Anatomical and functional changes in cardiovascular system during healthy ageing
In healthy ageing, the cardiovascular system undergoes a variety of anatomical and functional changes. Specifically, ageing has been linked to changes in the myocardial contractile characteristics, cardiac autonomic regulation deficiencies due to -adrenergic desensitisation, vascular dysfunction, and blood pressure baroreflex alterations. However, it is possible that some of these alterations may actually be acceptable secondary adaptations that provide the optimal autonomically controlled cardiovascular response to such fundamental physiological changes in the older people (Spranger, et al., 2015). Age-related changes in this system can play essential role in decreased cardiovascular response about physical activity that is seen in the elderly. Indeed, the exercise pressor reaction may be diminished in older people, according to a small number of investigations including handgrip exercise as well as occlusion of postexercise circulatory. The following essay will describe the impact of ageing on exercise pressor reflex.
Muscle contraction is triggered by activation of receptors that react to either the mechanical distortion or even metabolic by-products produced by training skeletal muscle, as the ‘exercise pressor response’ is well called. The stimulation of these receptors results in the generation of somatosensory signals, that are then transmitted to the central nervous system through afferent fibres of groups III and IV (which are mechanically sensitive predominantly) and unmyelinated group IV (which are metabolically sensitive predominantly) (Stone & Kaufman, 2015). Heart rate as well as blood pressure are elevated when the skeletal muscle in the afferent fibres is activated during contraction, and this is due to an increase in sympathetic nerve activity, which is the primary cause. This reflex has been the subject of intense research over the last 70 years, and it has contributed significantly to our knowledge of how the fundamental circulatory adaptations that occur during exercise are mediated. A greater focus has been placed on this reflex in recent years because of its probable involvement in the excessive cardiovascular response on exercise that is diagnostic of heart failure and hypertension (Smith, et al., 2019). It has been proposed that overactivity of the exercise pressor reflex is associated with decreased exercise tolerance as well as an increased risk of severe cardiac events as well as stroke at the time of exercise in both disease conditions.
In spite of a possible fivefold increase in vascular conductance during exercise, cerebral input from the skeletal muscle’s response keeps blood pressure stable or rises it during activity. In both electrically induced and voluntary activity, the exercise pressor reflex is shown by identical heart rate and blood pressure responses. Studies utilising pharmacological inhibition of lower limb muscle afferent neurons have shown the relevance of exercise pressor response in maintaining tight cardiovascular control during the dynamic exercise (Grotle, et al., 2020). When exercise is undertaken with decreased neural input, these trials demonstrate that the rise in blood pressure and cardiac output is attenuated. Additional research has shown that electrically produced exercise with paralysing epidural anaesthesia, as well as equivalent activity elicited in paraplegic patients, had no effect on blood pressure (BP) (Fadel, 2015). Furthermore, when the electrically induced exercise has performed in tetraplegic patients, blood pressure drops as a result. The absence of a rise in blood pressure during activity with paralysed legs is evident, despite the fact that electrical stimulation for muscles increases lactate production and decreases muscle glycogen levels. Consequently, exercise pressor reflex stimulates sympathetic activity as well as maintain perfusion pressure by restricting abdominal blood flow. However, because reflex ‘resets’ the arterial baroreceptor modulation of the vascular conductance, skin, brain, as well as muscle blood flow can also be affected during exercise. Blood pressure (BP) is the most tightly regulated cardiovascular variable during exercise.
Exercise pressor response and its role in maintaining cardiovascular control during exercise
In the study conducted by Troy A. et al., 2003, the scientists looked into effects of ageing on the human exercise pressor reflex, which they found to be positive. It is unknown whether or not ageing has an impact on this response, despite the fact that it is a key determinant of exercise flow regulation. A mismatch between muscular effort and blood flow causes the reflex to be elicited. The reflex was therefore engaged using a paradigm where the amount of labour performed remained constant while external impedance to the flow of muscle was progressively increased. (Nystoriak & Bhatnagar, 2018). We wanted to see if age had an effect on the blood pressure response to the reflex engagement, if the sympathetic responses of nerves to the reflex engagement were different in older and young people. The findings of these research lend support to the hypothesis that muscle reflex becomes less effective with age.
As a result of physical activity, sympathetic nervous system is engaged. This assists in the redistribution of blood flow for activating muscle and the prevention of blood pressure (BP) from dropping too low. Sympathetic activation is mediated by two brain systems: central command system, which includes a mechanism which is feed-forward, as well as a muscle reflex known as exercise pressor reflex. This is necessary for the muscle response to be activated when thin fibre afferents inside contracting muscle that are physically and metabolically sensitive increase overall discharge. During forearm activity, muscle reflex is activated when muscle becomes fatigued and when there is a mismatch among both the supply of blood as well as the demand for energy.
The current research looked at the effects of ageing on exercise pressor reflex in people, and the results were promising. It is unknown whether or not ageing has an impact on this response, despite fact which it is an important determinant in exercise flow control. A mismatch between muscular effort and blood flow causes the reflex to be elicited. For this reason, in order to activate reflex, a paradigm was used in which degree of labour was maintained constant while the amount of external resistance to muscle flow was gradually raised (Mcleod, Stokes & Phillips). They wanted to see whether age had an effect on the blood pressure response to the reflex engagement, if the responses of sympathetic nerve to the reflex engagement were different in young and older people. The findings of these research provide credence to the hypothesis that muscle reflex becomes less effective with age.
Researchers in another article investigated effect of ageing on role of the group III/IV of leg afferents in pressor reflex-mediated exercise for cardiovascular response at the time of dynamic exercise which is single-leg knee extensor using intrathecal fentanyl for temporarily attenuating the muscle afferent feedback at the time of dynamic single-leg knee extensor exercise. With no adverse effects on the cardiovascular system at the rest, fentanyl blockade reduced both cardiac output as well as quality of life at the time of exercise in the young, however in the elderly, drug-induced drop in the cardiac output was much less with no effect on QL (Chrysostomou, et al., 2014). The LVC and SVC of the elderly rose as a result of fentanyl blocking, but they decreased in the younger population. The contribution to the total response of blood pressure to the exercise from group III/IV remained consistent with age, despite the large age-related changes seen. Afferent feedback-related systems that contribute to MAP response to the exercise, on the other hand, seem to be influenced by age.
Significance of exercise pressor reflex in heart failure and hypertension
With respect to the exercise pressor reflex, while the cardiac output appears to account for the majority of group III/IV- MAP mediated responsee in the young, neural feedback on heart diminishes with age, as well as alterations in the SVC becomes prominent in terms of mediating the exercise pressor reflex in the elderly. It is noteworthy that, in terms of the peripheral hemodynamic, whereas group III/IV- feedback which is mediated clearly contributes to boosting LVC during the exercise in young, (Chrysostomou, et al., 2014) these afferents seem to be responsible for decreasing LVC in the old. Despite the fact that the present research cannot rule out the possibility of sex-related changes, this discovery may be useful in explaining the restricted exercise-induced peripheral vasodilation that is often linked with ageing.
Conclusion
To sum up that has been stated above, more than seven decades have been devoted to study of “exercise pressor response.” It has been postulated that overactivity of the exercise pressor reflex is related with lower exercise tolerance as well as an increased risk of serious cardiac events and stroke at the time of exercise in the patients having heart failure and high blood pressure, respectively. Exercise pressor reflex is a critical factor in the control of exercise flow during activity. Despite the fact that it is one of the most closely controlled cardiovascular variables during exercise – and may be impacted by it as well as age – little is known about the effects of ageing on this reaction. A fentanyl blockade lowered cardiac output and quality of life (QL) in young people who were exercising at high intensity. In the elderly, drug-induced decrease within cardiac output was significantly less severe, and there was no impact on quality of life. As a consequence of fentanyl blocking, the LVC and SVC of the older group increased, but they decreased in the younger population.
References
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Spranger, M. D., Krishnan, A. C., Levy, P. D., O’Leary, D. S., & Smith, S. A. (2015). Blood flow restriction training and the exercise pressor reflex: a call for concern. American Journal of Physiology-Heart and Circulatory Physiology, 309(9), H1440-H1452.
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