Slide 1 – Title & Context
Unit/Lecture: EXSS3070 | Advanced Exercise Programming & Delivery – “Respiratory (Patho)physiology – a Refresher”.
Presenter: Dr Troy J Cross, PhD, Senior Lecturer, Discipline of Exercise & Sport Science, The University of Sydney.
Signals that respiratory content underpins later exercise-for-asthma programming.
Slide 2 – Initial Learning Objectives
Purpose of breathing – gas exchange and non-respiratory roles.
Respiratory anatomy – conducting vs respiratory zones, airway walls.
Pulmonary function tests (PFTs) – spirogram, volume-time, flow-volume.
Disease spectrum – restrictive, obstructive, mixed.
Hallmark obstructive symptoms – cough & dyspnoea.
Slide 3 – Resources
ESSA position statements (link shown on slide) summarise best-practice assessment & exercise prescription for respiratory disorders. Download and file them for future clinical placement use.
SECTION 1 | Fundamentals of Breathing
Slide 4 – Respiratory Purpose
Primary goal: maintain arterial gases within narrow limits: PaO₂ ≈ 80–100 mmHg, PaCO₂ ≈ 35–45 mmHg; stabilises arterial pH at 7.35–7.45 via CO₂ buffering.
Requires tight V̇A/Q̇ (ventilation-perfusion) matching and intact alveolar–capillary diffusion.
Slide 5 – Non-Respiratory Roles
Valsalva-like maneuvers for emesis, defecation, parturition.
Airflow for phonation & swallowing.
Thoracic pump modulates venous return & cardiac output.
Thermoregulation via evaporative heat loss in expired air.
Slide 6 – Macro-Anatomy Overview
Upper airways: nasal/oral cavities → pharynx → larynx.
Lower airways: trachea → 1° bronchi → 23 generations of branching to alveolar sacs.
Distinct conducting vs respiratory zones introduced.
Slide 7 – Conducting vs Respiratory Zones
Zone | Structures | Function | Clinical Note |
Conducting | Mouth→terminal bronchioles | Warm, humidify, filter; anatomical dead space (~150 mL) | Obstruction here → ↑ airway resistance. |
Respiratory | Respiratory bronchioles, alveolar ducts/sacs | Gas exchange; surfactant lowers surface tension | Loss of surfactant (e.g., IRDS) → alveolar collapse (atelectasis). |
Slide 8 – Tracheal Cross-Section
C-shaped cartilage prevents collapse; posterior smooth muscle permits oesophageal expansion.
Mucociliary escalator sweeps debris cephalad; smoking destroys cilia → chronic cough.
Slide 9 – Airway Branching & Surface Area
23 generations create ~300 million alveoli; exchange surface ≈ 70–100 m².
Parallel branching multiplies cross-sectional area → velocity of airflow plummets distally, aiding diffusion & particle deposition.
Slide 10 – Airway Wall Layers
Inner mucosa: ciliated epithelium + goblet cells (mucus).
Submucosa & cartilage/CT: glands, vessels, nerves.
Airway smooth-muscle (ASM): constricts/relaxes lumen; hypertrophies in asthma.
SECTION 2 | Pulmonary Function Testing
Slide 11 – Spirogram Graph
Annotated lung volumes & capacities:
Static: TLC, FRC, RV.
Dynamic: VT (~500 mL), IRV, ERV, VC (~80% TLC).
Emphasise “capacity = two or more volumes”.
Slide 12 – Spirometric Definitions & Norms
TLC ≈ 6 L (♂) / 4.2 L (♀).
FRC = RV + ERV; baseline lung volume at end-tidal expiration.
Clinical: ↓TLC & VC with normal FEV₁/FVC suggests restriction; ↓FEV₁ & ratio suggests obstruction.
Slide 13 – Volume-Time Manoeuvre Protocol
Inspire to TLC.
Explode into forced expiration (no pause).
Continue ≥ 6 s or until plateau.
Optional reinspiration to TLC shows flow-volume loop closure.
Must coach maximal effort; sub-max blows under-diagnose obstruction.
Slide 14 – Key Indices from Volume-Time
FEV₁: volume exhaled in 1 s; ↓ in asthma/COPD.
FVC: maximal exhaled volume.
FEV₁/FVC (Tiffeneau index): < 0.70 (post-bronchodilator) ⇒ obstructive disease.
Slide 15 – Flow-Volume Loop Patterns
(Text not visible in preview; expanded for completeness)
Normal: rapid peak flow then linear descent.
Obstructive: scooped-out expiratory limb, ↓PEF.
Restrictive: narrow loop, PEF preserved, volumes compressed.
Loop analysis quickly differentiates pathologies during clinical screening.
SECTION 3 | Pulmonary Disorders
Slide 16 – Spectrum Overview
Disorders classified by predominant pathophysiology: restrictive, obstructive, mixed.
Flow-volume archetypes shown for each.
Slide 17 – Restrictive Disorders (Pathophysiology)
Intrinsic: interstitial fibrosis, pneumonitis → stiff parenchyma.
Extrinsic: kyphoscoliosis, neuromuscular weakness, pleural effusion.
Spirometry: ↓TLC, FRC, RV, VC; flows often normal/↑ relative to volume.
Slide 18 – Obstructive Disorders (Pathophysiology)
Primary issue = airflow limitation on expiration.
Episodic (asthma) vs chronic (COPD = chronic bronchitis + emphysema).
Hyperinflation ↑FRC/RV; diaphragm flattens.
Slide 19 – Mixed Patterns
Combines low volumes and low flows; e.g., pneumoconiosis with airway inflammation.
Slide 20 – Flow-Volume Morphology Examples
(Assumed visuals)
Learning point: recognise “coving” (obstruction) vs “compressed but tall” (restriction).
Slides 21 & 22 – Visual Chest X-ray/CT Comparisons
Restrictive: reticular opacities, small lung fields.
Obstructive: hyperlucent lungs, flattened diaphragms.
Slide 23 – Obstructive Disorders Focus (Asthma/COPD)
Transition to detailed mechanism slides.
Slide 24 – Airway Narrowing Mechanisms
Mucous plugging from goblet cell hyperplasia.
Wall thickening: ASM contraction + oedema + remodelling.
Loss of radial traction: parenchymal destruction removes tethering.
Slide 25 – Hallmark Obstructive Symptoms
Cough & Dyspnoea: shared across asthma, COPD, bronchiectasis.
Slide 26 – Cough Physiology
Protective reflex powered by rapid-flow “expiratory blast” (high intrathoracic pressure).
Effective cough clears secretions (expectoration).
Slide 27 – Acute vs Chronic Cough Aetiology
Acute (< 3 wk): viral URTI, allergic rhinitis.
Chronic (> 3 wk): smoking-related COPD, uncontrolled asthma, GORD, ACE-inhibitors.
Slide 28 – Intact Mucociliary Clearance
Healthy cilia transport ~100 mL mucus/day to oropharynx → swallow; cough frequency low.
Slide 29 – Impaired Ciliary Function
Smoking/pollutants destroy cilia → retained secretions → productive cough becomes main clearance route.
Slide 30 – Dyspnoea: Multidimensional Symptom
Sensory components: work/effort of breathing, air hunger, chest tightness.
Affective components: anxiety, fear, depression; dyspnoea-anxiety-dyspnoea spiral mirrors chronic pain cycles.
Slide 31 – Formal Definition
“Subjective experience of breathing discomfort comprising qualitatively distinct sensations varying in intensity.”
Slide 32 – The Dyspnoea Spiral
↓Activity → deconditioning → ↑ventilatory drive at low workloads → worse breathlessness → further inactivity. Exercise training aims to break this loop.
Slide 33 – Measuring Dyspnoea: Overview
Situational (during exercise) vs baseline (ADL).
Slide 34 – MRC & mMRC Scales
Grade 0 (no dyspnoea except strenuous exercise) → Grade 4 (too breathless to leave house).
mMRC widely used in COPD severity classification (GOLD guidelines).
Slide 35 – Visual Analog Scale (VAS)
100 mm line; patient marks perceived intensity. Reliable if standardised descriptors used.
Slide 36 – Category-Ratio 10 (Modified Borg)
Non-linear anchors: 0 = nothing, 10 = maximal.
CR10 preferred during incremental tests (e.g., CPET) because near-linear relation with log-ventilation.
Slide 37 – Multidimensional Dyspnoea Profile (MDP)
Separates sensory quality, immediate discomfort, emotional response.
Impractical mid-exercise but valuable in research or pulmonary rehab assessment.
Slide 38 – Learning Objectives Checkpoint (ticks)
Slide shows completed objectives; confirms end of physiology section.
SECTION 4 | Asthma Part 1 – Fundamentals
Slide 39 – New Title: “Exercise Considerations for Asthma”
Marks shift from generic respiration to asthma-specific programming.
Slide 40 – Asthma Section Objectives
Define asthma & prevalence.
Diagnostic pathway.
Pharmacological & non-pharmacological treatment.
Exercise programming nuances.
Slide 41 – Epidemiology
2 million Australians diagnosed; male bias (3:2) in childhood; prevalence peaks in first decade then stabilises.
Slide 42 – Definition & Core Pathology
Chronic inflammatory disorder of ASM → airway hyperresponsiveness (AHR) + reversible bronchoconstriction episodes.
Slide 43 – Common Triggers
Allergens (dust mite, pollen), cold dry air, respiratory infections, exercise, air pollutants, drugs (β-blockers, NSAIDs); chloramines in indoor pools, tobacco smoke.
Slide 44 – Exercise-Induced Bronchoconstriction (EIB)
Mechanism: high ventilatory rates → airway dehydration & cooling → ↑osmolarity → mediator release (leukotrienes, prostaglandins) → ASM contraction. Symptoms during or ~5–10 min post-exercise.
Slide 45 – Frequent Comorbidities
Rhinitis/rhinosinusitis, GORD, obesity, OSA, depression, anxiety. Addressing these improves asthma control.
Slide 46 – Mechanistic Triad of Airway Narrowing
ASM bronchoconstriction.
Wall thickening (inflammation, oedema).
Excess mucus production.
SECTION 5 | Asthma Part 2 – Diagnosis
Slide 47 – Diagnostic Step 1: Symptom History
Dyspnoea, cough, wheeze, chest tightness, nocturnal awakenings; ask about pattern & triggers.
Slide 48 – Step 2: Baseline Spirometry Decision Tree
Compare FEV₁, FVC, ratio to LLN (lower limit normal). Normal spirometry does not exclude asthma if quiescent.
Slide 49 – Step 3: Bronchodilator Reversibility
Post-salbutamol ↑FEV₁ or FVC > 10 % predicted (or > 200 mL absolute) = reversible obstruction.
Slide 50 – Step 4: Bronchoprovocation Testing
Required when baseline spirometry ± reversibility inconclusive.
Slide 51 – Direct Challenge (Methacholine/Histamine)
Escalating doses until FEV₁ falls 20 % (PD₂₀). High sensitivity; positive test confirms AHR but doesn’t prove active asthma.
Slide 52 – Indirect Exercise Challenge
6–8 min at 80–90 % HRmax breathing dry air (≤ 10 mg H₂O·L⁻¹). Serial spirometry @ 5, 10, 15, 30 min post. ≥ 10 % FEV₁ fall = EIB; classify mild < 25 %, moderate 25–49 %, severe ≥ 50 %.
Slide 53 – Additional Indirect Tests
Mannitol inhalation, eucapnic voluntary hyperventilation (EVH), hypertonic saline. Useful when exercise lab unavailable.
SECTION 6 | Asthma Part 3 – Management
Slide 54 – Management Goals
Symptom control, prevent exacerbations, maintain lung function, minimise medication side-effects.
Slide 55 – Pulmonary Function Monitoring
Document at diagnosis, again 3–6 months after therapy initiation, then periodically (≥ annually).
Slide 56 – Patient Responsibilities
Education on disease, inhaler technique, adherence (target > 80 % although typical ≈ 70 %), written action plan, peak-flow diary, regular medical reviews.
Slides 57 & 58 – Pharmacotherapy Ladder
(content implied)
Relievers: short-acting β₂-agonists (SABA).
Controllers: inhaled corticosteroids (ICS) ± long-acting β₂-agonists (LABA).
Add-on: leukotriene receptor antagonists, monoclonal antibodies for severe eosinophilic asthma.
Slide 59 – Exercise Training as Adjunct Therapy
Aerobic conditioning ↓V̇E (ventilation) at given workload → less airway dehydration → ↓EIB severity; improves QoL and anxiety.
SECTION 7 | Asthma Part 4 – Exercise Prescription
Slide 60 – “ExRx?” Prompt Slide
Sets stage to translate pathophysiology into FITT guidelines.
Slide 61 – Criteria for
Well-Controlled
Asthma
No nocturnal or morning symptoms, no rescue inhaler use, unrestricted ADL, no recent exacerbations. Only under these conditions follow standard ACSM guidelines.
Slide 62 – General FITT Recommendation
Frequency: 3–5 d·wk⁻¹.
Intensity: 40–59 % HRR progressing to 60–70 % as tolerated.
Time: 20–60 min; interval format (e.g., 10 min bouts) reduces EIB risk.
Type: Rhythmic large-muscle aerobic (cycling, brisk walking, swimming) + 2 resistance sessions/wk to offset corticosteroid myopathy.
Slide 63 – Medication Timing & Access
Administer controller & preventer meds ~(15 min) pre-exercise; carry reliever inhaler at all times during sessions.
Slide 64 – Mode/Environment Considerations
Swimming: warm, humid air → least “asthmagenic”; prefer non-chlorinated or outdoor pools (↓chloramines).
Cold/dry weather: encourage nose breathing or mask; schedule indoors on high-risk days; check bush-fire & thunderstorm asthma alerts.
Slide 65 – Pollution & Allergen Exposure
Road cycling → particulate matter (PM2.5) aggravates bronchoconstriction; choose low-traffic routes/times.
Slide 66 – Behavioural & Adherence Strategies
Individualise activities for enjoyment; include goal setting, symptom tracking, positive reinforcement.
Slide 67 – Over-Training Syndrome (OTS) Risk
Excessive load suppresses immunity → infection flare-ups; integrate periodisation & monitor RESTQ-Sport or HRV.
Slide 68 – Contra-Indications
No reliever available ⇒ cancel session.
Recent peak-flow or FEV₁ < 75 % personal best ⇒ reschedule.
Standard ACSM absolute/relative cardio contraindications also apply.
Slide 69 – Read ESSA Position Statement Prompt
Provides evidenced-based tables of exercise dosage, screening, and safety algorithms – download for quick reference before clinical placement.
SECTION 8 | Closing Slides
Slide 70 – Final Learning Objective Checklist
Visually confirms all asthma goals met (tick marks).
Slide 71 – Summary Graphic / Key Take-Home
“Asthma control → safe, beneficial exercise” emphasised; integrate physiology with programming.
Slide 72 – Questions / Discussion Cue
Prepare to discuss: adapting FITT for cold-weather sport, inhaler technique coaching, comorbidity management.
Slide 73 – Thank-You / Contact Details
Email: troy.cross@sydney.edu.au (assumed format).
Slides 74–77 – Spare / Backup (no core content)
Some presenters keep additional figures or references; not examinable unless explicitly shown in class.
Rapid-Reference Tables (optional paste into your study sheet)
Spirometry Interpretation Cheat-Sheet
FEV₁/FVC < 0.70 (post-BD) ⇒ obstructive.
FVC ↓ < 80 % predicted with normal ratio ⇒ restrictive.
Bronchodilator ↑FEV₁ ≥ 10 % pred (≥ 200 mL) ⇒ reversible.
EIB Severity Classification
| FEV₁ Fall from Baseline | Severity |
|———————––|–––––|
| 10–24 % | Mild |
| 25–49 % | Moderate |
| ≥ 50 % | Severe |
Modified Borg (CR10) Anchors
0 = nothing, 0.5 = just noticeable, 3 = moderate, 5 = severe, 7 = very severe, 10 = maximal.