Valsalva Maneuver

If you are lifting weights with any level of intensity, you have likely performed what is called the Valsalva maneuver, knowingly or unknowingly. The Valsalva maneuver is a physiological state that may or may not have an impact on performance and health; in this article, we will discover what the valsalva maneuver is, how it generally works, its usefulness, and its safety, but we will not be delving into depth on its physiological mechanisms.

What is the Valsalva Maneuver? Use?

The Valsalva maneuver is the state in which a person pushes air against a, typically, closed glottis for several moments (illustrations help in visualizing)[3]. More applicably, the Valsalva maneuver (also known as the Valsalva-Weber) is a conscious technique often used to create intra-abdominal pressure to brace the spine in heavy lifting; it is, however, also used during pooping as pressure from the top can translate downwards [2]. Of course, the Valsalva can be used and is used for many situations, even clinical ones, to measure and diagnose issues like equilibrating to sudden pressure changes (ex, diving, air travel, etc.) [1].

Valsalva Maneuver and Force Production

Before we go on, for those of us interested in weight lifting, there is some debate if the Valsalva maneuver truly provides a benefit in terms of force production [4][5]. The Valsalva does offer increased intra-abdominal pressure by increasing air volume forcefully, which, in its own right means a descending of the diaphragm and increased pressure between abdominal wall and spine, but this seems not to have an added effect on force production [4]. However, that said, although force production may be equal in Valsalva users and non-users, the condition still stands that for many exercises, abdominal pressure must remain and this may be made up for by simply tensing the abdominal muscles in controlling weight lifted in non-Valsalva lifters – however, this may be insufficient at high intensity loads (>80%1RM) in which Valsalva may be necessary to maintain pressure throughout a lift [6].

How does it function?

The Valsalva maneuver is made up of complex mechanical and neural components that end up working interchangeably to create 4 distinct stages [1][7]. Assuming a person closes their glottis and exerts air pressure upon that closed glottis, the 4 stages of the Valsalva maneuver go in this order of physiological occurrence:

Stage 1

The initial stage brings about an increase in blood pressure, but a slight drop in heart rate [1][7]. Vessel blood pressure increases proportionally to intra-abdominal and intra-thoracic pressure build up from air not being allowed to escape, as well as that air being forced upward against the closed glottis [1]. The aorta is rapidly compressed leading to quicker delivery of blood pressure change to the rest of the circulation to, presumably, equilibrate and protect circulation; this compression is induced by the baroreceptors of the aorta [1][8].  

What are baroreceptor?

Baroreceptors are neural assessment points on the aortic and carotid arteries that relay information to the rest of the nervous system and are major regulators in heart electrical conduction, blood pressure, heart rate, and a host of other cardiac functions [17].

Baroreceptors sense stretch (an indication of pressure on the artery walls) and send that signal to the brain to adjust different physiological processes to accommodate.

Stage 2

At this point, pressure has been set for a few seconds as the glottis remains closed, not allowing the relief of exhaling air back out of the body, so the pressure build up in the respiratory and cardiac areas of the trunk lead to a decrease in blood return to the heart as venous return moves  against trunk pressure back up the body via the inferior vena cava; not only that, the superior vena cava closes its lumen to decrease blood flow from the top-down back to the heart [1][13]. Blood, now restricted from returning to the heart finds its way to the periphery of the body and only when the pressure in the periphery exceeds intra-thoracic pressure can blood return to the heart [1][13]. The heart decreases its stroke volume (aka, amount of blood released per beat) by as much as 50% during this stage, likely due to a lack of blood return to the ventricles [1]. This, then, predictably increases heart rate to make up for the decrease in blood being pumped from the heart to the body; however, pressure is still making changes as parts of the periphery constrict and some parts remain open to equilibrate to these changes in pressure and decreases in flow [1].

As pressure builds inside the body, the image displays one of the vena cavae (inferior) closing to reduce return to the heart and increase circulation to the periphery.

Stage 3

In this step, the glottis opens and air is exhaled, leading to sudden drop in intra-thoracic pressure. This sudden drop in intra-thoracic pressure leads to the vena cavae expanding, due to an equilibration of blood pressure between the periphery and the thoracic trunk, allowing blood flow to increase to the heart again [1]. This increased blood flow and equilibration of blood pressure leads to a temporary sinking in peripheral blood pressure and this can lead to syncope (aka, passing out)[1].

Stage 4

This stage is dedicated to complete recovery and normalization of blood pressure by increasing blood flow through the heart and increasing cardiac output 40% over resting (cardiac overshoot) to quickly get blood pressure back to normal, resting levels [1].  This stage, ironically, is the stage in which there is the highest probability of stroke if stroke were to occur (covered in more detail in the next section).

As can be seen, blood pressure increases in stage 1 and heart rate decreases to accommodate, then in stage 2 blood pressure normalizes, but heart rate increases. In stage 3, there is a sudden drop in blood pressure as intra-thoracic pressure drops leading to a responsive drop in blood pressure (this can lead to syncope), and the body rapidly increases blood pressure to attenuate this sudden drop and avoid further hypotension in stage 4.

Is it safe?

So, after understanding the various stages in which the body regulates to attenuate these forced changes induced by the Valsalva we might be left with the question of its safety, especially considering the sheer dramatics of physiological change enacted within the body. Most clinical professionals would advise against the Valsalva maneuver for a few reasons, but do these reasons have merit?

The largest concern when involving the Valsalva maneuver is the impact on the brain, because although changes on the heart can seem dramatic, the brain is full of tiny veins and needs to be protected at all costs – so, will these sudden cardiac changes lead to brain damage of any sort? The answer is an intriguing one in that it would make common sense to imagine that if a person’s blood pressure rises over 300 mmHg, these vessels in the brain would cause immediate stroke; however, there are some interesting mechanisms that seem to protect the brain from the brunt of this pressure increase.

Diving into a bit of physics and physiology combined, talking about the Bernoulli and Monro-Kelli Principles, we know that the brain is regulated differently than the rest of the body in terms of blood pressure regulation [11][12][15]. As arterial pressure increases due to the Valsalva, the brain compensates by dilating vessels to allow more rapid blood flow to mitigate this increase in pressure occurring throughout the body. We can understand this better if we first understand how intra-cranial pressure is created.

There are three components to intra-cranial pressure as described by the Monro-Kelli Principle and these are brain tissue, cerebrospinal fluid, and blood [11]. The principle further mentions that if one or two increase, the remaining facets must decrease to compensate [11]. So, in the case of the Valsalva, two mechanisms are implemented – blood volume and cerebrospinal fluid regulation [11]. So, the Valsalva would normally increase blood volume as we know blood is kept in the periphery at points during the maneuver, but oddly enough, the brain compensates by decreasing the blood flow to itself via the carotic baroreceptors in the carotid artery which, in its own right decreases blood volume [9]. However, this is not enough and further changes occur as the cerebrospinal fluid is also moved into the spinal canal to relieve pressure [11]. Both of these mechanisms occur, not only to decrease total blood pressure effect, but to keep pressure stable between inside the blood vessels and outside as outlined by the Bernoulli Principle – this leads to a decreased risk of rupture that would be due to uneven pressure.

These mechanisms are most prevalent in the initial and middle stages, but once relaxation sets in and pressure is alleviated, the risk of stroke is highest, because the continued adaptation from low to high to low blood pressure leads to a risk of syncope (aka, passing out) all the way to a potential risk of stroke as the heart has an overshoot period where it attempts to reintroduce normal amounts of blood at the appropriate intensity and is difficult to compensate for in the brain as the carotid and superior vena cava return to their original states leaving, presumably, a discrepancy in pressure.
Investigating the literature in which weight lifting (aka, maximal or near maximal stress on the body) is performed and in which the Valsalva was used, there are varying conditions, but there are a few incidences in the literature implicating Valsalva for the hospitalization of 13 individuals throughout thousands [2]. So, there is a risk, but that risk is likely minimal for those who are young and/or healthy; however, if cardiovascular disease is common to you or you are older, it may be prudent to stay clear of the Valsalva even if it is necessary for intensities 80-85% of maximum [1][2][16].


Now we understand the Valsalva maneuver in all of its intricacies. The Valsalva, characterized by pushing pressure against a closed glottis, creating greater intra-abdominal and intra-thoracic pressure, does not seem to add to force production in comparison to some alternatives, although the Valsalva may be a necessity at high enough intensities (>80%). The Valsalva is a beautifully complex mechanism that has incredibly detailed impact on the heart and the surrounding vasculature with profound impact on the brain, as well. In terms of safety, many clinicians avoid the use of the Valsalva, but it would likely be a safe practice if found useful in healthy, younger populations – those with cardiovascular risk or older should likely avoid the Valsalva for a variety of reasons.

Writer: Nicolas Verhoeven
This is educational material only and not meant to be prescripton, consult your physician before making any changes.

[1] Pstras, L., Thomaseth, K., Waniewski, J., Balzani, I., & Bellavere, F. (2016). The Valsalva manoeuvre: physiology and clinical examples. Acta Physiologica, 217(2), 103-119. doi:10.1111/apha.12639

[2] Hackett, D. A., & Chow, C. (2013). The Valsalva Maneuver. Journal of Strength and Conditioning Research, 27(8), 2338-2345. doi:10.1519/jsc.0b013e31827de07d

[3] Junqueira, L. F. (2008). Teaching cardiac autonomic function dynamics employing the Valsalva (Valsalva-Weber) maneuver. AJP: Advances in Physiology Education, 32(1), 100-106. doi:10.1152/advan.00057.2007

[4] Hagins, M., Pietrek, M., Sheikhzadeh, A., & Nordin, M. (2006). The effects of breath control on maximum force and IAP during a maximum isometric lifting task. Clinical Biomechanics, 21(8), 775-780. doi:10.1016/j.clinbiomech.2006.04.003

[5] Ikeda, E. R., Borg, A., Brown, D., Malouf, J., Showers, K. M., & Li, S. (2009). The Valsalva Maneuver Revisited: The Influence of Voluntary Breathing on Isometric Muscle Strength. Journal of Strength and Conditioning Research, 23(1), 127-132. doi:10.1519/jsc.0b013e31818eb256

[6] MacDougall, J. D. (1992). Factors affecting blood pressure during heavy weight lifting and static contractions. Journal of Applied Physiology, 3(4), 1590-7. Retrieved from

[7] HAMILTON, W. F. (1936). PHYSIOLOGIC RELATIONSHIPS BETWEEN INTRATHORACIC, INTRASPINAL AND ARTERIAL PRESSURES. Journal of the American Medical Association, 107(11), 853. doi:10.1001/jama.1936.02770370017005

[8] Smith, S. A., Salih, M. M., & Littler, W. A. (1987). Assessment of beat to beat changes in cardiac output during the Valsalva manoeuvre using electrical bioimpedance cardiography. Clin. Sci, 72(4), 423-428. doi:10.1042/cs0720423

[9] Greenfield, J. C., Rembert, J. C., & Tindall, G. T. (1984). Transient changes in cerebral vascular resistance during the Valsalva maneuver in man. Stroke, 15(1), 76-79. doi:10.1161/01.str.15.1.76

[10] [10] Tiecks, F. P., Lam, A. M., Matta, B. F., Strebel, S., Douville, C., & Newell, D. W. (1995). Effects of the Valsalva Maneuver on Cerebral Circulation in Healthy Adults : A Transcranial Doppler Study. Stroke, 26(8), 1386-1392. doi:10.1161/01.str.26.8.1386

[11] Regulation of intracranial pressure under physiologic circumstances and in space-occupying lesions [PDF]. (n.d.). Retrieved from http://file:///C:/Users/Nic/Downloads/0019_2A_Neurologia_angol.pdf

[12] Mokri, B. (2001). The Monro-Kellie hypothesis: Applications in CSF volume depletion.Neurology, 56(12), 1746-1748. doi:10.1212/wnl.56.12.1746


[13] Gindea, A. J., Slater, J., & Kronzon, I. (1990). Doppler echocardiographic flow velocity measurements in the superior vena cava during the valsalva maneuver in normal subjects. The American Journal of Cardiology, 65(20), 1387-1391. doi:10.1016/0002-9149(90)91333-2

[14] MacDougall, D., Tuxon, D., Sale, D., Sexton, A., Moroz, J., & Sutton, J. (1985). Arterial blood pressure response to heavy resistance exercise. Journal of Applied Physiology, 58(3), 785-790. Retrieved from

[15] Nave, R. (n.d.). Bernoulli Equation. Retrieved from

[16] MacDougall, J. D. (1992). Factors affecting blood pressure during heavy weight lifting and static contractions. Journal of Applied Physiology, 73(4), 1590-1597. Retrieved from

[17] Swenne, C. A. (2012). Baroreflex sensitivity: mechanisms and measurement. Netherlands Heart Journal, 21(2), 58-60. doi:10.1007/s12471-012-0346-y


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