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310 D L TURNER,Introduction, The cardiorespiratory responses to the onset of mild or moderate exercise. phase 1 are rapid 0 15 s in fact so rapid that purely neural control mechanisms. are probably responsible for the initial actions of the various physiological. systems As exercise proceeds 15 s to 2 or 3min slower increases in the. cardiorespiratory variables occur phase 2 until a new steady state is reached. phase 3 3 min onwards Neural and humoral control mechanisms now combine. to bring about an appropriate response Fig 1, The two most important neural control systems responding during phase 1 are. 1 mechanical feedback reflexes originating from the active muscle mass and 2 a. centrally generated feedforward motor pattern In addition there may also be a. non neurally mediated cardiodynamic feedforward mechanism also operating. during phase 1 which could couple an increase in ventilation to an increase in. cardiac output, As the cardiovascular and respiratory systems more slowly begin to attain a. steady state response profile phase 2 each physiological system comes increas. ingly under the influence of further neural and humoral feedback control. mechanisms and central neural reverberation These feedback mechanisms may. arise either from neural afferent inputs originating in the lungs the heart the. carotid body and muscle chemoreceptors the arterial baroreceptors and thermor. eceptors or from humoral inputs blood borne substances acting directly on the. central nervous system or indirectly via peripheral receptor systems Furthermore. the control mechanisms predominant during phase 1 may still be operative. during phase 2 During the steady state phase 3 further prolonged exercise may. be compromised by thermoregulatory and fluid homeostatic control mechanisms. as well as changes in substrate utilization and delivery There may also be. modulation brought about by an array of hormones or other chemical substances. This review will describe the way in which each phase of physiological. adjustment to exercise is controlled and coordinated The intention is to produce. an up to date synthesis of recently obtained evidence of these control mechanisms. and then to discuss how they may be integrated into an overview of control. mechanisms operating during exercise,Control mechanisms operating during phase 1. The century old concept of a neural control mechanism operating during all. three phases of exercise commonly known as the exercise reflex has been. attributed to the German physiologist Zuntz Rowell 1986 Although numerous. addenda and modifications have been made the major core of the concept. remains intact Simply the reflex would be initiated within the active muscle mass. by a build up of metabolites due to a mismatch between perfusion and muscle. metabolism Chemoreceptors of some kind would sense this imbalance and the. increased firing rate in the chemosensitive afferent nerves would be detected in the. Control mechanisms during exercise 311, Fig 1 The cardiorespiratory responses to moderate sub maximal cycling exercise in.
humans Phase 1 lasts about 15 s from the onset of exercise phase 2 lasts for another. 2 3 min followed by a steady state phase 3 Recovery from exercise has qualitatively. similar periods of adjustment modified from Wasserman et al 1986. central nervous system and as a result the inadequacy of blood flow within the. muscle would be registered The appropriate increases of for example venti. tion central and peripheral components of perfusion and blood pressure would. be activated by the efferent arm of the reflex arc namely the autonomic. 312 D L TURNER, Table 1 Possible control mechanisms operating during exercise. Neurally mediated,1 Muscle receptor reflexes,2 Supramedullary command. 3 Cardiopulmonary mechanoreceptor reflexes,4 Baroreceptor reflexes. 5 Chemoreceptor reflexes,Non neurally mediated,1 Cardiodynamic coupling. 2 Cardiac Starling mechanism,3 Lung heart mechanical pumping assistance.
4 Heart lung mechanical pumping assistance,Neurohumorally mediated. 1 Decreased O2 partial pressure,2 Increased CO2 production. 3 Increased H production,4 Increased temperature,5 Increased catecholamine production. 6 Increased potassium release,Long term modulation. 1 Hormonal and opioid release,2 Exercise training,3 Other competing stresses.
nervous system This would result in a restoration of the metabolite concentrations. to normal levels The muscle chemoreflex has been implicated in the exercise. reflex since the 1930s in the pioneering work of Alam and Smirk 1937 up to the. present day for example in McArdle syndrome patients Lewis etal 1991. primarily because of the undisputed existence of chemosensitive nerve fibres that. originate in the muscle and act upon the medullary cardiorespiratory control. centres in the brainstem Mitchell and Schmidt 1983 In the context of phase 1. control the proven existence of mechanosensitive nerve fibres originating from. muscles is also particularly relevant, There is a growing body of direct and circumstantial evidence that for example. increases in ventilation heart rate and blood pressure can be elicited to a degree. even when the muscle chemoreflex is partially or wholly inoperative Hobbs 1982. Eldridge et al 1985 Galbo et al 1987 Eldridge and Waldrop 1991 This evidence. has led to the belief that supramedullary brain centres can confer a strong central. command primarily locomotor in nature which may also interact with respiratory. and cardiovascular control centres in the brainstem Krogh and Lindhard 1913. 1917 The result would be a cardiorespiratory response that is more or less. matched to the intensity of muscular activity and needed only fine continual. adjustment from the myriad of peripheral neural and neurohumoral receptor. mechanisms as exercise proceeded, A third completely different mechanism has been proposed for the linking o. Control mechanisms during exercise 313, tatantaneous increases in cardiac output and ventilation during phase 1 The idea. of a cardiodynamic coupling involves the direct activation of ventilation by a. signal from the heart itself or from within the blood flowing from it This may be. either chemical or mechanical Whipp and Ward 1982 Wasserman etal 1986. These three control mechanisms constitute the main methods by which the initial. fast component of cardiovascular and respiratory responses can be activated. during exercise Other non neural mechanisms may play minor roles. Neural mechanisms,Muscle sensory afferent fibres, The most important prerequisite for demonstrating a reflex neural control. system that arises within the skeletal muscle mass is the presence of afferent. sensory neurones There are four groups of sensory afferent nerves that arise from. muscle classified by roman numerals I IV Groups I III have nerve fibres with a. myelin sheath whilst group IV afferent nerves have nerve fibres that are non. myelinated Group I and II nerve fibres are relatively large in diameter generally. between 6 and 20 im with conduction velocities of more than 30ms 1 They. originate from within the muscle spindles where sensory endings are either. primary i e annulospiral endings in spindles or innervating Golgi tendon organs. mainly group I or secondary i e sensory endings on the intrafusal fibres mainly. group II Group I and II nerve fibres do not have a systematic important role in. chemoreception or cardiorespiratory control Kaufman et al 1982 Waldrop et al. 1984 and so will not be dealt with further in this review Group III and IV nerve. fibres are both thin between 1 and 6 im in diameter with correspondingly slower. conduction velocities 15 m s 1 than group I and II nerve fibres Most group III. and all group IV endings terminate as free nerve endings or as more recently. suggested unencapsulated nerve endings in the musculature Group III nerve. endings seem to be associated with collagen structures in the skeletal muscle. whilst the endings of group IV afferent nerves are more often associated with. blood and lymphatic vessels von During et al 1984 This anatomical distinction is. indicative of mechanoreceptive group III or chemoreceptive group IV func. tions Mitchell and Schmidt 1983, Within group III and IV nerve afferents there are nerve fibres that have.
receptors sensitive to non noxious stimuli such as muscular contraction or. movement local touch pressure and tendon or muscle stretch Kaufman et al. 1988 Stebbins etal 1988 These units have a low stimulus threshold are. commonly known as ergoreceptors and make up about 65 of group III. afferents and 45 of group IV afferents The remaining units in both groups are. particularly sensitive to more noxious stimuli and are thus commonly termed. nociceptors These units have a high stimulus threshold to mechanical distortion. and to chemical and thermal stimuli some even showing polymodal receptive. characteristics Kaufman etal 1988 Chemical stimulants include potassium. Rcreased pH bradykinin and arachidonic acid Kaufman etal 1988 Stebbins. 314 D L TURNER, Fig 2 The firing activity recorded from group III A and group IV B D fine. muscle afferent fibres in response to an induced muscular contraction lasting 40 45 s. filled bar and columns B and C represent the activity in two group IVfibresand D. represents the activity in a group IV afferent fibre whilst the muscle was kept. ischaemic before and during an induced contraction Note the instant strong response. of the group III fibre and also its rapid adaptation compared to the sustained weaker. response of the group IV fibres redrawn from Mitchell 1990. et al 1990 During exercise all of these stimuli may be present within the. receptive fields of the group III and IV nerve fibre endings and thus elicit a change. in afferent nerve firing rate, The immediate onset and rapid recovery of group III afferent activity during. induced muscular contraction is functionally consistent with a predominantly. mechanoreceptor function whilst the slower onset and more sustained activity. within group IV afferent units is functionally consistent with a more chemorecep. tive function Muscle ischaemia caused by upstream arterial occlusion or. increased intramuscular pressure during isometric contraction seems to stimulate. further the firing rate of afferent fibres during exercise Fig 2. There is ample evidence suggesting that the group III and IV muscle afferent. are heavily involved in the cardiovascular responses during all phases of exercis. Control mechanisms during exercise 315, increase in firing rate elicits an increase in blood pressure heart rate and. contractility as well as a significant and subtle redistribution of blood flow towards. the working muscle heart in cats at least and selected areas of the brain but. away from the kidneys McCloskey and Mitchell 1972 Mitchell et al 1977. Crayton et al 1979 Waldrop and Mitchell 1985 a pattern similar to that seen in. conscious exercising animals and humans Rowell 1986 Musch et al 1987. Armstrong 1988 Butler et al 1988 When most of the increase in afferent. information is blocked by dorsal root section the cardiovascular responses in. particular to muscular contraction are attenuated or abolished in anaesthetized. animals McCloskey and Mitchell 1972, The evidence for the role of muscle afferent input in eliciting the increase in. ventilation is not quite so compelling as it is for activation of the cardiovascular. system Certainly ventilation does increase and total pulmonary resistance is. reflexly decreased during electrically induced muscular contraction McCloskey. and Mitchell 1972 Bennett 1984 Rybicki and Kaufman 1985 and partial spinal. cord ablation in conscious ponies significantly attenuates the initial hyperpnoea. during phase 1 of low level voluntary exercise Taken together this evidence. implies at least some role for muscle afferent feedback in the control of ventilation. Pan et al 1990 However ventilation still increases in proportion to metabolic. rate during electrically induced muscular contraction in patients and anaesthetized. animals with complete spinal cord lesions where all sensory muscle afferent input. is presumably lost suggesting that muscle afferent information is not involved in. the ventilatory responses to exercise Cross et al 1982a Adams et al 1984 Brice. et al 1988 Muscle mechanoreceptor afferent information may contribute to the. linkage between respiratory frequency and locomotory gait which has been shown. to be present in several species during exercise Bramble and Carrier 1983. Group III and IV afferent nerves enter the spinal cord mainly through the dorsal. roots and disseminate throughout the dorsal horn of the segment of entry and also. neighbouring segments making synaptic connections with a group of spinal. neurones in laminae I V of the spinal cord the dorsal column nuclei and directly. in the nucleus tractus solitarius Kalia et al 1981 which together form part of a. pathway leading to integrative areas of the brain Suggested ascending neural. spinal pathways illuminated for example by retrograde horseradish peroxidase. labelling or lesioning include the lateral funiculus tract Kozelka et al 1987 and. spino thalamic and spino reticular tracts Putative neurotransmitters or neuro. modulators at the first synaptic relay point in the reflex arc include both substance. P and somatostatin Kaufman et al 1988 the release of which may be modulated. by opiates Hill and Kaufman 1990 acting at opiate receptor sites on the afferent. nerves Pomeroy et al 1986 In the central brain areas the spinal neurones. furnish information to a number of important regions of cardiorespiratory control. including the lateral reticular nucleus Ciriello and Calaresu 1977 Iwamoto et al. 1984 and possibly the cells of the lateral tegmental field which are both within the. u d a l ventrolateral region of the medulla Bauer et al 1990 Iwamoto et al 1989. Thus the muscle afferent nerve fibres can be structurally and functionally. 316 D L TURNER, identified from their origin in the collagen matrix and in the blood and.
vessels of the muscle through the spinal cord to their target brainstem areas and. the nuclei involved in eliciting the appropriate cardiovascular and respiratory. responses to muscular contraction,Central command, The evidence that afferent input can originate from supramedullary centres of. the central nervous system interact with medullary neurone pools and have an. influence on physiological responses to exercise in man is mainly circumstantial. Recent advances have been made in functionally dissecting central afferent input. from peripheral afferent input for example from muscle chemoreflexes using. partial neuromuscular blockade Concurrently in anaesthetized or decerebrate. animals lesion and or stimulation of putative nuclei conferring or relaying a. central command have also led to a significantly better understanding of the. complex central afferent command, Experiments involving human exercise The basic experimental protocol for. establishing the existence of the central component of the exercise response of. the cardiovascular system in particular heart rate and blood pressure is as. follows During partial neuromuscular blockade for example with tubocurarine. muscle isometric strength is reduced so that to obtain the same absolute isometric. force production there must be a greater central motor drive or effort Leonard. et al 1985 Locomotion respiration and cardiovascular responses can all be. elicited in parallel by stimulation of the central motor centres Eldridge et al. 1985 Therefore after partial neuromuscular blockade the increases in central. motor drive lead to greater increases in the cardiorespiratory variables than in the. control muscle contraction Fig 3 In this experimental condition the chemical. milieu of the contracting muscle is the same and is not therefore correlated to the. increases in ventilation heart rate and blood pressure When the same subjects. produced a contraction that represented the same relative proportion of in the. first instance the control maximal voluntary contraction MVC and in the. second instance the MVC measured during partial neuromuscular blockade the. central command was the same but the absolute force production and by. inference the muscle afferent information was less in the blocked state Heart rate. and blood pressure increased to the same extent in the non blocked and blocked. state i e were correlated to central command and not to the chemical milieu. existing in the contracting muscle and thus not to the neural activity of muscle. chemo and mechanosensors Mitchell 1990 The role of central command in. eliciting both locomotor and cardiovascular responses by parallel activation during. exercise is represented schematically in Fig 4, Recently heart rate and blood pressure have been shown to recover at different. rates after a subject has performed a powerful MVC If blood flow is occluded at. the end of the contraction heart rate returns to resting levels very quickly In. contrast blood pressure decreases to a level that is still significantly higher tha. that at rest and remains there until the occlusion is relieved The interpretation. Control mechanisms during exercise 317,0 1 2 3 4 5 0 1 2 3 4 5. Fig 3 The effect of partial neuromuscular blockade on heart rate and blood pressure. responses to static exercise In A the same absolute force is maintained without filled. curve or with open curve neuromuscular blockade whereas in B the same relative. percentage of the measured maximal voluntary contraction force is maintained without. filled curve or with neuromuscular blockade open curve See text for an. interpretation of these findings redrawn from Mitchell 1990. this finding is that heart rate is increased mainly by increased central command or. muscle mechanoreceptors via vagal withdrawal whereas blood pressure is. increased in part by central command and muscle mechanoreceptor feedback but. also in part by increased afferent input from muscle chemoreceptors sensing a. build up of metabolites during the MVC trapped in the muscle by occlusion. Fig 5 When an attempted contraction is performed during neuromuscular. blockade the build up of metabolites is not enough to stimulate the muscle. chemoreceptors and so blood pressure rapidly returns to normal even during. occlusion Rowell and O Leary 1990 The increases in blood pressure and heart. rate in response to moderate intensities of static contraction or dynamic contrac. tion when there is little or no build up of metabolites must be elicited primarily. by central command or muscle mechanoreceptors Gandevia and Hobbs 1990. Heart rate appears to be controlled more by central command via vagal. withdrawal and increased sympathetic drive than by muscle mechanoreceptors. during all intensities of static contraction Victor et al 1989 Hypnotic suggestion. has been used to increase the perception of muscular effort during a muscular. contraction and can lead to a hyperventilation Morgan et al 1973 This finding. agrees with the evidence concerning the role of central command in determining. the cardiovascular responses to exercise Evidence exists that the heart rate. sponse to exercise can be attenuated by behavioural conditioning Talan and. K lgel 1986 Perski et al 1985 The implication of this is that when the muscle. 318 D L TURNER,Motoneurone Light load,non blocked,Heavy load.
U UA non blocked,Light load,Blockade blocked,Vt A A A A i. Fig 4 A hypothesis in which descending central motor command activates in. parallel a recruitment of musclefibresand an appropriate cardiorespiratory response. be it blood pressure heart rate or ventilation The cardiorespiratory response is graded. to the degree of muscular contraction in the non blocked state However during. neuromuscular blockade the cardiorespiratory response is apparently stronger than the. muscular response This is due to a larger central motor command being necessary to. maintain the force production of the muscle mass adapted from Hobbs 1982 and. redrawn from Rowell 1986 Filled symbols represent active motoneurones and. muscle fibres unfilled ones represent inactive ones. afferent input is constant same absolute workload some cerebral influence on. the central motor command can still occur, Experiments involving electrical or chemical lesions and stimulation Obviously. the limitation of the experimental protocols described previously is that they offer. purely circumstantial evidence of a functional central command but they offer no. information about its anatomical location Traditionally the search for the. anatomical loci conferring the functional central afferent command has followed. two lines of enquiry First areas suspected of being involved in originating a. command can be rendered non functional by coarse or as techniques become. available fine lesion be it surgical or chemical Second those same areas can be. stimulated electrically or chemically and the consequent physiological responseji. monitored Spyer 1990,Control mechanisms during exercise 319. Fig 5 The partitioning of importance of central motor command muscle mechano. receptors and muscle chemoreceptors in bringing about a response in blood pressure. upper panel and heart rate lower panel during a muscular contraction filled bars. with B or without A neuromuscular blockade Arterial occlusion is initiated at the. end of the 3 min contraction to trap any released metabolites within the muscle In the. unblocked state blood pressure does not fall back to resting levels immediately after. the contraction because muscle chemoreceptor activation by metabolites maintains a. pressor reflex even in the absence of central command and muscle mechanoreceptor. control The muscle chemoreceptors do not appear to maintain an elevated heart rate. In the blocked state an attempted contraction does not produce a large enough build. up of metabolites to stimulate muscle chemoreceptors significantly and therefore. blood pressure falls rapidly back to resting levels during occlusion redrawn from. Rowell and O Leary 1990, The many nuclei within the central nervous system that have direct or indirect. influences on the cardiorespiratory centres in the medulla also have many. interconnections among themselves This makes unravelling individual roles for. each nucleus extremely difficult and any lesion or stimulation of one nucleus will. inevitably have repercussions for neural activity originating from other nuclei. Nevertheless a number of experiments has highlighted the importance of a large. number of brain areas The lesion of neurones in the subthalamic area of the brain. in primates has been shown to eliminate the increase in blood pressure during. exercise This finding implies that the descending command from the motor. cortex principally responsible for driving an orchestrated set of muscle fibre. contractions necessary for example during walking also sends a parallel drive to. cardiorespiratory control centres in the medulla Fig 4 Hobbs 1982 When the. intact subthalamic locomotor region is electrically or chemically stimulated in. unanaesthetized animals increases in ventilation blood pressure and heart rate as. d ell as a redistribution of blood flow can be elicited Similar responses can be. Jncited in animals that are deeply anaesthetized or paralysed and which obviously. 320 D L TURNER, do not walk DiMarco et al 1983 Eldridge etal 1985 Waldrop etal 1986a.
addition to the subthalamic locomotor region the neighbouring brain area known. as the fields of Florel can elicit when directly stimulated substantial increases in. blood pressure and heart rate coupled with increased phrenic nerve activity and a. bronchodilator response Together these two anatomically distinct regions have. been regarded as the main location for the functional central command Eldridge. et al 1985 McCallister et al 1988 Rybicki et al 1989 Interestingly lesions in the. fields of Florel do not alter the cardiorespiratory responses to running in conscious. dogs Ordway et al 1989 Thus merely abolishing the role of one important site. will not necessarily compromise the overall pattern of central neural feedforward. command or the resultant efferent outflow and pattern of responses This implies a. degree of redundancy or neural plasticity Superimposed on the drive from these. nuclei is the influence of the defence arousal system The perifornical region of the. hypothalamus and particularly the amygdala forms a functional centre receiving. projections from the hippocampus forebrain and brainstem summarized in. Spyer 1984 Efferent projections connect the hypothalamic defence area with the. medullary cardiorespiratory control areas Hilton 1982 Spyer 1990 and may. also relay information via the nucleus reticularis gigantocellularis Richard et al. Cardiopulmonary mechanoreceptor afferent information. Afferent fibres from the cardiopulmonary region course with the vagus nerve. towards the brain or alternatively with the sympathetic nerves which enter the. spinal cord Vagally mediated mechanoreceptors which have receptive fields in. the four chambers of the heart and also in the pulmonary artery are responsive to. distension brought about by the increase in end diastolic volume in the atria and. ventricles that may occur during exercise Plotnick et al 1986 or increased atrial. or pulmonary artery pressure Their activation could lead to a reduction in heart. rate and so would function as a peripheral feedback mechanism during exercise. However experimentally increased pulmonary artery pressure during maximal. exercise in humans did not result in any change in cardiac output heart rate or. ventilation D L Turner H Hoppeler C Noti H P Gurtner H Gerber and. G Ferretti in preparation nor did experimentally raised right ventricular. pressure in the anaesthetized dog Crisp etal 1988 Patients with denervated. heart and lungs through transplantation or cardiac denervated goats still demon. strate an appropriate ventilatory response to exercise but not an adequate. cardiovascular response Banner etal 1988 Brice et al 1991 Blocking of. sympathetically mediated information by removal of the left stellate ganglion does. not lead to major changes in cardiovascular responses to exercise apart from. possibly changing the distribution of blood flow across the myocardial wall Stone. 1983 Thus cardiac receptors probably at most only play a minor role during. exercise in normal environmental conditions Incidentally during exercise wit. peripheral pooling of blood for example brought about by lower body negati. Control mechanisms during exercise 321, e s s u r e cardiopulmonary mechanoreceptor afferent information may play a role. in maintaining blood pressure Mack etal 1990, The effect of chronic or acute hilar nerve section with a consequent loss of lung. volume afferent feedback to the medullary centres has been studied in dogs and. ponies Minute ventilation is not affected although the pattern by which it is. maintained may be altered Flynn et al 1985 Clifford et al 1986 This is similar to. the role ascribed to lung mechanoreceptors in exercising humans Lind and. Hesser 1984 Irritant or rapidly adapting receptors and J receptors also convey. afferent information via the pulmonary vagal nerves the former potentially. facilitating respiration during exercise The latter stimulated by pulmonary. congestion or oedema are situated in the alveolar wall and could potentially have. an important role during extreme exercise when pulmonary oedema is thought to. occur O Brodovich and Coates 1991 Neither appear to have a role in. controlling ventilation following vagotomy but again may be more important in. controlling the respiratory pattern Recently the ventilatory response to exercise. has been shown to persist even after heart or heart lung transplantation i e. cardiac or cardiopulmonary deafferentation and again indicates a relatively small. role for cardiopulmonary receptor control mechanisms during exercise. Baroreceptor afferent information, Recent evidence suggests that during exercise the baroreflex is reset to a higher. operating level during phase 1 as a result of a central command impinging upon the. baroreflex neuronal pool in the medulla Ludbrook 1983 Mitchell etal 1983. Rowell 1986 The maintenance of blood pressure at this new higher level is still. however adequately controlled by the reflex involving carotid sinus and aortic. baroreceptors and cardiac output and vascular resistance even during severe. exercise see later Rowell and O Leary 1990 Cardiac output is unaffected by. baroreceptor isolation in exercising dogs less afferent input with maintenance of. adequate blood pressure due to increased vascular resistance Walgenbach and. Donald 1983 During severe exercise this may even occur in the active muscle. Rowell and O Leary 1990,Chemoreceptor afferent information. During phase 1 of exercise the delay between measurable changes or errors in. the levels of blood gases and blood borne metabolites occurring in the contracting. muscles and their reception in peripheral or central arterial chemoreceptors. precludes a role of these receptive sites in initiating cardiorespiratory responses. However in humans relatively hypoxic and hypercapnic blood has been shown to. reach the pulmonary artery at the onset of exercise as a bolus from the inferior. vena cava before any return of venous blood from the exercising leg muscle. Casaburi etal 1989 The functional significance of this has yet to be fully. Pbtermined The central chemoreceptors have been ruled out as an important. 322 D L TURNER, source of afferent input in the control of ventilation or circulation in all phases.
exercise Casey etal 1987,Non neural mechanisms, An entirely different approach to the possible control of coupled cardiorespira. tory responses during exercise has been proposed The cardiodynamic coupling. hypothesis involves a direct linkage between cardiac output and ventilation. consisting of some kind of feedforward mechanism by which a pulmonary. circulatory stimulus or stimuli activates an increase in ventilation There is a. large body of evidence that lends circumstantial support to this hypothesis. Wasserman et al 1974 found that ventilation rose immediately and in proportion. to an induced increase in cardiac output Owing to the time delays between the. pulmonary artery and peripheral and central chemoreceptors the rise in venti. lation could not be mediated by a chemoreflex from these receptors In addition. in humans with resected carotid bodies cardiodynamic coupling is still present. during phase 1 of exercise Wasserman et al 1975 The activating stimulus for an. increase in ventilation secondary to an increase in cardiac output may be a. mechanical signal arising from distension of the right atrium and ventricle or even. the pulmonary artery Thus when stroke volume is increased for example by. increasing right ventricular work as a result of altered peripheral resistance and or. venous return ventilation increases accordingly and with the appropriate time. course Jones etal 1982 Incidentally altering heart rate only for example by. increasing the output of an artificial pacemaker does not affect ventilatory. responses to exercise Jones etal 1981 However the occurrence of this. feedforward cardiodynamic mechanism has been seriously questioned in studies of. exercising ponies Pan etal 1983 1984 and humans Adams etal 1987 Turner. et al 1991 and also in isolated subsystems involving the heart pulmonary arteries. and lungs Lloyd 1984, Stretching of the walls and therefore muscle fibres of the heart by an increase. in venous return may at least during mild exercise lead to an increase in stroke. volume and thus cardiac output via the Frank Starling mechanism Plotnick. et al 1986 The role of heart lung and lung heart mechanical pumping assistance. due to physical movement during exercise is potentially of importance but as yet. has not been thoroughly investigated Agostoni and Butler 1991 These two. mechanisms could occur without neural or neurohumoral involvement. Control mechanisms operating during phases 2 and 3. The neurohumoral drive, Phase 1 only lasts for a few seconds after which there is a slower increase in a. number of cardiorespiratory variables towards an asymptotic level Fig 1 The. phase 2 and 3 periods can obviously still be under the control of the mechanisms. operating during phase 1 However their delayed onset coincides roughly with t. delay for blood borne chemical transfer from muscles to heart pulmona. Control mechanisms during exercise 323, lungs carotid bodies and cerebral circulation Thus phases 2 and 3 have. long been associated with a number of possible humoral mediators of the. cardiorespiratory exercise responses The original synopsis of the two stage. neurohumoral control mechanism during exercise was popularised by Dejours. 1964 Humoral mediators can conceivably work directly upon target organs for. example the heart smooth muscle of the lungs or medullary centres or indirectly. via peripheral chemoreceptors from which neural pathways mediate control. Flandrois 1988,Humoral mechanisms, There are many possible candidates for the all important chemical blood borne.
mediator that may arise from the active muscle mass during exercise Increased. partial pressure or content of carbon dioxide decreased oxygen partial pressure. increased hydrogen ion concentration increased temperature increased catechol. amine concentrations and increased potassium concentration are all potential. signals that exist during exercise,Mixed venous chemoreceptors. During phase 3 of exercise there is a large increase in carbon dioxide flow. cardiac output x mixed venous carbon dioxide content to the heart and lungs. When the flow of carbon dioxide is decreased in non exercising humans. ventilation also decreases indicating a potentially strong direct role for carbon. dioxide flow in ventilatory control Dolan et al 1981 When the carbon dioxide. flow to the lungs during exercise is altered by removing or adding carbon dioxide. using a gas exchanger increased carbon dioxide flow is associated with an increase. in ventilation Wasserman et al 1986, There is possibly a vagally mediated pulmonary chemosensitivity to an increase. in carbon dioxide that may be an indirect humoral activator of ventilation during. exercise Green and Sheldon 1983 although other studies have shown that lung. denervation does not alter the total ventilatory response only the pattern by. which it is achieved Clifford et al 1986 Favier et al 1982 Unfortunately there. appears to be very little evidence suggesting the existence of mixed venous or. pulmonary arterial chemoreceptors and so their role as part of an indirect. Immorally activated reflex during exercise can be considered negligible Wasser. man et al 1986 Indeed the increases in venous carbon dioxide concentration and. ventilation can be disassociated by occlusion of the thigh during cycling exercise. Stanley et al 1985,Arterial chemoreceptors, During steady state exercise phase 3 arterial oxygen and carbon dioxide. partial pressures and pH are all maintained at normal levels and there will be no. mean increase in stimulus to the carotid body or central chemoreceptors Thus. hen the carotid body chemoreceptors are surgically resected in some humans. ventilatory responses during phase 3 are the same as those in normal.

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