Each of the 4 channels i. This is important in order to obtain data that are consistent among the 4 subjects. It minimizes variability between subjects that is due to differences among subjects in performing the activities within the treatments in the study thereby isolating the true effects of the treatments being measured.
During normal inspiration and expiration HR does indeed increase and decrease respectively, a phenomenon known as Respiratory Sinus Arrhythmia RSA , which has been amply demonstrated by many articles []. It cannot be overstated how critical it is to understand the phenomenon that is RSA. In this study we wanted to accentuate the conditions under which heart rate increases and decreases during RSA by having subjects maximally expire and inspire then hold breath for 15 seconds.
Indeed RSA was amplified but only during maximum inspiration during maximum expiration HR was also increased instead of decreasing as in regular expiration and this is well demonstrated in Figures 2,5,8,14 and 23 in which a significant difference was observed in the highest RR interval attained across all subjects during normal breathing versus expire-hold and normal breathing versus inspire-hold treatments.
P values for this comparison ranged from P Because it is not feasible to isolate the physical effects of thoracic pressure on HR; we allowed the participants to maximally inspire or expire then hold their breath for 15 seconds which maximized the effects of low and high thoracic pressure, respectively. Denver et al. For a long time, it has been deemed important to correct RSA for respiratory influences [18], yet there has been a paucity of research in this area [19]. Similar effects were observed with heart rate.
A comparison in HR during normal breathing versus expire-hold and normal breathing versus inspire-hold treatments demonstrated a significant difference in the maximum HR attained as indicated in Figures 3,6,9,15,21 and 24 where P values ranged from P Many studies have indicated that the RR Interval is shortened during inspiration higher HR and lengthened during expiration lower HR []. Exaggerating conditions during RSA amplifies this effect as we demonstrated in this study but only during maximum inspiration, during maximum expiration HR also increased instead of decreasing like it normally does during regular expiration.
It is very well established that the sinoatrial node SA node is the dominant pacemaker of the heart and regulates the frequency of heartbeat [20] and this was established a very long time ago [21]. However, one does not fail to attribute the faster heart rate to the intense physical activity just because it is the SA node that sets the beating rhythm and pace of the heart.
In similar fashion and reasoning we have designed our study to investigate the effects of breathing pattern manipulations on RSA. Bouairi and coworkers [22] stated that RSA in humans and in animals is mediated almost entirely through changes in parasympathetic cardiac vagal tone and this has been reported by many other studies [].
While fully cognizant of the fact that RSA is controlled by cardiac vagal tone, we wanted to investigate what happens to RSA when a person takes maximum inspiration and holds for 15 seconds and similarly when a person expires maximally and holds for 15 seconds. Indeed, we found that the normal RSA observations where HR increases during inspiration and decreases during expiration were not fully observed in our study in that HR increased significantly during maximum expiration held for 15 seconds.
We certainly feel that this is a novel and in fact exciting observation and we have put forward some plausible explanations for this observation. Our study demonstrated that indeed the RR Interval is significantly shortened during sustained maximum inspiration resulting in higher HR compared to normal breathing RR interval with lower HR. This is in agreement with our first hypothesis about sustained inspiration resulting in shorter RR intervals hence higher HR. However, we did not observe longer RR Intervals during sustained maximum expiration as expected based on our second hypothesis for sustained expiration.
In fact, we observed significantly shorter RR Intervals hence higher HR during maximum expiration which was the exact opposite of our second hypothesis. This may be because HR is influenced more by the amount of blood that is returned to the heart following the principles of Frank- Starling Law of the heart which states that during systole, the heart pumps out the volume of blood returned to it during diastole [ 29] rather than the mere physical mechanics of sub-atmospheric thoracic pressure during inspiration and supra-atmospheric thoracic pressure during expiration directly on the heart itself.
That is, the more stretching that occurs to the myocardium during ventricular filling, the greater the pressure generated by the heart, and thus the greater the stroke volume. Simply put; the heart beats faster when more blood is returned to it as the higher thoracic pressure during maximum expiration compresses the venae cavae and the pulmonary veins causing more blood to be deposited into the atria.
Furthermore, this may be a survival mechanism in which the body attempts to provide more O2 to the cells by pumping more blood from the heart during expiration, a time when the body is not taking in more O2. They further reported that respiratory parameters not only altered HF power but also strongly influenced the LF components of the R—R interval power spectrum, a component that previously was viewed to vary independently of changes in respiration Brown et al.
It also must be emphasized that HRV only provides an indirect assessment of cardiac autonomic activity and does not provide a direct measurement of either cardiac parasympathetic or sympathetic nerve activity. Thus, any relationship between HRV and cardiac autonomic regulation is qualitative rather than quantitative in nature.
In other words, a low or high amount of HRV may reflect a decreased or increased cardiac autonomic regulation but does not provide a quantification of the actual cardiac nerve firing rate. Furthermore and as previously noted, there is considerable debate as to the exact relationship between changes in cardiac autonomic activity and a particular branch of the autonomic nervous system Kollai and Mizse, ; Randall et al.
This is particularly true with regards to the relationship between LF power and cardiac sympathetic regulation Randall et al.
Low frequency power was found to be reduced by selective parasympathectomy and also was not totally eliminated when the denervation was combined with beta-adrenoceptor blockade Randall et al. Furthermore, interventions that would be expected to increase cardiac sympathetic activity, such as acute exercise or myocardial ischemia, not only failed to increase LF power but actually provoked significant reductions this variable Houle and Billman, Thus, LF component of HRV reflects both sympathetic, parasympathetic and other as yet unidentified factors.
Accordingly, LF power should not be used as an index of cardiac sympathetic regulation. Although the vast majority of the clinical and the experimental studies demonstrate a strong association between HF power and cardiac parasympathetic activity Appel et al.
Just as parasympathetic activation exerts profound influences on the LF component of HRV, sympathetic neural activity may modulate the HF component of the R—R interval variability Taylor et al.
Taylor et al. Thus, differences in cardiac sympathetic activation during a physiological challenge e. These data further demonstrate that HRV is a complex phenomenon that should not be solely attributed to changes in cardiac vagal efferent nerve traffic. In addition to autonomic influences, a portion of the HRV occurs as a consequence of the mechanical events due to stretch of the atria that results from both changes in cardiac filling and the changing thoracic pressure that occur during respiration as was first proposed by Bainbridge Thus, given the complex interactions between cardiac sympathetic and cardiac parasympathetic nerves that are confounded by the mechanical effects of respiration, HRV data should be interpreted with appropriate caution.
Heart rate variability has gained wide-spread acceptance as a clinical tool for the evaluation of cardiac autonomic changes in patients Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology, ; Bigger, ; Hohnloser et al.
A variety of cardiovascular risk factors and disease states have all been shown to reduce HRV, including diabetes Murray et al. Eppinger and Hess provide the first suggestion that HRV could be used to provide some insight in abnormalities in autonomic regulation in disease.
They further emphasized that pharmacological manipulation of the cholinergic system might provide an avenue for treatment Eppinger and Hess, However, the first reports of the applications of HRV in the clinic only began to appear in the mid s. Hon and Lee noted that fetal stress was preceded by reduction in the inter-beat interval even before any appreciable change in average heart rate could be detected. Fetal heart rate monitoring has now become the standard of care and has contributed to reductions in morbidity associated with fetal distress.
In the s, Ewing and co-workers used short-term changes in R—R interval in response to simple autonomic challenges to detect autonomic neuropathy in diabetic patients Murray et al. About the same time, Wolf was the first to demonstrate a relationship between HRV and mortality following myocardial infarction Wolf et al. Specifically, HRV is reduced in patients recovering from a myocardial infarction and, further, those patients with the greatest reduction in this variable also have the greatest risk for sudden death Myers et al.
Kleiger and co-workers Myers et al. The relative risk of mortality was 5. This finding has been subsequently confirmed by numerous more recent clinical studies; reductions in HRV following myocardial infarction now represent one of the strongest independent predictors of mortality following infraction.
La Rovere et al. To cite just one example, La Rovere et al. The greatest risk for mortality was observed in patients with a large reduction in both markers of cardiac vagal regulation La Rovere et al.
Similar results have also been obtained using animal model of human disease Billman, a. For example, HRV was reduced to a greater extent in animals susceptible to ventricular fibrillation as compared to animals resistant to these malignant arrhythmias Billman and Hoskins, ; Collins and Billman, ; Halliwill et al. In particular, the susceptible animals exhibited a much greater reduction withdrawal of cardiac vagal regulation in response to either submaximal exercise Billman and Hoskins, ; Halliwill et al.
Heart rate recovery and the reactivation of cardiac parasympathetic regulation following the termination of exercise were also impaired in the animals subsequently shown to prone to ventricular fibrillation Smith et al. For example, post-infarction patient with the slowest heart rate recovery following an exercise stress test also exhibited the highest mortality rate during the observation period up to 12 years; Cole et al.
Thus, despite the limitations noted in a previous section, HRV has proven to be an important tool for the identification of patients at risk for adverse cardiovascular events.
The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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