Comprehensive Physiology Wiley Online Library

Central Neural Control of Respiration and Circulation During Exercise

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Respiration
2 Circulation
3 Central Command Mechanisms
3.1 Central Drive of Locomotion
3.2 Locomotor Pattern Generator
3.3 Supraspinal Locomotor Sites
4 Central Command Control of Respiration and Circulation in Animals
4.1 Cerebral Cortex
4.2 Hypothalamic Locomotor Region
4.3 Mesencephalic Locomotor Region
4.4 Amygdala
4.5 Awake, Exercising Animal Studies
5 Short‐Term Potentiation
5.1 Respiration
6 Central Command Control of Respiration and Circulation in Humans
6.1 Respiration
6.2 Circulation
7 Interactions Between Central Command and Peripheral Feedback
8 Interaction of Central Command with Cardiorespiratory Reflexes
8.1 Baroreceptor Reflex
8.2 Hering‐Breuer Reflex
8.3 Chemoreceptor Reflexes
9 Conclusions
Figure 1. Figure 1.

Ventilation (V) increases in direct proportion to the workload during mild and moderate rhythmic exercise in humans such that arterial PO2, PCO2, and pH remain constant.

From Waldrop 254
Figure 2. Figure 2.

Examples of cardiovascular responses to (A) dynamic and (B) static exercise. The dynamic exercise was progressively increased to ; the static exercise was sustained at 30% of maximal voluntary contraction. Q, cardiac output; HR, heart rate; SV, stroke volume; ABP, systolic (top line), mean (middle line), and diastolic (bottom line) arterial blood pressure; TPR, total peripheral resistance.

From Mitchell and Raven 182
Figure 3. Figure 3.

Frontal and parasagittal drawings showing location of hypothalamic (subthalamic) and mesencephalic locomotor regions in the cat.

Adapted from Eldridge et al. 72
Figure 4. Figure 4.

Animal preparations utilized for studying exercise in the unanesthetized decorticate cat (A) and fictive locomotion in the paralyzed ventilated cat (B).

Adapted from Eldridge et al. 71
Figure 5. Figure 5.

Example of the respiratory, cardiovascular, and fictive locomotor responses elicited by stimulation in the hypothalamic locomotor region of a paralyzed cat.

From Eldridge et al. 71
Figure 6. Figure 6.

Hemodynamic and respiratory responses to electrical stimulation of the hypothalamic (subthalamic) locomotor region.

From Waldrop et al. 259
Figure 7. Figure 7.

Averaged changes in blood flow (as determined using the radioactive microsphere technique) to the heart, kidneys, diaphragm, and selected limb muscles of anesthetized cats during stimulation of the hypothalamic locomotor region.

From Waldrop et al. 259
Figure 8. Figure 8.

Responses (electromyographic recordings) of the triceps muscles to microinje GABA antagonists (A, picrotoxin; B, bicuculline) and a GABA agonist (muscimol) into pothalamic locomotor region of an anesthetized cat. Both antagonists produced rhythm nating bursts of left and right triceps activity that were reversed by the GABA agonist. 1 of the injections are denoted by filled triangles in C and D.

From Waldrop et al. 257
Figure 9. Figure 9.

Arterial pressure, heart rate, and skeletal muscle (triceps) responses to microinjection of a GABA antagonist [bicuculline methiodide (BMI)] into the hypothalamic locomotor region of an anesthetized cat. The responses evoked by the GABA antagonist were reversed by microinjection of a GABA agonist (muscimol) into the same hypothalamic site. The injection site is denoted by a filled triangle on the line drawing.

From Waldrop et al. 257
Figure 10. Figure 10.

Arterial pressure, heart rate, and sympathetic nerve (cervical nerve activity) responses to microinjection of a GABA antagonist (picrotoxin) into the hypothalamic locomotor region of an anesthetized cat. The increased activity (B) elicited by the injection was reversed by microinjection of a GABA agonist

muscimol, (C)]. [From Waldrop and Bauer 256
Figure 11. Figure 11.

Averaged changes in force, mean renal sympathetic nerve activity (MRNA), heart rate (HR), and mean arterial blood pressure (MAP) during two bouts of static exercise performed by a conscious cat.

From Matsukawa et al. 167
Figure 12. Figure 12.

Recording of phrenic nerve and integrated phrenic activity during control (left), during stimulation (bar) of a carotid sinus nerve, and during recovery in a paralyzed, vagotomized cat with partial pressures of CO2 and O2 kept constant by means of a servocontrolled ventilator. It shows the rapid increase of respiration at stimulus onset, further increase to a steady‐state within two breaths, and a rapid decrease on stimulus cessation followed by a slow recovery process (afterdischarge).

Figure 13. Figure 13.

Example of development and recovery of respiratory short‐term potentiation with stimulation of calf muscles (CM) in paralyzed, vagotomized cat with controlled PCO2. The animal had fortuitously developed apneustic breathing. The potentiation develops and decays according to its usual time course and is independent of the actual respirations.

Figure 14. Figure 14.

Effects of different modes of stimulating carotid sinus nerve on respiratory (phrenic) responses and recovery in paralyzed, vagotomized cat. A, Continuous stimulation. B, Expiratory‐only stimulation. C, Alternate‐cycle stimulation. Stimulated breaths of alternate‐cycle experiment are similar to those of continuous stimulation, and nonstimulated breaths are similar to those of expiratory stimulation. Despite differences in direct effects of stimulus, the amount of potentiation and the decay (afterdischarge) patterns are similar in all three experiments. Slowly rising activity during expiratory‐only stimulations represents increasing activation of potentiation. AP, arterial pressure.

From Eldridge and Gill‐Kumar 66
Figure 15. Figure 15.

Experiments showing that complete suppression of inspiratory activity during carotid sinus nerve (CSN) stimulation does not prevent potentiation in paralyzed, vagotomized cat. A, Control experiment showing baseline activity at left, effect of CSN stimulation of 30 s, and recovery. B, Baseline activity at left, effect of combined CSN and vagal stimulation, and recovery. Although inspirations are completely inhibited by vagal effects during combined stimulation, poststimulation respiratory activity is augmented, just as in control experiment, and decays with approximately the same time course.

From Eldridge and Gill‐Kumar 65
Figure 16. Figure 16.

Semilogarithmic plot of respiratory activity (units) vs. time during a stimulation (STIM.) and decay of potentiation (AFTERDISCHARGE) to show potential error in measurement of its time constant (τ). The true τ of the decay is 50 s. If the τ is measured as the 63% decay from the true starting level of 50 units, it will give the correct value of 50 s (point A). However, some of the total decrease, the loss of the direct effect of the stimulus, is not part of the exponential function. Thus, if the τ is measured as a 63% decay from the end‐stimulation level of 100 units, then an incorrect τ of only 15.3 s (point B) will be calculated.

Figure 17. Figure 17.

Computer‐generated neural inspiratory (phrenic equivalent) activity in a model that incorporates short‐term potentiation (onset τ, 10 s; offset τ, 50 s) and that mimicks constant blood gases and has no other feedback. Control at left, then a 4 min facilitatory stimulus (bar), and then 5 min of recovery. The STP has almost no effect on the pattern after the first 30 s of stimulation and little effect on the recovery after 2 min. (The irregular patterns in the tracing are pixel effects from the computer screen and have no physiological meaning.)

Figure 18. Figure 18.

Computer‐generated ventilation (liters per minute) and arterial, end‐tidal, and medullary PCO2 during rest (VO2 = 0.25 liter/min), 6 min of exercise ( = 1.0 liter/min), and recovery (see text and footnote for details of model). In panel A the model includes the usual short‐term potentiating (STP) mechanism (τ on = 10 s; τ off = 50 s); it yields a typical and normal ventilatory response to exercise. In panel B the STP has been removed, with the result that ventilation at the end of the 6 min of exercise is slightly less than in the model with STP, all PCO2 values are slightly higher, and there are increased oscillations of ventilation after both onset and cessation of exercise.

Figure 19. Figure 19.

Schematic representation of the ventilatory response to static (handgrip) exercise. Asterisks denote the onset and end of the exercise bout.

From Waldrop 255
Figure 20. Figure 20.

A, Experimental design for reducing the magnitude of central command required to achieve a muscle tension. The drawing shows how vibration is used to activate primary afferents from the contracting muscles, thereby contributing reflex excitation of the motoneurons innervating the muscle. The same amount of force can be generated as was true without the reflex excitation (on the left) but with a reduced central command component. B, Experimental design for increasing the magnitude of central command required to achieve a muscle tension. The drawing shows how vibration is used to activate primary afferents from a muscle (biceps) antagonist to the contracting muscles, thereby contributing reflex inhibition of the motoneurons innervating the contracting muscle. An increased central command component is required in order for the same amount of force to be generated as was true without the reflex inhibition (on the left).

Adapted from Goodwin et al. 104
Figure 21. Figure 21.

A, Reduction of central command. The blood pressure, heart rate, and ventilatory responses during a normal contraction are shown by the filled circles and continuous lines; the responses when vibration was used to reduce central command are shown by open circles and interrupted lines. B, Augmentation of central command. The blood pressure, heart rate, and ventilatory responses during a normal contraction are shown by the filled circles and continuous lines; the responses when vibration was used to increase central command are shown by open circles and interrupted lines.

Adapted from Goodwin et al. 104
Figure 22. Figure 22.

Schematic representation of the ventilatory response to static (handgrip) exercise. Asterisks denote the onset and end of the exercise bout.

From Waldrop 254
Figure 23. Figure 23.

Effect on heart rate and blood pressure responses to static exercise of neuromuscular blockade and of epidural anesthesia. Left, Comparison of each intervention to control at the same absolute force. Right, Comparison at the same relative force.

From Mitchell et al. 184
Figure 24. Figure 24.

Effect of intended contraction on heart rate and blood pressure in a totally paralyzed subject. Bars indicate the time when contractions were attempted with values for percentage of MVC.

From Gandevia et al. 97
Figure 25. Figure 25.

Heart rate and blood pressure responses and rating of perceived exertion (r.p.e. units on scale of 6–20) during progressive exercise to maximal. Filled circles represent exercise during the control study and open circles represent maximal effort as the neuromuscular blockade decreased. Values are means ± SEM.

From Galbo et al. 95
Figure 26. Figure 26.

Muscle sympathetic nerve activity (MSNA) and force. % MVC, percentage of maximal voluntary contraction. A study from one subject before and during partial neuromuscular blockade with curare.

From Victor et al. 248
Figure 27. Figure 27.

Effect of muscle fatigue on rating of perceived effort (RPE) and peak increase in skin sympathetic nerve activity [Skin SNA (%)] of the same handgrip force (kg). Data are mean ± SEM. Asterisks denote significant differences from previous handgrip contraction (P < 0.05).

From Vissing et al. 251
Figure 28. Figure 28.

Hemodynamic values at rest and during work rates of 10, 20, and 30 watts (W) performed with one leg and 2 × 20 W performed with two legs. Open circles represent voluntary dynamic exercise, filled triangles represent electrically induced exercise, and filled rectangles represent electrically induced exercise during epidural anesthesia. Values are mean ± SEM. Asterisk denotes differences between voluntary and electrically induced exercise before epidural anesthesia. Double asterisks denote differences between electrically induced exercise with and without epidural anesthesia.

From Strange et al. 234
Figure 29. Figure 29.

Cardiac output, heart rate, stroke volume, and blood pressure at rest and during one‐legged exercise at two workloads. Upper three panels in normal subjects with no weakness. (A, right leg; Δ, left leg). Lower four panels in subjects with one weak leg (•, normal leg; τ, weak leg). Values are means (± SD).

From Innes et al. 132
Figure 30. Figure 30.

Effects of static muscular contraction (elicited by ventral root stimulation) upon arterial pressure, heart rate, and the discharge frequency of a posterior hypothalamic neuron of an anesthetized cat. Note that contraction and other mechanical stimulation of the gastrocnemius muscles increased the discharge frequency of this neuron. Baroreceptor stimulation produced by a phenylephrine‐induced increase in arterial pressure had no significant effect upon this neuron. Location of the neuron is indicated by the filled triangle in the line drawing at bottom.

From Waldrop and Stremel 264
Figure 31. Figure 31.

Computer‐generated ventilatory and PCO2 responses to dynamic exercise. Panel A shows the normal responses with all mechanisms present. In panel B, only the central command component has been deleted. Notice the loss of the initial fast respiratory component but with the peak response differing little from that observed in panel A. The respiratory response is now dependent upon the rising PCO2. Details of the computer model are described in the text.



Figure 1.

Ventilation (V) increases in direct proportion to the workload during mild and moderate rhythmic exercise in humans such that arterial PO2, PCO2, and pH remain constant.

From Waldrop 254


Figure 2.

Examples of cardiovascular responses to (A) dynamic and (B) static exercise. The dynamic exercise was progressively increased to ; the static exercise was sustained at 30% of maximal voluntary contraction. Q, cardiac output; HR, heart rate; SV, stroke volume; ABP, systolic (top line), mean (middle line), and diastolic (bottom line) arterial blood pressure; TPR, total peripheral resistance.

From Mitchell and Raven 182


Figure 3.

Frontal and parasagittal drawings showing location of hypothalamic (subthalamic) and mesencephalic locomotor regions in the cat.

Adapted from Eldridge et al. 72


Figure 4.

Animal preparations utilized for studying exercise in the unanesthetized decorticate cat (A) and fictive locomotion in the paralyzed ventilated cat (B).

Adapted from Eldridge et al. 71


Figure 5.

Example of the respiratory, cardiovascular, and fictive locomotor responses elicited by stimulation in the hypothalamic locomotor region of a paralyzed cat.

From Eldridge et al. 71


Figure 6.

Hemodynamic and respiratory responses to electrical stimulation of the hypothalamic (subthalamic) locomotor region.

From Waldrop et al. 259


Figure 7.

Averaged changes in blood flow (as determined using the radioactive microsphere technique) to the heart, kidneys, diaphragm, and selected limb muscles of anesthetized cats during stimulation of the hypothalamic locomotor region.

From Waldrop et al. 259


Figure 8.

Responses (electromyographic recordings) of the triceps muscles to microinje GABA antagonists (A, picrotoxin; B, bicuculline) and a GABA agonist (muscimol) into pothalamic locomotor region of an anesthetized cat. Both antagonists produced rhythm nating bursts of left and right triceps activity that were reversed by the GABA agonist. 1 of the injections are denoted by filled triangles in C and D.

From Waldrop et al. 257


Figure 9.

Arterial pressure, heart rate, and skeletal muscle (triceps) responses to microinjection of a GABA antagonist [bicuculline methiodide (BMI)] into the hypothalamic locomotor region of an anesthetized cat. The responses evoked by the GABA antagonist were reversed by microinjection of a GABA agonist (muscimol) into the same hypothalamic site. The injection site is denoted by a filled triangle on the line drawing.

From Waldrop et al. 257


Figure 10.

Arterial pressure, heart rate, and sympathetic nerve (cervical nerve activity) responses to microinjection of a GABA antagonist (picrotoxin) into the hypothalamic locomotor region of an anesthetized cat. The increased activity (B) elicited by the injection was reversed by microinjection of a GABA agonist

muscimol, (C)]. [From Waldrop and Bauer 256


Figure 11.

Averaged changes in force, mean renal sympathetic nerve activity (MRNA), heart rate (HR), and mean arterial blood pressure (MAP) during two bouts of static exercise performed by a conscious cat.

From Matsukawa et al. 167


Figure 12.

Recording of phrenic nerve and integrated phrenic activity during control (left), during stimulation (bar) of a carotid sinus nerve, and during recovery in a paralyzed, vagotomized cat with partial pressures of CO2 and O2 kept constant by means of a servocontrolled ventilator. It shows the rapid increase of respiration at stimulus onset, further increase to a steady‐state within two breaths, and a rapid decrease on stimulus cessation followed by a slow recovery process (afterdischarge).



Figure 13.

Example of development and recovery of respiratory short‐term potentiation with stimulation of calf muscles (CM) in paralyzed, vagotomized cat with controlled PCO2. The animal had fortuitously developed apneustic breathing. The potentiation develops and decays according to its usual time course and is independent of the actual respirations.



Figure 14.

Effects of different modes of stimulating carotid sinus nerve on respiratory (phrenic) responses and recovery in paralyzed, vagotomized cat. A, Continuous stimulation. B, Expiratory‐only stimulation. C, Alternate‐cycle stimulation. Stimulated breaths of alternate‐cycle experiment are similar to those of continuous stimulation, and nonstimulated breaths are similar to those of expiratory stimulation. Despite differences in direct effects of stimulus, the amount of potentiation and the decay (afterdischarge) patterns are similar in all three experiments. Slowly rising activity during expiratory‐only stimulations represents increasing activation of potentiation. AP, arterial pressure.

From Eldridge and Gill‐Kumar 66


Figure 15.

Experiments showing that complete suppression of inspiratory activity during carotid sinus nerve (CSN) stimulation does not prevent potentiation in paralyzed, vagotomized cat. A, Control experiment showing baseline activity at left, effect of CSN stimulation of 30 s, and recovery. B, Baseline activity at left, effect of combined CSN and vagal stimulation, and recovery. Although inspirations are completely inhibited by vagal effects during combined stimulation, poststimulation respiratory activity is augmented, just as in control experiment, and decays with approximately the same time course.

From Eldridge and Gill‐Kumar 65


Figure 16.

Semilogarithmic plot of respiratory activity (units) vs. time during a stimulation (STIM.) and decay of potentiation (AFTERDISCHARGE) to show potential error in measurement of its time constant (τ). The true τ of the decay is 50 s. If the τ is measured as the 63% decay from the true starting level of 50 units, it will give the correct value of 50 s (point A). However, some of the total decrease, the loss of the direct effect of the stimulus, is not part of the exponential function. Thus, if the τ is measured as a 63% decay from the end‐stimulation level of 100 units, then an incorrect τ of only 15.3 s (point B) will be calculated.



Figure 17.

Computer‐generated neural inspiratory (phrenic equivalent) activity in a model that incorporates short‐term potentiation (onset τ, 10 s; offset τ, 50 s) and that mimicks constant blood gases and has no other feedback. Control at left, then a 4 min facilitatory stimulus (bar), and then 5 min of recovery. The STP has almost no effect on the pattern after the first 30 s of stimulation and little effect on the recovery after 2 min. (The irregular patterns in the tracing are pixel effects from the computer screen and have no physiological meaning.)



Figure 18.

Computer‐generated ventilation (liters per minute) and arterial, end‐tidal, and medullary PCO2 during rest (VO2 = 0.25 liter/min), 6 min of exercise ( = 1.0 liter/min), and recovery (see text and footnote for details of model). In panel A the model includes the usual short‐term potentiating (STP) mechanism (τ on = 10 s; τ off = 50 s); it yields a typical and normal ventilatory response to exercise. In panel B the STP has been removed, with the result that ventilation at the end of the 6 min of exercise is slightly less than in the model with STP, all PCO2 values are slightly higher, and there are increased oscillations of ventilation after both onset and cessation of exercise.



Figure 19.

Schematic representation of the ventilatory response to static (handgrip) exercise. Asterisks denote the onset and end of the exercise bout.

From Waldrop 255


Figure 20.

A, Experimental design for reducing the magnitude of central command required to achieve a muscle tension. The drawing shows how vibration is used to activate primary afferents from the contracting muscles, thereby contributing reflex excitation of the motoneurons innervating the muscle. The same amount of force can be generated as was true without the reflex excitation (on the left) but with a reduced central command component. B, Experimental design for increasing the magnitude of central command required to achieve a muscle tension. The drawing shows how vibration is used to activate primary afferents from a muscle (biceps) antagonist to the contracting muscles, thereby contributing reflex inhibition of the motoneurons innervating the contracting muscle. An increased central command component is required in order for the same amount of force to be generated as was true without the reflex inhibition (on the left).

Adapted from Goodwin et al. 104


Figure 21.

A, Reduction of central command. The blood pressure, heart rate, and ventilatory responses during a normal contraction are shown by the filled circles and continuous lines; the responses when vibration was used to reduce central command are shown by open circles and interrupted lines. B, Augmentation of central command. The blood pressure, heart rate, and ventilatory responses during a normal contraction are shown by the filled circles and continuous lines; the responses when vibration was used to increase central command are shown by open circles and interrupted lines.

Adapted from Goodwin et al. 104


Figure 22.

Schematic representation of the ventilatory response to static (handgrip) exercise. Asterisks denote the onset and end of the exercise bout.

From Waldrop 254


Figure 23.

Effect on heart rate and blood pressure responses to static exercise of neuromuscular blockade and of epidural anesthesia. Left, Comparison of each intervention to control at the same absolute force. Right, Comparison at the same relative force.

From Mitchell et al. 184


Figure 24.

Effect of intended contraction on heart rate and blood pressure in a totally paralyzed subject. Bars indicate the time when contractions were attempted with values for percentage of MVC.

From Gandevia et al. 97


Figure 25.

Heart rate and blood pressure responses and rating of perceived exertion (r.p.e. units on scale of 6–20) during progressive exercise to maximal. Filled circles represent exercise during the control study and open circles represent maximal effort as the neuromuscular blockade decreased. Values are means ± SEM.

From Galbo et al. 95


Figure 26.

Muscle sympathetic nerve activity (MSNA) and force. % MVC, percentage of maximal voluntary contraction. A study from one subject before and during partial neuromuscular blockade with curare.

From Victor et al. 248


Figure 27.

Effect of muscle fatigue on rating of perceived effort (RPE) and peak increase in skin sympathetic nerve activity [Skin SNA (%)] of the same handgrip force (kg). Data are mean ± SEM. Asterisks denote significant differences from previous handgrip contraction (P < 0.05).

From Vissing et al. 251


Figure 28.

Hemodynamic values at rest and during work rates of 10, 20, and 30 watts (W) performed with one leg and 2 × 20 W performed with two legs. Open circles represent voluntary dynamic exercise, filled triangles represent electrically induced exercise, and filled rectangles represent electrically induced exercise during epidural anesthesia. Values are mean ± SEM. Asterisk denotes differences between voluntary and electrically induced exercise before epidural anesthesia. Double asterisks denote differences between electrically induced exercise with and without epidural anesthesia.

From Strange et al. 234


Figure 29.

Cardiac output, heart rate, stroke volume, and blood pressure at rest and during one‐legged exercise at two workloads. Upper three panels in normal subjects with no weakness. (A, right leg; Δ, left leg). Lower four panels in subjects with one weak leg (•, normal leg; τ, weak leg). Values are means (± SD).

From Innes et al. 132


Figure 30.

Effects of static muscular contraction (elicited by ventral root stimulation) upon arterial pressure, heart rate, and the discharge frequency of a posterior hypothalamic neuron of an anesthetized cat. Note that contraction and other mechanical stimulation of the gastrocnemius muscles increased the discharge frequency of this neuron. Baroreceptor stimulation produced by a phenylephrine‐induced increase in arterial pressure had no significant effect upon this neuron. Location of the neuron is indicated by the filled triangle in the line drawing at bottom.

From Waldrop and Stremel 264


Figure 31.

Computer‐generated ventilatory and PCO2 responses to dynamic exercise. Panel A shows the normal responses with all mechanisms present. In panel B, only the central command component has been deleted. Notice the loss of the initial fast respiratory component but with the peak response differing little from that observed in panel A. The respiratory response is now dependent upon the rising PCO2. Details of the computer model are described in the text.

References
 1. Abrahams, V. C., S. M. Hilton, and A. W. Zbrozyna. Active muscle vasodilation produced by stimulation of the brain stem: its significance in the defence reaction. J. Physiol. (Lond.) 154: 491–513, 1960.
 2. Adams, L., H. Frankel, J. Garlick, A. Guz, K. Murphy, and S. J. G. Semple. The role of spinal cord transmission in the ventilatory response to exercise in man. J. Physiol. (Lond.) 355: 85–97, 1984.
 3. Adams, L., J. Garlick, A. Guz, K. Murphy, and S. J. G. Semple. Is the voluntary control of exercise in man necessary for the ventilatory response? J. Physiol. (Lond.). 355: 71–83, 1984.
 4. Adams, L., A. Guz, J. A. Innes, and K. Murphy. The early circulatory and ventilatory response to voluntary and electrically induced exercise in man. J. Physiol. (Lond.) 383: 19–30, 1987.
 5. Ahmed, M., G. G. Giesbrecht, C. Serrette, D. Georgopoulos, and N. R. Anthonisen. Respiratory short‐term potentiation (after‐discharge) in elderly humans. Respir. Physiol. 93: 163–173, 1993.
 6. Alam, M., and F. H. Smirk. Unilateral loss of a blood pressure raising, pulse accelerating, reflex from voluntary muscle due to a lesion of the spinal cord. Clin. Sci. 3: 247–258, 1938.
 7. Aminoff, M. J., and T. A. Sears. Spinal integration of segmental, cortical and breathing inputs to thoracic respiratory motoneurons. J. Physiol. (Lond.) 215: 557–575, 1971.
 8. Ashbridge, K. M., S. Jennett, and J. B. North. The absence of post‐hyperventilation in the wakeful state. J. Physiol. (Lond.) 230: 52P, 1973.
 9. Asmussen, E. Ventilation at transition from rest to exercise. Acta Physiol. Scand. 89: 68–78, 1973.
 10. Asmussen, E. Control of ventilation in exercise. Exerc. Sport Sci. Rev. 11: 24–54, 1983.
 11. Asmussen, E., S. H. Johansen, M. Jorgensen, and M. Nielsen. On the nervous factors controlling respiration and circulation during exercise. Experiments with curarization. Acta Physiol. Scand. 63: 343–350, 1965.
 12. Asmussen, E., and M. Nielsen. Experiments on nervous factors controlling respiration and circulation during exercise employing blocking of the blood flow. Acta Physiol. Scand. 60: 103–111, 1964.
 13. Asmussen, E., M. Nielsen, and G. Wieth‐Pedersen. Cortical or reflex control of respiration during muscular work? Acta Physiol. Scand. 6: 168–175, 1943.
 14. Asmussen, E., M. Nielsen, and G. Wieth‐Pedersen. On the regulation of the circulation during muscular work. Acta Physiol. Scand. 6: 353–358, 1943.
 15. Badr, M. F., J. B. Skatrud, and J. A. Dempsey. Determinants of poststimulus potentiation in humans during NREM sleep. J. Appl. Physiol. 73: 1958–1971, 1992.
 16. Baev, K. V., V. K. Berezovskii, T. T. Kebkalo, and L. A. Savos'kina. Forebrain projections to the hypothalamic locomotor region in cats. Neirofiziologiya 17: 255–263, 1985.
 17. Baev, K. V., V. K. Berezovskii, T. T. Kebkalo, and L. A. Savos'kina. Projections of neurons of the hypothalamic locomotor region to some brainstem and spinal cord structures in the cat. Neirofiziologiya 17: 817–823, 1985.
 18. Barman, S. M. Descending projections of hypothalamic neurons with sympathetic nerve‐related activity. J. Neurophysiol. 64: 1019–1032, 1990.
 19. Barman, S. M., and G. L. Gebber. Hypothalamic neurons with activity patterns related to sympathetic nerve discharge. Am. J. Physiol. 242 (Regulatory Integrative Comp. Physiol. 11): R34–R43, 1982.
 20. Bauer, R. M., G. A. Iwamoto, and T. G. Waldrop. Discharge patterns of ventrolateral medullary neurons during muscular contraction. Am. J. Physiol. 259 (Regulatory Integrative Comp. Physiol. 28): R606–R611, 1990.
 21. Bauer, R. M., G. A. Iwamoto, and T. G. Waldrop. Ventrolateral medullary neurons modulate pressor reflex to muscular contraction. Am. J. Physiol. 257 (Regulatory Integrative Comp. Physiol. 26): R1154–R1161, 1989.
 22. Bauer, R. M., M. B. Vela, T. Simon, and T. G. Waldrop. A GABAergic mechanism in the posterior hypothalamus modulates baroreflex bradycardia. Brain Res. Bull. 20: 633–641, 1988.
 23. Bauer, R. M., T. G. Waldrop, G. A. Iwamoto, and M. A. Holzwarth. Properties of ventrolateral medullary neurons that respond to muscular contraction. Brain Res. Bull. 28: 167–178, 1992.
 24. Bedford, T. G., P. K. Loi, and C. C. Crandall. A model of dynamic exercise—the decerebrate rat locomotor preparation. J. Appl. Physiol. 72: 121–127, 1992.
 25. Benchitrit, G., and T. Pham Dinh. Analyse d'une étude statistique de las ventilation cycle par cycle chez l'homme aur repos. Biom. Humaine 8: 7–19, 1973.
 26. Benchitrit, G., and T. Pham Dinh. Un essai d'analyse statistique de séries de données respiratoires. Rev. Stat. Appl. 12: 51–68, 1974.
 27. Berezovskii, V. K., T. G. Kebkalo, and L. A. Savos'kina. Afferent brainstem projections to the hypothalamic locomotor region of the cat brain. Neurophysiology 16: 279–286, 1984.
 28. Birzis, L., and A. Hemingway. Shivering as a result of brain stimulation. J. Neurophysiol. 20: 91–99, 1957.
 29. Boothby, W. M. Absence of apnoea after forced breathing. J. Physiol. (Lond.) 45: 328–333, 1912.
 30. Borst, C., A. P. Hollander, and L. N. Bouman. Cardiac acceleration elicited by voluntary muscle contractions of minimal duration. J. Appl. Physiol. 32: 70–77, 1972.
 31. Brice, A. G., H. V. Forster, L. G. Pan, A. Funahashi, T. F. Lowry, C. L. Murphy, and M. D. Hoffman. Ventilatory and Paco2 responses to voluntary and electrically induced leg exercise. J. Appl. Physiol. 64: 218–225, 1988.
 32. Budzinska, K. Respiratory cycle as an index of CNS excitability. Warsaw: University of Warsaw, Ph.D. thesis, 1978.
 33. Calaresu, F. R., and J. Ciriello. Projections to the hypothalamus from buffer nerves and nucleus tractus solitarius in the cat. Am. J. Physiol. 239 (Regulatory Integrative Comp. Physiol. 8): R130–R136, 1980.
 34. Casey, K., J. Duffin, and G. V. McAvoy. The effect of exercise on the central‐chemoreceptor threshold in man. J. Physiol. (Lond.) 383: 9–18, 1987.
 35. Cerretelli, P., R. Sikand, and L. E. Fahri. Readjustments in cardiac output and gas exchange during onset of exercise and recovery. J. Appl. Physiol. 21: 1345–1350, 1966.
 36. Clarke, N. P., and R. F. Rushmer. Tissue uptake of 86Rb with electrical stimulation of hypothalamus and midbrain. Am. J. Physiol. 213: 1439–1444, 1967.
 37. Clarke, N. P., O. A. Smith, and D. W. Shearn. Topographical representation of vascular smooth muscle of limbs in primate motor cortex. Am. J. Physiol. 214: 122–129, 1968.
 38. Conway, J., D. J. Patterson, E. S. Peterson, and P. A. Robbins. Changes in arterial potassium and ventilation in response to exercise in humans. J. Physiol. (Lond.) 399: 36P, 1988.
 39. Coote, J. H., S. M. Hilton, and J. F. Perez‐Gonzalez. Inhibition of the baroreceptor reflex on stimulation in the brain stem defence centre. J. Physiol. (Lond.) 288: 549–560, 1979.
 40. Corfield, D. R., K. Murphy, and A. Guz. Does cortical activation of the human diaphragm act via brainstem respiratory centres? J. Physiol. (Lond.) 467: 17P, 1993.
 41. Cunningham, D. J. C., B. B. Lloyd, and J. M. Patrick. The relation between ventilation and end‐tidal Pco2 in man during moderate exercise with and without CO2 inhalation. J. Physiol. (Lond.) 169: 104–106, 1963.
 42. Cunningham, D. J. C., E. S. Petersen, R. Peto, T. G. Pickering, and P. Sleight. Comparison of the effect of different types of exercise on the baroreflex regulation of heart rate. Acta Physiol. Scand. 86: 444–455, 1972.
 43. D'Angelo, E., and G. Torelli. Neural stimuli increasing respiration during different types of exercise. J. Appl. Physiol. 30: 116–121, 1971.
 44. Dean, C., and J. H. Coote. Discharge patterns in postganglionic neurones to skeletal muscle and kidney during activation of the hypothalamic defence areas in the cat. Brain Res. 377: 271–278, 1986.
 45. Dejours, P. Control of respiration in muscular exercise. In: Handbook of Physiology, Respiration, edited by W. O. Fenn and H. Rahn. Washington, DC: Am. Physiol. Soc., 1964, p. 631–648.
 46. Delaney, K. R., R. S. Zucker, and D. W. Tank. Calcium in motor nerve terminals associated with post‐tetanic potentiation. J. Neurosci. 9: 3558–3567, 1989.
 47. Dempsey, J. A., E. H. Vidruk, and S. M. Mastenbrook. Pulmonary control systems in exercise. Federation Proc. 39: 1498–1505, 1980.
 48. Diepstra, G., W. Gonyea, and J. H. Mitchell. Distribution of cardiac output during static exercise in the conscious cat. J. Appl. Physiol. 52: 642–646, 1982.
 49. Dillon, G. H., C. A. Shonis, and T. G. Waldrop. Hypothalamic GABAergic modulation of respiratory responses to baroreceptor stimulation. Respir. Physiol. 85: 289–304, 1991.
 50. Dillon, G. H., and T. G. Waldrop. Responses of feline caudal hypothalamic cardiorespiratory neurons to hypoxia and hypercapnia. Exp. Brain Res. 96: 260–272, 1993.
 51. Dimarco, A. F., J. R. Romaniuk, C. von Euler, and Y. Yamamoto. Immediate changes in ventilation and respiratory pattern with onset and offset of locomotion in the cat. J. Physiol. (Lond.) 343: 1–16, 1983.
 52. DiMicco, J. A., V. M. Abshire, K. D. Hankins, R. H. B. Sample, and J. H. Wible. Microinjection of GABA antagonists into the posterior hypothalamus elevates heart rate in anesthetized rats. Neuropharmacology 25: 1063–1066, 1986.
 53. Duffin, J., R. R. Gechbache, R. C. Goode, and S. A. Chung. The ventilatory response to carbon dioxide in hyperoxic exercise. Respir. Physiol. 40: 93–105, 1980.
 54. Duncan, G., R. H. Johnson, and D. G. Lambie. Role of sensory nerves in the cardiovascular and respiratory changes with isometric forearm exercise in man. Clin. Sci. 60: 145–155, 1981.
 55. Dutton, R. E., W. A. Hodson, D. G. Davies, and A. Fenner. Effect of rate of rise of carotid body Pco2 on the time course of ventilation. Respir. Physiol. 3: 367–379, 1967.
 56. Dutton, R. E., R. S. Fitzgerald, and N. Gross. Ventilatory response to square‐wave forcing of carbon dioxide at the carotid bodies. Respir. Physiol. 4: 101–108, 1968.
 57. Eklund, B., and L. Kaijser. Blood flow in the resting forearm during prolonged contralateral isometric handgrip and muscle effort. J. Physiol. (Lond.) 227: 359–366, 1978.
 58. Eldridge, F. L. Posthyperventilation breathing: different effects of active and passive hyperventilation. J. Appl. Physiol. 34: 422–430, 1973.
 59. Eldridge, F. L. Central neural respiratory stimulatory effect of active respiration. J. Appl. Physiol. 37: 723–735, 1974.
 60. Eldridge, F. L. Central neural stimulation of respiration in unanesthetized decerebrate cats. J. Appl. Physiol. 40: 23–28, 1976.
 61. Eldridge, F. L. Maintenance of respiration by central neural feedback mechanisms. Federation Proc. 36: 2400–2404, 1977.
 62. Eldridge, F. L. Subthreshold central neural respiratory activity and afterdischarge. Respir. Physiol. 39: 327–343, 1980.
 63. Eldridge, F. L. Phase resetting of respiratory rhythm—experiments in animals and models. In: Springer Series in Synergetics, Vol. 55. Rhythms in Physiological Systems, edited by H. Haken and H. P. Koepchen. Berlin: Springer‐Verlag, 1991, p. 165–175.
 64. Eldridge, F. L. Overview: role of neurochemicals and hormones. In: Control of Breathing and its Modeling Perspective, edited by Y. Honda, et al. New York: Plenum Press, 1992, p. 187–196.
 65. Eldridge, F. L., and P. Gill‐Kumar. Lack of effect of vagal afferent input on central neural respiratory afterdischarge. J. Appl. Physiol. 45: 339–344, 1978.
 66. Eldridge, F. L., and P. Gill‐Kumar. Central neural respiratory drive and afterdischarge. Respir. Physiol. 40: 49–63, 1980.
 67. Eldridge, F. L., and P. Gill‐Kumar. Central neural drive mechanisms and respiratory afterdischarge—the “T‐pool” concept. In: Central Nervous Control Mechanisms in Breathing, edited by C. von Euler and H. Lagercrantz. Oxford: Pergamon Press, 1980, p. 101–113.
 68. Eldridge, F. L., P. Gill‐Kumar, and D. E. Millhorn. Input‐output relationships of central neural circuits involved in respiration in cats. J. Physiol. (Lond.) 311: 81–95, 1981.
 69. Eldridge, F. L., J. P. Kiley, and D. Paydarfar. Dynamics of medullary hydrogen ion and respiratory responses to square‐wave change of arterial carbon dioxide in cats. J. Physiol. (Lond.) 383: 627–642, 1987.
 70. Eldridge, F. L., and D. E. Millhorn. Oscillation, gating, and memory in the respiratory control system. In: Handbook of Physiology, The Respiratory System, Control of Breathing, edited by N. S. Cherniack and J. G. Widdicombe. Bethesda, MD: Am. Physiol. Soc., 1986, p. 93–114.
 71. Eldridge, F. L., D. E. Millhorn, J. P. Kiley, and T. G. Waldrop. Stimulation by central command of locomotion, respiration and circulation during exercise. Respir. Physiol. 59: 313–337, 1985.
 72. Eldridge, F. L., D. E. Millhorn, and T. G. Waldrop. Exercise hyperpnea and locomotion: parallel activation from the hypothalamus. Science 211: 844–846, 1981.
 73. Eldridge, F. L., and T. G. Waldrop. Neural control of breathing during exercise. In: Exercise: Pulmonary Physiology and Pathophysiology, edited by B. Whipp and K. Wasserman. New York: Marcel Dekker, Inc., 1991, p. 309–370.
 74. Eliasson, S., P. Lindgren, and B. Uvnas. Representation in the hypothalamus and the motor cortex in the dog of the sympathetic vasodilator outflow to the skeletal muscles. Acta Physiol. Scand. 27: 18–27, 1952.
 75. Emptage, N. J., and T. J. Carew. Long‐term synaptic facilitation in the absence of short‐term facilitation in Aplysia neurons. Science 262: 253–256, 1993.
 76. Engwall, M. J. A., L. Daristotle, W. Z. Niu, J. A. Dempsey, and G. E. Bisgard. Ventilatory afterdischarge in the awake goat. J. Appl. Physiol. 71: 1511–1517, 1991.
 77. Engwall, M. J. A., C. A. Smith, J. A. Dempsey, and G. E. Bisgard. Ventilatory afterdischarge and central respiratory drive interactions in the awake goat. J. Appl. Physiol. 76: 416–423, 1994.
 78. von Euler, C. Brain stem mechanisms for generation and control of breathing pattern. In: Handbook of Physiology, The Respiratory System, Control of Breathing, edited by N. S. Cherniack and J. G. Widdicombe. Bethesda, MD: Am. Physiol. Soc., 1986, p. 1–67.
 79. Fernandes, A., H. Galbo, M. Kjaer, J. H. Mitchell, N. H. Secher, and S. N. Thomas. Cardiovascular and ventilatory responses to dynamic exercise during epidural anaesthesia in man. J. Physiol. (Lond.) 420: 281–293, 1990.
 80. Fernandes, A., H. Galbo, M. Kjær, N. H. Secher, F. W. Bach, H. Galbo, D. R. Reeves, Jr., and J. H. Mitchell. Hormonal, metabolic, and cardiovascular responses to static exercise in humans: influence of epidural anesthesia. Am. J. Physiol. 261 (Endocrinol. Metab. 24): E214–E220, 1991.
 81. Fink, B. R. Influence of cerebral activity in wakefulness on regulation of breathing. J. Appl. Physiol. 16: 15–20, 1961.
 82. Fink, G. R., L. Adams, J. D. G. Watson, J. A. Innes, B. Wuyam, I. Kobayashi, D. R. Corfield, K. Murphy, R. S. J. Frackowiak, T. Jones, and A. Guz. Motor cortical activation in exercise‐induced hyperpnoea in man: evidence for involvement of supra‐brainstem structures in control of breathing. J. Physiol. (Lond.) 473: 58P, 1993.
 83. Fitzhugh, R. Impulses and physiological states in theoretical models of nerve membrane. Biophys. J. 1: 445–466, 1961.
 84. Folgering, H. Beta‐adrenergic drugs do not affect phrenic nerve afterdischarge. Pflugers Arch. 391: 355–356, 1981.
 85. Fordyce, W. E., F. M. Bennett, S. K. Edelman, and F. S. Grodins. Evidence in man for a fast neural mechanism during the early phases of exercise hyperpnea. Respir. Physiol. 48: 27–43, 1982.
 86. Forsyth, R. P. Hypothalamic control of the distribution of cardiac output in the unanesthetized rhesus monkey. Circ. Res. 26: 783–794, 1970.
 87. Fregosi, R. F. Short‐term potentiation of breathing in humans. J. Appl. Physiol. 71: 892–899, 1991.
 88. Fregosi, R. F., and J. A. Dempsey. Arterial blood acid–base regulation during exercise in rats. J. Appl. Physiol. 57: 396–402, 1984.
 89. Freund, P. R., L. B. Rowell, T. M. Murphy, S. F. Hobbs, and S. H. Butler. Blockade of the pressor response to muscle ischemia by sensory nerve block in man. Am. J. Physiol. 237 (Heart Circ. Physiol. 6): H433–H439, 1979.
 90. Freyschuss, V. Cardiovascular adjustments to somatomotor activation. Acta Physiol. Scand. Suppl. 342: 1–63, 1970.
 91. Friedman, D. B., J. Brennum, F. Sztuk, O. B. Hansen, P. S. Clifford, F. W. Bach, L. Arendt‐Nielsen, J. H. Mitchell, and N. H. Secher. The effect of epidural anaesthesia with 1% lidocaine on the pressor response to dynamic exercise in humans. J. Physiol. 470: 681–691, 1993.
 92. Friedman, D. B., C. Peel, and J. H. Mitchell. Cardiovascular responses to voluntary and nonvoluntary static exercise in humans. J. Appl. Physiol. 73: 1982–1985, 1992.
 93. Fritsch, G., and J. E. Hitzig. Uber die elektrische Erregbarkeit des Grooshirns. Archives fur anatome, physiologie und wissenschaftliche Medizin, 1870, p. 300–332.
 94. Gage, P. W., and J. I. Hubbard. An investigation of the post‐tetanic potentiation of end‐plate potentials at a mammalian neuromuscular junction. J. Physiol. (Lond.) 184: 353–375, 1966.
 95. Galbo, H., M. Kjaer, and N. H. Secher. Cardiovascular, ventilatory and catecholamine responses to maximal dynamic exercise in partially curarised man. J. Physiol. (Lond.) 389: 557–568, 1987.
 96. Gandevia, S. C., and S. F. Hobbs. Cardiovascular responses to static exercise in man: central and reflex contributions. J. Physiol. (Lond.) 430: 105–117, 1990.
 97. Gandevia, S. C., K. Killiam, D. K. McKenzie, M. Crawford, G. M. Allen, R. B. Gorman, and J. P. Hales. Respiratory sensations, cardiovascular control, kinaesthesia and transcranial stimulation during paralysis in humans. J. Physiol. (Lond.) 470: 85–107, 1993.
 98. Gandevia, S. C., and J. C. Rothwell. Activation of the human diaphragm from the motor cortex. J. Physiol. (Lond.) 384: 109–118, 1987.
 99. Garcia‐Rill, E. The basal ganglia and the locomotor regions. Brain Res. Rev. 11: 47–63, 1986.
 100. Garcia‐Rill, E., R. D. Skinner, and J. A. Fitzgerald. Chemical activation of the mesencephalic locomotor region. Brain Res. 330: 43–54, 1985.
 101. Gebber, G. L. Central determinants of sympathetic nerve discharge. In: Central Regulation of Autonomic Functions, edited by A. D. Loewy and K. M. Spyer. New York: Oxford University Press, 1990, p. 126–144.
 102. Georgopoulos, D., Z. Bshouty, M. Younes, and N. R. Anthonisen. Hypoxic exposure and activation of the afterdischarge mechanism in conscious humans. J. Appl. Physiol. 69: 1159–1164, 1990.
 103. Gesell, R., C. R. Brassfield, and M. A. Hamilton. An acid‐neurohumoral mechanism of nerve cell activation. Am. J. Physiol. 136: 604–608, 1942.
 104. Goodwin, G. M., D. I. McCloskey, and J. H. Mitchell. Cardiovascular and respiratory responses to changes in central command during isometric exercise at constant muscle tension. J. Physiol. (Lond.) 226: 173–190, 1972.
 105. Graham Brown, T. The intrinsic factors in the act of progression in the mammal. Proc. R. Soc. Lond. 84B: 308–319, 1911.
 106. Graham Brown, T. The phenomenon of “narcosis progression” in mammals. Proc. R. Soc. Lond. 86B: 140–164, 1913.
 107. Graham Brown, T. On the nature of the fundamental activity of the nervous centres; together with an analysis of the conditioning of rhythmic activity in progression, and a theory of the evolution of function in the nervous system. J. Physiol. (Lond.) 48: 18–46, 1914.
 108. Green, H. D., and E. C. Hoff. Effects of faradic stimulation of the cerebral cortex on limb and renal volumes in the cat and monkey. Am. J. Physiol. 118: 641–658, 1937.
 109. Grodins, F. S. Exercise hyperpnea. The ultra secret. Adv. Physiol. Sci. 10: 243–251, 1981.
 110. Grossman, R. G. Effects of stimulation of non‐specific thalamic system on locomotor movements in cat. J. Neurophysiol. 21: 85–93, 1958.
 111. Guyenet, P. G. Role of the ventral medulla oblongat in blood pressure regulation. In: Central Regulation of Autonomic Functions, edited by A. D. Loewy and K. M. Spyer. New York: Oxford University Press, 1990, p. 145–167.
 112. Haldane, J. S., and J. G. Preistly. The regulation of lung ventilation. J. Physiol. (Lond.) 32: 225–266, 1905.
 113. Hastings, A. B., F. C. White, T. M. Sanders, and C. M. Bloor. Comparative physiological responses to exercise stress. J. Appl. Physiol. 52: 1077–1083, 1982.
 114. Henderson, Y. Acapnia and shock. IV. Fatal apnoea after excessive respiration. Am. J. Physiol. 25: 310–333, 1910.
 115. Hilton, S. M. Central nervous origin of vasomotor tone. Adv. Physiol. Sci. 8: 1–12, 1981.
 116. Hilton, S. M., J. M. Marshall, and R. J. Timms. Ventral medullary relay neurons in the pathway from the defence areas of the cat and their effect on blood pressure. J. Physiol. (Lond.) 345: 149–166, 1983.
 117. Hilton, S. M., and W. S. Redfern. A search for brain stem cell groups integrating the defence reaction. J. Physiol. (Lond.) 378: 213–228, 1986.
 118. Hilton, S. M., K. M. Spyer, and R. J. Timms. The origin of the hind limb vasodilatation evoked by stimulation of the motor cortex in the cat. J. Physiol. (Lond.) 287: 545–557, 1979.
 119. Hilton, S. M., and A. W. Zbrozyna. Amygdaloid region for defence reactions and its efferent pathway to the brain stem. J. Physiol. (Lond.) 165: 160–173, 1963.
 120. Hobbs, S. F. Central command during exercise: parallel activation of the cardiovascular and motor systems by descending command signals. In: Circulation, Neurobiology and Behavior, edited by O. A. Smith, R. A. Galosy, and S. M. Weiss. Amsterdam: Elsevier Science Publishers, 1982, p. 217–231.
 121. Hobbs, S. F., and S. C. Gandevia. Cardiovascular responses and the sense of effort during attempts to contract paralyzed muscles: role of the spinal cord. Neurosci. Lett. 57: 85–90, 1985.
 122. Hobbs, S. F., and D. I. McCloskey. Effect of spontaneous exercise on reflex slowing of the heart in decerebrate cats. J. Auton. Nerv. Syst. 17: 303–312, 1986.
 123. Hoff, E. C., J. F. Kell, Jr., and M. N. Carroll, Jr.. Effects of cortical stimulation and lesions on cardiovascular function. Physiol. Rev. 43: 68–114, 1963.
 124. Hollander, A. P., and L. N. Bouman. Cardiac acceleration in man elicited by a muscle‐heart reflex. J. Appl. Physiol. 38: 272–278, 1975.
 125. Holstege, G. Some anatomical observations on the projections from the hypothalamus to brainstem and spinal cord: an HRP and autoradiographic tracing study in the cat. J. Comp. Neurol. 260: 98–126, 1987.
 126. Horn, E. M., and T. G. Waldrop. Modulation of the respiratory responses to hypoxia and hypercapnia by synaptic input onto caudal hypothalamic neurons. Brain Res. 664: 25–33, 1994.
 127. Hornbein, T. F., S. C. Sørensen, and C. R. Parks. Role of muscle spindles in lower extremities in breathing during bicycle exercise. J. Appl. Physiol. 27: 476–479, 1969.
 128. Huang, Z.‐S., G. L. Gebber, S. M. Barman, and K. J. Vatner. Forebrain contribution to sympathetic nerve discharge in anesthetized cats. Am. J. Physiol. 252 (Regulatory Integrative Comp. Physiol. 21): R645–R652, 1987.
 129. Huang, Z.‐S., K. J. Varner, S. M. Barman, and G. L. Gebber. Diencephalic regions contributing to sympathetic nerve discharge in anesthetized cats. Am. J. Physiol. 254 (Regulatory Integrative Comp. Physiol. 23): R249–R256, 1986.
 130. Hugelin, A., and M. I. Cohen. The reticular activating system and respiratory regulation in the cat. Ann. N. Y. Acad. Sci. 109: 586–603, 1963.
 131. Hultman, E., and H. Sjoholm. Blood pressure and heart rate response to voluntary and non‐voluntary static exercise in man. Acta Physiol. Scand. 115: 499–501, 1982.
 132. Innes, J. A., S. C. De Cort, P. J. Evans, and A. Guz. Central command influences cardiorespiratory response to dynamic exercise in humans with unilateral weakness. J. Physiol. (Lond.) 448: 551–563, 1992.
 133. Johansson, J. E. Uber die Einwirkung der Musdeltatigkeit auf die Atmun und die Herztatigkeit. Skand. Arch. Physiol. 5: 20–66, 1893.
 134. Kaczmarek, L. K., and F. Strumwasser. The expression of long lasting afterdischarge in peptidergic neurons of Aplysia bag cell neurons. J. Neurosci. 1: 626–634, 1981.
 135. Kao, F. F. An experimental study of the pathways involved in exercise hyperpnea employing cross‐circulation techniques. In: The Regulation of Human Respiration, edited by D. J. C. Cunningham and B. B. Lloyd. Philadelphia: F. A. Davis Company, 1963, p. 461–502.
 136. Karczewski, W. A., K. Budzinska, H. Gromysz, R. Herczynski, and J. R. Romaniuk. Some responses of the respiratory complex to stimulation of its vagal and mesencephalic inputs. In: Respiratory Centres and Afferent Systems, edited by B. Duron. Paris: INSERM, 1976, p. 107–115.
 137. Karczewski, W. A., and J. R. Romaniuk. Neural control of breathing and central nervous system plasticity. Acta Physiol. Pol. Suppl. 20: 1–10, 1980.
 138. Katz, B., and R. Miledi. The role of calcium in neuromuscular facilitation. J. Physiol. (Lond.) 195: 481–492, 1968.
 139. Kelly, M. A., M. D. Laufe, R. P. Millman, and D. D. Peterson. Ventilatory response to hypercapnia before and after athletic training. Respir. Physiol. 55: 393–400, 1984.
 140. Khoo, M. C. K., A. Gottschalk, and A. I. Pack. Sleep‐induced periodic breathing and apnea: a theoretical study. J. Appl. Physiol. 70: 2014–2024, 1991.
 141. Khoo, M. C. K., R. E. Kronauer, K. P. Strohl, and A. S. Slutsky. Factors inducing periodic breathing: a general model. J. Appl. Physiol. 53: 644–659, 1982.
 142. Kiley, J. P., W. D. Kuhlman, and M. R. Fedde. Respiratory and cardiovascular responses to exercise in the duck. J. Appl. Physiol. 47: 112–136, 1979.
 143. Kjær, M., G. Perko, N. H. Secher, R. Boushel, N. Beyer, S. Pollack, A. Horn, A. Fernandes, T. Mohr, S. F. Lewis, and H. Galbo. Cardiovascular and ventilatory responses to electrically induced cycling with complete epidural anaesthesia in humans. Acta Physiol. Scand. 151: 191–207, 1994.
 144. Kjær, M., N. H. Secher, F. W. Bach, H. Galbo, D. R. Reeves, Jr., and J. H. Mitchell. Hormonal, metabolic, and cardiovascular responses to static exercise in humans: influence of epidural anesthesia. Am. J. Physiol. 261 (Endocrinol. Metab. 24): E214–E220, 1991.
 145. Kjær, M., N. H. Secher, F. W. Bach, S. Sheikh, and H. Galbo. Hormonal and metabolic responses to dynamic exercise in man: effect of sensory nervous blockade. Am. J. Physiol. 257 (Endocrinol. Metab. 20): E95–E101, 1989.
 146. Kleyntjens, F., K. Koizumi, and C. McC. Brooks. Stimulation of suprabulbar reticular formation. Arch. Neurol. Psychiatry 73: 425–438, 1955.
 147. Krogh, A., and J. Lindhard. The regulation of respiration and circulation during the initial stages of muscular work. J. Physiol. (Lond.) 47: 112–136, 1913.
 148. Krogh, A., and J. Lindhard. A comparison between voluntary and electrically induced muscular work in man. J. Physiol. (Lond.) 51: 182–201, 1917.
 149. Langhorst, P., M. Lambertz, G. Schultz, and G. Stock. Role played by amygdala complex and common brainstem system in integration of somatomotor and autonomic components of behavior. In: Organization of the Autonomic Nervous System: Central and Peripheral Autonomic Mechanisms. New York: Alan R. Liss, Inc., 1987, p. 347–361.
 150. Larabee, M. G., and D. W. Bronk. Prolonged facilitation of synaptic excitation in sympathetic ganglia. J. Neurophysiol. 10: 139–154, 1947.
 151. Lawson, E. E., and W. A. Long. Central neural respiratory response to carotid sinus nerve stimulation in newborns. J. Appl. Physiol. 56: 1614–1620, 1984.
 152. Leonard, B., J. H. Mitchell, M. Mizuno, N. Rube, B. Saltin, and N. H. Secher. Partial neuromuscular blockade and cardiovascular responses to static exercise in man. J. Physiol. (Lond.) 359: 365–379, 1985.
 153. Li, P., and T. A. Lovick. Excitatory projections from hypothalamic and midbrain defense regions to nucleus paragigantocellularis lateralis in the rat. Exp. Neurol. 89: 543–553, 1985.
 154. Lind, A. R., G. W. McNicol, R. A. Bruce, H. R. MacDonald, and K. W. Donald. The cardiovascular responses to sustained contractions of a patient with unilateral syringomyelia. Clin. Sci. 35: 45–53, 1968.
 155. Lind, A. R., and J. S. Petrofsky. Amplitude of the surface electrocardiogram during fatiguing isometric contractions. Muscle Nerve 2: 257–264, 1979.
 156. Lind, A. R., S. R. Taylor, P. W. Humphreys, B. M. Kennelly, and D. W. Donald. Circulatory effects of sustained muscle contraction. Clin. Sci. 27: 229–244, 1964.
 157. Lipski, J., A. Bektas, and R. Porter. Short latency inputs to phrenic motoneurones from the sensorimotor cortex in the cat. Exp. Brain Res. 61: 280–290, 1986.
 158. Llinas, R., T. L. McGuinnes, C. S. Leonard, M. Sugimori, and P. Greengard. Intraterminal injection of synapsin I or calcium/calmodulin‐dependent protein kinase II alters neurotransmitter release at the squid giant synapse. Proc. Natl. Acad. Sci., U. S. A. 82: 3035–3039, 1985.
 159. Loeschcke, H. H., J. DeLattre, M. E. Schlafke, and C. O. Trouth. Effects on respiration and circulation of electrically stimulating the ventral surface of the medulla oblongata. Respir. Physiol. 10: 184–197, 1970.
 160. Lovick, T. A. Projections from the diencephalon and mesencephalon to nucleus paragigantocellularis lateralis in the cat. Neuroscience 14: 853–861, 1985.
 161. Luiten, P. G. M., G. J. Ter Horst, H. Karst, and A.B. Steffens. The course of paraventricular hypothalamic efferents to autonomic structures in medulla and spinal cord. Brain Res. 329: 374–378, 1985.
 162. Magleby, K. L. Synaptic transmission, facilitation, augmentation, potentiation, depression. In: Encyclopedia of Neuroscience, edited by G. Edelman. Boston: Birkhauser, 1987, p. 1170–1174.
 163. Magleby, K. L., and J. E. Zengel. A quantitative description of stimulation‐induced changes in transmitter release at the frog neuromuscular junction. J. Gen. Physiol. 80: 613–638, 1982.
 164. Mark, A. L., R. G. Victor, C. Nerhed, and B. G. Wallin. Microneurographic studies of the mechanisms of sympathetic nerve responses to static exercise in humans. Circ. Res. 57: 461–469, 1985.
 165. Marshall, J. M., and R. J. Timms. Experiments on the role of the subthalamus in the generation of the cardiovascular changes during locomotion in the cat. J. Physiol. (Lond.) 301: 92–93 P, 1980.
 166. Maskati, H. A. A., and A. W. Zbrozyna. Cardiovascular and motor components of the defense reaction elicited in rats by electrical and chemical stimulation in amygdala. J. Auton. Nerv. Syst. 28: 127–132, 1989.
 167. Matsukawa, K., J. H. Mitchell, P. T. Wall, and L. B. Wilson. The effect of static exercise on renal sympathetic nerve activity in conscious cats. J. Physiol. (Lond.) 434: 453–467, 1991.
 168. McCloskey, D. I. Centrally‐generated commands and cardiovascular control in man. Clin. Exp. Hypertens. 3: 369–378, 1981.
 169. McCloskey, D. I., and J. H. Mitchell. Reflex cardiovascular and respiratory responses originating in exercising muscle. J. Physiol. (Lond.) 224: 173–186, 1972.
 170. McNaughton, B. L. Long‐term synaptic enhancement and short‐term potentiation in rat fascia dentata act through different mechanisms. J. Physiol. (Lond.) 324: 249–262, 1982.
 171. Meah, M. S., and W. N. Gardner. Post‐hyperventilation apnoea in conscious humans. J. Physiol. (Lond.) 477: 527–538, 1994.
 172. Mel'nikova, Z. L. Connections of the subthalamic and mesencephalic “locomotor regions” in rats. Neirofiziologiya 9: 275–280, 1977.
 173. Melton, J. E., Q. P. Yu, J. A. Neubauer, and N. H. Edelman. Modulation of respiratory responses to carotid sinus nerve stimulation by brain hypoxia. J. Appl. Physiol. 73: 2166–2171, 1992.
 174. Miller, S., and F. G. A. van der Meche. Coordinated stepping of all four limbs in the high spinal cat. Brain Res. 109: 395–398, 1976.
 175. Millhorn, D. E., F. L. Eldridge, and T. G. Waldrop. Pharmacologic study of respiratory afterdischarge. J. Appl. Physiol. 50: 239–244, 1981.
 176. Millhorn, D. E., F. L. Eldridge, and T. G. Waldrop. Effects of medullary area I(s) cooling on respiratory response to chemoreceptor input. Respir. Physiol. 49: 23–39, 1982.
 177. Millhorn, D. E., F. L. Eldridge, T. G. Waldrop, and J. P. Kiley. Diencephalic regulation of respiration and arterial pressure during actual and fictive locomotion in cat. Circ. Res. 61 (Suppl. I): I‐53–I‐59, 1987.
 178. Mills, J. N. Hyperpnea induced by forced breathing. J. Physiol. (Lond.) 105: 95–116, 1946.
 179. Mitchell, G. S., T. T. Gleeson, and A. F. Bennett. Ventilation and acid base balance during graded activity in lizards. Am. J. Physiol. 238 (Regulatory Integrative Comp. Physiol. 7): R27–R37, 1981.
 180. Mitchell, J. H. Cardiovascular control during exercise: central and reflex neural mechanisms. Am. J. Cardiol. 55: 33D–41D, 1985.
 181. Mitchell, J. H. Neural control of the circulation during exercise. Med. Sci. Sports Exer. 22: 141–154, 1990.
 182. Mitchell, J. H., and P. B. Raven. Cardiovascular response and adaptation to exercise. In: Physical Activity, Fitness and Health: International Proceedings and Consensus Statement, edited by C. Bouchard, R. Shephard, and T. Stephens. Champaign, IL: Human Kinetics Publishers, 1994, p. 286–298.
 183. Mitchell, J. H., D. R. Reeves, Jr., H. B. Rogers, and N. H. Secher. Epidural anaesthesia and cardiovascular responses to static exercise in man. J. Physiol. (Lond.) 417: 13–24, 1989.
 184. Mitchell, J. H., D. R. Reeves, Jr., H. B. Rogers, N. H. Secher, and R. G. Victor. Autonomic blockade and the cardiovascular responses to static exercise in partially curarized man. J. Physiol. (Lond.) 413: 433–335, 1989.
 185. Mitchell, J. H., B. Schibye, F. C. Payne, III, and B. Saltin. Response of arterial blood pressure to static exercise in relation to muscle mass, force development, and electromyographic activity. Circ. Res. 48 (Suppl. I): I‐70–I‐75, 1981.
 186. Mori, S., H. Nishimura, C. Kurakami, T. Yamamura, and M. Aoki. Lower brainstem “locomotor region” in the mesencephalic cat. In: Integrative Control Function of the Brain, edited by M. Ito. Tokyo: Kodansha Press, 1978.
 187. Mosso, A. La physiologie de l'apnée etudiée chez l'homme. Arch. Ital. Biol. 40: 1–30, 1903.
 188. Murray, J. F. The Normal Lung. Philadelphia: W. B. Saunders Company, 1976.
 189. Muza, S. R., L.‐Y Lee, R. L. Wiley, S. McDonald, and F. W. Zechman. Ventilatory responses to static handgrip exercise. J. Appl. Physiol. 54: 1457–1462, 1983.
 190. Myhre, K., and K. L. Andersen. Respiratory responses to static muscular contraction. Respir. Physiol. 12: 77–89, 1971.
 191. Nolan, P. C., J. A. Pawelczyk, and T. G. Waldrop. Neurons in the ventrolateral medulla receive input from descending “central command” and feedback from contracting muscles. Physiologist 35: 240, 1992.
 192. Ochwadt, B., E. Bücherl, H. Kreuzer, and H. H. Loeschcke. Beeinflussing der Atemsteigerung bei Muskelarbeit durch partiellen neuromuscularen Block (Tubocurarine). Pflugers Arch. 269: 613–621, 1959.
 193. O'Hagan, K. P., L. B. Bell, S. W. Mittelstadt, and P. S. Clifford. Effect of dynamic exercise on renal sympathetic nerve activity in conscious rabbits. J. Appl. Physiol. 74: 2099–2104, 1993.
 194. Ordway, G. A., T. G. Waldrop, G. A. Iwamoto, and B. J. Gentile. Hypothalamic influences on cardiovascular response of beagles to dynamic exercise. Am. J. Physiol. 257 (Heart Circ. Physiol. 28): H1247–H1253, 1989.
 195. Orlovskii, G. N. Spontaneous and induced locomotion of the thalamic cat. Biophysics (USSR—English translation) 14: 1154–1162, 1969.
 196. Orlovskii, G. N. Connexions of the reticulo‐spinal neurones with the “locomotor sections” of the brain stem. Biofizika 15: 171–177, 1970.
 197. Pan, L. G., H. V. Forster, G. E. Bisgard, R. P. Kaminski, S. M. Dorsey, and M. A. Busch. Hyperventilation in ponies at the onset and during steady‐state exercise. J. Appl. Physiol. 54: 1394–1402, 1983.
 198. Patterson, D. J. Potassium and ventilation in exercise. J. Appl. Physiol. 72: 811–820, 1992.
 199. Peano, C. A., C. A. Shonis, G. H. Dillon, and T. G. Waldrop. Hypothalamic GABAergic mechanism involved in the respiratory response to hypercapnia. Brain Res. Bull. 28: 107–113, 1992.
 200. Petro, J. K., A. P. Hollander, and L. N. Bouman. Instantaneous cardiac acceleration in man induced by a voluntary muscle contraction. J. Appl. Physiol. 29: 794–798, 1970.
 201. Pickar, J. G., J. M. Hill, and M. P. Kaufman. Stimulation of vagal afferents inhibits locomotion in mesencephalic cats. J. Appl. Physiol. 74: 103–110, 1993.
 202. Pitt, R. F., and D. W. Bronk. Excitability cycle of the hypothalamus‐sympathetic neurone system. Am. J. Physiol. 135: 504–525, 1942.
 203. Pitts, R. F., M. G. Larrabee, and D. W. Bronk. An analysis of hypothalamic cardiovascular control. Am. J. Physiol. 134: 359–383, 1941.
 204. Plum, F., H. W. Brown, and E. Snoep. The neurological significance of posthyperventilation apnea. JAMA, 181: i050–1055, 1962.
 205. Priban, I. P. An analysis of some short‐term patterns of breathing in man at rest. J. Physiol. (Lond.) 166: 425–434, 1963.
 206. Redgate, E. S. Hypothalamic influence on respiration. Ann. N. Y. Acad. Sci. 109: 606–618, 1963.
 207. Richter, D. W., H. Camerer, and U. Sonnhof. Changes in extracellular potassium during the spontaneous activity of medullary respiratory neurones. Pflugers Arch. 376: 139–149, 1978.
 208. Romaniuk, J. R., S. Kasicki, and U. Borecka. The Breuer‐Hering reflex at rest and during electrically induced locomotion in the decerebrate cat. Acta Neurobiol. Exp. 46: 141–151, 1986.
 209. Rosenthal, J. Post‐tetanic potentiation at the neuromuscular junction of the frog. J. Physiol. (Lond.) 203: 121–133, 1969.
 210. Rushmer, R. F. Structure and Function of the Cardiovascular System. Philadelphia: W. B. Saunders Company, 1972, p. 94–97, 142–144, 220–243.
 211. Rybicki, K. J., R. W. Stremel, G. A. Iwamoto, J. H. Mitchell, and M. P. Kaufman. Occlusion of pressor responses to posterior diencephalic stimulation and static muscular contraction. Brain Res. Bull. 22: 306–312, 1989.
 212. Saito, M., H. Abe, S. Iwase, and T. Mano. Responses in muscle sympathetic nerve activity in sustained and rhythmic muscle contraction. Environ. Med. 33: 33–41, 1989.
 213. Saito, M., T. Mano, and S. Iwase. Sympathetic nerve activity related to local fatigue sensation during static contraction. J. Appl. Physiol. 67: 980–984, 1989.
 214. Saito, M., M. Nato, and T. Mano. Different responses in skin and muscle sympathetic nerve activity to static muscle contraction. J. Appl. Physiol. 69: 2085–2090, 1990.
 215. Saper, C. B., A. D. Loewy, L. W. Swanson, and W. M. Cowan. Direct hypothalamo‐autonomic connections. Brain Res. 117: 305–312, 1976.
 216. Schibye, B., J. H. Mitchell, F. C. Payne, and B. Saltin. Blood pressure and heart rate response to static exercise in relation to electromyographic activity and force development. Acta Physiol. Scand. 113: 61–66, 1981.
 217. Schlafke, M. E., and H. H. Loeschcke. Lokalization einer an de regulation von Atmung und Kreislauf betieligten Gebietes an de ventralen Oberflack der Medulla Oblongata durch Kalte blockage. Pflugers Arch. 297: 205–220, 1967.
 218. Seals, D. R. Influence of force on muscle and skin sympathetic nerve activity during sustained isometric contractions in humans. J. Physiol. (Lond.) 462: 147–159, 1993.
 219. Seals, D. R., and R. M. Enoka. Sympathetic activation is associated with increases in EMG during fatiguing exercise. J. Appl. Physiol. 66: 88–95, 1989.
 220. Senapati, J. M. Effect of stimulation of muscle afferents on ventilations of dogs. J. Appl. Physiol. 21: 242–246, 1966.
 221. Shea, S. A., L. P. Andres, D. C. Shannon, and R. B. Banzett. Ventilatory responses to exercise in humans lacking ventilatory chemosensitivity. J. Physiol. (Lond.) 468: 623–640, 1993.
 222. Sherrington, C. Lecture II. Co‐ordination in the simple reflex. In: The Integrative Action of the Nervous System, 2nd ed. New Haven, CT: Yale University Press, 1947, p. 36–69.
 223. Shik, M. L., and G. N. Orlovskii. Neurophysiology of locomotor automatism. Physiol. Rev. 56: 465–501, 1976.
 224. Shik, M. L., F. V. Severin, and G. N. Orlovskii. Control of walking and running by means of electrical stimulation of the midbrain. Biofizika 11: 659–666, 1966.
 225. Shik, M. L., and A. S. Yagosditsyn. The pontobulbar locomotor strip. Neurophysiology 9: 72–74, 1977.
 226. Shik, M. L., and A. S. Yagosditsyn. Unit responses in the locomotor strip of the cat hindbrain to microstimulation. Neurophysiology 10: 373–379, 1978.
 227. Skinner, R. D., and E. Garcia‐Rill. The mesencephalic locomotor region (MLR) in the rat. Brain Res. 323: 385–389, 1984.
 228. Smith, C. A., G. S. Mitchell, L. C. Jameson, T. I. Musch, and J. A. Dempsey. Ventilatory response of goats to treadmill exercise: grade effects. Respir. Physiol. 54: 331–341, 1983.
 229. Smith, O. A., Jr., R. E. Rushmer, and E. P. Lasher. Similarity of cardiovascular responses to exercise and to diencephalic stimulation. Am. J. Physiol. 198: 1139–1142, 1960.
 230. Splengler, C. M., D. von Ow, and U. Boutellier. The role of central command in ventilatory control during static exercise. Eur. J. Appl. Physiol. 68: 162–169, 1994.
 231. Spyer, K. M. Neural organisation and control of the baroreceptor reflex. Rev. Physiol. Biochem. Pharmacol. 88: 23–124, 1981.
 232. Steeves, J. D., and L. M. Jordan. Autoradiographic demonstration of the projections from the mesencephalic locomotor region. Brain Res. 307: 263–276, 1984.
 233. Steeves, J. D., L. M. Jordan, and N. Lake. The close proximity of catecholamine‐containing cells to the mesencephalic locomotor region (MLR). Brain Res. 100: 663–670, 1973.
 234. Strange, S., N. H. Secher, J. A. Pawelczyk, J. Karpakka, N. J. Christensen, J. H. Mitchell, and B. Saltin. Neural control of cardiovascular responses and of ventilation during dynamic exercise in man. J. Physiol. (Lond.) 470: 693–704, 1993.
 235. Stremel, R. W., and I. G. Joshua. Disinhibition of posterior hypothalamic neurons elicit splanchnic microvascular constriction. Soc. Neurosci. Abstr. 19: 958, 1993.
 236. Swanson, G. D., D. S. Ward, and J. W. Bellville. Posthyperventilation isocapnic hyperpnea. J. Appl. Physiol. 40: 592–596, 1976.
 237. Sykova, E. Activity‐related fluctuations in extracellular ion concentrations in the central nervous system. News Physiol. Sci. 1: 57–61, 1986.
 238. Tansey, K. E., A. K. Yee, and B. R. Botterman. Force modulation due to firing rate variation in single motor units during centrally evoked muscle contractions. Soc. Neurosci. Abstr. 16: 115, 1990.
 239. Tansey, K. E., and B. R. Botterman. Recruitment order and discharge patterns among pairs of motor units evoked by brainstem stimulation. Soc. Neurosci. Abstr. 15: 919, 1989.
 240. Tawadrous, F. D., and F. L. Eldridge. Posthyperventilation breathing patterns after active hyperventilation in man. J. Appl. Physiol. 37: 353–356, 1974.
 241. Thomas, M. R., and F. R. Calaresu. Responses of single units in the medial hypothalamus to electrical stimulation of the carotid sinus nerve in the cat. Brain Res. 44: 49–62, 1972.
 242. Thomas, M. R., and F. R. Calaresu. Hypothalamic inhibition of chemoreceptor‐induced bradycardia in the cat. Am. J. Physiol. 225: 201–208, 1973.
 243. Valbo, A. B., R.‐E. Hagbarth, H. E. Torebjörk, and B. G. Wallin. Somatosensory proprioceptive and sympathetic activity in human peripheral nerves. Physiol. Rev. 59: 919–957, 1979.
 244. Varner, K. J., S. M. Barman, and G. L. Gebber. Cat diencephalic neurons with sympathetic nerve‐related activity. Am. J. Physiol. 254 (Regulatory Integrative Comp. Physiol. 23): R257–R267, 1988.
 245. Victor, R. G., S. L. Pryor, N. H. Secher, and J. H. Mitchell. Effects of partial neuromuscular blockade on sympathetic nerve responses to static exercise in humans. Circ. Res. 65: 468–476, 1989.
 246. Victor, R. G., and D. R. Seals. Reflex stimulation of sympathetic outflow during rhythmic exercise in humans. Am. J. Physiol. 257 (Heart Circ. Physiol. 26): H2017–H2024, 1989.
 247. Victor, R. G., D. R. Seals, and A. L. Mark. Differential control of heart rate and sympathetic nerve activity during dynamic exercise. Insight from intraneural recordings in humans. J. Clin. Invest. 79: 508–516, 1987.
 248. Victor, R. G., N. H. Secher, T. Lyson, and J. H. Mitchell. Central command increases muscle sympathetic nerve activity during intense intermittent isometric exercise in humans. Circ. Res. 76: 127–131, 1995.
 249. Vis, A. Dynamic aspects of the regulation of breathing. Nijmegen: The Netherlands, Katholieke University, Ph.D. thesis, 1981.
 250. Vis, A., and H. Folgering. Phrenic nerve afterdischarge after electrical stimulation of the carotid sinus nerve in cats. Respir. Physiol. 45: 217–227, 1981.
 251. Vissing, S. F., U. Scherrer, and R. G. Victor. Stimulation of skin sympathetic nerve discharge by central command. Differential control of sympathetic outflow to skin and skeletal muscle during static exercise. Circ. Res. 69: 228–238, 1991.
 252. Wagner, P. G. Further characterization of the central nervous system mechanism involved in the generation of a respiratory afterdischarge. Chapel Hill, NC: University of North Carolina at Chapel Hill, Ph.D. thesis, 1990.
 253. Wagner, P. G., and F. L. Eldridge. Development of short‐term potentiation of respiration. Respir. Physiol. 83: 129–140, 1991.
 254. Waldrop, T. G. Respiratory responses and adaptations to exercise. In: Scientific Foundations of Sports Medicine, edited by C. C. Teitz. Toronto: B. C. Decker, Inc., 1989, p. 59–76.
 255. Waldrop, T. G. Posterior hypothalamic modulation of the respiratory response to CO2 in cats. Pflugers Arch. 418: 7–13, 1991.
 256. Waldrop, T. G., and R. M. Bauer. Modulation of sympathetic discharge by a hypothalamic GABAergic mechanism. Neuropharmacology 28: 263–269, 1989.
 257. Waldrop, T. G., R. M. Bauer, and G. A. Iwamoto. Microinjection of GABA antagonists into the posterior hypothalamus elicits locomotor activity and a cardiorespiratory activation. Brain Res. 444: 84–94, 1988.
 258. Waldrop, T. G., F. L. Eldridge, and D. E. Millhorn. Prolonged post‐stimulus inhibition of breathing following stimulation of afferents from muscle. Respir. Physiol. 50: 239–254, 1982.
 259. Waldrop, T. G., M. C. Henderson, G. A. Iwamoto, and J. H. Mitchell. Regional blood flow responses to stimulation of the subthalamic locomotor region. Respir. Physiol. 64: 93–102, 1986.
 260. Waldrop, T. G., and G. A. Iwamoto. Neurons in the insular cortex are responsive to muscular contraction and have sympathetic and/or cardiac‐related discharge. Soc. Neurosci. Abstr. 20: 1370, 1994.
 261. Waldrop, T. G., D. C. Mullins, and M. C. Henderson. Effects of hypothalamic lesions on the cardiorespiratory responses to muscular contraction. Respir. Physiol. 66: 215–224, 1986.
 262. Waldrop, T. G., D. C. Mullins, and D. E. Millhorn. Control of respiration by the hypothalamus and by feedback from contracting muscles in cats. Respir. Physiol. 64: 317–328, 1986.
 263. Waldrop, T. G., and J. P. Porter. Hypothalamic involvement in respiratory and cardiovascular regulation. In: Regulation of Breathing, edited by J. A. Dempsey and A. I. Pack. New York: Marcel Dekker, Inc., 1995, p. 315–364.
 264. Waldrop, T. G., and R. W. Stremel. Muscular contraction stimulates posterior hypothalamic neurons. Am. J. Physiol. 256 (Regulatory Integrative Comp. Physiol. 25): R348–R356, 1989.
 265. Wall, P. D., and K. H. Pribram. Trigeminal neurotomy and blood pressure responses from stimulation of lateral cerebral cortex of Macaca mulatta. J. Neurophysiol. 13: 409–412, 1950.
 266. Waller, W. H. Progression movements elicited by subthalamic stimulation. J. Neurophysiol. 3: 300–307, 1940.
 267. Wang, S. C., and S. W. Ranson. Descending pathways from the hypothalamus to the medulla and spinal cord. Observations on blood pressure and bladder responses. J. Comp. Neurol. 71: 457–472, 1939.
 268. Wasserman, K., B. J. Whipp, and R. Casaburi. Respiratory control during exercise. In: Handbook of Physiology, The Respiratory System, Control of Breathing, edited by N. S. Cherniack and J. G. Widdicombe. Bethesda, MD: Am. Physiol. Soc., 1986, p. 595–619.
 269. Weil, J. V, E. Byrne‐Quinn, I. E. Sodal, J. S. Line, R. E. McCollough, and G. F. Filley. Augmentation of chemosensitivity during mild exercise in normal man. J. Appl. Physiol. 33: 813–819, 1972.
 270. Weinrich, D. Ionic mechanism of post‐tetanic potentiation at the neuromuscular junction of the frog. J. Physiol. (Lond.) 212: 431–446, 1971.
 271. Whipp, B. J. The control of exercise hyperpnea. In: Regulation of Breathing, Part I. New York: Marcel Dekker, Inc., 1981, p. 1069–1139.
 272. Wible, J. H., F. C. Luft, and J. A. DiMicco. Hypothalamic GABA suppresses sympathetic outflow to the cardiovascular system. Am. J. Physiol. 254 (Regulatory Integrative Comp. Physiol. 22): R680–R687, 1988.
 273. Wiley, R. L., and A. R. Lind. Respiratory responses to sustained static muscular contractions in humans. Clin. Sci. 4: 221–234, 1971.
 274. Yamamoto, W. S. Looking at the regulation of ventilation as a signalling process. In: Muscular Exercise and the Lung, edited by J. A. Dempsey and C. E. Reed. Madison, WI: University of Wisconsin Press, 1977, p. 137–149.
 275. Younes, M. The physiological basis of central apnea and periodic breathing. Curr. Pulmonol. 10: 265–326, 1989.
 276. Zucker, R. S. Short‐term synaptic plasticity. Annu. Rev. Neurosci. 12: 13–31, 1989.
 277. Zuntz, N., and J. Geppert. Uber die Natur der normalen Atemreize und den Ort ihrer Wirkung. Arch. Ges. Physiol. 38: 337–338, 1886.

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Tony G. Waldrop, Frederic L. Eldridge, Gary A. Iwamoto, Jere H. Mitchell. Central Neural Control of Respiration and Circulation During Exercise. Compr Physiol 2011, Supplement 29: Handbook of Physiology, Exercise: Regulation and Integration of Multiple Systems: 333-380. First published in print 1996. doi: 10.1002/cphy.cp120109