Cardiovascular control in exercise, the contribution of central command and muscle afferents

Cardiovascular control in elabo post, the contribution of central command and vigor afferentsCardiovascular Control in Exercise, the contribution of Central Command and Muscle Afferents The human body has the ability to easily adapt when mould begins with many of these adaptations occurring in the cardiovascular system. It is well put down that at the onset of practice heart rate (HR), blood pressure (BP) and energy sympathetic nerve activity progressively increase to higher levels (Lind et al, 1964). These cardiovascular adaptations argon controlled by either central (Central Command) or peripheral device (exercise pressor reflex) mechanisms (McCloskey Mitchell, 1972). Central Command (CC) is thought to be a feed-forward process controlling some(prenominal) HR and respiration, twain(prenominal) of which are known to increase in the anticipation of exercise (Secher, 2007). CC originates from higher areas of the brain (motor cortex and subcortical areas) and works in parall el with both the locomotor and cardiorespiratory systems during exercise (Green et al, 2007). The feed-forward efferent input converges on the cardiovascular centres of the brainstem along with feedback returning from afferents located in the active agent skeletal muscle providing the changes seen at the onset of exercise (Fisher et al, 2005). The changes inside the cardiovascular system during exercise are helped via peripheral mechanisms as well as CC. CC inhibits the parasympathetic nervous system by decreasing vagal tone allowing HR to rise, the sympathetic nervous system eventually takes over to allow but increases. Activation of the sympathetic nervous system is produced via feedback from muscle afferents, mainly mechanoreceptors (Murata and Matsukawa, 2001), and forms the sensory arm of the exercise pressor reflex. Muscle afferents are split into two specialize classes, group III and group IV. Group III afferents, classified as mechanoreceptors, are stimulated via muscle load up, condensate or pressure (Kaufman et al, 1983) whereas group IV afferents, classified as metaboreceptors, are chemically sensitive (Gladwell and Coote, 2002). Afferents are also said to be polymodal and can respond to both mechanical and chemical stimuli (Mense and Meyer, 1985). The exercise pressor reflex is evoked when afferents become sensitised allowing feedback to the cardiovascular centres within the brain. This then allows adequate perfusion of the muscles by increasing cardiac output and constricting the vascular beds (OLeary, 1993). A number of studies aim to distinguish between the role of CC and muscle afferent feedback in humans during exercise. When the blood supply to an exercising muscle is impede CC is non present, this process known as post exercise circulatory occlusion (PECO) activates metaboreceptors (Gandevia and Hobbs, 1990). Electrically evoked exercise also bypasses CC so when this method is used CC is redundant (Kaufman and Rybicki, 1987). These tw o methods allow the elimination of CC showing muscle afferents provide all feedback which could evoke a cardiovascular response. CC is activated in proportion to the intensity of the exercise results from a study by Williamson et al (2002) have shown this through hypnosis. Originally an individuals comprehend exertion during exercise was thought to be independent of any force creation produced, allowing the magnitude of CC to be seen (Gandevia et al, 1993). Williamson et al (2002) obtained results related to this idea they put together that the level of CC activated was related to an individuals sense of effort independently of any force being produced. Increases in HR were found during hypnosis despite no exercise being performed and increases were therefore independent of feedback from afferents within the active limb. Passively stretching muscles allows cardiovascular responses to be evoked within humans two studies by Gladwell and Coote (2002) and Fisher et al (2005) have pro posed opposing ideas. Gladwell and Coote (2002) activated mechanoreceptors in the triceps surea to measure the effectuate on HR and BP. Voluntary isometric contraction of the plantar flexor muscle followed by a sustained stretch of the triceps surea by dorsiflexion were performed. Fisher et al (2005) used a similar protocol but blood supply was occluded throughout and different percentages of maximal wilful contraction were used. They aimed to see whether cardiovascular response to sustained muscle stretch was altered by varying metabolites within the muscle. Gladwell and Coote (2002) found HR increased soon after the onset of muscle contraction with part of the HR response being mediated via mechanoreceptors since stimulation of receptors via stretch decreased parasympathetic activity. Fisher et al (2005) found that HR and BP were untouched by levels of metabolite accumulation, therefore stretch was seen to activate mechanically sensitive afferents which are unaffected by the m etabolic condition. This studys use of occlusion shows that the response to stretch is purely from muscle afferents as it is known that CC is not present in these conditions. Gladwell and Coote (2002) did not use occlusion and though cardiac vagal tone activity was measured throughout stretch there is no way to as accredited whether CC was present. The conclusion bony by Fisher et al (2005) is more reliable as the cardiovascular response seen is entirely down to mechanoreceptors, it must be certain that CC has been authorized in Gladwell and Cootes (2002) study in the lead the results can be taken into consideration. The use of stimulated and voluntary exercises is an easy way to directly compare the effects of CC and muscle afferent feedback on the cardiovascular system. An early study by Krogh and Lindhard (1917) showed through electrical stimulation that an increase in pulse rate was reflexly induced (by muscle afferent) whereas increases in voluntary exercise originated fro m cerebral impulses (CC). Alam and smile (1937) took this further and looked into the changes in BP during muscular work when circulatory occlusion was applied. A cuff placed around the thigh occluded flow whilst knee raises were performed at repeated intervals using only the calf muscle. BP rose as a result of the exercise and dropped when the exercise stopped, however it remained at an elevate level compared to rest. BP did not return to resting level until PECO was ceased. Mental efforts which are associated with muscular work are not the main reason for the rise in BP when no cuff was placed around the leg increases in BP were less or abolished. Therefore the keen fall in BP whilst PECO is still in place is due to the cessation of mental activity concerned with muscular exercise and muscle afferents must be causing the cardiovascular response thereafter. The studies indicated previously provided the basis for the concept that CC and muscle afferents affect cardiovascular resp onse in separate ways. More young studies by Coote et al (1971) and Bull et al (1989) have looked further into the effects of voluntary and stimulated exercise. Bull et al (1989) compared the pressor reflex during and following voluntary and involuntary contraction of the triceps surea whilst under occlusion. When voluntary contraction ended but PECO was maintained BP rapidly fell to a lower though still elevated level compared with rest. It was thought that the initial drop was attributed to the removal of CC, matching the results of Alam and Smirk (1937). The immediate drop in HR back to resting level seen post exercise whilst still under PECO suggests that it cannot be the metabolites which cause the increase in HR, if this were the case HR would stay elevated in PECO. The study concludes that the elevated BP following both types of contractions (electrical and voluntary) were due to circulatory arrest caused by trapped metabolites within the muscle. This suggests that the cardi ovascular responses of HR and BP must be controlled by two separate mechanisms, CC and peripheral feedback respectively. Coote et al (1971) looked at the pressor reflex response to muscular exercise in cats. The cats were anaesthetised and contraction of the hindlimb was elicited by electrical stimulation of the ventral germ, CC was not activated as electrical stimulation bypasses the brain. An increase in BP was still seen without CC being present therefore the conclusion was drawn that cardiovascular response arises from within the contracting muscles themselves, either mechanically or chemically, rather than from CC. Evidence for a chemical stimulus within humans has come from Alam and Smirk (1937) which can provide the link that results drawn from cats can be similar to those that occur in humans. It was also found that the pressor reflex was proportional to the latent hostility developed by the contraction and so the stronger the contractions the large the pressor reflex is l ikely to be. Distinguishing between CC and muscle afferent feedback can also be undertaken through neuromuscular blockade (NMB) and anaesthesia. Two studies employing this technique are by Gandevia and Hobbs (1990) and Iwamoto et al (1987) both looked at cardiovascular response in man, McCloskey and Mitchell (1972) also assiduous this technique but investigated cats. The latter study sought to provide evidence that NMB would abolish the cardiovascular response in exercise. Cats triceps surea were electrically stimulated via the ventral root with two nerve blocking techniques being used anodal blockage was used to eliminate large myelinated nerve fibres and anaesthesia was used to eliminate small and unmyelinated nerve fibres. Anodal block did not change the pressor reflex from the control condition this is due to only the large fibres being blocked which are predominantly muscle spindles and Golgi tendon organs. However under anaesthetic the cardiovascular responses were abolishe d. This is due to small and unmylinated fibres being blocked which are predominantly mechano- and metaboreceptors. The fact that only anaesthesia affects the cardiovascular response shows that the response is entirely due to the pressor reflex as no CC could be present. Iwamoto et al (1987) did a similar study but experimented on both cats and humans. The cat procedure was the same as McCloskey and Mitchell (1972) whilst humans performed voluntary and evoked knee extensions before and after NMB (tubocurarine). In cats blockade eliminated all cardiovascular responses compared with the control condition. In human voluntary contraction HR increased and cleverness was large, NMB reduced strength but allowed further increases in HR. Stimulated contraction reduced strength but HR was as large as in voluntary exercise though increased from the second R-R interval, NMB reduced strength further but HR still increased from second heart beat. BP increased in both types of exercise but to a l esser extent in stimulated exercise, NMB further reduced BP. As HR was unaffected by NMB it is suggested that it is governed by processes foreign the muscle (CC) this is in line with Sechers (1985) findings. However BP was affected suggesting that muscle afferent feedback plays a role in the control of BP within the cardiovascular response, this matches the McCloskey and Mitchells (1972) conclusion drawn from cats. Gandevia and Hobbs (1990) looked at changes in HR and BP to graded contraction in man with the use of anaesthesia. Handgrip contractions were performed with a period of 3min PECO, arm muscles were then acutely paralysed via anaesthesia and the exercise performed again. HR and BP increased in line with the preceding contraction with PECO showing the degree to which the metaboreflex was activated. BP increased in direct relation to the preceding contraction but HR did not. In paralysis graded increases in HR were seen but not in BP, suggesting CC controls HR response. The se results are consistent with in Iwamoto (1987) who found NMB to reduce BP response but which had little effect on HR response to voluntary contraction. Both studies show that cardiovascular response must be due to a combination of CC and chemoreflex. Gandevia and Hobbs (1990) showed that during anaesthesia HR was controlled by CC as muscle afferent would have been blocked, as BP did not increase with anaesthesia it could be concluded that muscle afferents control the modulation of BP. Conclusions can be drawn from all the relevant literature that CC and muscle afferent feedback have overlapping tendencies and that the different aspects of the cardiovascular response, though controlled via both mechanisms, lean towards one aspect more than the other. Therefore HR could be controlled to a greater extent by CC (Gandevia and Hobbs, 1990 Iwamoto et al, 1987 and Bull et al, 1989) whereas muscle afferent feedback could control BP response (Alam and Smirk, 1937 and Coote et al, 1971).