Biomedical subjects
Publications and source records attributed to Philippe Haouzi.
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For over a century of creative research, many theories on the possible mechanisms controlling respiration during exercise have been developed and discussed. One of the most enduring questions is certainly related to the mechanisms that can prevent P(a)(CO(2)) rising when CO(2) production increases. As multiple systems and structures are capable of increasing ventilation (V (E)), not all the mechanisms controlling respiration can provide a proper answer to this question. Indeed, exercise is a complex physiological condition combining motor activity with a change in metabolic rate. The most intriguing aspect of exercise is that when the changes in metabolism are dissociated from the motor and locomotor activity, the strategy 'chosen' by the respiratory control system is to follow the metabolic rate (or more precisely factors temporally associated with the pulmonary gas exchange rate) regardless of the motor act. The strategy used by the respiratory system during exercise therefore appears to select from among various sources of information the most relevant to follow the rate at which CO(2) is ultimately exchanged by the lungs. Yet, the nature of the signal(s) which prevents CO(2)/H(+) disturbance during exercise is the fundamental question addressed by this simple observation and remains to be clarified. This review illustrates the attempts of many physiologists to collect experimental evidence for theories which could provide satisfactory mechanisms accounting for the matching between ventilation and the rate at which CO(2) leaves the tissues and is exchanged at the lungs. More recent models based on somatic information of circulatory origin are presented and discussed.
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The ventilatory response to electrically induced rhythmic muscle contractions (ERCs) was studied in six urethane-chloralose-anaesthetized sheep, while arterial oxygen and carbon dioxide pressure (P(a,O(2)) and P(a,CO2)) and perfusion pressure were maintained constant at the known chemoreception sites. With cephalic P(a,CO2) held constant, the response to inhaled CO2 was virtually abolished (0.03 +/- 0.04 l min(-1) Torr(-1)). During low-current ERC, which doubled the metabolic rate ( increased from 192 +/- 23 to 317 +/- 84 ml min(-1), P < 0.01), followed the change in closely (from 5.24 +/- 1.81 to -9.27 +/- 3.60 l min(-1), P < 0.01) in the absence of any chemical error signal occurring at carotid and central chemoreceptor level (Deltacephalic P(a,CO2)=-0.75 +/- 1 Torr). Systemic P(a,CO2) decreased by -2.47 +/- 1.9 Torr (P < 0.01). Both heart rate and systemic blood pressure increased significantly by 18.6 +/- 5.5 beats min(-1) and 7.0 +/- 9.3 mmHg, respectively. When the CO2 flow to the central circulation was reduced during ERC by blocking venous return ( decreased by 102 +/- 45 l min(-1), P < 0.01), ventilation was stimulated (from 11.99 +/- 4.11 to 13.01 +/- 4.63 l min(-1), P < 0.05). The opposite effect was observed when the arterial supply was blocked. Finally, raising the CO2 content and flow in the systemic blood did not significantly stimulate ventilation provided that the peripheral and central chemoreceptors were unaware of the changes in blood CO2/H+ composition. Our results support the existence of a system capable of controlling blood P(a,CO2) homeostasis when the metabolism increases independently of peripheral and central respiratory chemoreceptors. Information from the skeletal muscles related to the local vascular response provides the central nervous system with a respiratory stimulus proportional to the rate at which gases are exchanged in the muscles, thereby coupling ventilation to the metabolic rate.
The sites and forms of interactions between voluntary breathing acts and automatic respiratory rhythm generation are the subject of considerable research interest. We report here observations of the control of breathing in a patient suffering from an advanced form of progressive supranuclear palsy (Steele-Richardson-Olszewski syndrome). This patient demonstrated a severely compromised ability to perform volitional respiratory acts upon command, despite exacerbated behavioural and automatic control of respiration. The presence of residual volitional control of breathing in this patient provided interesting insights concerning the interaction between the automatic and the voluntary control of respiration. We observed that (1) when the subjects was asked to inspire voluntarily he could at best mobilize a volume similar to spontaneous VT and only very slowly; (2) automatic breathing movements persisted, superimposed onto the active voluntary movements, with an amplitude that decreased when the inspiratory activity, albeit weak, reached its maximal level; (3) during breath holding both the amplitude and the frequency of the basal spontaneous rhythmic activity were depressed. This observation therefore supports the idea of a strong interaction between volitional and automatic breathing in the form of an inhibition of automatic activity during voluntary breathing. Although, the site of interaction (spinal versus supraspinal) could not be determined during volitional inspiration, the effect of breath holding on the frequency of the spontaneous breathing activity supports the view that a volitional breathing arrest has some inhibitory effects on the respiratory oscillator at the medullary level. Finally, in an attempt to reconcile the persistence of a rhythmic activity during voluntary inspiration and expiration with previous data from the literature, it is proposed that the normal suppression of the automatic activity during voluntary inspiration relies on cortical and sub-cortical structures involved in the planning, i.e. the praxic component, of a respiratory task rather than on projections originating from the primary motor cortex.
This study was designed to test the hypothesis that the frequency response of the systems controlling the motor activity of breathing and walking in quadrupeds is compatible with the idea that supra-spinal locomotor centres could proportionally drive locomotion and ventilation. The locomotor and the breath-by-breath ventilatory and gas exchange (CO2 output (VCO2) and O2 uptake (VO2)) responses were studied in five sheep spontaneously walking on a treadmill. The speed of the treadmill was changed in a sinusoidal pattern of various periods (from 10 to 1 minute) and in a step-like manner. The frequency and amplitude of the limb movements, oscillating at the same period as the treadmill speed changes, had a constant gain with no phase lag (determined by Fourier analysis) regardless the periods of oscillations. In marked contrast, when the periods of speed oscillations decreased, the amplitude (peak-to-mean) of minute ventilation (VE) oscillations decreased sharply and significantly (from 6.1 +/- 0.4 l min(-1) to 1.9 +/- 0.2 l min(-1)) and the phase lag between ventilation and treadmill speed oscillations increased (to 105 +/- 25 degrees during the 1 min oscillation periods). VE response followed VCO2 very closely. The drop in VE amplitude ratio was proportional to that in VCO2 (from 149 +/- 48 ml min(-1) to 38 +/- 5 ml min(-1)) with a slightly longer phase lag for ventilation than for VCO2. These results show that beyond the onset period of a locomotor activity, the amplitude and phase lag of the VE response depends on the period of the walking speed oscillations, tracking the gas exchange rate, regardless of the amplitude of the motor act of walking. Locomotion thus appears unlikely to cause a simple parallel and proportional increase in ventilation in walking sheep.
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This review examines the evidence that skeletal muscles can sense the status of the peripheral vascular network through group III and IV muscle afferent fibers. The anatomic and neurophysiological basis for such a mechanism is the following: 1) a significant portion of group III and IV afferent fibers have been found in the vicinity and the adventitia of the arterioles and the venules; 2) both of these groups of afferent fibers can respond to mechanical stimuli; 3) a population of group III and IV fibers stimulated during muscle contraction has been found to be inhibited to various degrees by arterial occlusion; and 4) more recently, direct evidence has been obtained showing that a part of the group IV muscle afferent fibers is stimulated by venous occlusion and by injection of vasodilatory agents. The physiological relevance of sensing local distension of the vascular network at venular level in the muscles is clearly different from that of the large veins, since the former can directly monitor the degree of tissue perfusion. The possible involvement of this sensing mechanism in respiratory control is discussed mainly in the light of the ventilatory effects of peripheral vascular occlusions during and after muscular exercise. It is proposed that this regulatory system anticipates the chemical changes that would occur in the arterial blood during increased metabolic load and attempts to minimize them by adjusting the level of ventilation to the level of muscle perfusion, thus matching the magnitudes of the peripheral and pulmonary gas exchange.
The aim of our study was to develop and validate a simple surgical model in the sheep which allows control of the gas composition of the blood supplying the carotid and central chemosensitive area independently of the rest of the body. This approach was made possible due to the specific features of the cranial circulation in the sheep. An extracorporeal circuit, consisting of a pump and a gas exchanger, was placed at the level of the two common carotid arteries to create a pressure gradient between the carotid and the systemic systems and to reverse blood flow in the vertebral vessels via the occipital arteries. When a pressure gradient of about 40 Torr was created between the systemic and carotid circulation, we found that no blood could reach the carotid bodies and the medulla without passing though the extracorporeal circulation. This was established (1) by measuring vertebral blood flow; and (2) by injecting either a coloured suspension or particles labelled with (99m*)Tc into the systemic or the carotid circulation. The slope of the relationship between minute ventilation (V(E)) and systemic arterial P(CO2) (P(a,CO2)) during high CO(2) inhalation in seven hyperoxic vagotomised and anaesthetised sheep was dramatically reduced, but remained above zero, when P(a,CO2) was maintained constant in the cephalic circuit (0.11 +/- 0.15 vs. 0.70 +/- 0.35 l min(-1) Torr(-1) for the control tests). This residual V(E) response to CO(2) inhalation remains to be explained since it could not be accounted for by any of the chemical or circulatory changes occurring in the cephalic circulation. Nevertheless, this preparation provides an easy method of maintaining chemical and circulatory homeostasis at the chemoreceptor level.
The aim of this study was to identify some of the mechanisms that could be involved in blunted ventilatory response (VE) to exercise in the supine (S) position. The contribution of the recruitment of different muscle groups, the activity of the cardiac mechanoreceptors, the level of arterial baroreceptor stimulation, and the hemodynamic effects of gravity on the exercising muscles was analyzed during upright (U) and S exercise. Delayed rise in VE and pulmonary gas exchange following an impulselike change in work rate (supramaximal leg cycling at 240 W for 12 s) was measured in seven healthy subjects and six heart transplant patients both in U and S positions. This approach allows study of the relationship between the rise in VE and O2 uptake (VO2) without the confounding effects of contractions of different muscle groups. These responses were compared with those triggered by an impulselike change in work rate produced by the arms, which were positioned at the same level as the heart in S and U positions to separate effects of gravity on postexercising muscles from those on the rest of the body. Despite superimposable VO2 and CO2 output responses, the delayed VE response after leg exercise was significantly lower in the S posture than in the U position for each control subject and cardiac-transplant patient (-2.58 +/- 0.44 l and -3.52 +/- 1.11 l/min, respectively). In contrast, when impulse exercise was performed with the arms, reduction of ventilatory response in the S posture reached, at best, one-third of the deficit after leg exercise and was always associated with a reduction in VO2 of a similar magnitude. We concluded that reduction in VE response to exercise in the S position is independent of the types (groups) of muscles recruited and is not critically dependent on afferent signals originating from the heart but seems to rely on some of the effects of gravity on postexercising muscles.