR value, it is unlikely that
the renal vasoconstriction observed was due predominantly to metaboreflex
engagement.
In the graded handgrip contraction protocol, subjects performed 15-s bouts of handgrip exercise at workloads of 10, 30, 50, and 70%. An increase in RVR was noted during the 6- to 10- and 11- to 15-s time periods, and renal vasoconstriction was seen at the two highest workloads. BP was elevated at the time that renal vasoconstriction was noted. Thus the vasoconstrictor response observed had an MVC threshold, and the observed vasoconstrictor response had an onset latency of between 6 and 10 s. These findings also suggest that the vasoconstrictor response is not likely due to engagement of the muscle metaboreflex and is likely due to an increase in central command, engagement of the mechanoreflex, or myogenic vasoconstriction.
Biceps contraction also led to a renal vasoconstriction response. This effect was seen clearly during the 6- to 10- and 11- to 15-s time periods. We did observe a main effect for constriction during the first 5 s, although none of the individual workload values were different from baseline measurements. The increase in RVR was seen at a lower MVC workload than was observed during handgrip exercise, which suggests an inverse relationship between muscle mass and the tension necessary to evoke the reflex (15, 30). Importantly, in this protocol, we observed increases in RVR without changes in BP. These results suggest that a myogenic reflex did not cause the observed vasoconstriction. Thus the results of this paradigm are consistent with engagement of either central command or the muscle mechanoreflex.
Involuntary biceps contraction evoked an increase in RVR values. This finding suggests that central command was not needed to evoke renal vasoconstriction. The increase in RVR was therefore due to either the muscle metaboreflex or the muscle mechanoreflex. Because the response was seen within the first few seconds after the target tension was achieved, we believe that muscle mechanoreflex engagement was responsible for the increase in RVR values.
Prior Reports on This Topic
These findings support a number of prior reports on animals that suggest a role for mechanically sensitive afferents in increasing renal sympathetic nerve activity and in causing renal vasoconstriction. Our report is consistent with prior literature by Mueller et al. (26), which suggests that the increase in RVR early in exercise is due to a sympathetic vasoconstrictor response. Work by Victor et al. (37) suggests that hindlimb contractions induced by electrical stimulation of the tibial nerve in chloralose-anesthetized cats evokes an increase in renal sympathetic nerve activity that is due to stimulation of mechanically sensitive muscle afferents. Our findings are also consistent with earlier work that suggests there is a relationship between the tension developed and the magnitude of the increase in renal sympathetic nerve activity (21). An additional area of agreement of this report with prior work is that we observed that the metaboreceptors contribute to the reflex increase in RVR (22).
In prior work by Middlekauff et al.
(24), PET scanning techniques
were used to examine renal cortical blood flow during a variety of handgrip
exercise interventions in human subjects. PET scanning is a reliable and
regionally sensitive method. With the use of this methodology, this research
team demonstrated that handgrip exercise evokes renal vasoconstriction. The
authors' report suggests that the metaboreflex as well as either the
mechanoreflex and/or the central command contribute to the reflex engagement.
Our report adds to this study by demonstrating the beat-by-beat time course of
the vasoconstriction in humans, the effects of tension and mass on the reflex,
as well as the relative contributions of the muscle reflex and central command
to the renal vasoconstrictor response. Our report disagrees with the findings
of Middlekauff et al. in that they found that the increases in RVR were
similar with handgrip exercise at 30% MVC and during PHG-CA. Thus this earlier
report could be interpreted to suggest that muscle metaboreflex engagement is
a crucial determinant of renal vasoconstriction during static handgrip
exercise. In addition, the prior report demonstrated similar renal vascular
responses "early" in 10% MVC (first 2 min of a 2.5-min
contraction) and "late" in 30% MVC (last 2 min of a 3.5-min
contraction). The reasons for these differences between the earlier report and
this study are not entirely clear but may relate to the differences in
methodologies used to measure renal blood flow. For this reason, some mention
of the comparative strengths and weaknesses of the PET and Doppler methods are
necessary. PET is reliable and regionally sensitive. Its major limitation is
the time necessary to obtain each data point. Doppler methods provide measures
of flow velocity but not volume of flow. Moreover, it could be argued that
this method does not have the regional sensitivity necessary to understand and
interpret RBV responses to muscle contraction. However, it must be emphasized
that renal cortical blood flow comprises 90% of total renal blood flow.
Cortical blood flow responses are more sensitive to sympathetic nerve
stimulation than are medullary blood flow responses. Moreover, Leonard et al.
(19) have shown that both
cortical and medullary vasoconstriction occur with sympathoexcitation. Thus
PET flow and Doppler velocity should yield similar directional responses to an
intervention.
Limitations
In these studies, we were not able to precisely measure renal artery diameter using ultrasound methodology. This is because spatial resolution decreases as the frequency of the ultrasound transducer decreases (17). To obtain an optimal velocity signal from the renal artery, a low-frequency (2.5-MHz) transducer was employed. At this frequency level, spatial resolution of the technique is not sufficient to precisely measure diameter changes that would be seen in the relatively small renal artery.
In conclusion, when all of the protocols are viewed collectively, they suggest that in intact conscious humans, muscle contraction evokes renal vasoconstriction. The voluntary biceps contraction protocol demonstrates that an increase in BP and engagement of the myogenic reflex are not necessary for renal vasoconstriction to occur with muscle contraction. The involuntary biceps contraction paradigm results suggest that central command is also not necessary to evoke renal vasoconstriction with muscle contraction. The primary stimulus for renal vasoconstriction is not likely to be chemical in nature, because the PHG-CA response represents only a small percentage of the total vasoconstrictor response (during the fatiguing static handgrip protocol); vasoconstriction was observed early in all contraction protocols. Thus each protocol can be explained by a variety of different mechanisms. However, muscle mechanoreflex engagement is the only mechanism that can explain each and every protocol presented.
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DISCLOSURES |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESREFERENCES |
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ACKNOWLEDGMENTS |
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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. Section 1734 solely to indicate this fact.
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