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Human Physiology · Nervous system and exercise

The Autonomic Nervous System

The autonomic nervous system controls the heart, vessels, gut, bladder, pupils and glands without conscious effort. This page explains its two divisions, their transmitters and receptors, how they adjust to exercise and posture, and autonomic emergencies in spinal cord injury.

11Sections
5Figures
2Tables
10Questions

Part 9 · Nervous System and Exercise · Chapter 45 of 47

Learning objectives

By the end of this page you should be able to:

  • Compare the sympathetic and parasympathetic divisions.
  • Name the main transmitters and receptors.
  • Describe autonomic effects on the main organs.
  • Explain autonomic control of heart rate in exercise and recovery.
  • Recognise orthostatic hypotension and autonomic dysreflexia.
  • Apply heart-rate recovery and autonomic safety in practice.

Why it matters

Physiotherapists change posture, load and activity, all of which challenge autonomic control. Dizziness on standing, abnormal heart-rate responses and autonomic emergencies happen in the gym and on the ward.

Knowing the physiology lets you predict and prevent them.

Organisation

Figure 1 · Two divisions, two layouts

Sympathetic and parasympathetic pathways with ganglion position and transmitters Sympathetic fibres leave from T1 to L2, with short preganglionic fibres to chain ganglia and long noradrenergic postganglionic fibres. Parasympathetic fibres leave from cranial nerves and sacral segments, with long preganglionic fibres to ganglia near the organ and short cholinergic postganglionic fibres. Sympatheticthoracolumbar outflow (T1–L2)short preganglioniclong postganglionicAChnoradrenalineganglia in chain beside the spineParasympatheticcraniosacral outflow (III, VII, IX, X; S2–S4)long preganglionicshortAChAChganglia in or near the organExceptions: sweat glands use sympathetic ACh; adrenal medulla acts as a modified ganglion
All preganglionic fibres use acetylcholine. The postganglionic transmitter and receptor decide the effect on each organ.
ReceptorTransmitterMain locations and effects
NicotinicAcetylcholineAll autonomic ganglia; adrenal medulla
MuscarinicAcetylcholineParasympathetic targets: heart slows, gut and bladder contract; sweat glands
α1NoradrenalineVasoconstriction; pupil dilation
β1Noradrenaline, adrenalineHeart rate and force up
β2AdrenalineBronchodilation; muscle vessel dilation

Beta-blockers blunt heart-rate response to exercise, so heart-rate targets must be adjusted. Rating of perceived exertion is often more useful in these patients.

Effects on organs

Figure 2 · Effects on organs

Sympathetic and parasympathetic effects on major organs Sympathetic activity raises heart rate and force, dilates bronchi and pupils, slows the gut, relaxes the bladder wall, constricts skin and gut vessels, dilates muscle vessels in exercise and releases glucose. Parasympathetic activity slows the heart, constricts bronchi and pupils, speeds the gut and empties the bladder. Sympathetic: fight or flightParasympathetic: rest and digestHeartrate and force uprate downBronchidilateconstrictPupildilatesconstrictsGutmotility downmotility and secretion upBladderrelaxes wall; holds urinecontracts wall; voidsSkin and gut vesselsconstrictlittle effectMuscle vesselsdilate in exerciselittle effectGlucoseliver releases glucose—
Mostly opposing, always balanced. Most organs receive both inputs; the balance shifts with posture, exercise, eating and stress.

The hypothalamus and brainstem coordinate autonomic output. Reflexes such as the baroreflex keep blood pressure stable from moment to moment.

Exercise and recovery

During exercise, heart rate rises partly through withdrawal of vagal tone [1]. Sympathetic drive adds to it as intensity increases. After exercise, the early fall in heart rate reflects vagal reactivation [1].

Figure 3 · Heart-rate recovery

Heart rate falling quickly or slowly in the first minutes after exercise Heart rate rises during exercise. After stopping, it normally falls quickly as vagal activity returns. An abnormal recovery is a fall of 12 beats per minute or less in the first minute. peak exercise1 min-2024680120160Minutes (0 = end of exercise)Heart rate (beats/min)Normal: fast recoveryAbnormal: fall of 12 or lessin the first minute [1]
A simple vagal test. Recovery in the first minute reflects parasympathetic reactivation [1]. Schematic curves.

Cole and colleagues followed 2,428 adults after exercise testing for six years [1]. A fall of 12 beats per minute or less in the first minute predicted death, independent of fitness and other risks [1].

Figure 4 · Slow recovery predicts death

Relative risk of death with abnormal heart-rate recovery Among 2,428 adults followed for six years, 26 per cent had abnormal heart-rate recovery. Their relative risk of death was 4.0 unadjusted and 2.0 after adjusting for age, workload, perfusion defects and risk factors. RR 4.0UnadjustedRR 2.0Adjusted for age, workload,perfusion and risk factorsno extra risk2,428 adultsfollowed 6 years26%had abnormal recovery213 deaths
Vagal function matters. A delayed fall in heart rate was a powerful predictor of mortality, independent of workload [1].

Posture and orthostatic hypotension

Standing pools blood in the legs. Baroreceptors detect the fall in pressure and trigger sympathetic vasoconstriction and a faster heart rate.

When this fails, as after bed rest, with some drugs, diabetes, Parkinson disease or spinal cord injury, blood pressure falls on standing and the patient feels dizzy or faints.

Practical skill · first sit-up

Measure blood pressure lying, then after sitting and standing. Progress head-up position gradually, use leg exercises, compression and abdominal binders where appropriate, and stop if symptoms appear.

Autonomic dysreflexia

In spinal cord injury at or above about T6, a stimulus below the lesion can trigger a dangerous rise in blood pressure. Krassioukov and colleagues reviewed 31 studies on its management [2].

Figure 5 · Autonomic dysreflexia

Mechanism and first response in autonomic dysreflexia after high spinal cord injury In injury at or above T6, a trigger below the lesion such as a full bladder causes an unchecked sympathetic surge with vasoconstriction and very high blood pressure. The baroreflex slows the heart and causes flushing and headache above the lesion, but descending inhibition cannot pass. First response is to sit upright, loosen clothing and remove the trigger. cordinjury at or above T6Trigger below injuryfull bladder, bowel, pressuresore, tight clothingUnchecked sympathetic surgevessels constrict below injury:blood pressure soarsBaroreflex responds above injuryslow heart, flushing, headacheinhibition cannotpass the lesionFirst response [2]sit the person uprightloosen tight clothingfind and remove triggermonitor blood pressure
An emergency. Initial non-drug management is supported by consensus and physiology; drugs are used if blood pressure stays high [2].

Sitting the person upright, loosening clothing and removing the trigger are the first steps [2]. Drugs such as prazosin are used when blood pressure remains high [2].

Clinical relevance for the physiotherapist

  • Heart-rate recovery. Note the first-minute fall after exercise tests [1].
  • Beta-blockers. Use perceived exertion rather than heart rate alone.
  • Orthostatic hypotension. Measure lying and standing blood pressure before mobilising.
  • Spinal cord injury. Recognise autonomic dysreflexia and act at once [2].
  • Breathing. Slow breathing raises vagal activity and can calm anxiety.

Assessment and application

SituationInterpretationAction
Heart rate falls only 8 beats in the minute after a testAbnormal recovery [1]Report; consider supervised programme
Dizziness on first standing after a week in bedOrthostatic hypotensionSit down; graded verticalisation
Tetraplegic patient with pounding headache and flushingAutonomic dysreflexia [2]Sit up, loosen clothing, check bladder
Patient on beta-blocker cannot reach target heart rateBlunted responseUse perceived exertion

Common mistakes

  • Laying a patient with autonomic dysreflexia flat [2].
  • Ignoring slow heart-rate recovery [1].
  • Using heart-rate targets in patients on beta-blockers.
  • Standing a deconditioned patient without blood pressure checks.
  • Forgetting that tight straps or splints can be triggers.

Exam preparation

Long answer

Compare the sympathetic and parasympathetic nervous systems.

  • Outflow, ganglia and fibre lengths (Figure 1).
  • Transmitters and receptors (table).
  • Organ effects (Figure 2).
  • Control of heart rate in exercise (Figure 3) [1].
  • Autonomic dysreflexia (Figure 5) [2].

Short notes

  • Adrenergic receptors.
  • Orthostatic hypotension.
  • Heart-rate recovery [1].
  • Autonomic dysreflexia [2].

Viva and practical

  • “Which transmitter acts at all autonomic ganglia?” — acetylcholine.
  • “What is abnormal heart-rate recovery?” — a fall of 12 or less in one minute [1].
  • “First action in autonomic dysreflexia?” — sit the person up [2].
  • OSCE: measure lying and standing blood pressure.

Current evidence

Exam and traditional teaching

The autonomic system is a simple on-off balance of two divisions.

What the evidence adds

Heart-rate recovery is a powerful marker of vagal health and survival [1].

Autonomic dysreflexia management relies on simple first steps and selected drugs [2].

What the student should understand

Every exercise session tests autonomic control. Watch heart rate and blood pressure, not just effort.

Check yourself

10 questions on this page. Tap one to see the answer and the reasoning.

Q1. Heart-rate recovery in the first minute after exercise mainly reflects:
  1. (A) Sympathetic activation
  2. (B) Vagal reactivation
  3. (C) Adrenal cortex
  4. (D) Thyroid hormone

Answer: (B) Recovery of heart rate immediately after exercise is a function of vagal reactivation [1].

Q2. An abnormal heart-rate recovery was defined as a fall of:
  1. (A) 12 beats/min or less in the first minute
  2. (B) 50 beats/min in 10 seconds
  3. (C) Any fall
  4. (D) More than 40 beats/min

Answer: (A) Abnormal was a reduction of 12 beats/min or less from peak at one minute [1].

Q3. What proportion of patients had abnormal heart-rate recovery?
  1. (A) 2.6%
  2. (B) 26%
  3. (C) 62%
  4. (D) 96%

Answer: (B) 639 patients, 26% [1].

Q4. After adjustment, the relative risk of death with abnormal recovery was about:
  1. (A) 1.0
  2. (B) 2.0
  3. (C) 10
  4. (D) 0.5

Answer: (B) Adjusted relative risk 2.0 (1.5 to 2.7) [1].

Q5. The increase in heart rate during exercise is partly due to:
  1. (A) Increased vagal tone
  2. (B) Reduced vagal tone
  3. (C) Lower body temperature
  4. (D) Reduced adrenaline

Answer: (B) The rise is due in part to a reduction in vagal tone [1].

Q6. The initial non-drug management of autonomic dysreflexia includes:
  1. (A) Lying flat with legs raised
  2. (B) Sitting upright, loosening clothing and removing the trigger
  3. (C) Cold water immersion
  4. (D) Exercise

Answer: (B) Positioning upright, loosening tight clothing and eliminating the stimulus [2].

Q7. The evidence for the initial non-drug management of autonomic dysreflexia comes mainly from:
  1. (A) Large RCTs
  2. (B) Clinical consensus and physiological data
  3. (C) Animal studies only
  4. (D) No evidence

Answer: (B) It is supported by consensus and physiological data (level 5) [2].

Q8. Which drug had level 1 evidence for sustained high blood pressure in autonomic dysreflexia?
  1. (A) Prazosin
  2. (B) Aspirin
  3. (C) Insulin
  4. (D) Salbutamol

Answer: (A) Prazosin was supported by level 1 evidence [2].

Q9. Common triggers of autonomic dysreflexia include:
  1. (A) The urogenital system
  2. (B) Bright light only
  3. (C) Reading
  4. (D) Music

Answer: (A) Common triggers include the urogenital system and surgery [2].

Q10. How many studies were assessed in the autonomic dysreflexia review?
  1. (A) 3
  2. (B) 31
  3. (C) 310
  4. (D) 3,100

Answer: (B) Thirty-one studies including 6 RCTs [2].

Quick review

Key takeaways

  • Sympathetic: T1–L2, short pre, long noradrenergic post.
  • Parasympathetic: cranial and sacral, long pre, short cholinergic post.
  • Exercise heart-rate rise starts with vagal withdrawal [1].
  • Fall of 12 or less in one minute after exercise predicts death [1].
  • Orthostatic hypotension: check lying and standing blood pressure.
  • Autonomic dysreflexia: sit up, loosen, remove trigger [2].

Further reading

SourceWhy it earns its place
Cole CR et al. — NEJM, 1999Heart-rate recovery and mortality [1]
Krassioukov A et al. — Arch Phys Med Rehabil, 2009Autonomic dysreflexia management [2]
Guyton and Hall, Textbook of Medical PhysiologyAutonomic nervous system

References

  1. Cole CR, Blackstone EH, Pashkow FJ, Snader CE, Lauer MS. Heart-rate recovery immediately after exercise as a predictor of mortality. New England Journal of Medicine. 1999;341(18):1351–1357. doi:10.1056/NEJM199910283411804 PMID 10536127 Prospective cohort study
  2. Krassioukov A, Warburton DE, Teasell R, Eng JJ. A systematic review of the management of autonomic dysreflexia after spinal cord injury. Archives of Physical Medicine and Rehabilitation. 2009;90(4):682–695. doi:10.1016/j.apmr.2008.10.017 PMID 19345787 Systematic review

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