Aerobic training · understand the whole system
What happens in your body with aerobic training?
You become better at delivering oxygen, using it and sustaining work. The change emerges from the interaction between blood, heart, vessels and muscles, at different speeds and with different responses from person to person.
01 / From air to muscle work
Fitness is a chain of functions.
Muscle uses ATP when producing force. ATP stores are limited, so the molecule must continually be regenerated. During sustained exercise, carbohydrate and fat oxidation provide much of the energy. This requires both oxygen delivery to muscle and the cellular capacity to process fuel.
Aerobic means that oxygen participates in energy metabolism. Other energy systems remain active. During an acceleration, phosphocreatine and glycolysis contribute rapidly while oxidative metabolism increases its contribution. Very hard intervals can therefore stimulate aerobic adaptation.
Figure 01 / The oxygen journey
Air → lungs → blood → heart → muscle → mitochondria → ATP
Select a stage to highlight it. This is a functional sequence; anatomical structures are not drawn to scale.
Explore the mechanism
Air · oxygen starts outside the body
Inspired air contains about 21% oxygen at sea level. Differences in partial pressure drive subsequent diffusion. Becoming fitter does not change the oxygen fraction in air.
Acute response
During a session, heart rate, ventilation and energy turnover increase. Blood is redistributed, and existing transport proteins are activated or relocated. These are immediate responses to the current task.
02 / Central adaptations
Delivery: lungs, blood and heart.
“Central” is a practical grouping of oxygen supply and transport. It is not a strict biological boundary: the heart depends on venous return, and flow also depends on vessels within muscle.
Figure 02 / The pump equation
Heart rate × stroke volume = cardiac output
beats/min
mL/beat
L/min · after ÷ 1,000
Flow indicator · scale 0–33 L/min.
Respiration · air in, CO₂ out
What is it? Ventilation moves air to and from the alveoli. Oxygen diffuses into the blood here, while carbon dioxide travels in the opposite direction. Ventilation, oxygen uptake and lung size are different measurements.
Why does it change? Exercise immediately increases the need for gas exchange. After training, the same workload can produce less metabolic and ventilatory disturbance without requiring larger lungs.
How does it change? Respiratory muscles and the control of breathing can adapt. However, aerobic training does not generally produce a large increase in resting lung volumes in healthy adults.
Why it matters. Feeling less breathless at the same pace can reflect a lower relative demand on the whole system. It does not prove that the lungs have grown.
Heart · a pump that remodels
What is it? The heart consists of two pumps in series. The right side sends blood to the lungs; the left sends oxygenated blood around the body. Filling and contraction determine how much blood each beat ejects.
Why does it change? Repeated endurance exercise exposes the heart to recurring changes in blood return, pressure and pumping work.
How does it change? Over months, chamber size, muscle mass and filling properties can change. Remodelling develops gradually and depends on the training dose. Right and left ventricles do not necessarily follow the same timetable.
Why it matters. Early improvements do not require visible anatomical growth. Blood volume and filling can improve before clear structural changes are detectable.
Stroke volume · more blood per beat
What is it? Stroke volume is the amount of blood a ventricle ejects with each beat, usually expressed in mL/beat. It is the difference between ventricular volume before and after contraction.
Why does it change? Delivering more blood to working muscles requires greater flow. Ejecting more blood with each beat is one way to provide it.
How does it change? An expanded blood volume can increase venous return and cardiac filling. Within the physiological range, the Frank–Starling mechanism links greater filling to greater ejection. Longer-term cardiac remodelling can also contribute.
Why it matters. A lower heart rate at the same workload can coexist with unchanged blood flow because each beat moves more blood. Greater stroke volume does not necessarily mean a higher ejection fraction.
Cardiac output · flow per minute
What is it? Cardiac output, Q̇, is blood flow from the heart in L/min: heart rate multiplied by stroke volume. It is a flow rate, not the total quantity of blood in the body.
Why does it change? At maximal exercise, greater pumping capacity can increase oxygen delivery per minute. At the same submaximal workload, the requirement may remain approximately unchanged.
How does it change? A greater stroke volume can raise Q̇max without a higher maximal heart rate. At a fixed workload, a larger stroke volume and lower heart rate can offset each other. If tissues extract more oxygen, the required flow can even be lower.
Why it matters. Always ask whether flow was measured at rest, at the same watts, at the same percentage of capacity, or at maximum. A correct number can become a misleading explanation when its measurement condition is omitted.
Heart rate · fewer beats may be enough
What is it? Heart rate is the number of beats per minute. The sinus node generates the rhythm, while autonomic regulation adjusts it to current demands.
Why does it change? At a fixed workload, greater stroke volume and a smaller relative physiological disturbance can reduce the required heart rate. Resting heart rate may also fall.
How does it change? Autonomic changes and adaptations in intrinsic pacemaker activity can contribute. D’Souza et al. identified HCN4-channel changes in trained rodents: useful mechanistic animal evidence, but not a complete explanation for human heart rate. Maximal heart rate typically does not increase as fitness improves. [24]
Why it matters. Compare similar temperature, hydration, medication, sleep and measurement conditions. A single lower reading does not establish a lasting training adaptation.
Blood volume · more circulating blood
What is it? Blood volume comprises plasma and blood cells. Plasma is the fluid component; red blood cells contain the haemoglobin carrying most of the oxygen.
Why does it change? Repeated exercise challenges circulatory filling and heat dissipation. Fluid and protein regulation can expand plasma volume; producing additional red blood cells takes longer.
How does it change? Plasma volume can change early, whereas a lasting increase in red-cell volume requires erythropoiesis. The different components therefore do not share one adaptation deadline.
Why it matters. More circulating volume can support stroke volume and temperature regulation. It does not imply a proportional increase in blood pressure.
Haemoglobin · concentration is not mass
What is it? Haemoglobin is the oxygen-binding protein in red blood cells. Haemoglobin concentration describes the amount per volume of blood; total haemoglobin mass describes the amount across the body.
Why does it change? If training increases red-cell volume over time, the total oxygen-carrying capacity can grow. This also depends on sufficient materials for blood-cell production.
How does it change? Rapid plasma expansion can dilute the blood: concentration can fall even when total haemoglobin mass is unchanged or greater. Arterial oxygen content depends especially on haemoglobin concentration and oxygen saturation, not on total mass alone.
Why it matters. A routine haemoglobin concentration cannot by itself show whether training has improved oxygen transport. An automatic “haemoglobin concentration ↑” arrow is misleading.
Blood pressure · flow and resistance
What is it? Blood pressure is the pressure inside arteries. In a simplified model, mean pressure depends on cardiac output multiplied by total peripheral resistance. Systolic and diastolic pressure describe different phases of the heartbeat.
Why does it change? During dynamic exercise, systolic pressure typically rises to support increased flow. With regular training, resting and 24-hour blood pressure can fall, especially when initially elevated.
How does it change? Changes in vascular function, autonomic regulation and hormonal control can reduce resistance. Greater blood volume and lower resting blood pressure can therefore coexist.
Why it matters. Cardiovascular health and aerobic fitness are related but distinct outcomes. Lower resting pressure does not require a reduction in maximal pumping capacity.
VO₂max · the ceiling of the whole system
What is it? VO₂max is the highest rate at which the body can take up and use oxygen during maximal exercise. L/min expresses absolute uptake; mL/kg/min relates it to body mass.
Why does it change? The ceiling can rise when oxygen delivery and/or the ability to extract oxygen improves. The Fick equation connects these contributions.
How does it change? Gas exchange is measured during an exercise test with increasing work. VO₂peak is the highest observed value; claiming VO₂max requires stronger evidence that maximal capacity was reached. Exercise mode and testing protocol affect the result.
Why it matters. A faster 5 km also depends on running economy and the fraction of VO₂max that can be sustained. Relative VO₂max can increase through weight loss even if absolute oxygen uptake is unchanged.
03 / Connecting delivery and use
The Fick equation connects the system.
Oxygen uptake equals blood flow multiplied by the amount of oxygen removed from each litre of blood. Total oxygen use can increase through greater flow, greater extraction, or both. These physiological processes are connected.
Figure 03 / Fick equation
VO₂ = cardiac output × a-vO₂ difference
L blood/min
mL O₂/L blood
L O₂/min
The model holds arterial oxygen content at 200 mL O₂/L blood. Extraction is 60 %; venous content is 80 mL O₂/L blood.
04 / Peripheral adaptations
Use: inside the muscle fibre.
Delivered oxygen must reach the cell, be released and be used. Glucose and fatty acids also need transport and metabolism. Muscle adapts its supply network, transport proteins and metabolic machinery.
Figure 04 / Muscle cross-section
One cross-section. Four different functions.
Capillaries · around the muscle fibre
Vessels surround the fibre. More capillary contacts can improve exchange area and distribution. “After” illustrates a principle, not a counted biopsy.
The pale circles are myofibrils: the contractile apparatus. Amber dots represent myoglobin, blue gates represent GLUT4, and rust-coloured ovals represent mitochondria.
Structures are greatly enlarged and simplified. Counts or percentage changes cannot be inferred from this drawing. [9] [10] [12] [22]
Mitochondria · greater oxidative capacity
What is it? Mitochondria are dynamic structures within muscle cells. They couple fuel oxidation to ATP production, supporting contraction and ion pumping. Oxygen is the final electron acceptor in the respiratory chain.
Why does it change? Repeated periods of high ATP turnover alter energy status and calcium signalling. The cell responds by regulating gene activity and protein turnover.
How does it change? Signalling networks involving PGC-1α support mitochondrial biogenesis and remodelling. Volume, protein content and function are more informative than simply counting “power stations”.
Why it matters. A given ATP demand can be supported by more oxidative machinery. Mitochondrial content, measured respiratory capacity and whole-body VO₂max remain different outcomes.
Oxidative enzymes · capacity for reactions
What is it? Enzymes are proteins that catalyse chemical reactions. Citrate synthase is often used as a marker of mitochondrial content; β-HAD reflects part of fatty-acid oxidation.
Why does it change? Repeated aerobic ATP demand can increase synthesis of relevant enzymes alongside other mitochondrial components.
How does it change? Laboratories often measure maximal enzyme activity in a biopsy under standardised conditions. This estimates capacity, not the actual reaction rate inside a running person.
Why it matters. The muscle has more capacity to process fuel aerobically. Glycolytic enzymes do not follow one universal “unchanged” rule either; their response depends on the protocol. [13]
Capillaries · more exchange surfaces
What is it? Capillaries are the smallest blood vessels. They provide the interface for oxygen and nutrient exchange between blood and tissue. Capillarisation describes development of this network.
Why does it change? Repeated contractions alter flow, mechanical forces and local signals, including VEGF. These can stimulate vascular growth around active fibres.
How does it change? Additional capillary contacts can expand exchange area and improve oxygen access. Capillaries per fibre, capillaries per mm² and fibre size are different measurements.
Why it matters. Oxygen delivery also depends on distribution close to cells. A shorter average diffusion path is a possible functional advantage, not something that can be calculated from a capillary-density arrow alone. [25]
Myoglobin · oxygen inside the fibre
What is it? Myoglobin is an oxygen-binding protein inside muscle cells. It can buffer local oxygen availability and facilitate oxygen movement towards mitochondria, especially at low oxygen pressure.
Why does it change? Its function makes adaptation biologically plausible. Plausibility does not establish that concentration always increases in trained humans.
How does it change? A muscle can develop greater oxidative capacity without every component of oxygen transport increasing in parallel.
Why it matters. Myoglobin appears in the muscle illustration because it matters to the system. Its amount does not automatically increase in the “after training” view.
GLUT4 · moving glucose into muscle
What is it? GLUT4 is a transport protein that moves glucose across the muscle-cell membrane. It may be stored in intracellular vesicles or positioned at the membrane.
Why does it change? Active muscle needs fuel. Contraction can move existing GLUT4 towards the membrane through signalling pathways that do not require the same insulin activation as resting uptake.
How does it change? Acute translocation moves existing protein. Training can also increase the total amount of protein. A larger cellular pool does not mean every transporter is permanently positioned at the surface.
Why it matters. Greater transport capacity can support glucose uptake during work and replenishment afterwards. GLUT4 alone is not a measure of whole-body insulin sensitivity.
Glycogen · storage and use are different
What is it? Glycogen consists of branched glucose chains. Muscle glycogen is a local fuel store supporting both rapid and oxidative ATP production.
Why does it change? Repeated depletion and replenishment can alter storage capacity. Changes in fat and carbohydrate oxidation can also alter how quickly the store is used at a particular workload.
How does it change? Store size depends on carbohydrate intake and time since the previous session. A biopsy immediately after exercise answers a different question from one taken after several days of recovery.
Why it matters. A store can last longer because it is larger, because the task consumes it more slowly, or both. High-intensity work still requires substantial carbohydrate turnover.
Muscle fibres · function before labels
What is it? Types I, IIa and IIx primarily describe contractile protein profiles. Type I fibres are generally slower and more fatigue-resistant. Type II fibres can produce faster force and also adapt metabolically.
Why does it change? Recruitment and repeated loading change the proteins that fibres maintain. Fibre type and oxidative capacity are related but distinct characteristics.
How does it change? A type IIa fibre can increase its mitochondrial content without becoming type I. Shifts away from IIx or hybrid profiles can occur, but an automatic IIx → IIa → I sequence is too categorical.
Why it matters. A key functional benefit is more sustained ATP supply in recruited fibres. Becoming more enduring does not require every fibre to change type.
Blood flow · delivery where it is needed
What is it? Muscle blood flow depends on pressure differences and vascular resistance. It is not automatically a fixed proportion of cardiac output.
Why does it change? Exercise repeatedly exposes vessel walls to the frictional force of flowing blood, called shear stress, and exposes muscles to local metabolic signals.
How does it change? The endothelium can change its ability to regulate dilation, and vessels can remodel. Meanwhile, circulation must maintain blood pressure and supply the brain, skin and other organs.
Why it matters. Maximal delivery capacity and distribution can improve. At the same submaximal workload, more flow is not necessarily required if oxygen extraction improves.
a-vO₂ difference · oxygen removed from blood
What is it? The arterial–venous oxygen difference is arterial minus mixed-venous oxygen content, expressed, for example, in mL O₂ per litre of blood. It concerns content, not the difference in oxygen pressure.
Why does it change? With better exchange and oxidative capacity, active muscles may extract more oxygen from each litre of blood under some conditions.
How does it change? Capillary supply, local flow distribution, haemoglobin unloading and mitochondrial metabolism work together. Mixed-venous blood combines contributions from many tissues; it does not isolate one muscle’s mitochondria.
Why it matters. A larger maximal oxygen difference can increase VO₂max, but it is not observed in every training study. The Fick equation describes a relationship; by itself it does not prove the mechanism.
Fat oxidation · more energy from fatty acids
What is it? Fat oxidation breaks down fatty acids to support oxidative ATP production. Transport into muscle, mitochondrial access and enzyme capacity all contribute.
Why does it change? Repeated sustained exercise can increase the capacity to obtain energy from fat at a fixed moderate workload, potentially reducing glycogen use.
How does it change? Training can increase fatty-acid transport and oxidative capacity. Actual fuel selection still depends on intensity, diet, fuel stores and training status.
Why it matters. Greater fat oxidation during a test does not demonstrate greater body-fat loss. Nor does it make fat the preferred fuel at maximal intensity.
Lactate · a circulating fuel
What is it? Lactate is formed from pyruvate, helping regenerate NAD⁺ so glycolysis can continue. It is produced even when oxygen is available and can be transported to other tissues and oxidised.
Why does it change? Adaptations in oxidative ATP supply and transport can change the balance between lactate appearance and removal.
How does it change? Blood lactate concentration is a net result. A lower concentration can reflect lower appearance, greater clearance, or both. Concentration is not a direct measure of production.
Why it matters. A higher workload can often be sustained before lactate accumulates substantially. This does not make lactate waste, mean the body is “acid-free”, or imply that maximal lactate must decrease.
Insulin sensitivity · more response to a signal
What is it? Insulin sensitivity describes how strongly tissue responds to a given insulin exposure. In muscle, this includes glucose uptake and storage.
Why does it change? Replenishing fuel stores is important after exercise. Repeated activity can also change transport capacity, vascular function and glucose metabolism.
How does it change? A single session can improve insulin action in the exercised muscles; repeated training adds structural and protein adaptations. Measurements therefore need to specify time since the last session. [23]
Why it matters. Improved glucose regulation is a benefit in its own right. It need not be proportional to the change in VO₂max or to weight loss.
05 / The comparison that matters
The same pace. A different relative demand.
Submaximal exercise is below maximal capacity. After training, a fixed speed or power output can represent a smaller percentage of VO₂max and cause less metabolic disturbance. Heart rate, ventilation and perceived exertion may therefore be lower.
Maximal exercise tests the capacity ceiling. After training, the body may perform more work at maximal effort. “Lower heart rate” and “greater oxygen uptake” can therefore describe different comparisons: the same submaximal task and a new maximal test.
Figure 05 / Before vs after training
Choose the comparison before interpreting the number.
Illustrative calculations. Values were selected to explain Fick and the pump equation. They are not study data, predicted individual changes or training targets.
Before training
L O₂/min
Q̇:
L/min
a-vO₂:
mL O₂/L blood
After training
L O₂/min
Q̇:
L/min
a-vO₂:
mL O₂/L blood
Why can it feel easier?
Greater reserve, more oxidative capacity and altered fuel and lactate metabolism can make sustained work easier. If movement economy also improves, oxygen demand at the same pace can fall. That is a separate adaptation and does not automatically follow from a higher VO₂max. [4] [17]
What should stay comparable?
Compare the same route or watts under similar temperature, equipment, duration and recovery conditions. “60% of VO₂max” before and after describes different absolute workloads if VO₂max has changed. A trained person can therefore have the same heart rate at a new, faster pace.
06 / Intensity, time and the measured outcome
HIIT and continuous training have overlapping adaptations.
Intervals
Work interspersed with recovery can accumulate time at high oxygen uptake and recruit more fibres under heavy demand. Long aerobic intervals, brief intense intervals and all-out sprints are different stimuli. HIIT is not one standardised treatment.
Continuous exercise
A continuous session can accumulate more exercise time at a lower demand per minute. It also stimulates mitochondria, capillaries and metabolism. Outcomes depend on completed dose, progression and initial training status.
Figure 06 / One study, two outcomes
Which adaptation do you call “best”?
Daussin et al.: 11 sedentary adults, six men and five women, completed eight weeks of each training method in a randomised crossover design, separated by 12 weeks of detraining. Work and training time were matched. [26]
% change in VO₂max
VO₂max increased by 9% after continuous training and 15% after interval training.
The outcome determines the question.
VO₂max, capillary density, glucose regulation and sustainable pace are different outcomes. A protocol can produce a larger change in one and a smaller change in another. Small, short studies cannot rank all training methods for everyone.
Longer aerobic intervals, moderate exercise and very brief intense sessions all produced documented adaptations in these studies. Compare total time, recoveries and feasibility as well as the number of hard minutes. [4] [13] [18] [26]
07 / Different biological timelines
How quickly do adaptations develop?
This timeline shows when changes were observed in selected studies. It does not identify an exact onset or guarantee a waiting time. Training status, dose and measurement method affect the timetable.
Hours
GLUT4 can move during exercise, and muscle insulin responsiveness can improve afterwards. In a study of seven young men, exercise of one leg increased insulin-stimulated glucose clearance in that leg three hours later. This is an acute response. [22] [23]
A few sessions → weeks
Molecular signals recur. Some oxidative enzymes and protein markers can change within the first few sessions. Measurable plasma expansion was present at two weeks in Montero et al.’s time-course study. [6] [8]
4–8 weeks
Studies document capillary growth and greater red-cell volume within this period. Stroke volume and fitness can improve before fully developed anatomical cardiac remodelling. [3] [6] [11]
Months
Continued progression can further change cardiac dimensions and function. In the one-year study, left-ventricular volume first increased significantly after six months. [2]
What happens with detraining?
When the stimulus is reduced or removed, some adaptations decline. Circulatory filling and stroke volume can change early, while enzymes and structures follow other time courses. A break does not necessarily erase everything at once.
Coyle et al. followed seven endurance-trained people after complete training cessation. VO₂max declined by 7% in the first 21 days and was about 16% lower after 56 days. Stroke volume fell early; a lower a-vO₂ difference contributed later. Capillarisation remained elevated through 84 days. [19]
A small, older study of complete cessation in trained people. These figures are not predictions for an active holiday, reduced training or bed rest, which impose different stimuli.
Why do responses vary?
The same programme does not impose the same internal demand. Initial capacity, completed dose, biological differences, nutrition, recovery, illness and measurement uncertainty all contribute. A VO₂max change is not a complete measure of someone’s response.
HERITAGE examined 481 previously sedentary adults from 98 families during 20 weeks of standardised cycling. Mean VO₂max increased by about 0.4 L/min, with wide variation and greater similarity within families. The maximal heritability estimate was 47%. Shared environment also contributes to family resemblance. This estimate does not mean that 47% of your improvement is predetermined; the original analysis also involved a restricted ancestry group. [20]
Why aerobic fitness improves
More capacity for the same task.
Training can increase the oxygen delivered by blood and heart and improve how muscles distribute and use it. Fuel metabolism and regulation adapt too. You can therefore sustain a given workload for longer or perform more work at high effort. No single upward arrow explains the whole change.
08 / Clear definitions
A glossary of the system.
- Stroke volume
- Blood ejected per heartbeat, usually mL/beat. Depends on filling, contraction and the resistance to ejection.
- Cardiac output
- Blood flow from the heart per minute: heart rate × stroke volume, usually L/min.
- VO₂max
- The maximal rate of oxygen uptake and use during demanding exercise, not the amount of air the lungs can hold.
- a-vO₂ difference
- Arterial minus mixed-venous oxygen content: the average amount of oxygen removed from each litre of blood.
- Mitochondria
- Dynamic cellular structures involved in oxidative ATP production. Their content and function are assessed in different ways.
- Capillarisation
- Development of the capillary network around tissue. Capillaries per fibre and capillaries per mm² are different measurements.
- Myoglobin
- An oxygen-binding protein inside muscle fibres. It differs from haemoglobin, which is found in red blood cells.
- GLUT4
- A protein that transports glucose across the cell membrane. Both its location and total amount matter.
- Lactate
- A product of pyruvate metabolism that can be transported and used as fuel. Blood concentration reflects appearance relative to removal.
- Insulin sensitivity
- The tissue response to a given insulin exposure, such as increased glucose uptake.
- ATP
- Adenosine triphosphate: a molecule coupling energy metabolism to work, including muscle contraction. It is continually regenerated.
- Absolute versus relative workload
- The same watts or pace is an absolute comparison. The same percentage of VO₂max is a relative comparison and may involve more work after training.
09 / Research and limitations
Read the sources behind the explanation.
This is a research-based narrative explanation using selected primary studies, not an exhaustive systematic review. Classic experiments are included because they measured blood flow, sampled muscle or directly manipulated a mechanism. Several are small and predominantly involve young men. Results from one muscle, population or protocol are not universal reference values.
Improvement in a before-and-after study without an inactive control provides weaker causal evidence than a randomised comparison. Enzyme activity, mitochondrial content, biopsy respiration and whole-body VO₂ are different endpoints. Where only an abstract was accessible, protocol details and results are limited to what could be verified there.
These are original educational illustrations. Only Figure 06 displays results from a training experiment. Figures 02, 03 and 05 show calculated examples; the others are qualitative. General adaptation arrows have been re-examined against the sources, particularly for myoglobin, haemoglobin, blood flow and fibre types.
- Miyachi & Katayama · 1999 ↗ Respiration during 12 weeks of interval training
- Arbab-Zadeh et al. · 2014 ↗ Cardiac remodelling over one year of training
- Bonne et al. · 2014 ↗ Blood volume and maximal cardiac output
- Helgerud et al. · 2007 ↗ Four training protocols over eight weeks
- Montero et al. · 2015 ↗ Blood, muscle and VO₂peak after six weeks
- Montero et al. · 2017 ↗ Plasma and red blood cells over eight weeks
- Lopes et al. · 2021, EnRicH ↗ Randomised trial in resistant hypertension
- Perry et al. · 2010 ↗ Repeated molecular signals and mitochondrial proteins
- Little et al. · 2010 ↗ Six interval sessions: mitochondria, GLUT4 and glycogen
- Andersen & Henriksson · 1977 ↗ Capillary adaptation in human thigh muscle
- Jensen, Bangsbo & Hellsten · 2004 ↗ Capillary growth after local interval training
- Svedenhag et al. · 1983 ↗ Oxidative enzymes increased; myoglobin did not
- Scribbans et al. · 2014 ↗ Fibre-specific adaptation to two training methods
- Tinken et al. · 2010 ↗ An experimental test of vascular shear stress
- Spina et al. · 1993 ↗ Central and peripheral contributions in older adults
- Talanian et al. · 2007 ↗ Fat oxidation after two weeks of intervals
- Bergman et al. · 1999 ↗ Lactate production, transport and clearance
- Houmard et al. · 2004 ↗ STRRIDE: exercise dose and insulin sensitivity
- Coyle et al. · 1984 ↗ Detraining over 84 days
- Bouchard et al. · 1999 ↗ HERITAGE: variation between people and families
- Montero & Lundby · 2017 ↗ Responses to an increased training dose
- Kennedy et al. · 1999 ↗ Acute GLUT4 translocation in human muscle
- Wojtaszewski et al. · 1997 ↗ Insulin action after a single exercise session
- D’Souza et al. · 2014 ↗ Sinus-node adaptation: animal experiments
- Jensen et al. · 2004 ↗ VEGF signalling after muscle exercise
- Daussin et al. · 2008 ↗ Continuous versus interval training: crossover study