Chapter Overview
Functional rehabilitation depends on the body's ability to deliver oxygen to working tissues and remove metabolic waste. Limb strength, balance, and gait all fail when the cardiorespiratory system cannot meet demand. This chapter reviews the physiology that underpins exercise tolerance, describes how dysfunction presents clinically, and outlines assessment and staged management for physiotherapists.
Core Physiology: Oxygen Transport
Oxygen uptake (VO₂) is governed by the Fick equation: VO₂ = cardiac output × (arterial − mixed venous oxygen content difference). Cardiac output equals heart rate multiplied by stroke volume. At rest, cardiac output is approximately 5 L/min. During maximal exercise in a fit adult it may exceed 20 L/min. Stroke volume typically plateaus at moderate intensities, so heart rate drives most of the early increase in output.
Hemoglobin carries roughly 1.34 mL O₂ per gram when fully saturated. Anaemia therefore reduces oxygen content without any primary cardiac or lung disease, and it must be considered whenever exercise tolerance is unexpectedly poor.
Respiratory Mechanics
The diaphragm is the primary inspiratory muscle, supported by the external intercostals, scalenes, and sternocleidomastoid during increased demand. Expiration is passive at rest and becomes active through the abdominal muscles and internal intercostals during exercise. Ventilation rises from roughly 6 L/min at rest to over 100 L/min in maximal exertion in healthy adults.
Ventilation-perfusion matching determines gas exchange efficiency. Dead space ventilation (V_D/V_T) normally falls to about 0.2–0.3 with exercise. Its failure to fall, or a rising ventilatory equivalent for CO₂ (VE/VCO₂), signals inefficient gas exchange and is an important prognostic marker in heart failure.
Autonomic and Exercise Responses
Exercise produces a rapid vagal withdrawal followed by sympathetic activation. Heart rate and contractility increase, peripheral vasoconstriction redistributes blood toward working muscle, and the baroreflex maintains arterial pressure. Systolic blood pressure should rise progressively with workload, typically to 160–200 mmHg in healthy adults at peak effort. Diastolic pressure should remain stable or fall slightly.
Heart rate recovery (HRR) reflects parasympathetic reactivation. A fall of less than 12 bpm at one minute after peak exercise is associated with increased mortality (Cole et al., 1999).
Clinical Presentation of Dysfunction
Cardiorespiratory limitation usually presents as one or more of the following:

Cardiorespiratory limitation often shows as dyspnoea out of proportion to the workload, graded with the mMRC scale (0–4) or Borg CR10.
- Dyspnoea out of proportion to workload, graded with the Modified Medical Research Council (mMRC) scale (0–4) or Borg CR10.
- Exercise-induced desaturation (SpO₂ falling by 4% or more, or below 88%).
- Early fatigue with preserved limb strength, suggesting a central or ventilatory limit.
- Chest pain, presyncope, or palpitations during activity, which require urgent screening.
- Orthostatic symptoms, defined by a drop of at least 20 mmHg systolic or 10 mmHg diastolic within three minutes of standing (Freeman et al., 2011).
Typical conditions include chronic obstructive pulmonary disease (COPD), heart failure, post-myocardial infarction, post-cardiac surgery, pulmonary embolism, deconditioning after critical illness, and long COVID.
Assessment
Resting Vital Signs and Normative Values
- Heart rate: 60–100 bpm
- Blood pressure: normal below 120/80 mmHg; stage 1 hypertension 130–139/80–89 mmHg; stage 2 at or above 140/90 mmHg (Whelton et al., 2018)
- Respiratory rate: 12–20 breaths/min
- SpO₂: 95–100% on room air
Estimated maximum heart rate is calculated as 208 − (0.7 × age) (Tanaka et al., 2001), which is more accurate than the older 220 − age formula.
Functional Capacity Tests
- 6-Minute Walk Test (6MWT): Standard distance is measured on a 30 m course. Healthy adults typically walk 400–700 m. A change of 25–30 m is considered the minimal clinically important difference in COPD (Holland et al., 2014). Distances below 350 m are associated with worse outcomes in chronic disease.
- 30-Second Chair Stand (Rikli & Jones, 1999): Below-average scores for women aged 60–64 are fewer than 12 stands, and for men aged 60–64 fewer than 14.
- Two-Minute Step Test: Counts steps with knee height target; compare against HR and SpO₂ response.
- Incremental Shuttle Walk Test: Used when sensitivity to change is needed.
- Cardiopulmonary Exercise Testing (CPET): Gold standard. Key outputs include peak VO₂ (ml/kg/min), anaerobic threshold, VE/VCO₂ slope (above 34 is poor prognosis in heart failure), and oxygen pulse.
Respiratory and Cardiac Measures
- Spirometry: Obstruction is defined as post-bronchodilator FEV₁/FVC below 0.70. GOLD grades severity by FEV₁ percent predicted: GOLD 1 at or above 80%, GOLD 2 at 50–79%, GOLD 3 at 30–49%, GOLD 4 below 30% (GOLD, 2024).
- Maximal inspiratory pressure (MIP): Measured against predicted values, with reduced values indicating respiratory muscle weakness.
- Heart failure classification: NYHA I–IV, and ejection fraction (HFrEF ≤40%; HFpEF ≥50%).
Management: Staged Protocols and Dosage
Exercise prescription should follow ACSM principles of frequency, intensity, time, and type (FITT), within a safety framework (Liguori et al., 2021).
Stage 1: Acute or Early Recovery (Days to Weeks)
- Goal: Safe mobilisation, prevention of deconditioning.
- Intensity: 3–4 on the Borg CR10 scale, or 11–12 on the Borg 6–20 scale; talk test passed.
- Duration: 5–10 minutes, 2–3 bouts per day.
- Mode: Sit-to-stand, walking, bed-based limb exercise, and breathing control (pursed-lip breathing).
Stage 2: Progressive Aerobic Conditioning (Weeks 2–8)
- Intensity: 40–59% heart rate reserve (HRR) or RPE 11–13, progressing to 60–75% HRR.
- Duration: Increase by 1–2 minutes per session to a target of 20–30 minutes.
- Frequency: 3–5 days/week, targeting 150 minutes per week of moderate activity.
- Mode: Interval walking or cycling, with work-to-rest ratios such as 1:1 for low-capacity patients.

Stage 2 builds to 20–30 minutes at 40–59% heart rate reserve or RPE 11–13. Low-capacity patients can use interval cycling at a 1:1 work-to-rest ratio.
Stage 3: Strength and Functional Integration (Weeks 6–12)
- Resistance training: 2–3 days/week, 8–12 repetitions at 40–70% of 1-repetition maximum, 1–3 sets.
- Functional circuits: stair climbing, carrying, and transfers at target heart rate.
- Respiratory muscle training may be added for patients with reduced MIP, at 30% of maximal inspiratory pressure initially, progressing as tolerated.
Stage 4: Maintenance and Self-Management
- Transition to home programs, community exercise, or cardiac or pulmonary rehabilitation Phase IV.
- Reassess the 6MWT and sit-to-stand at 6–12 weeks to document change.
Stop Criteria During Exercise
- Chest pain or pressure
- Systolic pressure falling by 10 mmHg or more despite increasing workload
- SpO₂ below 88%
- Dizziness, confusion, or pallor
- Abnormal arrhythmia or symptoms out of proportion to effort
Contraindications
- Absolute: Unstable angina, uncontrolled symptomatic arrhythmia, decompensated heart failure, acute myocarditis or pericarditis, severe symptomatic aortic stenosis, recent (less than 48 hours) suspected pulmonary embolism.
- Relative: Resting SBP above 200 mmHg or DBP above 110 mmHg, significant electrolyte abnormality, uncontrolled diabetes, recent syncope.
Clinical Pearls
- Always check the medication list. Beta-blockers blunt heart rate response, so use RPE or the talk test rather than HR targets.
- Measure SpO₂ at rest, during, and after activity. Desaturation below 88% during a 6MWT is a clinical trigger for supplemental oxygen assessment.
- Use HRR, not percentage of predicted maximum, when beta-blockers or pacing are present.
- Watch for orthostatic hypotension in patients with heart failure, autonomic neuropathy, or after prolonged bed rest. Test lying, sitting, and standing blood pressure before standing exercise.
- Dyspnoea should guide progression, not just heart rate. A Borg dyspnoea rating of 3–4 is a useful target in pulmonary conditions.
- Re-screen if symptoms change. New chest pain, unexplained weight gain, or rising oedema should prompt referral before continuing.
Summary
Cardiorespiratory function determines how effectively the body meets the metabolic demands of functional movement. Oxygen transport depends on cardiac output, hemoglobin, ventilation, and gas exchange, all coordinated by autonomic control. Dysfunction presents as disproportionate dyspnoea, desaturation, early fatigue, or abnormal blood pressure response. Physiotherapists should use validated measures, including the 6MWT, 30-second chair stand, spirometry, and HRR, to establish baselines and track progress. Staged exercise programmes, guided by the FITT principles, safety thresholds, and clear stop criteria, allow patients to progress from early mobilisation to independent functional activity. Recognising contraindications and red flags is essential to safe practice.
References
- Liguori G, Feito Y, Fountaine CJ, Roy B, eds. ACSM's Guidelines for Exercise Testing and Prescription. 11th ed. Philadelphia: Wolters Kluwer; 2021.
- Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults. Hypertension. 2018;71(6):e13–e115.
- Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global Strategy for the Diagnosis, Management, and Prevention of COPD. 2024 Report. Available at: goldcopd.org.
- Holland AE, Spruit MA, Troosters T, et al. An official European Respiratory Society/American Thoracic Society technical standard: field walking tests in chronic respiratory disease. Eur Respir J. 2014;44(6):1428–1446.
- Cole CR, Blackstone EH, Pashkow FJ, Snader CE, Lauer MS. Heart-rate recovery immediately after exercise as a predictor of mortality. N Engl J Med. 1999;341(18):1351–1357.
- Rikli RE, Jones CJ. Development and validation of a functional fitness test for community-residing older adults. J Aging Phys Act. 1999;7(2):129–161.
- Freeman R, Wieling W, Axelrod FB, et al. Consensus statement on the definition of orthostatic hypotension, neurally mediated syncope and the postural tachycardia syndrome. Clin Auton Res. 2011;21(2):69–72.
- Tanaka H, Monahan KD, Seals DR. Age-predicted maximal heart rate revisited. J Am Coll Cardiol. 2001;37(1):153–156.