Is it possible to train an autonomic reflex

Thus a well functioning autonomic N. At the same time, the autonomic N. A great example of this is the role of the autonomic N. We typically breathe without thinking about it, thankfully but we do have the ability to speed up or slow down our breathing at will and ideally with relative speed and ease. A strong autonomic nervous system intelligently uses aspects of both the sympathetic and parasympathetic and is able to switch gears when needed without taxing the body.

We can consciously train our nervous system to seamlessly make this shift between stimulation and relaxation, and this will help keep our cardiovascular system strong and supple and facilitate muscle recovery. Most modern humans spend significant time in situations and engaged in activities that stimulate the sympathetic nervous system to a mild degree.

This constant low-grade stimulation can become a habit, leading to missed cues that our body is neither resting nor fully engaged. This can happen to all of us occasionally, and its not a big problem until it begins to manifest consistently when it will weaken our nervous system and its ability to shift from the sympathetic N. Diaphragmatic breathing is the easiest way to turn on the parasympathetic response. When you breathe well, your shoulders relax, your whole abdominal wall gently expands degrees and there is a slight pause between the inhale and exhale.

Your diaphragm is one of your largest back muscles. In order to draw air into the deepest part of the lungs, it has to contract during inhalation. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer.

In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. The autonomic nervous system is the primary mechanism for short-term blood pressure BP regulation on a beat-by-beat basis. In normal physiological conditions, very precise control of BP levels is achieved through a complex combination between central neural and reflex influences, leading to a continuous modulation of efferent sympathetic and parasympathetic nerve activity and the associated activity of neurohormonal systems primarily regulated by the hypothalamus.

Several studies using direct methodologies for the assessment of overall and regional sympathetic cardiovascular CV drive have demonstrated the association between chronic activation of the sympathetic nervous system and the development, establishment and progression of essential hypertension.

In the frequency domain, current spectral analysis techniques allow for quantification of the power of HR variations in the very-low VLF, 0. Indeed, significant improvements in indices of autonomic cardiac modulation derived from the analysis of HRV reflecting increases in cardiac vagal modulation have been reported after the achievement of BP control with antihypertensive treatment 13 , 14 and in response to non-pharmacological interventions such as regular physical training.

Further information on the clinical applicability of HRV analysis in the assessment of the effects of physical exercise is provided by the paper by Cozza et al. This study assessed the effects of a week protocol of aerobic physical training min treadmill exercise, three times a week on autonomic cardiac modulation as assessed by means of spectral analysis of HRV in a group of sedentary, non-treated subjects with mild essential hypertension.

During the follow-up, physical training promoted significant reductions of resting HR in all study subgroups and a reduction of mean BP levels in both treated and non-treated hypertensive subjects. Some caution is required, however, for a proper interpretation of these results because LF and HF powers, despite being considered indices of sympathetic and parasympathetic cardiac modulation, respectively, may be influenced by a number of other cardiovascular regulatory mechanisms.

Thus, HR HF power is considered a satisfactory, but incomplete, measure of parasympathetic cardiac control. The specificity of HR LF power 0. In the study by Cozza et al. Aside from the assessment of changes in the sympathovagal balance induced by the shift from supine to standing a possible marker of autonomic balance rearrangement , this measure also provides information on the integrity of the reflex arc involved in the autonomic response to orthostatic stress.

The additional significant improvement in the autonomic response to passive tilting observed in the group of treated hypertensives who shared similar profiles of autonomic response with normotensive subjects before starting the physical training protocol led investigators to conclude that physical exercise may provide further improvements in autonomic CV modulation even in hypertensive patients under active treatment with an angiotensin-converting enzyme inhibitor an intervention previously demonstrated to improve autonomic cardiac modulation itself.

Important as they are, the findings obtained by the study by Cozza et al. Moreover, in recognition that autonomic modulation of the CV system takes place in a network of intricate interactions between several regulatory systems, a general concern has been raised that for a comprehensive assessment of autonomic CV modulation, information provided by HRV analysis might not be specific enough and should be integrated with the analysis of variability in other biological signals.

An example of this is represented by the assessment of HRV along with analysis of BPV from beat-to-beat BP recordings, which complements the information provided by HRV analysis by providing indices of vascular autonomic modulation. In addition, by applying modeling approaches which focus on the relationship between fluctuations of HR and BP either in time or in the frequency domain , 26 , 27 it is also possible to assess other mechanisms of major importance for autonomic CV control such as the degree of spontaneous cardiac baroreflex sensitivity.

Such an approach may provide a more comprehensive analysis of cardiovascular regulation mechanisms than that represented by the separate analysis of BP and HR variability alone. In conclusion, the data by Cozza et al.

They also emphasize the usefulness of spectral analysis for dynamically tracking changes in neurally modulated HRV parameters induced by exercise over time. It should be emphasized, however, that the combination of HRV analysis with analysis of the variability of other cardiorespiratory parameters might offer deeper and more specific insights into this complex issue. Mark AL. The sympathetic nervous system in hypertension: a potential long-term regulator of arterial pressure.

These tell us how they are responding to their training and lifestyle. The information is especially valuable both for long-term health and performance results. How does their body respond to this day, week, and block of training?

How do they respond to various types of training? These are very important factors to be sure and have been discussed in other HRV articles; consider reading more on that topic. What sort of interventions can we use to create a desirable response in our athletes? It would be very easy to look past these questions and only consider the biomechanical and physiological components of preparing the athlete for competition—like priming the CNS and prepping movement patterns or tissues.

If we look a little more closely at competition, we see other factors at play that can affect outcomes. The sympathetic state allows for increases in short-term performance.

The purpose of the fight or flight response is to increase our abilities in a situation where our life might be at risk so we can succeed against our foe. This means that our body will do such things as:. With an acute threat, the body prioritizes necessary acute responses over long-term processes increased blood flow for delivery of nutrients and oxygen over digestion. I had heard that Steve collected saliva samples from his athletes and gathered data. He observed that his athletes had differences in how quickly and efficiently they transitioned in and out of the sympathetic state.

Especially considering that some athletes take up to 24 hours to recover completely from a workout or practice, as shown in this study on HRV in sport. The challenge is that athletes might need to be classified and treated differently in this regard. Steve used the terms warrior and worrier which he may have borrowed from Henk Kraijenhoff , and it gave me a bit of an Aha!

This athlete is pretty chilled out most of the time. On the flipside, the worrier is often sympathetic and is generally stressed out about many things. Plugging your athlete into one of these categories can really help you customize their competition preparation.

The warrior needs to be activated. This athlete needs a more rigorous and competitive warm up to enter the sympathetic state and achieve the stress response we want. The worrier may become too agitated and active. Remember, we only want to activate for competition or the repeated stress response could be detrimental to health and performance. This athlete should probably be controlled more throughout their pre-competition routines.

One group of athletes needs a push, and one needs a pull. What I can do, though, is be an observant coach through training and competition. Luckily, providing your athlete with tools to aid their recovery is one of the easiest things you can do. Here are some common ways to influence and activate the ANS. These are a list of popular parasympathetic interventions to help your athletes relax and recover. Deep Breathing One of the simplest and most common solutions is deep diaphragmatic breathing.

Deep breathing also gets the diaphragm working. Consider implementing deep breathing a few times a day to calm nerves and aid recovery. If you fit one in early in the day, your diaphragm should be humming along nicely. Meditation Meditation has slowly become more common with both athletes and non-athletes. Blood samples were collected in heparinized syringes at 0 before glucose administration , 5, 15, 30 and 45 min after the glucose administration.

As previously described [ 29 ], surgical longitudinal incisions were made on the anterior cervical region. Under the dissection microscope, the nerve bundle of the left superior branch of the upper vagus nerve was severed from the carotid artery close to the trachea. The nerve trunk was pulled with a fine cotton line, and a pair of recording silver electrodes 0. The nerve was covered with silicone oil to prevent dehydration.

During all data acquisition, the animals were placed in a Faraday cage to avoid any electromagnetic interference. Nerve activity was analyzed as the number of spikes during 5 sec. After stabilization of the signal for 2 min, 20 record frames of 15 sec from each animal were randomly chosen for spike counting. The average number of spikes was used as the nerve firing rate for each rat.

The branch of the sympathetic nerve from the lumbar plexus that innervates the retroperitoneal white fat tissue, which may be called the greater splanchnic nerve, was dissected from another batch of anesthetized rats from all experimental groups, as described above.

The electrode was placed under the greater splanchnic nerve, close to the retroperitoneal area. Firing rates from the nerve were obtained as described for the vagus nerve. The retroperitoneal fat pads were removed and weighed. The fat mass of this tissue was used as a simple reliable estimation of total body fat in normal and obese rodents.

Probability values less than. Tests were performed using GraphPad Prism version 5. However, the exercise training was able on improves the glucose intolerance of the SL rats. Intravenous glucose tolerance test ivGTT. The upper panel of each figure represents the area under the curve of glycemia during the ivGTT.

The representative records of each nerve discharge, which illustrate the data for each experimental group, are given in the Figure 3 C. Electrical activity of the autonomic nervous system. The vagus A and greater splanchnic nerve B electrical activity.

Representative records of each nerve discharge, which illustrate the data for each experimental group, are given in the Figure 3 C. As expected, a reduction in litter size during the suckling phase induced obesity in adult rats, as indicated by increased bw and increased fat tissue accumulation.

Confirming data reporting that this experimental model of obesity is caused by the overfeeding behavior of young rats during lactation [ 30 ], this metabolic imprinting model displays glucose intolerance, insulin resistance, hyperphagia among others important metabolic disturbances [ 6 , 31 ]. The afferent vagus projects from the periphery to the nucleus of the solitary tract in the brainstem, a brain region situated in the dorsal vagal complex that functions as a port of entry for visceral information to the brain.

Interestingly, the incoming peripheral signals about glucose levels can be modified by central glucose-sensing neurons at nearly every level of the central nervous system [ 32 ], and populations of neurons in the ventromedial and lateral hypothalamus are reported to increase their firing rates in response to the application of glucose [ 33 ].

The balance of the ANS is important to maintain constant glycemia. Overall, the parasympathetic stimulates insulin secretion, whereas the sympathetic inhibits it, which can produces decreases and increases in glycemia that are dependent on the glucose demand of cells, skeletal muscles and fat tissue. The data of the current research reveal, for the first time, that higher vagal nerve activity is observed in obese rats induced by early overfeeding.

Our group also observed this feature in other different model of obesity [ 19 , 20 , 27 , 34 ], in all of these obesity model high fasting insulinemia and insulin resistance were observed. The method used in the present work cannot discriminate afferent from efferent signals; however, the firing rates from control rats are very similar to those reported by other authors [ 35 , 36 ]. Thus, in the current work we suggest that autonomic dysfunction could be indirectly responsible by the large fat pad accumulation in the SL rats, through the insulin lipogenesis action.

The most important find in the present work, is the observation that ANS may be modulated by the low-intensity and moderated exercise training, even in rats ran until puberty, and rats that start to run at begin of adulthood that includes later stages of developmental plasticity.

Interestingly, using the swimming training protocol at the same periods of life that were used in the present work, we showed that MSG-obese mice displayed the metabolic ameliorations, however it was more prominent in mice that began to swim at weaning and stopped to do it at the end of puberty or at day-old.

Swimming training protocol did not improve the metabolic changes in mice swam between and day-old, like as is observed in early stages of life [ 24 ]. In agreement with, it has been demonstrated that exercise applied immediately after weaning is able to improve the cognitive ability of rats and it is correlated with high neuronal density in the neurons of the hippocampal area [ 37 , 38 ]. Concerning, in previous studies we reported that the puberty is one important phase of life in which metabolic changes can happen similar to those occur early in perinatal phases [ 19 , 20 ], which can be an important window to either malprogramming or deprogramming the metabolism.

It is known that physical exercise is a potent attenuator of obesity, activating energy expenditure, promoting lipolysis and increasing the consumption of fatty acids by peripheral tissues to reduce body fat deposits [ 39 — 41 ]. The peripheral metabolic adaptations promoted by physical exercise are activated by the hypothalamic neural pathways involved in the regulation of the sympathetic nervous system [ 40 ]. Our data demonstrate that physical exercise was able to improve the imbalanced parasympathetic activity of SL-obese rats, which was observed to be closely associated with reduction on the fat pad deposition in these obese rats.

Interestingly, beyond high vagus nerve tonus no difference was observed in sympathetic activity of these overfeeding rats. On the same line the improvement of vagus nerve tonus was able in ameliorate the disrupted glucose homeostasis and fat pad stores, independent of the time exercise training protocol had begun.

In previous studies, using the same exercise training protocol applied throughout life, we showed that obese rats induced by high-fat diet restores the imbalanced autonomic function beyond other metabolic dysfunctions [ 27 ].

Similar results were obtained in rats fed hypercaloric diets that ran voluntarily [ 39 ]. Although our study to be a phenomenological study, our data are suggestive that autonomic changes are modulating the increased energy expenditure, the mobilization of fat stores, and the reduction in bw.