Physiology and Teleology; the body’s ‘needs’ and ‘wants’ and the nature of what really controls physiological systems

(Some exam-answering advice for Physiology students)

One widespread feature of student exam answers and lab reports, as well as far too many textbooks, is the tendency to invoke teleological rather than physiological ‘explanations’. The former, a philosophical term, means assuming a process is explained in terms of the ‘result’ or the ‘final outcome’ it produces. The sorts of phrase that litter such writing are: ‘the heart beats faster because it needs to increase cardiac output’, ‘the body tries to keep blood pressure up’, ‘more blood reaches the tissues because they need more oxygen’, and so forth. What is implied here is that the needs and wants of the body or its tissues are - in some mystical way - the very cause of the responses observed. (Odd, since the 16th Century at least, we are no longer vitalists - surely not?). However, we have ever–better and more comprehensive physiological explanations; these are formulated in terms of sequences of cause and effect that involve known (or knowable) biological processes. In fact, the ‘needs’, as usually mentioned, actually tend to be the result or outcome of what goes on in the body (e.g. blood pressure is maintained, tissues receive greater blood flow) rather than any sort of cause, as such. Nobody loses exam marks simply for dropping such teleological phrases, we all resort to this form of words very easily. But too often they are the only ‘explanation’ on offer; I hope you soon see that they are completely inadequate as explanations. I also hope, especially if you find the following commentary novel, that you can usefully carry this concept into all your scientific and medical studies and eventually into practice in the lab or ward.

Let us take an example. How are you expected to answer, say, a question about haemorrhage and the homeostatic responses that are involved? You can easily avoid the teleological remarks (‘needs to’, ‘wants to’) by stating that: blood pressure is relatively well maintained because cardiac output (CO) is nearly sustained while total peripheral resistance (TPR) rises. However, the terms in italics need further explanation.

(a) blood pressure; this is more precisely and informatively, mean arterial pressure, MAP. AS we explore later, this is the key variable that is regulated and, if maintained adequately, is what ensures that tissue perfusion is sustained.
(b) because; this word means that what is described next in the sentence is the physiological cause of what happens.
(c) nearly sustained; more detail on that detail is given later.

Now we can give some detail; because MAP=CO x TPR, MAP can be sustained, at least to some degree and for some time, so long as CO and TPR alter suitably. Changes to both these variables are initiated and controlled largely by the autonomic nervous system, especially through the raised activity of the Sympathetic NS. This response, in this scenario, is initiated principally by the baroreceptor reflex. (You could give brief details: baroreceptors are located in the walls of the aortic arch and carotid sinus, lower MAP means a reduced activity – a reduced rate of sensory impulse frequency in those autonomic sensory endings - is reported to the medulla oblongata where the CVS integrative and control centres are located. A reflex rise in efferent sympathetic tone (i.e. increased sympathetic neurone firing rates) follows; this is what raises heart rate and heart beat strength. Activity in different sympathetic efferents causes: arteriolar constriction (thereby raising TPR), venoconstriction (thereby increased venous return by reducing peripheral pooling, especially in the large, capacitance veins) and increases the release of catecholamines (i.e. adrenaline and noradrenaline) from the adrenal medulla. The circulating catecholamines act mostly to raise TPR and to venoconstrict. (Remember that the cardiac effects of circulating catecholamines, despite what too many books report, are minor, only becoming significant at extreme levels of aerobic exertion – see companion document: ‘The Surge of Adrenaline’). This scenario of maintained MAP cannot be sustained indefinitely since a net volume loss continues with the continuing haemorrhage. However, the compensatory responses tend successfully to maintain MAP and thus to maintain basic tissue perfusion and capillary function. (Note that the near maintenance of MAP is the physiologically successful outcome of the regulatory processes; maintaining MAP is not the cause and nor is it informative to say that the ‘need’ to maintain it is the cause either. The core point for the negative feedback control loop operating here is that, once a fall in MAP is detected, the autonomic reflexes that are triggered tend to reverse the fall). It is also worth noting in passing that some organs such as the heart itself and the brain, in particular, show strong autoregulation; their perfusion rate is maintained even if MAP falls. This is because the resistance offered in these organs continues to fall as their arterioles dilate (local controls dominate here) in such a way that flow rate is sustained. Again, this is a ‘desirable’ physiological outcome but not helpfully ‘explained’ as being because the heart and brain ‘need’ or ‘want’ their blood supply maintained!

A further feature of CVS behaviour during haemorrhage perhaps nails this point better. When blood pressure (MAP) falls, it disturbs the balance of osmotic and hydrostatic forces (the Starling forces) acting on fluid movements across the capillary walls. In the capillaries, the osmotic gradient inwards now slightly exceeds the outward hydrostatic gradient. At normal MAP, the reverse is the case, so a slight net leak of fluids from the bloodstream into the tissues occurs. if MAP is raised above normal, this effect becomes greater. If MAP (and thus capillary hydrostatic pressure) falls, the net effect is for fluid to enter the capillary blood stream from the tissues. If the local arterioles constrict for whatever reason – haemorrage being just one provocation - capillary blood pressure will also fall even if the general MAP was constant. The result of this is that with low MAP, the total volume of the blood increases. If no changes to blood vessels occurred, this alone would raise blood pressure. However, these fluid movements are entirely ‘passive’ in the sense that there is no direct control over them. The movements are simply the consequence of the complex balance of local blood pressure and osmotic forces across the capillary. Apart from gross effects on capillary permeability by agents such as histamine, these processes are not controlled in the responses to haemorrhage. So the desirable physiological outcome, in one sense, simply ‘happens’.

Note that all of the section above explains what it happening, which systems are involved and what causes what to happen. There is actually little use in resorting the ‘needs to’, ‘wants to’, ‘tries to’ phrases since they contain no information about the physiology involved i.e. mechanisms, causes or effects. In an important sense, the teleological ‘explanations’ are also positively misleading in most cases. The physiological control systems often do not detect, or respond to, the triggers that the teleological ‘explanation’ might lead you to expect. Thus, when the perfusion of tissues initially becomes inadequate to meets the metabolic ‘demands’ (e.g. in exercising muscles during sustained, moderate to strenuous activity), there is little or no significant chemo-information fed back to the CNS to control the heart or blood vessels. Whatever the state of the blood that returns from tissues in the veins (to the right heart and lungs), arterial blood composition pumped back to the tissues is normally maintained as a result of lung function (for the respiratory gases and pH). Other regulatory adjustments to bllod composition follow during each circuit through organs such as the liver, kidneys etc. Furthermore, it is essentially only arterial blood chemistry that is sensed by peripheral and central chemoreceptors. The heart and lungs, therefore, cannot ‘know’ what is ‘needed’ or ‘wanted’ by the tissues since the blood emerging from the tissues is not ‘sensed’.

The reason the CVS responds as it does (cardiac output increases and most of the ‘extra’ output ends up going to the exercising tissues themselves) is that vascular resistance falls selectively in active tissues. This reflects the actions of local factors (pH, temperature, adenosine, raised [K+] etc.), produced within the tissue and acting directly on the adjacent vascular smooth muscle of arterioles and pre-capillary sphincters. These local factors provoke relaxation and thus arteriolar dilatation and this results in greater capillary blood flow. The reduced TPR in a vascular bed results in a small fall in MAP overall. If many such beds reduce their resistance, the fall in MAP will be greater. Any significant fall in MAP is detected by arterial baroreceptors. They feed information (coded as a reduced firing frequency if pressure falls) via autonomic sensory nerves to the autonomic CVS and respiratory control centres in the medulla oblongata. It is the integrative processes there that raise sympathetic activation with the result that MAP is restored, largely by the various mechanisms dealt with above. Raised respiration (=breathing) rates will compensate any arterial O2/CO2 changes.

So, as far as the heart, the lungs and most blood vessels are concerned, you can see that they have no specific information about whether they are responding to haemorrhage or to simple exercise, whether the whole body is involved or just the arms or just one leg or one small muscle. In that sense, no information about ‘needs’, nor a scenario whereby the heart ‘tries to’ do anything specific, emerges here. However, the strength of the autonomic reflexes invoked, as well as subtle features of their precise form, will tend to match the magnitude and detailed features of the particular physiological challenge. This is coded in the scale of changes in MAP, circulating volume, core temperature, arterial blood chemistry, proprioceptive feedback, conscious inputs, motor activity, emotion etc. that are all involved.

The homeostatic process in many animals, especially the birds and mammals (including us), has evolved in complexity and subtlety in such a way that the features of the system ensure (meaning ‘result in’) all tissues being supplied according to their ‘needs’ but without that ‘need’ actually being monitored. (Natural selection, of course defines what systems survive to reproduce and are thus - in evolutionary terms - 'successful'. We could broaden this analysis of physiological mechanisms not being teleological to Natural Selection itself; once again the outcome of the selection process is survival to reproduce rather than survival being the response to the ‘need’ to reproduce better. Even dear old David Attenborough so often seems to get that wrong, despite it being the most fundamental concept in modern biology!) This control system, ensuring adequate tissue perfusion by blood, holds in the face of multiple physiological challenges, provided that the key features of MAP and arterial blood chemistry are maintained ‘normal’ by the responses triggered by any local change. Of course, there are important additional, generalised and specific responses that are non–local; in exercise or haemorrhage for example, circulating catecholamines will be released and trigger responses e.g. in the liver, kidney, airways and CNS in various ways. Other hormonal and neural responses will raise or lower the rate of supporting physiological mechanisms. Furthermore, there is an increasing recognition by researchers that many of our autonomic responses appear to be ‘learned’. We seem able to ‘judge’ (albeit unconsciously) the severity of a challenge (such as a meal or a given physical exercise) and respond with a ‘suitable’ scale of response. Part of that is pre-emptive; your cardiac output and breathing rate will generally rise to ‘match’ the physiological demands anticipated for the staircase you are about to climb, just before you actually start. This means that experience and learning seem able to refine the autonomic reflexes. Generally, a smooth accommodation by physiological systems is ensured as we routinely change our physical activity levels, move from fasting to digestion/absorbtion etc. Similar learned behaviour applies to proprioceptive information so that body movement, limb placement, load-lifting etc is usually unconsciously, but accurately, ‘judged’ to meet the task. When we misjudge a load’s weight, or where our feet are when we are walking, the ‘surprise’ effect is considerable! Increasingly, this ‘autonomic learning’ is seen to be an important element contributing, for example, to the health benefits offered to western societies by aerobic fitness and appetite control.

I hope this rather detailed exposition helps you appreciate how the refinements of response and reflex, as orchestrated by the autonomic system, and how can give a convincing impression of being ‘need’ driven. The teleological type of ‘explanation’ is a naïve response. It often does look compellingly like the organs and tissues indeed ‘know’ what to do and ‘try’ to do it. But, again, the outcomes that give the appearance of resolving ‘needs’ and ‘wants’ are merely the consequence of the operating characteristics of the system as a whole. In modern terms, this consequence is described as an emergent property of a complex system. It is akin to consciousness itself which many of us believe is merely (albeit still amazingly!) the outcome of cerebral function rather than some stand-alone entity in itself. Nevertheless, it is easy for any one of us to slip into using the ‘needs, wants’ phrases as a kind of shorthand, so be on your guard for it.

Jogging and Global Warming – or - The Nike-Adidas CO2 footprint

(this item first appeared in Physiology News, the magazine of the Physiological  Society  - Spring 2008 No 70, p53 - see www.physoc.org/site/cms/contentChapterView.asp?chapter=151)

Have you ever wondered how much CO2 all those frantic joggers add to the global warming problem? And how does it compare with travel by the vilified car? Given the result of some simple physiological calculations, I suspect some will be surprised.

A car running at about 40 mpg and 100 km per hour – very achievable for modern vehicles – will generate about 150g CO2 per km (according to published data that you can check in any recent car advert). For an exercising, efficient human we can assume a near-maximum, steady-state, oxygen consumption of about 50ml O2 per kg body weight per minute. Let’s take the conventional ‘textbook’ 70kg man; that equate with 3.5 litres of O2 consumed per minute. Assume, at this stage, that he’s running his metabolism on carbohydrate; the respiratory quotient (RQ) for this substrate is about 1.0. This means his oxygen consumption will result in about 3.5 litres of CO2 breathed out per minute. The density of CO2 is nearly 2g per litre (under standard conditions) which means a CO2 production of 7g per minute. He will also be running at close to his maximum, sustainable, aerobic speed. If our runner is pretty fit ( … very fit!), he might be running at 5 minutes per mile rate, or approximately 3 minutes per kilometre. Thus, to run a kilometre, he will generate (3 x 7) = 21g of CO2. Of course, if he was less fit or efficient, he’d be producing more CO2 to cover each kilometre, and also taking longer over it.

So, if our car was carrying 4 people, over a 100 km trip it would generate some (150 x 100)/1000 = 15kg of CO2. If those same 4 passengers were to run the 100 km instead of riding, they would generate about (4 x 21 x 100)/1000 = 8.4kg between them, a little over half as much as taking the car. But we have overlooked something. After about an hour, when the car arrives and stops, it ceases to produce any more CO2. However, our passengers will still be respiring at their resting rate as will our runners too (once they have stopped puffing after their 100 km ‘jog’). Thus, they carry on producing at least 30g of CO2 per hour, day and night. Indeed they were still producing that much, even when being driven in the car. In 24 hours, after just one 100km trip, our 4 travellers by car will generate 2.9kg themselves and their car 15kg; a total of just under 18kg for the day. The runners, who spent 5 hours running and 19 at rest, will produce (8.4 + (4 x 19 x 0.03)) = 10.7kg for the day. So, the car journey only produced an ‘extra’ CO2 output comparable with 4 or 5 people sitting around doing nothing for a few days. If the journey were shorter, the CO2 ‘gap’ would obviously be less remarkable too. And furthermore, unlike the car, in order to run at this speed, our joggers would have to be jogging almost daily to keep fit between trips too; ‘training’ generates still more CO2 .

What’s the alternative? If our travellers continued sitting around doing nothing, thereby becoming couch potatoes, they would not travel or run as far, but they would reduce their global CO2 ‘footprint’ by 75% for the day. But there is a further bonus. The term ‘couch potato’ is misleading because our idlers would lay down fat, not starch. Adipose tissue is surely an excellent way of sequestering carbon. The metabolic rate of adipose tissue, once built, is pretty close to zero. And when they do eventually come to burn it off, either in exercise or, I suppose, eventually in a crematorium, remember that the RQ for fat is only 0.7. Less CO2 production in the end too!

More cynically still, has Gaia perhaps found the right strategy to save the planet by changing the shape and reducing the life expectancy of the average American (because they can’t be persuaded out of their SUVs)? This is not for the squeamish: achieving ideal carbon sequestering requires an early death for our tubbies, ideally from an abrupt cause since wasting diseases rather defeat the objective (I said this was cynical). Obesity–driven CVS problems fit the remit. And finally, disposal of the body demands an hermetically-sealed mode of burial to avoid carbon recycling.

The arithmetic implies we should eat more and exercise less to help save the planet. I rather suspect a better answer lies elsewhere!

Sydney Ringer - Father of physiological saline

Sydney Ringer (1836-1910) FRS, MD

Physiologist, Pharmacologist & Professor of Medicine, University College London

Parishioner and Benefactor of St Mary's, Lastingham, North Yorkshire

Sydney Ringer lies buried in the churchyard of St Mary's, together with his wife Ann (née Darley) and their elder daughter Annie, in whose memory the church was extensively restored in 1879. Ringer is the scientist and clinician most properly credited with 'inventing' physiological saline, now most familiar as the 'drip' seen in operating theatres and hospital wards. Physiological saline is the salt solution that allows the body's tissues to function for a time, even when isolated from their blood supply. It can replace blood in many clinical circumstances. A one of the scientific fathers of this life-saving liquid, Ringer deserves to be as well known as others whose names are associated with the great advances of medical science.

This is the opening paragraph of an illustrated booklet describing the life and times of Ringer, one of my scientific heroes. It is published by the Physiological Society; a free pdf can be downloaded at: 

www.physoc.org/site/cms/contentDocumentLibraryView.asp?chapter=103&category=382