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Neural Regulation of Respiration During Exercise -Beyond the Conventional Central Command and Afferent Feedback Mechanisms

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Neural Regulation of Respiration During Exercise -Beyond the Conventional Central Command and Afferent Feedback Mechanisms J Phys Fitness Sports Med, 1(2): 235-245 (2012) JPFSM: Review Article Neural regulation of respiration during exercise -Beyond the conventional central command and afferent feedback mechanisms- Koji Ishida1* and Miharu Miyamura2 1 Research Center of Health, Physical Fitness and Sports, Nagoya University, E5-2(130), Fro-cho, Chikusa-ku, Nagoya 464-8601, Japan 2 Faculty of Human Science, Kanazawa Seiryo University, Gosho-Machi, Kanazawa 920-8620, Japan Received: April 16, 2012 / Accepted: June 3, 2012 Abstract Ventilation increases rapidly and significantly in proportion to workload or metabolic rate during dynamic exercise. This increase is called “exercise hyperpnea.” During light to mod- erate step load exercise, ventilation increases from the first breath and reaches a plateau within 20 s (Phase I), during which metabolites do not reach chemoreceptors; thus Phase I is solely caused by neurogenic drives. It is worthwhile to clarify the aspects of Phase I in order to identify the mechanism of neurally mediated exercise hyperpnea. Until 2000, the mechanisms of exercise hyperpnea during light to moderate step load exercise were assumed to have been derived from two conventional neurogenic drives, “central command,” coming from the motor cortex or the hypothalamus, and “peripheral neural reflex,” originating mainly from the mechanoreceptors in muscles through group III afferents. For about a century there have been a large number of exper- iments trying to illuminate which mechanism is the cause of exercise hyperpnea. Although central command is thought to be the more likely key source, the consensus is that both central and pe- ripheral neurogenic drives operate ventilation redundantly, building a multiple regulation system during exercise. Recent advantages in technology have enabled us to examine exercise hyperpnea in novel ways. Peripheral neurogenic drive through group III and IV afferents again enters into the limelight by using selective blockers for these afferents without augmenting central com- mand. The vascular distension hypothesis has advocated that a rapid increase in peripheral blood flow is sensed as a plethysmometric change by the mechanoreceptors around the venule near the contracting muscles, stimulating the respiratory center through group IV afferents so as to match ventilation with metabolic rate. On the other hand, “learning” is attracting a growing interest from a central neurogenic point of view. Two types of learning have been proposed: “long term modulation (LTM),” serotonin mediated synaptic adaptation to repeated combined exercise and other stimuli such as an increase in dead space, and “volitional control,” a behavioral and learned response with cognitive function by way of the cerebrum and cerebellum. Nevertheless, these two pathways were derived from, not direct, but circumstantial evidence. The question, “What causes ventilation to increase during exercise?” is not likely to be solved in the near future. Keywords : Exercise hyperpnea, Central command, Peripheral neural reflex, Learning, Phase I Two representative pathways are humoral inputs from the Introduction peripheral and/or central chemoreceptors (chemorecep- Ventilation increases rapidly and greatly from the first tor reflex), and neural inputs from the higher center and/ breath at the onset of dynamic exercise, and this ventila- or peripheral receptors. Arterial CO2 partial pressure, a tory increase is tightly coupled with a change in workload powerful stimulator for the chemoreceptors, shows little or metabolic rate. This increase is called “exercise hy- change during light to moderate exercise; so it is assumed perpnea,” and the mechanisms that control it have been that the chemoreceptors don’t provide the primary drive a matter of debate in the field of exercise physiology for for exercise hyperpnea, but rather a fine tuning of venti- about a century. A change in breathing occurs when out- lation during exercise1). Neural regulation of ventilation put signals are sent to the respiratory muscles from the thus plays a dominant role during light to moderate ex- respiratory center in the medulla oblongata, and is regu- ercise. In this review, the aspects of ventilatory response lated by various input signals to the respiratory center. to exercise, produced by neural factors, are mentioned, after which comes an overview of the conventional well- *Correspondence: [email protected] accepted mechanisms for exercise hyperpnea. In addition, 236 JPFSM: Ishida K, et al. several novel concepts regarding exercise hyperpnea are Phase I than exercise load. For example, faster treadmill demonstrated. speed produced greater Phase I response, compared to steeper treadmill grade5). As for the subject’s posture, Phase I was more attenuated in the supine position than Characteristics of the neural components of exercise that in an upright one6). It is interesting to note that pas- hyperpnea sive limb movement exerted by electrically-induced mus- Before reviewing the mechanisms for the neural com- cular contraction, or mimic movement by the experiment- ponents of exercise hyperpnea, we need to elucidate ers without muscular contraction (e.g. tandem cycling) the characteristics of the neurally mediated ventilatory also produce a rapid increase in ventilation at the start of response to exercise, because it should shed light on its movement, even during sleep7). Our research group has mechanisms. It is well known that ventilation increases been demonstrating Phase I responses to both voluntary abruptly at the onset of light to moderate step load exer- exercise and passive movement. Phase I response to vol- cise from the first breath and shows a brief plateau until untary exercise and passive movement by the arms were about 20 s (Phase I), thereafter increasing exponentially larger than those by the legs8). Delayed onset muscle (Phase II), and finally reaching a steady state within 3-5 soreness caused by eccentric exercise induced augmented + min (Phase III). Since metabolites (e.g. CO2, H ) cannot Phase I response to voluntary exercise and passive move- reach the peripheral chemoreceptor (carotid bodies) with- ment9). As for the effect of deconditioning, Phase I re- in 20 s at the onset of exercise, and Phase I accounts for sponse to voluntary exercise was attenuated after bed rest almost half of the full response as shown in Fig.1, eluci- for 20 days; but showed no change after unilateral lower dation of the features of Phase I enables us to simplify the limb suspension for 20 days, while passive movement mechanism for exercise hyperpnea solely into the neural exhibited no difference in Phase I after both decondition- factor. ing10). As for different subject groups, our research group Several researchers have observed Phase I under vari- revealed that Phase I response to voluntary exercise and ous conditions. As compared with dynamic step load ex- passive movement was attenuated in the elderly, as shown ercise from rest, static exercise2), ramp and sinusoidal load in Fig. 111), pre-teenage children12), endurance runners13), exercise3), and exercise starting from pre-exercise such as and sprinters (only passive)14) as compared with normal unloaded cycling4), produced little or no Phase I response. adults around twenty years in age. There was no gender Limb movement frequency was a greater determinant for difference in Phase I response to voluntary exercise or 䞉 VI Voluntary Passive 18 (l/min) 18 (l/min) 15 15 12 12 䞉 䞉 9 9 Rest Exercise Recovery Rest Movement Recovery 6 6 -20 0 20 40 -20 0 20 40 Time (s) Time (s) 120 Exercise Movement (%) 50 (%) Steady state value of 100 3 min Exercise 40 80 30 60 20 40 * * * * 10 * 20 * * * * * * * * * * * * 0 * 0 * * Rest 5 10 15 20 Rest 5 10 15 20 Time (s) Time (s) Fig. 1 Elderly (66.8yr) Young (22.9yr) ・ Fig. 1 Absolute (upper) and relative (lower) changes of inspiratory minute ventilation (VI) responses to voluntary leg extension exercise (left) and passive movement (right) for 20 s in the elderly (●) and the young (△). As for the relative change, 100% indicates the steady state value of the same exercise for 3 min in voluntary exercise and 0% indicates resting value. * repre- sents significant difference between the elderly and the young. Data modified from Ishida et al.11) JPFSM: Neural regulation for exercise hyperpnea 237 passive movement15). These results will either be suc- rogenic drive,” “peripheral neural reflex,” and “afferent cessfully explained by the mechanisms mentioned in the feedback.” The latter is incorrect as feedback is defined following sections, or suggest a new concept for exercise as a self-regulating system where the output signal loops hyperpnea. back to an input circuit, which is not the case here. As mentioned in the Phase I section above, passive limb movement produces a rapid increase in ventilation at the Classic neurogenic mechanisms for exercise hyperpnea initial stage of movement, indicating the involvement In 1996, the classic concepts of central and peripheral of afferent neurogenic drives from moving limbs as the neural regulation of ventilation during exercise were el- cause of exercise hyperpnea. This mechanism is strongly egantly and thoroughly summarized by Waldrop et al.16) supported by experiments showing that increased ventila- and Kaufman and Foster1), respectively, in the “Handbook tion induced by electrical stimulation or manual passive of Physiology.” Additionally, in the 1990s, Mateika and limb movement disappeared in partial spinal cord resect- Duffin17),
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