Chronic Exercise-Induced Cardio-Respiratory Adaptations

Creating the right environment for improved fitness

Hans Selye's General Adaptation Syndrome has often been used to illustrate how exercise that overloads, or stresses, the cardio-respiratory system will elicit subsequent adaptations in the component parts of that system. [Read more on Selye here]

The challenge for those that prescribe exercise is to create a programme that creates the right amount of stress, or alarm, without creating exhaustion which can be detrimental to the production of positive adaptations.

Why the need to understand physiological adaptations?

For coaches and exercise professionals to be able to produce effective conditioning programmes, a knowledge of the underpinning adaptations that occur with training is important so that training variables can be optimised accordingly. 

This resource page gives an overview of the key adaptations that result from endurance training and also contains links to further reading for more advanced readers. 

Maximal Oxygen Uptake (VO2max)

Maximal oxygen uptake is one of the gold standards of aerobic fitness testing and increases during training due to increases in stroke volume (SV), cardiac output (Q) and a small increase in arteriovenous difference. Aerobic exercise will elicit the greatest changes in VO2max and in the first six months of training increases of 10-30% are often seen. The more highly trained an athlete is however, the less potential there remains for further increases in VO2max. It also becomes a weaker predictor of performance than other measures such as lactate threshold and running economy. See Paula Radcliffe’s data here for insight into the importance of VO2max.

Adaptations of the Heart 

Increased Stroke Volume 

Endurance training causes the heart's stroke volume to increase during rest and physical activity. 

The key factors in this adaptation are increased LV volume, reduced cardiac and arterial stiffness, increased diastolic filling time and improved cardiac contractile function.

Increased Preload

The increase in stroke volume mentioned above is predominantly a result of an increased amount of blood in the ventricles and this is dependent on venous return. (more on preload).

Left Ventricular eccentric hypertrophy

During prolonged aerobic exercise the resulting increase in venous return and cardiac preload causes periods where the heart's chambers are expanded and this in turn will cause myocardial tissue to adapt. If the associated adaptations are a result of increased preload then subsequent adaptations will result in stronger ventricle walls and a larger capacity whereas if the heart had to work harder to overcome a high afterload (eg in the presence of arteriosclerosis in the peripheral circulatory system) then the result can be a pathologically disproportionate increase in chamber wall thickness in relation to chamber volume increase.

While strength-trained athletes may see a somewhat increased wall thickness in proportion to chamber volume, this is not as large an increase in those with cardiomyopathies.

Increased Frank-Starling Mechanism

The ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return is called the Frank-Starling mechanism. This mechanism is enhanced with training as the hypertrophic and chamber volume adaptations that result from regular endurance exercise are made by the addition of new sarcomeres in the cardiac muscle that maintain or even increase the stretching action of the tissue during diastole (filling).

Increased myocardial contractility

The cardiac hypertrophy mentioned above can result in a more forceful contraction which in turn can assist with ventricular emptying. For more on the cardiac adaptations of athletes from a range of sports see Pluim et al, 2000.

Training-induced bradycardia

Bardycardia is a low resting heart rate (<60 beats per minute) and when present in healthy, trained individuals is a consequence of increased stroke volume with unchanged cardiac output at rest or submaximal intensities. A lower heart rate for any given cardiac output allows for longer periods of filling (diastole) which in turn can increase stroke volume as the larger ventricles can be used to their full potential.

Read More: See Baggish et al (2008)

Adaptations of the Blood

Increased Total Blood Volume

Increased total blood volume is a critical adaptation that allows stroke volume to increase via the Frank-Starling mechanism.

Plasma Volume Increase

During exercise, plasma volume can decrease by around 10% while resistance training and up to 20% while training aerobically. As blood pressure increases with exercise, water is forced from the blood into the interstitial spaces and with increased duration of exercise, fluid loss from perspiration can cause further decreases in plasma volume.

With even the first workout however, adaptations occur that increase the plasma volume post-workout. Within the first few weeks of a new training programme plasma volume can increase 12-20% and endurance athletes can have blood volumes ~35% greater than untrained individuals.

Increased Red Blood Cells

Initially, there are no changes in the number of rbcs and the increase in blood volume that occurs in the first few days of training is a result of the increases in plasma mentioned above. Eventually, rbc count does increase to ensure that the oxygen carrying capacity of the blood is maintained however the percentage increase does not match that of plasma, reducing the haematocrit and decreasing blood viscosity which in turn is an aid to improved blood flow.

Arteriogenesis and Angiogenesis

Endurance training can result in exercise induced vascular remodelling. Arteriogenesis is the enlarging of existing arterial vessels and allows for increased blood flow to the periphery of the vascular system. Angiogenesis is the formation of new capillaries and this denser capillary network results in improved gas diffusion and an increased mean transit time for red blood cells that travel through the exercising muscle, both features which contribute to higher O2 extraction levels in trained individuals. Angiogenesis can also allow for greater nutrient delivery over a longer period of time.

See Laughlin & Roseguini (2008) for more on the mechanisms for exercise training-induced increases in skeletal muscle blood flow capacity.

Improved Blood Distribution

During exercise, blood flow is redistributed to ensure that the working muscles are supplied with adequate amounts of oxygen and nutrients and blood flow is restricted to areas such as the abdomen and kidneys. With prolonged endurance training the body becomes more efficient at submaximal intensities of exercise and therefore requires relatively less redistribution of blood flow allowing for less restriction of blood flow to the abdominal organs and kidneys. This could be beneficial in metabolising glucose which can in turn be used for fuelling exercise.

Part of the mechanism for controlling blood flow is related to endothelial function and for more on exercise-related changes in endothelial function see Di Francescomarino et al, 2009

Reduced Blood Pressure

An individual with normal blood pressure may not see much change in BP following aerobic training, however a hypertensive individual may see small but significant decreases. Research suggests that both aerobic training and resistance training can have a beneficial effect on blood pressure, with aerobic training reducing SBP by 3-5 mmHg and DBP by 2-3mmHg with just a 3 mmHg reduction in BP decreasing the risk of CV disease by 5-9% and stroke by 8-14% (Pescatello et al, 2004)

Adaptations of the Lungs

There is little change in lung volumes and capacities with endurance training. Although Tidal Volume and Pulmonary Diffusion do not change at rest or during sub-maximal exercise, endurance training can increase the capacity of both at maximal intensities.

For more on exercise-induced respiratory adaptations see Wagner (2005)

Adaptations of Skeletal Muscle

Increased Mitochondrial Mass

Approximately 4-7% of skeletal muscle volume comprises mitochondria and aerobic training can increase the mitochondrial density in muscle by up to 40%. There are exercise-induced biochemical and morphological changes that take place and both combine to increase the oxidative capacity of skeletal muscle.

For more on the mitochondrial adaptations that occur in skeletal muscle see Lundby and Jacobs (2016).

For a CrossTalk published debate on mitochondrial adaptations, see the following four articles MacInnis et al (2019), Bishop et al (2019) and their rebuttals https://doi.org/10.1113/JP278328, https://doi.org/10.1113/JP278329 

For more on the skeletal muscle determinants of endurance exercise see van der Zwaard et al (2021).

Time-course & Individual Difference

Changes that result from endurance training occur at different rates as do subsequent changes that result from de-training or sedentary behaviour (see image below). 

There are also a range of factors that influence the degree of adaptive response such as initial fitness level, training intensity, frequency and duration.

How Adaptations Vary with Type of Training

Over time many of these adaptations will occur however there may be greater changes to come than others, depending on the type of training that predominates. A well-rounded training programme will often incorporate all of these types of training at some point however, when done in isolation the following changes are linked to the three main types of training:

Recap/Overview of Adaptations

Recommended Reading (Textbooks)

Haff, G. G., & Triplett, N. T. (Eds.). (2015) Essentials of Strength Training and Conditioning (4th Ed.) Champaign, IL: Human Kinetics. (Ch 6 by Swank & Sharp)

Jeffreys, I., & Moody, J. (Eds.). (2016) Strength and Conditioning for Sports Performance. Routledge.

McArdle, W. D., Katch, F. I., & Katch, V. L. (2015) Exercise physiology: nutrition, energy, and human performance (8th Ed). Lippincott Williams & Wilkins.Ch 21

Ratamess, N. A. (2012) ACSM's foundations of strength training and conditioning. Lippincott Williams & Wilkins.

References and Further Reading

Baggish, A. L., Wang, F., Weiner, R. B., Elinoff, J. M., Tournoux, F., Boland, A., ... & Wood, M. J. (2008). Training-specific changes in cardiac structure and function: a prospective and longitudinal assessment of competitive athletes. Journal of applied physiology, 104(4), 1121-1128. https://doi.org/10.1152/japplphysiol.01170.2007   

Bishop, D. J., Botella, J., & Granata, C. (2019). CrossTalk opposing view: Exercise training volume is more important than training intensity to promote increases in mitochondrial content. The Journal of physiology, 597(16), 4115-4118. https://doi.org/10.1113/jp277634 

Bishop, D. J., Botella, J., Genders, A. J., Lee, M. J., Saner, N. J., Kuang, J., ... & Granata, C. (2019). High-intensity exercise and mitochondrial biogenesis: current controversies and future research directions. Physiology, 34(1), 56-70. https://doi.org/10.1152/physiol.00038.2018 

CDC (1996) Physical Activity and Health: A Report of the Surgeon General Ch 3: Physiologic responses and long-term adaptations to exercise https://www.cdc.gov/nccdphp/sgr/pdf/chap3.pdf

Dawson, E. A., Cable, N. T., Green, D. J., & Thijssen, D. H. (2018). Do acute effects of exercise on vascular function predict adaptation to training?. European journal of applied physiology, 118(3), 523-530. https://doi.org/10.1007/s00421-017-3724-8 

Di Francescomarino, S., Sciartilli, A., Di Valerio, V., Di Baldassarre, A., & Gallina, S. (2009). The effect of physical exercise on endothelial function. Sports Medicine, 39(10), 797-812.

George, K., Whyte, G. P., Green, D. J., Oxborough, D., Shave, R. E., Gaze, D., & Somauroo, J. (2012). The endurance athletes heart: acute stress and chronic adaptation. Br J Sports Med, 46(Suppl 1), i29-i36. http://bjsm.bmj.com/content/46/Suppl_1/i29

Green, D. J., Hopman, M. T., Padilla, J., Laughlin, M. H., & Thijssen, D. H. (2017). Vascular adaptation to exercise in humans: role of hemodynamic stimuli. Physiological Reviews, 97(2), 495-528. https://doi.org/10.1152/physrev.00014.2016 

Hawley, J. A., Lundby, C., Cotter, J. D., & Burke, L. M. (2018). Maximizing cellular adaptation to endurance exercise in skeletal muscle. Cell Metabolism, 27(5), 962-976. https://doi.org/10.1016/j.cmet.2018.04.014 

Heinicke, K., Wolfarth, B., Winchenbach, P., Biermann, B., Schmid, A., Huber, G., ... & Schmidt, W. (2001). Blood volume and hemoglobin mass in elite athletes of different disciplines. International journal of sports medicine, 22(07), 504-512.

Heinonen, I., Kalliokoski, K. K., Hannukainen, J. C., Duncker, D. J., Nuutila, P., & Knuuti, J. (2014). Organ-specific physiological responses to acute physical exercise and long-term training in humans. Physiology, 29(6), 421-436. http://physiologyonline.physiology.org/content/29/6/421

Heil, M., Eitenmüller, I., Schmitz‐Rixen, T., & Schaper, W. (2006). Arteriogenesis versus angiogenesis: similarities and differences. Journal of Cellular and Molecular Medicine, 10(1), 45-55.

Hellsten, Y., & Nyberg, M. (2015). Cardiovascular adaptations to exercise training. Comprehensive Physiology.6(1), 1-32.[abstract]

Jones, A. M. (2006). The physiology of the world record holder for the women's marathon. International Journal of Sports Science & Coaching, 1(2), 101-116.

Joyner, M.J. and Coyle, E.F. (2008) Endurance exercise performance: the physiology of champions. Journal of Physiology. Vol. 586, 35-44 https://doi.org/10.1113/jphysiol.2007.143834

Laughlin, M. H., Bowles, D. K., & Duncker, D. J. (2011). The coronary circulation in exercise training. American Journal of Physiology-Heart and Circulatory Physiology 302(1) https://doi.org/10.1152/ajpheart.00574.2011 

Laughlin, M. H., & Roseguini, B. (2008). Mechanisms for exercise training-induced increases in skeletal muscle blood flow capacity: differences with interval sprint training versus aerobic endurance training. Journal of Physiology and Pharmacology, 59(Suppl 7), 71.

Lavie, C. J., Arena, R., Swift, D. L., Johannsen, N. M., Sui, X., Lee, D. C., ... & Blair, S. N. (2015). Exercise and the cardiovascular system: clinical science and cardiovascular outcomes. Circulation research, 117(2), 207-219. https://doi.org/10.1161/CIRCRESAHA.117.305205   

Lundby, C., & Jacobs, R. A. (2016). Adaptations of skeletal muscle mitochondria to exercise training. Experimental Physiology, 101(1), 17-22.

MacInnis, M. J., & Gibala, M. J. (2017). Physiological adaptations to interval training and the role of exercise intensity. The Journal of Physiology, 595(9), 2915-2930. http://onlinelibrary.wiley.com/doi/10.1113/JP273196/full 

MacInnis, M. J., Skelly, L. E., & Gibala, M. J. (2019). CrossTalk proposal: Exercise training intensity is more important than volume to promote increases in human skeletal muscle mitochondrial content. The Journal of physiology, 597(16), 4111-4113. https://doi.org/10.1113/JP277633 

Moore, R. L. (2006). The cardiovascular system: cardiac function. In Tipton, C.M. (Ed) ACSM’s Advanced Exercise Physiology. Lippincott Williams and Wilkins, Philadelphia, 326-342.

Pescatello, L. S., Franklin, B. A., Fagard, R., Farquhar, W. B., Kelley, G. A., & Ray, C. A. (2004). Exercise and hypertension. Medicine & Science in Sports & Exercise, 36(3), 533-553.

Pluim, B. M., Zwinderman, A. H., van der Laarse, A., & van der Wall, E. E. (2000). The athlete’s heart. Circulation, 101(3), 336-344.

van der Zwaard, S., Brocherie, F., & Jaspers, R. T. (2021). Under the hood: skeletal muscle determinants of endurance performance. Frontiers in Sports and Active Living, 213. https://doi.org/10.3389/fspor.2021.719434 

Wagner, P. D. (2005). Why doesn’t exercise grow the lungs when other factors do?. Exercise and Sport Sciences Reviews, 33(1), 3-8.