MSNA- muscle sympathetic nerve activity
this following is a part of my review i am going to send for a renowned journal.
Comparison of impacts of activation of SNA via metaboreflex & chemoreflex (21)
Bothdynamic and static exercise are associated with a metaboreflex activation of sympathetic activity. Both dynamic and static exercises are associated with a metaboreflex activation of sympathetic activity. Arterial hypoxemia is associated with a peripheral chemoreflex-mediated increase in sympathetic activity. Symathoexcitation manifests by increases in heart rate, blood pressure, and ventilation.
Characteristics of metaboreflex induced SNA: Increases in ventilation and heart rate being most prominent during dynamic exercise and blood pressure most prominent during static exercise.
Characteristics of chemoreflex induced SNA: Increases in ventilation and heart rate, but no change in blood pressure. Although an increase in systolic blood pressure has been reported in subjects who performed dynamic exercise in hypoxic conditions, the effects of static exercise on blood pressure in hypoxia are not well documented.
Interaction between metaboreflex & chemoreflex mechanisms in sympathoexcitation
At least 3 previous studies (Hanada A et al, Saito M et al, Seals DR et al), that these two mechanisms may interact in producing the autonomic responses. All three studies indicate that the sympathetic response to exercise during hypoxia is greater than to exercise or to hypoxia separately.
Arterial (high pressure) baroreceptors
Baroreceptors & Baroreflex:
Baroreceptors act in response to detected stretch on the blood vessel walls to elicit a negative feedback system called the baroreflex. This stretch on blood vessel wall signals to the nervous system. The output is by means of increase or decrease total peripheral resistance and cardiac output. Further because of these adjustments; as soon as there is a change from the usual blood pressure, return to the pressure to a normal level. However, they represent only a short term blood pressure regulation mechanism & over a period of 1-2 days they reset to a new BP value.
Typpes of baroreflex:
Baroreceptors can be divided into two categories
1. High pressure arterial baroreceptors and
2. Low pressure baroreceptors.
We are more concerned with the arterial baroceptors in the present context of discussion.
Arterial (high pressure) baroreceptors
Arterial baroreceptors are present in the aortic arch and the carotid sinuses of the left and right internal carotid arteries. They are vastly scattered sensory nerve endings lying in the tunica adventitia of the artery, not drug-binding molecules as the term 'receptor' may suggest. A depolarisation of these sensory endings which results in action potentials is a result of change in the mean arterial pressure. These action potentials are conducted to the central nervous system by axons and have a direct effect on the cardiovascular system through autonomic neurons. Baroreceptors are present in carotid arteries & aorta and are called carotid baroreceptors & aortic baroreceptors respectively. The efferent inputs from these baroreceptors travel through 9th & 10th cranial nerve respectively.
Baroreflex & MSNA (23, 25, 26):
Many researches have found that baroreflex is a major determinant of sympathetic discharge during exercise especially static exercise. But there is a lot of argument which baroreceptors are the major contributors i.e. the sinoaortic (receptors of aortic arch) or the caroid. Researchers Walgenbach & Donald (1983) has found during exercise, the carotid baroreflex acts to balance finely the opposing effects of sympathetic vasoconstriction and metabolic vasodilation25. However according to sherrer U & colleagues it is the sinoaortic baroreceptors which plays the dominant role. Further they also have shown in their study that in healthy humans sinoaortic baroreflex acts an effective buffer to the reflex sympathetic action caused by static muscle action23.
ABR function is impaired in hypertension and many other cardiovascular diseases. In clinical setting impaired baroreceptor function may lead to exaggerated increases in the sympathetic outflow & arterial pressure during exercises in patients with hypertension, heart failure & advancing age23. However, according to Giulliano G et al physical training improves ABR sensitivity in neurally mediated syncope patients and could be applied as a non-pharmacological therapeutic alternative for these patients26.
Thermal stress, ABR & MSNA:
At rest, whole-body heating enhances arterial baroreflex control of MSNA. This occurrence is likely to afford protection against potential decreases in arterial blood pressure in an effort to preserve orthostatic tolerance during heat stress 24.
Comparison of impacts of activation of SNA via metaboreflex & chemoreflex (21)
Bothdynamic and static exercise are associated with a metaboreflex activation of sympathetic activity. Both dynamic and static exercises are associated with a metaboreflex activation of sympathetic activity. Arterial hypoxemia is associated with a peripheral chemoreflex-mediated increase in sympathetic activity. Symathoexcitation manifests by increases in heart rate, blood pressure, and ventilation.
Characteristics of metaboreflex induced SNA: Increases in ventilation and heart rate being most prominent during dynamic exercise and blood pressure most prominent during static exercise.
Characteristics of chemoreflex induced SNA: Increases in ventilation and heart rate, but no change in blood pressure. Although an increase in systolic blood pressure has been reported in subjects who performed dynamic exercise in hypoxic conditions, the effects of static exercise on blood pressure in hypoxia are not well documented.
Interaction between metaboreflex & chemoreflex mechanisms in sympathoexcitation
At least 3 previous studies (Hanada A et al, Saito M et al, Seals DR et al), that these two mechanisms may interact in producing the autonomic responses. All three studies indicate that the sympathetic response to exercise during hypoxia is greater than to exercise or to hypoxia separately.
Arterial (high pressure) baroreceptors
Baroreceptors & Baroreflex:
Baroreceptors act in response to detected stretch on the blood vessel walls to elicit a negative feedback system called the baroreflex. This stretch on blood vessel wall signals to the nervous system. The output is by means of increase or decrease total peripheral resistance and cardiac output. Further because of these adjustments; as soon as there is a change from the usual blood pressure, return to the pressure to a normal level. However, they represent only a short term blood pressure regulation mechanism & over a period of 1-2 days they reset to a new BP value.
Typpes of baroreflex:
Baroreceptors can be divided into two categories
1. High pressure arterial baroreceptors and
2. Low pressure baroreceptors.
We are more concerned with the arterial baroceptors in the present context of discussion.
Arterial (high pressure) baroreceptors
Arterial baroreceptors are present in the aortic arch and the carotid sinuses of the left and right internal carotid arteries. They are vastly scattered sensory nerve endings lying in the tunica adventitia of the artery, not drug-binding molecules as the term 'receptor' may suggest. A depolarisation of these sensory endings which results in action potentials is a result of change in the mean arterial pressure. These action potentials are conducted to the central nervous system by axons and have a direct effect on the cardiovascular system through autonomic neurons. Baroreceptors are present in carotid arteries & aorta and are called carotid baroreceptors & aortic baroreceptors respectively. The efferent inputs from these baroreceptors travel through 9th & 10th cranial nerve respectively.
Baroreflex & MSNA (23, 25, 26):
Many researches have found that baroreflex is a major determinant of sympathetic discharge during exercise especially static exercise. But there is a lot of argument which baroreceptors are the major contributors i.e. the sinoaortic (receptors of aortic arch) or the caroid. Researchers Walgenbach & Donald (1983) has found during exercise, the carotid baroreflex acts to balance finely the opposing effects of sympathetic vasoconstriction and metabolic vasodilation25. However according to sherrer U & colleagues it is the sinoaortic baroreceptors which plays the dominant role. Further they also have shown in their study that in healthy humans sinoaortic baroreflex acts an effective buffer to the reflex sympathetic action caused by static muscle action23.
ABR function is impaired in hypertension and many other cardiovascular diseases. In clinical setting impaired baroreceptor function may lead to exaggerated increases in the sympathetic outflow & arterial pressure during exercises in patients with hypertension, heart failure & advancing age23. However, according to Giulliano G et al physical training improves ABR sensitivity in neurally mediated syncope patients and could be applied as a non-pharmacological therapeutic alternative for these patients26.
Thermal stress, ABR & MSNA:
At rest, whole-body heating enhances arterial baroreflex control of MSNA. This occurrence is likely to afford protection against potential decreases in arterial blood pressure in an effort to preserve orthostatic tolerance during heat stress 24.
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