It’s long been considered important to balance your sympathetic and parasympathetic nervous systems, but in reality most athletes don’t even try. Ian Craig explores this complex topic, which actually has some simple take homes.

In 2014 (1), I wrote an article on the hypothalamus-pituitary-adrenal (HPA) axis, primarily focussing on the regulation and support of the endocrine system. It’s now the turn of the nervous system for deeper scrutiny. With this article, it is my intension to give you a physiological reminder of the functions and activities of the autonomic nervous system (ANS), to explain how it interacts with and influences endocrine and immune function, and with health, physical performance and longevity in mind, provide you with some practical suggestions of how to keep this vital system well balanced in our daily hectic lives.

Autonomic, in a sense, stands for involuntary, although even that meaning has been challenged by some scientists. It’s involved in the regulation of vital functions such as temperature, blood pressure, heart rate and contractility, and hormonal output; processes that in most cases we have no voluntary control over. There are two major sub-divisions of the ANS; the noradrenaline secreting sympathetic nervous system (SNS), which has been labelled as ‘fight or flight’ and the acetyl choline (ACh) secreting parasympathetic nervous system (PNS), which has been labelled as ‘relax and repair’ or ‘rest and digest’.

Represented in this way, from a Chinese medicine perspective, the SNS and PNS represent the concept of yin-yang very nicely: when we want something done, the SNS is intense and stimulating and when we need to recover, the PNS takes control of the situation. In reality however, like most things physiological, the ANS isn’t quite that simple. Scientists have found that instead of assuming this normal SNS/PNS yin-yang balance, we need to be very function specific in our understanding. I’ll give a few examples (2):

  • - The adrenal medulla (secretes adrenaline and noradrenaline) and most blood vessels only receive SNS innervation.
  • - The sublingual glands (secretes saliva in the mouth) are only innervated by the PNS.
  • - The male sex organs require the PNS to obtain an erection, while they rely on the SNS for ejaculation.
  • - Heart rate and contractility is increased by the SNS, but decreased by the PNS.
  • - Intestinal motility is decreased by the SNS and increased by the PNS.


Figure 1 - overview of sympathetic and parasympathetic physiological effects

As you can see from my list of examples plus Figure 1, sometimes the SNS and PNS help each other, sometimes they oppose each other and at other times, they act independently from one another. Cohen & Sherman (2) term this relationship between the two divisions of the ANS, ‘cooperative integrative action’.

Hypothalamus - the juncture between nervous and endocrine

In terms of autonomic nervous function, the hypothalamus is considered by physiologists as the major conduit for nerve pathways between the brain and the body. Of course other brain centres are involved in certain processes (e.g. respiration), but the hypothalamus deserves some serious air time in this regard. You should also be aware that the hypothalamus is often considered the ‘master gland’ when it comes to endocrine function (1). So, although the nervous and endocrine systems are usually considered separately, the proximity of hypothalamic nerves with the ANS means that hormone outputs of the hypothalamus coordinate closely with the activities of the sympathetic and parasympathetic nervous systems. For example; corticotropin-releasing hormone (CRH), in addition to being a hormone-releaser that activates adrenal hormone output, is also now considered as a neurotransmitter (3). It stimulates sympathetic nervous output from the brain and spinal cord, while concurrently inhibiting the parasympathetic nervous system, thereby activating a stimulating action via both endocrine and nervous systems.

The immune system as a communication network

According to old school physiology (2), the ANS influences the immune system in two ways:

  • - CRF from the hypothalamus stimulates the release of ACTH (adrenocorticotropic hormone) from the pituitary, which activates the adrenal output of cortisol, which   has an immune modulating effect. Physiological levels of cortisol are thought to support immunity, whereas long-term elevation of stress hormones will likely suppress the immune system (4).
  • - The thymus, spleen, lymph nodes, bone marrow and vasculature are all innervated by nerves and therefore influenced by outputs of the ANS.

But we now know that the interaction of the nervous and immune systems are a lot more complex than presented. For example, the observation that receptor sites for neuropeptides exist on the surface of white blood cells (5 - Chopra or Pert) suggest in very real terms that our thoughts and emotions directly affect our immune strength. Additionally, studies have illustrated that the degree of tone of the SNS, via several mechanisms, is closely correlated with the levels of inflammatory cytokines, such as interleukin-1, interleukin-6 and tumour necrosis factor (6). If you take a look at Figure 2, parasympathetic (vagal) nerves plus sensory fibres act as detectors of local inflammation, which if the stimulus is strong enough, will feedback to the central nervous system (CNS), resulting in a SNS response, with a net anti-inflammatory action. Overall, however, we cannot classify the SNS, and the noradrenaline that it secretes, as pro- or anti-inflammatory. According to Pongratz & Straub (6), “noradrenaline modulates immune function in a context-dependent manner.”


Figure 3 - ANS modulation of inflammation (6)

If we take rheumatoid arthritis (RA) as a model, in general RA patients have an autonomic imbalance with an overly active SNS and reduced PNS activity (7) and in line with this observation, it has been suggested that stress may aggravate disease activity. Interestingly, experimental stimulation of the vagus nerve has shown beneficial effects in RA patients.

Why would we consider a disease state such as RA in a sports nutrition magazine? Simply because it is a model of a stress state, just like we experience during heavy training. The effect of the training stress state has been beautifully illustrated by a nine month longitudinal study of seven Italian national rowers who were following a periodised training regime towards the Junior World Rowing Championships. Iellamo et al (8) noted that in healthy young subjects, there is consistent evidence that parasympathetic activity increases with fitness levels, but they wanted to see what happened in world class athletes during strenuous training. They measured their athletes a total of four times at 3-monthly intervals; the first just after time off from the previous season, the middle two when they were at approximately 75 per cent of maximum training load, and the last measurement was taking during their peak training load, 20 days before the World Championships.

To assess sympathetic and parasympathetic balance, they measured heart rate variability (HRV), which is described on pp20-22 of this magazine. As expected, fitness levels (Peak VO2) increased from 5600 ml to 5800ml during the nine months of the study. Their resting heart rate (RHR) decreased progressively and their HRV increased progressively from measurement session 1 to 3, meaning a shift towards parasympathetic dominance. However, by they time they reached their final measurement (at peak training load), they experienced a marked increase in RHR and a decrease in HRV, indicating a shift into sympathetic dominance. Since this study, HRV has been demonstrated as a potential early indicator of overtraining syndrome (e.g. 9,10).

It has therefore been observed that heavy training can shift an athlete into a sympathetic dominant state. It has also been also been observed that, in clinical settings, an imbalance between sympathetic and parasympathetic tone can increase systemic inflammation. These observations fit in with the study of cytokine sickness, an over-production and/or intolerance to interleukin-6 and other cytokines, which is thought to influence under-performance syndrome (UPS), another name for overtraining syndrome (11). This suggestion has been supported by Robson-Ansley et al (12), who noted that an acute period of intensified training can suppress the innate immune system and chronically increase IL-6 levels. These elevated cytokines can in-turn increase fatigue and malaise, which are related to the cytokine theories of UPS.

The human body, particularly when you introduce the dynamics of stress and heavy training, is complex. But these central integrated functions, which collectively in nutritional therapy and functional medicine have become known as the communication systems, seem to go round in circles and heavily influence one another. I have to admit that stepping into these very detailed immune-CNS research papers really stretched my mind, because I struggled to find concrete physiological rules to pin my discussions around. However, stepping back and reading enough research from a variety of subject fields, has brought us to this: The hypothalamus gland is indeed an excellent starting point for the understanding of these communication systems because of the obvious neural-endocrine integration that it represents, plus the body conductor role that it so eloquently plays. It receives neural feedback from our body, information that it uses to conduct SNS/PNS and HPA outflow, which in turn heavily influences the endocrine, immune and inflammatory activities. From an ANS point of view, we can’t say that the SNS is stimulatory and PNS is relaxing; it’s not that simple. But, what we can say is that most of the time we want the systems to be in relative balance and when they are out of balance, it should be only be for a short period of time. But to truly understand our body systems, we need to step up to a higher level in the brain and to study some stuff that is really complex on one hand, but incredibly simple on the other.

Higher centres and allostatic control

Although we may consider the hypothalamus to be a central focus in the nervous and endocrine systems, anatomically it is near the base of the the brain and from a traditional hierarchical point of view, perhaps it has some big brothers. This thinking leads us into the realms of psychoneuroimmunology, psychoneuroendocrinology and psychoneuroendoimmunology, research fields that were introduced to us by Dr Alex Concorde (13) in FSN, which reach beyond our nerves and into the grey matter of the higher brain centres, plus our spirit beyond. To simplify: the hypothalamus conducts our body processes fluently, but it has to answer to higher centres - our unconscious mind and out conscious mind. In effect, it is like a bridge between our mind and body.

According to psychobiologist Dr Philip Hayes (14), we transduct the energy of mental experience in our mind into the energy of physiological signs and symptoms in our body in our limbic-hypothalamus system. The example he gives is of anger being transduced into myocardial contraction and the production of stress hormones. The limbic system is the oldest part of our cortex and has historically been labelled as the mediation of emotional behaviour, with a flow of information into the hypothalamus (2).

Additionally, nerves from the prefrontal cortex (used for logic, planning and organisation) project to the limbic system and hypothalamus, meaning that our hypothalamus, and therefore body, receive their inputs from areas of logical AND emotional thought. If it were left to our hypothalamus to make the final decisions, we would simply slow down when our physiology was being over-worked, such as in an over-training scenario. However, our conscious and unconscious minds, and don’t forget spirit, are shaped by years of psychological conditioning; why else do some people train themselves to the bone, while others are bone idol? In both scenarios, the higher centres are over-riding/over-looking the physiological messages that are coming back to the hypothalamus.

ANS re-conditioning

Because we are taking about enthusiastic athletes here, we’ll stick with the over-training, as opposed to under-training scenario. How therefore do we give them daily tools to modulate the activities of the ANS and therefore all the physiological functions that it influences, such as endocrine, immune and inflammatory imbalances? After all, if we can merely reduce post-exercise inflammation by introducing some daily behaviours, we can potentially speed up recovery as hinted by Robson-Ansley et al (12).

According to our rowing scientists (8), even in top-level athletes, sub-maximal exercise training enhances vagal tone and tends to decrease sympathetic cardiac stimulation. So most exercise is good for balance, but to a point. The first three points that I would like to make with regards to ANS balance are all in this magazine. Firstly, as noted by the article on HRV (pp20-22), it helps if you can measure your SNS and PSN activity. HRV is now a widely available technology; it is criticised by some scientists as not being reliable enough, but when you talk to practitioners using the devices, it tallies well with what state they perceive the athlete to be in. In this regard, as long as you back up the use of technology with perceptional observation (either that of the athlete or coach), it can be particularly helpful within a training programme.

Secondly, sleep is the ultimate parasympathetic stimulator, which is unfortunately often compromised due to athletes trying to fit training sessions into already compacted days. Sleep quality is also vital and you can find out more with Craig Lewis on pp28-30. Thirdly, excessive systemic inflammation can be an aspect of SNS/PSN imbalance: in addition to knowing what anti-inflammatory herbs (p32) and oils to use, an athlete’s diet needs to focus on micro and phytonutrient density and not just the big macronutrients. Sugars and refined carbs and oils, plus excessive saturated products from dairy products and meats, can accelerate a pro-inflammatory flame that has already been initiated by the physiological stresses of hard training.

My final point is that of training balance. As an endurance coach, my modern thinking is to find out how an athlete can perform at their best with the least amount of training. Not only that; the inclusion of restorative training, such as flowing yoga or Tai Chi, is not in my mind optional. For example, Streeter et al (15) proposed a theory that the decreased PNS and GABAergic activity that underlies stress-related disorders can be corrected by yoga practices. This thinking can also be applied to heavy training being a stress-related disorder: yoga or Tai Chi serves as an active restorative process that allows the active body to spend more hours of the day in a parasympathetic state.


  1. Craig I (2014). The Hypothalamus-Pituitary Axis. Functional Sports Nutrition. Jan-Feb 2014.
  2. Cohen DH & Sherman SM (1988). The Nervous System. In: Physiology. Ed: Berne RM & Levy MN. 2nd Edition. C.V. Mosby Company.
  3. Pacak K (2000). Stressor-specific activation of the hypothalamic-pituitary-adrenocortical axis. Physiol Res. 49(Suppl 1):S11-S17.
  4. Jefferies WM (1991). Cortisol and immunity. Med Hypotheses. 34(3):198-208.
  5. Chopra or Pert
  6. Pongratz G & Straub RH (2014). The sympathetic nervous response in inflammation. Arthritis Research & Therapy. 16:504.
  7. Koopman FA et al (2011). Restoring the balance of the autonomic nervous system as an innovative approach to the treatment of rheumatoid arthritis. Mol Med. 17(9-10):937-948.
  8. Iellamo et al (2002). Conversion from vagal to sympathetic predominance with strenuous training in high-performance world class Circulation. 105:2719-2724.
  9. Kiviniemi AM et al (2014). Altered relationship between R-R interval and R-R interval variability in endurance athletes with overtraining syndrome. Scand J Med Sci Sports. 24(2):e77-e85.
  10. Baumert M et al (2006). Heart rate variability, blood pressure variability, and baroreflex sensitivity in overtrained athletes. Clin J Sport Med. 16(5):412-417.
  11. Robson P (2003). Elucidating the unexplained underperformance syndrome in endurance athletes: the interleukin-6 hypothesis. Sports Med. 33(10):771-781.
  12. Robson-Ansley PJ et al (2007). Elevated plasma interleukin-6 levels in trained male triathletes following an acute period of intense interval training. Eur J Appl Physiol. 99(4):353-360.
  13. Concorde A (2014). Psychoneuroendoimmunology: the holy grail of performance gain in sports. Functional Sports Nutrition. July/Aug 2014.
  14. Hayes P (2002). The psychobiology of stress and healing. Part 1 (of 3): A framework for modern Stress News. (14)2.
  15. Streeter CC et al (2012). Effects of yoga on the autonomic nervous system, gamma-aminobutyric-acid, and allostasis in epilepsy, depression, and post-traumatic stress disorder. Med Hypotheses. 78(5):571-579.