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Vol. 83, Issue 5, 1454-1460, 1997
Department of Cardiac Physiology, National Cardiovascular Center Research Institute, Suita, Osaka 565, Japan
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES
ABSTRACT 
Sadamoto, Tomoko, and Kanji Matsukawa. Cardiovascular
responses during spontaneous overground locomotion in freely moving
decerebrate cats. J. Appl. Physiol.
83(5): 1454-1460, 1997.
To examine whether the cerebrum is
essential for producing the rapid cardiovascular adjustment at the
beginning of overground locomotion, we examined heart rate (HR), mean
arterial blood pressure (MAP), and integrated electromyogram (iEMG) of
the forelimb triceps brachialis muscle in freely moving decerebrate
cats during locomotion. Two to four days after decerebration surgery
performed at the level of the precollicular-premammillary body, the
animals spontaneously produced coordinated overground locomotion,
supporting body weight. HR began to increase immediately before the
onset of iEMG, and MAP began to rise almost simultaneously with the
iEMG onset. Their increases in HR and MAP (24 ± 3 beats/min and 22 ± 4 mmHg) were sustained during locomotion. Sinoaortic denervation
(SAD) did not affect the abrupt changes in HR and MAP at the beginning
of locomotion (0-4 s from the onset of iEMG), whereas SAD had a
contrasting effect during the subsequent period, a decrease in the HR
response (9 ± 1 beats/min) and an increase in the MAP response (30 ± 3 mmHg). These results suggest that the cerebrum and the rostral part of the diencephalon are not essential for producing the rapid cardiovascular adjustment at the beginning of spontaneous overground locomotion. The arterial baroreflex does not contribute to this rapid
adjustment but plays an important role in regulating the cardiovascular
responses during the later period of spontaneous locomotion.
heart rate; arterial blood pressure; rapid adjustment; central
control; sinoaortic denervation
INTRODUCTION VOLUNTARY DYNAMIC EXERCISE such as locomotion increases
heart rate (HR), arterial blood pressure (ABP), and sympathetic nerve activity in conscious animals and humans. Two neural mechanisms responsible for these cardiovascular responses have been hypothesized. One is a feed-forward control because of central descending output from
higher brain centers, and the other is a feedback control because of
peripheral afferent signals arising from the contracting skeletal
muscle. Recent studies in conscious animals (11, 18) have shown that
renal sympathetic nerve activity (RSNA) and HR increase immediately
before or at the onset of voluntary static exercise and dynamic
treadmill exercise, suggesting that this rapid cardiovascular
adjustment at the onset of exercise is predominantly controlled by
central descending output from higher brain centers. Although the
cerebral cortex is believed to have an important role in controlling
somatic movements during voluntary exercise, it is unknown whether the
cerebrum is also essential for producing central descending signals
responsible for the rapid cardiovascular adjustment at the beginning of
voluntary exercise. Previous studies reported that several sites of the
brain stem outside the cerebrum can produce both somatomotor behaviors
and cardiovascular adjustments. Chemical stimulation of neurons in the
hypothalamus involving the posterior hypothalamus, the lateral
hypothalamus, and a part of the field of Forel, which is called the
"locomotor area," induced both cardiorespiratory changes and
locomotor movements (5-7, 20, 23). It was also shown that neurons
in the localized areas of the hypothalamus and the midbrain
periaqueductal gray matter, which are called the "defense area,"
were capable of producing both cardiovascular changes and defense body
movements (2, 10, 21). Therefore, we hypothesized that areas of the
brain stem outside the cerebrum can produce the rapid cardiovascular adjustment associated with spontaneous overground locomotion.
To verify the aforementioned hypothesis, we examined the time course of
the responses in HR and ABP at the onset of overground locomotion in
freely moving cats, which were decerebrated at the level of the
precollicular-premammillary body. These kinds of decerebrate cats
could induce spontaneous locomotion without any artificial stimulation
in the same way as intact awake cats performed voluntary locomotion. In
addition, to identify whether the cardiovascular adjustment at the
beginning of spontaneous locomotion in decerebrate cats was
independent of the arterial baroreflexes, we examined the effect of
sinoaortic denervation (SAD) on the responses of HR and ABP during
spontaneous overground locomotion. It has been hypothesized that tonic
inhibitory effects of the arterial baroreflexes are suppressed (9)
and/or the operating point of the baroreflexes is shifted
during dynamic exercise (4, 15), which, in turn, may contribute to the
increases in HR and ABP at the onset of voluntary exercise. If so, SAD
may diminish the cardiovascular responses at the onset of spontaneous
overground locomotion, as found during treadmill exercise in
conscious dogs (15) and rabbits (4, 9).
METHODS
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RESULTS
and
, Onset and offset of iEMG, respectively. HR began to increase before onset of iEMG and gradually reached a peak during overground locomotion. ABP showed a rapid increase with onset of iEMG and reached
an initial peak (*) and thereafter a late peak (
) in subsequent
period of overground locomotion.
The duration of locomotion varied among animals before and after SAD (range 10-32 s before and 10-29 s after SAD) as shown in Table 1. The average duration of locomotion was 21 ± 4 s (n = 5 cats) before SAD, which corresponded to 14 ± 3 cm/s in the speed of locomotion. The average duration and speed after SAD were 22 ± 3 s and 14 ± 3 cm/s, respectively. In a given animal, the duration of locomotion seemed quite constant because there was no significant difference in the locomotor duration obtained before and after SAD (Table 1), and the coefficient of variation of the duration was low (23 ± 6% before and 24 ± 6% after SAD). Time course of changes in HR and MAP during locomotion. A typical example of HR and ABP in response to spontaneous overground locomotion is shown in Fig. 1. HR began to increase before the onset of iEMG and continuously increased, reaching a peak in the later period of spontaneous locomotion. ABP increased concurrently with the onset of iEMG and often showed two peaks during spontaneous locomotion, as shown in Fig. 1. Immediately after the end of overground locomotion, HR showed an abrupt drop and ABP gradually returned to the baseline value. The early and late peaks of the pressor response to overground locomotion were observed in 52 (80%) of 65 locomotor trials performed by 5 cats before SAD. The early peak of the pressor response was 13 ± 2 mmHg and appeared at 3.8 ± 0.2 s from the onset of iEMG, and the late peak of the pressor response was 26 ± 3 mmHg at 15.5 ± 1.1 s from the iEMG onset. In the following analysis of the average time course of the cardiovascular responses, all data in 65 trials were collected and averaged. The baseline values of HR and MAP and their maximum changes during spontaneous locomotion in individual cats are summarized in Table 1. The overall baseline values of HR and MAP were 168 ± 7 beats/min and 118 ± 4 mmHg (n = 5 cats), respectively. HR increased by 15-36 beats/min and MAP increased by 5-60 mmHg during spontaneous overground locomotion produced by decerebrate cats (Table 1). The average time course of the increases in HR and MAP at the beginning of spontaneous locomotion was analyzed as shown in Fig. 2A. A significant increase in HR occurred 1 s before the onset of iEMG and reached the maximum value of 24 ± 3 beats/min at 13 s from the onset of iEMG. Also, a significant increase in MAP occurred 1 s after the onset of iEMG and reached the maximum of 22 ± 4 mmHg at 15 s.
The time course of changes in HR and MAP after the cessation of spontaneous locomotion is shown in Fig. 2B. The changes in HR and MAP began to decrease as soon as locomotion ended, despite the presence of increased iEMG. HR showed a quick drop of 14 beats/min within 5 s, which was followed by a gradual decline toward the baseline level in the subsequent 80-s recovery period. In contrast, MAP decreased by 18 mmHg within 10 s and remained at this level. Effect of SAD. The effects of SAD on the baseline values of HR and MAP varied among cats (Table 1), and the overall changes in these baseline values were not significant before and after SAD. During spontaneous locomotion after SAD (Fig. 3), there were significant increases in HR and MAP. In the initial period of locomotion (0-4 s from the onset of iEMG), the average time course and magnitude of the increases in HR and MAP were identical before and after SAD (Fig. 3). However, in the subsequent period of locomotion, SAD had a significant effect on the magnitude of increases in HR and MAP. SAD attenuated the peak increase of HR (21 ± 2 beats/min observed at 15 s before SAD vs. 9 ± 1 beats/min observed at 12 s after SAD) but augmented the peak increase in MAP (13 ± 2 mmHg observed at 16 s before SAD vs. 30 ± 3 mmHg observed at 16 s after SAD). These contrasting effects of SAD on the peak increases in HR and MAP were similarly observed in individual cats (Table 1). Conversely, the time in which HR and MAP peaked in the average time course analysis was not different before and after SAD.
Indeed, in 33 (63%) of 52 trials performed by 4 cats after SAD, the early and late peaks of the pressor response were discriminated. In the trials the early peak of the pressor response was 11 ± 1 mmHg and appeared at 3.6 ± 0.2 s from the iEMG onset, indicating that there was no significant difference in the amplitude and time of the early peak of MAP. In contrast, the late peak amplitude of the pressor response was significantly greater after SAD (33 ± 3 mmHg at 14.9 ± 1.3 s from the iEMG onset) than that before SAD (26 ± 3 mmHg at 15.5 ± 1.1 s from the iEMG onset). In the 80-s recovery period (Fig. 3B), the time courses of the changes in HR observed before and after SAD were almost identical, but the HR level after SAD was shifted to a lower value than that before SAD. The time course of the changes in MAP in the recovery period was also similar before and after SAD, except for a brief period immediately after the end of locomotion. Histology. From the histological analysis (n = 6 cats), it was observed that the transection occurred in the middle of the hypothalamus in the sagittal plane, as shown in Fig. 4. In all cats, it was found that the cerebrum and the rostral part of the hypothalamus (the anterior hypothalamic area, supraoptic nucleus, and rostral part of the lateral hypothalamic area) were disconnected from the brain stem. However, the caudal part of the hypothalamus (the posterior hypothalamic area and the caudal parts of the lateral hypothalamic area, and the ventromedial nucleus of the hypothalamus) were intact.
DISCUSSION
The time course of the cardiovascular responses during spontaneous overground locomotion was studied before and after SAD in freely moving decerebrate cats. Our major new finding is that HR began to increase immediately before the onset of iEMG and MAP began to rise almost at the onset of iEMG. The time course and magnitude of the increases in HR and MAP observed in the initial period of locomotion were identical before and after SAD. These results suggest that the rapid adjustment of HR and MAP occurs in parallel with locomotor movement in animals without the cerebrum and the rostral part of the diencephalon and that the neural mechanism responsible for this adjustment is independent of the arterial baroreflexes.
The present finding that the increase in HR preceded the onset of EMG activity of the forelimb triceps brachialis muscle and the rise in ABP occurred almost simultaneously with the iEMG onset suggests that this rapid cardiovascular adjustment is directly initiated by descending signals from higher brain centers, although it cannot be excluded that a reflex originating from receptors in the exercising muscle may contribute further to the cardiovascular adjustment after the start of locomotion (8, 13). Furthermore, SAD did not affect the increases in HR and MAP at the initial period of spontaneous overground locomotion (before and within 4 s after the iEMG onset). Taken together, it is likely that central descending signals were capable of generating the rapid cardiovascular adjustment at the onset of spontaneous locomotion in decerebrate cats without feedback signals from the contracting muscles and arterial baroreceptors. Our idea is supported by previous findings using unanesthetized decerebrate cats showing that responses in HR, MAP, and RSNA occurred during spontaneous fictive locomotion (5-7).
In intact awake animals, such rapid cardiovascular adjustment has been observed during static and dynamic exercises and other voluntary behaviors. RSNA and HR began to increase immediately before or at the onset of voluntary static exercise in cats (12) and at the first step of treadmill exercise in rabbits (18). The instantaneous adjustment of RSNA and HR was also observed during eating (12), grooming (12), and defense reactions (1) in conscious cats. Because the rapid cardiovascular adjustment that decerebrate cats produced during spontaneous overground locomotion seems identical to the results observed in intact awake animals, the cerebrum and the rostral part of the diencephalon may not be essential for generating direct descending signals responsible for the rapid cardiovascular adjustment during locomotion in awake animals.
Possible sites in the brain stem producing both cardiovascular adjustment and somatomotor behavioral changes have been reported. Chemical stimulation of neurons in the hypothalamus involving the posterior hypothalamus, the lateral hypothalamus, and a part of the field of Forel induced both cardiorespiratory changes and locomotor movements (5-7, 20, 23). Neurons in the localized areas of the hypothalamus and the midbrain periaqueductal gray matter were capable of producing both cardiovascular changes and body defense movements (2, 10, 21). These sites of the brain stem may be responsible for generating direct descending signals for the rapid cardiovascular adjustment during spontaneous locomotion evoked by decerebrate cats.
Because stimulation of arterial baroreceptors induced by injection of norepinephrine inhibited the increase in RSNA during voluntary static exercise in awake cats (11), it is assumed that when MAP increases considerably during locomotion, the arterial baroreflexes decrease sympathetic efferent nerve activity and thereby counteract the pressor response. If the inhibition of the baroreflexes is eliminated, the pressor response during locomotion will be enhanced. Indeed, we found that SAD augmented the response in MAP observed in the late period of locomotion, whereas the denervation did not affect the rapid increases in HR and MAP in the initial 4-s period of locomotion. Stimulation of the sympathetic nervous system is likely to increase MAP in the initial period of spontaneous locomotion, which in turn may inhibit sympathetic nerve activity and counteract the pressor response. However, a time lag from a decrease in sympathetic nerve activity to a change in MAP mediated via a relaxation of vascular smooth muscles should be taken into account because the time lag was ~6 s when an increase in RSNA during static exercise in the conscious cat was followed by a rise in MAP (11). On the other hand, the augmenting effect of SAD on the late increase in MAP suggests that the arterial baroreflexes can counteract the increase in MAP in the late period of spontaneous locomotion in decerebrate cats. This effect is in agreement with the previous findings made during dynamic exercises in conscious dogs (19, 24). In addition, the augmented response in MAP is presumably caused by a marked increase in sympathetic vasomotor activity to peripheral vascular beds because the HR response was decreased after SAD.
In contrast, the opposite effect on the HR response of SAD was found. SAD reduced the increase in HR in the late period of spontaneous locomotion. This attenuated HR response might be caused by the loss of vagal efferents to the heart because we cut the vagal nerve in some cats during the denervation surgery. However, this is unlikely because the cats with and without vagotomy showed the same reduction of the HR response after SAD (Table 1). Alternatively, to explain the contrasting effect of SAD on the responses in HR and MAP, we considered that the two (cardiac and vasomotor) components of the arterial baroreflexes are controlled differently during spontaneous locomotion. The cardiac component of the arterial baroreflexes may be inhibited during spontaneous locomotion, whereas the vasomotor component of the arterial baroreflexes is operating. If the inhibition of the cardiac component of the arterial baroreflexes contributes to cardiac acceleration during locomotion, the lack of arterial baroreceptors with SAD will result in a decreased HR response. In support of this explanation, previous studies showed that the cardiac component of the arterial baroreflexes was inhibited by electrical stimulation of muscle afferent fibers (14, 17) or by stimulation of the central nervous system (16). Thus the attenuating effect on the HR response of SAD suggests that the cardiac component of the arterial baroreflexes is inhibited during locomotion, which in turn contributes to an increase in HR observed in the late period of spontaneous locomotion.
In conclusion, it is likely that the increase in HR obtained immediately before the onset of spontaneous locomotion in decerebrate cats is caused by direct descending signals that couple with locomotor activity and not by a reflex arising from the contracting muscle and from arterial baroreceptors. It is concluded that some central site, other than the cerebrum and the rostral part of the diencephalon, generates a central descending signal that can increase HR before spontaneous locomotion.
ACKNOWLEDGEMENTS
This study was supported by a Grant-in-Aid for Scientific Research from the Ministry of Education, Science and Culture of Japan, and by research grants from the Japan Heart Foundation and from the Japan Cardiovascular Research Foundation.
FOOTNOTES
Address for reprint requests: T. Sadamoto, Dept. of Sport Science, Faculty of Letters, Nara Women's Univ., Kitauoyanishi-machi, Nara 630, Japan.
Received 20 December 1996; accepted in final form 18 July 1997.
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