If we look at the relationship between cardiac output and heart rate, we see that without the influence of the autonomic nervous system the CO would decrease at higher frequencies due to a respectively shorter diastole and insufficient atrial filling, but positive initropy and chronotropy mostly go hand in hand without one having to be sacrificed thanks to the sympathetic nervous system, such as during exercise, orthostasis or a fight or flight response. I'm wondering if a HR increase without sympathetic activation is physiologically or pathologically possible, and if yes does it make sense (at higher frequencies this would mean a decrease in CO)?
I ran into the information that mild exercise can stimulate a decrease in vagal tone, allowing heart rate to increase without SNS activation. At lower frequencies (< ~80 bpm) a HR increase causes a linear CO increase, so it makes sense for this to happen during mild activity. But I ran into this without a paper/author reference or a source. Does a decrease in vagal tone without SNS activation really occur?
There is stress. Systems that implement it are associated with activation of the SNS. This is the humoral mechanisms. Therefore, an increase (decrease) in heart rate in the range of no stress factors are sold through baroreflex mechanisms. The stress factor that ensures the inclusion of the SNS (central mechanisms, adrenal cortex, and others.), Leads to a decrease (or off) baroreflex mechanisms.
The decrease vagal activity with a load of low intensity is possible due to activation of tissue metabolism, when the impact factor does not reach the level of stress.
It´s possible during certain types of arrhythmias, where the generation of the stimulus is altered
This is a very interesting question. The answer is complicated, I think. The fundamental characteristic of autonomic influences on the heart is its ying-yang nature. SNS stimulation of the heart increases HR, contractility and conduction velocity, whereas PNS stimulation of the heart has opposite effects. Under normal conditions, it seems impossible to have both SNS and PNS going to the same direction. However, HR is regulated by not only the ANS, but also neurotransmitters, hormones, exercise, and stress, etc. Pathological conditions make the HR regulation more complicated. And an imbalance of SNS and PNS is, of course, problematic. For example, AF, VT/VF, SAN dysfunction, even thyroid dysfunction and hyper/hypothermia can lead to pathological HR change.
Yes, of course it can. Quick changes in heart rate are mediated by vagal withdrawal. The only measure of vagal "tone" that really means that is the use of atropine which results in a heart rate increase to about 100 bpm. Strongly suggest you check out Stephen Porges writings about polyvagal theory.
You should read "Autonomic neural control of heart rate during dynamic exercise: revisited." by White et al in Journal of Physiology 2014 vol 592. They talk about parasympathetic withdrawal resulting in HR increase with mild exercise. As an interesting side note - appropriately timed vagal stimuli can in fact increase sinus node firing rate as Jalife showed but not sure whether this would ever occur in normal physiology.
Another avenue you might pursue is the heart rate response of the transplanted heart, which has lost both parasympathetic and sympathetic innervation. As already intimated, the resting heart rate is dominated more by a parasympathetic (vagal) brake than sympathetic output. A transplanted heart generally has a resting rate +/- 20 bpm higher than normal. And as you have noted the initial heart rate response in exercise (unless being pursued by a bear?!) is probably due to reduced vagal tone.
There are internal mechanisms within the heart associated with changes in rate (in either direction) Rapid atrial filling of the denervated heart is associated with an increase in rate, possibly via stretch stimulation of conducting tissue, and rapid decrease in atrial filling is associated with a decrease in heart rate. Someone is bound to mention the Bezold Jarisch reflex (forgive the spelling if wrong) if I don't, which is a (paradoxical?) slowing of the heart following sudden emptying but this may be a local cholinergic reflex associated with ischaemia.
Another area of interest would be heart rate changes associated with the rapid onset of high spinal anaesthesia, which takes out the traffic from the sypathetic chain, but leaves the vagal input intact. One would expect this to result in a bradycardia, which can occur and is quite common particularly in the elderly, but in pregnant patients the commonest immediate response is a tachycardia, perhaps due to rapid reduction in venous return.
a fascinating and time-consuming question. good luck!
Chris
PS don't try the bear experiment!
PPS
Apropos the issue of rate and CO, look for the effect of electrical pacing on the denervated heart. there is an ultimate fall-off in CO, but this might be explained by ischaemia rather than simple volume-rate considerations.
In addition to late literature (tx to J Ashton Auckland), you may have a look into the early literature : Braunwald Circ Res 1966, 19, 400-11. there are in there two enlightening schemas with opposing views on the cardiac para vs the cardiac sympathetic systems. we are we any further ? I would welcome an answer from the panel.
regarding the cardiac vagal withdrawal in the setting of preparation to exercise or mild exercise you might also read the schema by de boer AJP 1987 253 H680-9 : the take home message is that the vagus primarily affect the n (or the n+1) beat, ie its act within one beat, via an intra cellular action : see Jalife, Circ Res, 1979, 45, 595-607. look into Karemaker Cardiovascular Engineering 2008 8 23-9 for an overview and coming papers from this last group.
There are two phenomena which would raise HR by 10 to 15 ppm from resting rates. One is to put your whole body weight on one leg (with a slighly bent knee) for a short while and then move your body weight slowly to the other leg, and repeat many times. If you do it slower than your brain’s movement detection threshold and without impact, Both SNS and PNS will not be activated. Actually, this is the old long form taichi done before 1956. The other phenomenon is when you get into your REM sleep cycle, your dream can also bring your HR up by 10 to 15 ppm from resting rate (during sleep which is lower than the daytime rate). If your dream is not a nightmare, both SNS and PNS will not be activated. With a near empty stomach, I believe that both phenomena is the key to our brain perfusion and microcirculations to other internal organs, based on my observations. I call it a heart rate stimulation therapy.
Article “Rapid Eye Movement In REM Sleep Is Slow Motion Taichi ” - T...
We may get proof by asking the question from contradiction, i.e. “Is a heart rate DECREASE possible without any influence of the sympathetic nervous system?”
"Yes" is then the answer, because cardiac Na+/K+ ATPase inhibitor (e.g. digoxin) and in particular funny channel inhibitor (e.g. ivabradin) can decrease heart rate in a sympathetic or parasympathetic independent fashion. It is believed that the direct heart rate reduction by these medicines does not involve central, ganglionic, or peripheral receptor mechanism at all, which initiates or transmits neural signals. In this regard, One may comfortably say that without systemic change in sympathetic or vagal nervous system, heart rate can be altered by mechanisms that control the local ion channels across the membrane of the cardiac pacemaker cells.
I may have this briefly mentioned in my previous paper http://www.sciencedirect.com/science/article/pii/S1568163708000524
Thank you all for your contributions. There were very diverse and valuable pieces of information regarding not only the vagal withdrawal with a resulting increase in heart rate and its occurrences but also various other mechanisms independent of the ANS that can alter HR such as,
- internal mechanisms within the denervated heart (rapid atrial filling)
- certain arrhythmia
- direct T3 effect on the heart (nuclear and extranuclear)
- direct Na+/K+ ATPase inhibitor and Funny Channel inhibitor effect and other mechanisms that control the local ion channels across cardiac pacemaker cell membranes
- Slow Motion Taichi and REM Sleep, although I believe here regardless of the content of the dream there is usually a significant increase in HR that is SNS induced, since REM is a SNS dominated cycle whereas N3 (deep sleep) is dominated by the PNS.
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