Figure Index

Every figure from every lecture, with its caption, in lecture order.

37 figures from 10 lectures.

Lecture 1: Basics in Exercise Physiology and Immunology - Key Concepts, Homeostasis and Hormesis

Homeostasis

Homeostasis refers to the dynamic equilibrium of the internal environment, maintained through regulatory mechanisms that counteract disturbances. Physical activity is a significant disturbance to homeostasis, triggering rapid regulatory responses.

Heart rate Ventilation

Example for acute disturbance of the homeostasis by acute physical stress. Heart rate and ventilation increase during exercise and return after the end of the exercise. Light blue lines: Physical rest before exercise, red lines: Incremental graded maximal cycle ergometer exercise, dark blue lines: physical rest after the end of exercise.

Homeostasis time-course

Homeostasis time-course: the IL-6 peak, delayed IL-10/IL-1Ra counter-response, functional capacity dip, and the set-point reference line, with annotated phase zones.

Hormesis dose-response

Hormesis dose-response: the full J-curve (URTI risk), bell-shaped adaptive benefit, and monotonically rising inflammatory load, with the three dose zones (sub-threshold / hormetic / overload) shaded.

Lecture 2: Exercise and Immune System, Limits of Performance, Energy Balance

Limits of physical performance capacity — Power and running speed Limits of physical performance capacity — Age and mortality

Limits of performance with age: relating MET, V̇O₂max, physical-activity behaviour and mortality/morbidity [%] across the lifespan — from physical inactivity (1 MET, 3.5 mL·min⁻¹·kg⁻¹) to very fast running (~26 METs, ~90 mL·min⁻¹·kg⁻¹) — demonstrates age-dependent changes in maximal performance capacity.

ATP flow rate cycling

Adenosine-triphosphate (ATP) flow rates versus time. P — cycling performance on a bicycle ergometer; RPE — ratings of perceived exertion (Borg scale 6–20).

Energy time oxygen

Time course of energy generation.

Performance lactate 4h Performance energy lactate 4h Performance energy heart rate 4h Performance energy 4h Performance cortisol 4h Performance cortisol 4h amount Performance adrenaline 4h Performance adrenaline 4h amount Performance 100s lactate adrenaline cortisol

Cycle-ergometer exercise of different intensities and durations, showing performance, lactate generation and hormone secretion built up step by step. Male subjects with a V̇O₂max of 60–65 mL·min⁻¹·kg⁻¹.

Exercise strain lactate CHO FAT AA Exercise strain lactate HPA SNS CHO Fat AA

Overview of hormonal regulation and energy supply at different loads and load durations. RPE — rating of perceived exertion (Borg scale value).

Lecture 3: Energy Expenditure, MET-concept, Thresholds, Determine Exercise Intensity

Predicted basal metabolic rate as a function of body mass

The FAO/WHO/UNU equations plotted for the two adult age bands. BMR rises linearly with body mass, and the sex difference is larger than the age difference across the whole range. Worked example: a 30-year-old man of 75 kg is predicted at 7.62 MJ·day⁻¹ ≈ 1821 kcal·day⁻¹ (FAO/WHO/UNU 2004).

MET zones for physical activity and the effect of an individual RMR correction

Left: physical activity classification by MET range, after the Compendium of Physical Activities (Ainsworth et al. 2011), with the corresponding ACSM V̇O₂ cut-points on the upper axis. Right: the same activities recalculated for an individual whose resting metabolic rate is 2.8 instead of the conventional 3.5 mL·kg⁻¹·min⁻¹ — every tabulated MET value rises by 25 %.

Blood lactate and ventilatory equivalents against work rate, with T1 and T2 marked

The same two thresholds read from two different signals on one work-rate axis. Top: blood lactate first rises above baseline at T1 and reaches the maximal lactate steady state at T2. Bottom: V̇E/V̇O₂ turns upward at the first ventilatory (gas-exchange) threshold and V̇E/V̇CO₂ follows at the respiratory compensation point. The shaded band between them is the transition zone in which metabolism is neither purely aerobic nor sustainably anaerobic (Faude et al. 2009; Meyer et al. 2005).

Lecture 4: Basics of Biochemistry Principles of Exercise

ATP resynthesis rate of the three energy systems against effort duration

The three energy systems compared by the two properties that matter in practice: how fast they resynthesise ATP, and how long they can keep it up. ATP–PCr delivers the highest rate but is spent within 5–10 s, glycolysis peaks over 30–90 s, and oxidative phosphorylation sustains a moderate rate for effectively unlimited duration. Note the logarithmic time axis.

Cellular respiration

After uptake into the cell, glucose is phosphorylated and passes through glycolysis down to pyruvate. Under anaerobic conditions, pyruvate is converted to lactate to regenerate the NAD⁺ required for glycolysis, and lactate is typically released by the cells (2 mol ATP per mol glucose). Under aerobic conditions, pyruvate enters the mitochondria and is converted to acetyl-CoA by oxidative decarboxylation, feeding the citrate cycle; it is broken down to CO₂ and the reduction equivalents NADH/H⁺ and FADH₂, whose oxygen-dependent reoxidation yields water and is coupled to ATP synthesis from ADP and Pᵢ, giving ≈ 30 mol ATP per mol glucose.

ATP yield per mole of substrate and the resulting Pasteur effect

Left: ATP yield per mole of substrate on a logarithmic scale — 2 for anaerobic glycolysis, ~31 for the complete aerobic oxidation of glucose, and 106 for palmitate. Right: the direct consequence, the Pasteur effect. Because the anaerobic yield is roughly 15-fold lower, about 15× as much glucose must be consumed anaerobically to liberate the same amount of ATP (Nelson & Cox 2013).

Relative contribution of fat and carbohydrate to energy supply across exercise intensity

The crossover from fat to carbohydrate as exercise intensity rises. At low intensity the CHO:fat ratio is about 30:70, near 50:50 at moderate intensity, and 85:15 at high intensity. FAT_max — the intensity at which absolute fat oxidation peaks — lies at roughly 45–65 % V̇O₂max, well below the intensity at which carbohydrate begins to dominate the mixture.

Lecture 5: Teaching Anaerobic Threshold

Aerobic-anaerobic transition during incremental exercise

Schematic representation of the aerobic–anaerobic transition (grey zone). Top: blood-lactate curve with aerobic threshold (AeS) and individual anaerobic threshold (IAS ≙ MLSS). Bottom: pulmonary ventilation with the two ventilatory thresholds VT1 and VT2 (RCP). Redrawn after Kindermann (2004).

Determination of the IAT after Stegmann et al. (1981)

Lactate–velocity curve during incremental exercise (red) and lactate–time curve during recovery (blue). The dashed grey line marks L_end. The descending recovery curve crosses L_end at ≈ 2.7 min post-exercise (linear interpolation between R1 = 10.0 mmol/L at 1 min and R2 = 8.8 mmol/L at 3 min → L = 9.0 at t ≈ 2.7 min): this is the anchor. The dashed green line is the tangent from the anchor to the ascending exercise curve; the tangent contact on the exercise curve is the IAT. Vertical and horizontal projections give v_IAT and L_IAT respectively.

Training zones as % of IAS

Typical blood-lactate ranges encountered during the four endurance-training zones, expressed as a percentage of the individual anaerobic threshold (IAS). Redrawn after Kindermann (2004).

Lecture 6: Lactate – From Metabolic Waste Product to Central Metabolite

Lactate turnover flux relative to glucose, fed versus fasted

Both bars sit above the line at which the two fluxes would be equal — lactate, not glucose, is the primary circulating carbohydrate fuel. Feeding brings the two close together; fasting pulls them apart, and lactate then turns over two and a half times as fast as glucose. After Hui et al., Nature 551: 115–118 (2017).

Blood lactate and glucose after a 75 g oral glucose load

The enteric rise from intestinal metabolism of the ingested carbohydrate appears while blood glucose is still at its fasting value; the larger systemic rise follows, synchronous with the glucose peak, and accounts for roughly 38 % of the 75 g load. Glycolysis is not the emergency route — it is the ordinary one. Schematic after Leija et al. (2024); the ordering and timing of the two rises are the finding.

Lecture 7: Cardiorespiratory Fitness measured in metabolic equivalent task

CRF and Mortality Risk — JAMA 2009

Cardiorespiratory fitness and mortality risk. Each 1-MET increment in exercise capacity is associated with a 14–15 % reduction in all-cause mortality, plotted here relative to the 7.9-MET reference. Shaded band = 95 % CI. Meta-analysis of 33 studies (n = 102,980; Kodama et al. 2009).

All-cause mortality by fitness category — Cleveland Clinic and Veterans Affairs cohorts

All-cause mortality hazard ratios by fitness category on a common logarithmic axis. Left: Cleveland Clinic cohort (n = 122,007); the above-average vs. below-average hazard ratio of 1.41 equates to the excess mortality risk of smoking or diabetes, and the Low-to-Elite gradient exceeds 5-fold (Mandsager et al. 2018). Right: US Veterans Affairs cohort (n = 750,302; mean follow-up 10.2 years) with a ≈4-fold Very-Low to Very-High gradient and no ceiling risk at the top; error bars = 95 % CI (Kokkinos et al. 2022).

Meta-Analysis 2024: METs versus direct VO₂ max — participants, imbalance and effect size

Data imbalance between METs-based CRF and direct VO₂ max evidence. a: >99 % of outcome-linked participants contributed MET data; <1 % contributed direct VO₂ max data. b: The same imbalance as a relative participant count — 234-fold more participants in the MET arm. c: Point estimates for cardiovascular mortality reduction are remarkably similar (≈14 %), confirming construct validity — but the evidence base rests almost entirely on METs (Swain and Franklin 2024).

Lecture 8: Exercise Snacks

Evidence-based effects of Exercise Snacks

Summary of evidence-based effects on energy metabolism, muscular adaptations, aerobic capacity and immunological signalling pathways of Exercise Snacks (created in BioRender; Puta C, 2025).

Postprandial blood glucose with and without pre-meal exercise snacks

Left: blood glucose after a meal preceded by six one-minute exercise snacks versus a no-exercise control; the shaded area is the difference in glycaemic excursion. Right: the two summary effects — a ~1.4 mmol·L⁻¹ lower 3-hour postprandial peak after breakfast and a ~0.7 mmol·L⁻¹ lower 24-hour mean glucose, in insulin-resistant adults (Carter & Solomon 2020).

Mortality risk reduction with VILPA by dose pattern and outcome

Reduction in mortality risk associated with vigorous intermittent lifestyle physical activity, by outcome. Three separate bouts of 1–2 min per day are associated with larger reductions than a single daily bout of 4.4 min, and the effect is largest for cardiovascular mortality. UK Biobank, n = 25,241 non-exercisers, mean age 61.8 y (Stamatakis et al. 2022).

Exercise Snack protocols and anti-inflammatory efficacy

Exercise Snack protocols and anti-inflammatory efficacy (data: literature analysis). HIIT: high-intensity interval training.

Energy metabolism signalling

Exercise Snacks — energy-metabolism signalling. Both the GLUT4 and LPL axes operate insulin-independently via AMPK, converging on reduced insulin resistance and lower cardiovascular risk.

Muscle structure and function signalling

Exercise Snacks — muscle signalling: three staggered phases from acute AMPK/PGC-1α through mTORC1-driven protein synthesis to satellite-cell hypertrophy.

Aerobic capacity signalling

Exercise Snacks — aerobic-capacity signalling: central (CO) and peripheral (a-vO₂ diff) adaptations framed by the Fick equation, with snacks disproportionately targeting the peripheral side.

Immunological signalling pathways

Exercise Snacks — immunological signalling: three parallel axes (myokines, transcriptional reprogramming, microbiome metabolites) converging on NF-κB suppression.

Timescales of the four adaptation domains after a short exercise bout

The four domains on a shared logarithmic time axis, from the stimulus to the adaptation. Energy metabolism responds within minutes to hours, immune signalling over hours to weeks, muscle structure over hours to months, and aerobic capacity only after weeks — which is why a single snack is measurable in glucose but not in V̇O₂max. Central mediators are named below each bar.

Lecture 9: Protein Intake in Sport - How Much Is Appropriate?

Daily protein intake ranges by population and athletic discipline

Recommended daily protein intake by population and exercise type, against the general-population RDA of 0.8 g·kg⁻¹·d⁻¹ and the evidence-based ceiling of 1.6 g·kg⁻¹·d⁻¹. The shaded region above 1.5 g·kg⁻¹·d⁻¹ marks the range in which leucine-driven mTORC1 activation in macrophages has been described. Puta C (2025), based on Egan (2016); Delany et al. (2025); Jäger et al. (2017).

Training vs Protein Effects

What is the principal driver for building muscle mass and strength? The training stimulus, not protein intake per se. Without a training stimulus, extra protein moves lean mass and maximal strength barely at all; with it, the increment from extra protein is real but small next to the increment from training. Puta C (2025), based on Egan (2016); Delany et al. (2025); Jäger et al. (2017).

Muscle protein synthesis and macrophage mTORC1 signalling against protein per meal

Two dose–response curves on one axis. Muscle protein synthesis saturates at roughly 25–30 g of protein per meal — beyond the plateau, further protein in the same meal adds no measurable anabolic response. Leucine-driven mTORC1 signalling in macrophages rises steeply across the same dose range, so the point at which extra protein stops helping muscle is also the point at which it begins to act elsewhere (Zhang et al. 2024).

Lecture 10: Infection-Associated Chronic Illness and Wearable Data

Wearable data analysis of the match cohort

From Ledebur et al. (2025): https://www.nature.com/articles/s41746-025-01456-x/figures/3. Wearable data analysis of the match cohort. Z-transformed mean RHR (average of all 15-min RHR measurements within the last seven days) relative to the seasonal mean RHR with respect to the mean and standard deviation up to 7 days prior to the date of the reported test of all individuals in the M-COVID-19[+]PS (pink), M-COVID-19[+]NS (blue) and M-COVID-19[−] (black) cohorts. The difference between the maximum and minimum z-transformed RHR within 14 to and 20 days after the date of the reported SARS-CoV-2 test was more pronounced (1.3 vs 1.0) and more prolonged for M-COVID-19[+]PS than for M-COVID-19[+]NS. Shading indicates standard errors. The inset shows the average RHR relative to the SARS-CoV-2 test date. Already prior to the SARS-CoV-2 test, M-COVID-19[+]PS-individuals showed an increased RHR compared to M-COVID-19[+]NS and M-COVID-19[−].