Lectures

Introduces foundational concepts of physical activity and exercise in relation to energy expenditure and metabolic strain. Covers short-term homeostatic balancing during exercise, including cardiovascular, respiratory, metabolic and thermoregulatory responses. Presents homeostasis and hormesis as complementary frameworks for exercise-induced inflammation, contrasting negative feedback dynamics with biphasic dose-response adaptation, and discussing implications for healthy athletes and clinical populations (ME/CFS, Long COVID). Explores the physiology of sleep and wakefulness, including sleep architecture, NREM/REM cycles, and the bidirectional relationship between exercise and sleep quality.

Examines the immune system's role in protecting bodily integrity, covering innate and adaptive immunity, the four-phase inflammatory cascade, acute vs. chronic inflammation, and the effects of acute and chronic exercise on immune regulation. Defines the physiological and sports-medical limits of physical performance, including the influence of ageing, the primary and secondary determinants of performance capacity, and the extended definition incorporating age-related mortality. Introduces bioenergetics and energy balance — energy-supply systems and their flow rates, ATP as the energy currency, gross vs. physiological energy values, and the metabolic roles of carbohydrates, lipids and proteins.

Examines resting heart rate as a prognostic marker — its linear dose–response with mortality, what survives adjustment for fitness, the evidence behind proposed mechanisms, and the distinction between a risk marker and a treatment target. Follows how a wearable produces the number — from reflectance photoplethysmography and its processing chain to head-to-head validations against ECG and the heart-rate-derived sleep stages whose accuracy claims depend on base rates. Asks whether the resting value in use is actually known, comparing clinic and wearable definitions, photoplethysmography against ECG, the individual baseline as reference, and deviation from that baseline during and after infection. Treats maximal heart rate as the denominator under every intensity zone, from the criteria of a maximal test and the 1971 origin of 220 − age to the modern equations, their individual spread and the eighty-five-per-cent rule. Presents heart-rate recovery as an autonomic response whose cut-off belongs to the protocol, with its mortality association in referral cohorts and the general population, its threshold-shaped risk curve and minimum reporting standards.

Provides a detailed treatment of energy expenditure, from basal and resting metabolic rate through total daily energy expenditure (TDEE) to the Weir formula and respiratory exchange ratio (RER). Links oxygen uptake (V̇O₂) to daily behaviour, physical activity levels, and energy supply under normoxic and hypoxic conditions, including the MET concept and MET-minutes. Covers threshold concepts — ventilatory, lactate, and anaerobic thresholds — and their physiological significance for exercise prescription and performance diagnostics. Presents standardised exercise intensity terminology (Very Low to Very High) based on the joint ACSM/ESSA consensus, with methods for determining and monitoring cardiorespiratory and resistance exercise intensity using metabolic thresholds, RIR, and RPE.

Traces the evolution of lactate from a metabolic byproduct to a central regulator of human physiology, highlighting its continuous aerobic production, role as a primary fuel source, and function as a signaling molecule across cellular and systemic levels. It also introduces lactate-based performance diagnostics, emphasizing individualized thresholds and curve analysis to assess training adaptation, endurance capacity, and metabolic dysfunction in conditions such as Long COVID and ME/CFS.

Evidence-based comparison of cardiorespiratory fitness (CRF) measured in METs versus VO₂ max, based on Eric Topol's *Ground Truths* analysis and reconstructed figures from major cohort studies. Demonstrates that CRF/METs underpins >99% of the outcome literature linking fitness to all-cause and cardiovascular mortality, drawing on the JAMA 2009 meta-analysis (n=102,980), the Cleveland Clinic cohort (n=122,007), and the Veterans Affairs cohort (n=750,302). Critically evaluates consumer wearable VO₂ max estimates (7–16% MAPE) and the data imbalance between METs-based and direct VO₂ max evidence, concluding that METs are clinically superior for most healthy adults.

Presents the concept and clinical evidence base for Exercise Snacks — isolated, brief, intense bouts repeated through the day — across four domains, namely glycaemic control, muscular adaptation, cardiovascular mortality (VILPA) and immune regulation. Develops the underlying physiological mechanisms — the AMPK-convergent GLUT4 and LPL axes, the three phases of muscular adaptation, the Fick-equation framework for aerobic gains, and the three immunological axes converging on NF-κB suppression. Translates the evidence into prescription, with intensity anchors (%HRmax, RPE CR10), an example one-day protocol, and the safety limits that apply in cardiac rehabilitation and post-exertional malaise.

Frames sleep as an active, quantifiable performance reserve with dose-response effects on strength, glucose tolerance and immune function. Frames sleep as an active, quantifiable performance reserve with dose-response effects on strength, glucose tolerance and immune function. Situates the circadian system — from the SCN pacemaker to peripheral muscle oscillators — as a regulatory layer that exercise can entrain or disrupt depending on timing. Presents Saner et al.'s finding that acute sleep restriction impairs mitochondrial respiration, glucose tolerance and muscle protein synthesis. Demonstrates that a structured HIIE protocol can partially rescue these deficits, while emphasising that exercise serves as mitigation rather than a substitute for sleep, with distinct implications for athletes and clinical populations.

Frames prediabetes as an active cardiometabolic risk state rather than a benign waiting period, emphasising physical inactivity as a primary driver through reduced GLUT4 translocation, visceral adiposity and low-grade inflammation. Introduces continuous glucose monitoring as a teaching tool for illustrating postprandial dynamics, counter-regulatory hormone responses and the acute glucose-lowering effect of exercise. Explains the dual insulin- and contraction-mediated GLUT4 pathways, highlighting that the contraction-mediated route remains functional in insulin-resistant muscle and forms the molecular rationale for exercise prescription. Distinguishes obese phenotypes by visceral fat and insulin sensitivity rather than BMI alone, and presents waist circumference as a practical frontline diagnostic for cardiometabolic risk stratification.

Reframes NAFLD as MAFLD to reflect its identity as a hepatic manifestation of systemic metabolic dysfunction, and maps the disease spectrum from simple steatosis through fibrosis to cirrhosis. Explains the mechanisms by which HIIT reduces hepatic fat — enhanced fatty acid oxidation via PGC-1α, PPAR-α and AMPK, reduced de novo lipogenesis, and indirect adipose-mediated signalling — alongside anti-inflammatory Kupffer cell phenotype shifts. Presents the 4×4 HIIT protocol as the best-evidenced exercise prescription for MAFLD, with documented improvements in liver fat, ALT, insulin sensitivity and V̇O₂max, and outlines practical screening and progression considerations. Introduces protein-adequate dietary patterns as a complementary intervention supporting muscle mass and hepatic regeneration, and summarises the ESSA position statement endorsing aerobic exercise, resistance training and sedentary-time reduction as first-line lifestyle management.

Frames IBD as a chronic immune-dysregulation disease in which disrupted mucosal barrier function, Th1/Th17 dominance and microbiota cross-talk create a therapeutic opening for exercise. Presents Jones et al.'s meta-analytic evidence that structured exercise reduces disease activity scores and reliably improves fatigue, psychological wellbeing and physical function, mediated through exerkine signalling, SCFA-producing microbiome shifts, vagal tone enhancement and visceral fat reduction. Distinguishes the acute immune signatures of MICT, HIIT and resistance training, and maps appropriate exercise modality to disease state — from light walking during flares to combined HIIT and resistance training in established remission. Highlights the clinical significance of SCFA-fatigue and TNF-α-quality-of-life correlations, and introduces a 13-component pathway model underwriting multimodal exercise prescription as a disease-modifying behaviour in IBD.

Establishes the disease-state-specific prescription principle for IBD, distinguishing flare, moderate remission and established remission as three distinct clinical contexts requiring different exercise doses. Presents operational prescriptions for each state — from brief light walking at low intensity during flares, through moderate continuous cycling, to vigorous 8×30-second interval blocks in established remission — with practical notes on modality, accumulation and symptom monitoring. Outlines a worked weekly programme architecture for both stable remission and flare recovery, and defines progression rules based on duration-before-intensity sequencing and a 10% weekly volume cap. Provides a five-step decision algorithm integrating disease activity, fitness baseline, and patient readiness to guide prescription selection, progression and de-escalation.

Establishes the immunological foundations - the structure and cellular components of the innate and adaptive immune systems, the chronological immune response to viral infections, the role of dendritic cells, NK cells, and lymphocytes, and the principles of laboratory diagnostics at three levels of complexity.

Defines the anaerobic threshold as the upper border of the aerobic–anaerobic transition (MLSS), compares fixed (4 mmol/L) and individualised threshold concepts, walks through a Stegmann tangent worked example, and derives heart-rate–anchored training zones — with a critical look at why %VO₂max and %HRmax fall short as prescription anchors.

Introduces the three energy systems (ATP-PCr, glycolytic, oxidative) by time-course, ATP rate and capacity, and the concept of metabolic thresholds. Treats glucose biochemistry after Lehninger — the four fates of glucose and three fates of pyruvate, glycolysis regulation, the Pasteur and Warburg effects, GLUT4 and type 1 diabetes, fermentation and the Cori cycle, gluconeogenesis, and the pentose phosphate pathway. Covers substrate utilisation across exercise intensities and its hormonal control by catecholamines, insulin/glucagon and cortisol/growth hormone. Develops the lactate paradigm shift — production and clearance, MCT transport and the lactate shuttle, GPR81 signalling, histone lactylation, and the lactate threshold. Closes with fibre-type biochemistry, endurance vs resistance adaptations (AMPK, mTOR, PGC-1α), ROS and hormesis, recovery metabolism (EPOC, glycogen resynthesis, muscle protein synthesis), and exercise as medicine.