January 22, 2009


Posted in Health at 7:46 am by Edwin

Alberto Concu
Institute of Human Physiology,
School of Sports Medicine,
University of Cagliari, Medical School,

Stroke volume (SV) is the blood volume ejected from ventricles into the arterial bed at each cardiac cycle. SV, together with heart rate (HR), determines cardiac output (CO), which is to say the blood volume that outflows from the ventricles towards the vascular bed in a given period. In fact, CO depends on how many times ventricles eject a fraction of their blood content into the arteries, either aorta or pulmonary, in one minute. During exercise, oxygen intake increases. Since oxygen delivery to active muscles depends on CO, the importance of the response of both SV and HR to the fuel requirements of exercising muscles is evident. However, while HR is seen to change almost linearly with work rate, induced SV changes at a given work rate can, on the contrary, be quite different, depending on intrinsic, individual characteristics and extrinsic circumstances. In this topic, the effects of different exercising conditions on SV are reviewed.

Stroke Volume Response To Acute Exercise

The same innate variables that condition SV at rest, i.e., age, sex, height, weight and lean body mass, also represent the basis of SV behavior when acute physical exercise is performed. However, extrinsic factors pertaining to environmental conditions (consider for instance possible changes in atmospheric PO2 and PCO2, which influence nervous reflexes from chemoreceptors controlling circulatory activity), body posture (when exercising in a standing position gravitational forces draw blood to the lower body, thus subtracting it from the central hematic volume and causing a reduction in end diastolic ventricular volume with SV consequently lower than in the supine position) and exercise characteristics (frequency, duration and intensity of muscle contraction) interact with innate factors and produce the individual SV response to a given exercise.
In particular, the SV response to acute exercise among subjects with identical physical characteristics and exercising with the same body posture and energy expenditure may be quite different, both with static and dynamic exercises. To explain these different SV responses to static and dynamic exercise we must recall the Frank-Starling law linking tension developed to length reached by muscle fibers. The Frank-Starling law states that when the external load applied to a contracting muscle approaches the maximum of the force producible by sarcomeres, the shortening of the muscle at each contraction approaches zero. This implies that, while maintaining the duration of muscle contraction constant, the time during which the muscle remains isometrically contracted before beginning to shorten is directly proportional to the external load applied to the muscle. Considering that when the muscle is isometrically contracted all the mechanical energy produced is expressed in terms of mechanical pressure, this results in the maximum compression of the arteriae within and surrounding the muscle, with a great increase in their hydraulic resistance. On the contrary, when reducing the load applied to the contracting muscle, its shortening increases proportionally and part of the mechanical energy produced is kinetic, arriving at a reduction of mechanical pressure on the muscle arteriae with a consequent reduction in their hydraulic resistance.
These considerations lead us to conclude that during acute exercise, the higher the load applied to the muscle the longer the isometric condition during contraction lasts and the greater the increase in the hydraulic resistance of its arteriae. Greater arterial hydraulic resistance produces higher ventricle after¬load, which may reduce SV, since afterload is the mechanical tension developed in the ventricle wall during the systole and depends on the hydraulic impedance met by the blood flow at the arterial input. Thus prevalently static or prevalently dynamic exercise certainly leads to differences in SV behavior.

Effects Of Acute Static Exercise On Stroke Volume

In everyday activities, static exertion may often occur suddenly and unexpectedly. Such acute events result from almost isometric contractions of large groups of muscles and produce work load-dependent mechanical compression in muscle arteries which, by increasing local vessel resistance, reduces local blood flow. However, relative hypoxia in working tissues increases the local concentration of vasoactive metabolites and induces vasodilatation. Thus, during an isometric contraction, the vessel resistance of active skeletal muscle is the product of two opposite events: one is the mechanical compression of vessels by contracting skeletal muscles and the other is vessel dilatation due to the activity of muscle effort-dependent vasoactive metabolites. However, it must be considered that in any case a vessel occlusion due to mechanical compression occurs at 60% to 70% of maximum voluntary muscle contraction. Nevertheless, the increase in arterial resistance induced by isometric exercise leads to increased aorta input impedance or increased left ventricle afterload. As a consequence, diastolic pressure in the aorta tends to rise, thus reducing the ventricle-to-aorta pressure gradient, with the result that both velocity and duration of ventricle blood ejection may be reduced, and this leads to a fall in SV.
As an example, Table 1 represents the cardiocirculatory picture during and after an isometric effort in a standing young man (18 years), obtained by utilizing the non-invasive method of impedance cardiography. By flexing his elbow to an angle of 90 degrees he pulled a floor-locked metal spring with his right hand. The effort produced by the biceps muscle was about 50% of its maximum isometric force. This static effort lasted until the subject gave signals of discomfort (140 s).
As expected, 40s after the start of exercise total peripheral vascular resistance (TPR) increased, thus impeding the reduction of arterial blood pressure during diastole. In fact, diastolic arterial blood pressure (DBP) increased, and this led to an increase in both systolic (SBP) and mean (MBP) arterial blood pressures, thus maintaining the rest ventricle-to-aorta pressure gradient (see the Frank-Starling law applied to the heart).
On the basis of the following well-known relation: CO = MBP/TPR, despite increasing MBP, CO fell because of the greater TPR increase. Since HR did not diminish, the CO fall depended entirely on a SV reduction. This SV reduction resulted in part from reduction in both duration and velocity of ventricle blood ejection due to increased arterial input impedance. However, even Valsalva maneuvers (respiratory maneuvers consisting of expiratory efforts made without changing lung volume by closing the glotis, thus greatly increasing intra- thoracic pressure) could be induced by this isometric muscular strength, thus producing compression of heart and aorta which not only contributed to enhancing ventricular afterload, but also impeded diastolic ventricle wall distension with a reduction in end diastolic ventricle volume (EDVV) or ventricle preload (ventricle preload in fact is due to diastolic stretch of the ventricle, or to its filling at end diastole). Ventricular contractility (the contractile state of the myocardium conditions the rate of increase in intraventricular pressure during the systole), indexed as mean systolic ejection rate (MSER), may also be reduced by the ventricle wall deformations thus induced. Therefore, at 40s from the start of isometric exercise all the changes described above led to a SV fall of 21% and, in correspondence with the end of this static effort (140s), the variables considered continued to further change, thus arriving at a SV reduction of -34%.
Because of high arterial blood pressures, HR showed a moderate increase during this isometric effort. This was due to an inhibitory action exerted by increased nervous activity traveling from the baroreceptors in the aorta and carotid bodies to the nervous structures controlling circula¬tion in the brain stem. This, together with the reduced SV, contributed to the not negligible fall in CO at the end of this isometric exercise.
This experiment demonstrates that the cardiocirculatory system did not adapt its activity to supporting for a longer period of time the fuel supply required by the acutely and isometrically contracted muscles mainly because of an SV failure.

Effects Of Acute Dynamic Exercise On Stroke Volume.

Dynamic, as well as static, exercises are part of our every day activities. When we perform rhythmic exercises of moderate intensity, muscles shorten at each contraction and, compared to static exercise, there is a lower mechanical compression of muscle vessels due to a partial shift of the sarcomere-produced energy from the potential (i.e. pressure) to the kinetic (i.e. flow) type, while metabolically induced vasodilatation by muscle contraction persists. This results in a net vasodilatation and leads to a reduction in muscle vessel resistance, with a fall in diastolic aortic pressure. Consequently, the ventricle-to-aorta pressure gradient increases, enhancing both velocity and duration of blood ejection and resulting in an increased SV.
On the other hand, rhythmic muscle contractions act as an external pump exerting a compression on capacitance vessels (i.e. large veins) which increases venous return and thus end diastolic ventricle volume. This contributes to enhancing SV on the basis of the Frank-Starling mechanism.
Furthermore, since stress induced by exercise enhances nervous orthosympathetic activity towards the cardiocirculatory system, myocardial contractility is also increased and adds its contribution to the exercise-induced SV increase.
As an example, Table 2 shows changes in SV and related variables in an untrained young male subject (24 years) during a dynamic-type physical performance consisting of a progressive (10W/min) cycle ergometer exercise up to a work rate (200W) at which he manifested some discomfort. We can see that on reaching just 20% of Wmax, SV had already increased and continued to do so up to 50% of Wmax. This was due to favorable interactions among SV determinants since the afterload index (TPR) progressively fell and both preload (EDVV) and contractility (MESR) indices increased. When the work rate progressively approached its maximum, the SV decreased to a value lower than at rest on reaching 100% of Wmax, since TPR progressively increased once again and both EDVV and MESR fell with respect to previous peak values.
This experiment shows that SV increased initially since preload, afterload and contractility all contribute to this occurrence. Nevertheless, as the dynamic exercise became heavier and work rate approached Wmax, the isometric component of muscle contraction persisted longer and the Valsalva maneuver was often produced, as were those effects on preload, afterload and contractility, as in the previously studied static exercise. Thus, SV progressively fell to values lower than at rest and, despite a high HR increase, CO also decreased with respect its previous peak.
Contrary to what took place during static exercise, MBP did not increase further during dynamic exercise. Thus inhibitory nervous afferent activity from arterial baroreceptors to brain stem cardiovascular controllers was irrelevant and HR increased more. But although HR reached a higher level when dynamic exercise became heavier, the consequent shortening of diastolic duration reduced ventricle filling, thus contributing to the fall in SV, and thus to the final reduction of CO with respect to its previous peak value.
In any case, as happens with static effort, in dynamic exercise exhaustion is also reached because the cardiocirculatory system is incapable of further supplying the required fuel to working muscles mainly because of a SV impairment.

Stroke Volume Adaptation To Chronic Exercise

When acute physical exertion is performed, changes induced in SV depend not only on the kind of exercise but can be greatly influenced by the type and degree of physical training in which the subject is engaged, if any. In fact, the long-lasting (i.e., chronic) practice of stereotyped physical exercise, either for strength or endurance or strength-endurance together, induces characteristic morpho-functional adaptations in the cardio-circulatory system which obviously condition cardiovascular responses to acute exercise in such a way as to produce the best response to exercise schedules closest to those habitually performed. The latter can be considered the effects of chronic exercise on response of SV to acute exercise.

Effects Of Chronic Static Exercise On Stroke Volume.

There are several sports, such as weight lifting, body building, wrestling, throwing events, sprint races, broad jumping and others, in which the training regimen comprises high-resistance static exercise. Since top athletes engaged in these sports train almost every day, they chronically perform isometric exercises included in their training schedules, and this results in a left ventricle pressure overload leading to typical morpho-functional changes in their cardiocirculatory apparatus. In fact, at-rest echocardiography of these strength athletes often shows an increase in left ventricle mass mainly associated with increased left ventricular wall thickness, while left ventricular volume reduces or at least does not increase, i.e. left ventricle concentric hypertrophy. This permits the reaching of higher systolic blood pressure, which may sustain blood flow during an isometric effort despite increased arterial input impedance since, as Laplace’s law states, increased ventricle wall thickness not accompanied by a proportional increase in ventricle radius of curvature results in increased internal pressure during the systole. However, diastolic function is not favored by this concentric type of ventricle hypertrophy, since both reduced volume and compliance of left ventricle may reduce diastolic filling and thus ventricle preload.
Nevertheless, an improvement in myocardial contractility may be considered one of the adaptive cardiocirculatory responses in subjects who chronically train by performing almost exclusively strength exercises, since high arterial input impedance evokes the homeometric regulatory mechanism of SV, which is to say the mechanism that increases SV by increasing the ejection fraction. Moreover, since chronically performed strength exercise improves maximum metabolic vascular dilatatory capacity in trained mu¬scles, this represents another adaptive response to strength training and, by leading to a relative reduction in ventricular afterload, it contributes to improving SV response to an acute, almost isometric exercise.
In conclusion, adaptations that occur in well-trained strength athletes certainly allow an improved fuel supply to their activated muscles when a short but intense isometric effort is made. In fact, previous experiments have shown that when cardio¬circulatory responses to static exercise in weight-lifters are compared with those of appropriately matched untrained subjects, the former were able to keep their SV from returning to its rest value for a longer period of time.
Nevertheless, if strength athletes are engaged in heavy, prolonged exercise, as for instance was the case of well-trained sprinters performing a progressive cycle ergometer exercise in our laboratory, they, like untrained subjects, reached a modest Wmax (200 W) since the response of their cardiocirculatory system in practice did not differ from that observed in the controls.

Effects Of Chronic Dynamic Exercise On Stroke Volume.

Dynamic exercises represent the main component in the training schedule of so called “endurance athletes”. The goal to be reached by these athletes is that of sustaining at length rhythmic exercises such as middle and long distance running and swimming, Nordic skiing, endurance rowing, cycling etc. Since long-lasting rhythmic exercise requires an increase in oxygen transport by the blood so as to meet the energy requirement of exercising muscles, in top athletes who perform dynamic exercises every day, this leads to a chronically volume overloaded left ventricle causing specific morpho-functional adaptations in their cardiocirculatory apparatus. The main feature of cardiovascular adaptations to endurance training is an increase in SV both at rest and at any given level of oxygen uptake. In endurance-trained athletes, echocardiographic assessment revealed a ventricular volume which can increase by more than 30% compared to sedentary subjects. This depends on eccentric left ventricle hypertrophy in these athletes and consists of a proportional increase in both wall thickness and internal volume of the left ventricle, allowing a greater increase in left ventricle end diastolic volume without altering, according to Laplace’s law, ventricle pressure developing during the systole.
Moreover, since endurance training increases parasympathetic activity which causes bradycardia at rest and also decreases HR at any given level of oxygen uptake, this leads to an augmented diastolic filling period which concurs, together with enhanced ventricular volume, in increasing left ventricle preload.
Nevertheless, increased preload alone does not account for the very high CO reached by endurance athletes (up to 40 l/min). In fact, afterload reduction is also a crucial component of integrated cardiovascular responses to aerobic training. Reduction in arteriole hydraulic resistance, due both to regulatory and anatomical adaptation, seems to be the main cause of low afterload both at rest and during exercise in these athletes. In fact, a release in systemic vasoconstrictor activity and an enhanced intrinsic capacity of the skeletal muscle vasculature to be dilated by local metabolites seems to occur as a regulatory adaptation to endurance training. Moreover, the anatomical adaptation represented by proliferation in the skeletal muscle capillary bed also concurs in this reduced peripheral vascular resistance, due to augmented conduits connected in parallel.
Furthermore, studies of myocardial performance in intact animals and man, as well as observations on open-chest animals, isolated hearts, and isolated papillary muscle confirm an association of increased contractile state with rhythmic exercise training.
Thus, regarding the effects on SV played by practicing prolonged dynamic exercise, it may be concluded that this practice improves preload, contractility and afterload responses in such a way as to adequately increase SV to better sustain prolonged exercise by utilizing aerobic mechanisms. On the other hand, when long-distance runners were submitted to a static effort they, contrary to what occurs in strength athletes, showed a lack of increase in ventricular contractility, thus confirming the connection between training schedule and heart response to exercise.

Effects Of Static-Dynamic Chronic Exercise On Stroke Volume.

Between the two extremes of training, almost exclusively static and almost exclusively dynamic, there are several categories of athletes whose training schedules comprise both static and dynamic exercises. Most of these athletes are engaged in the so-called “situation games” such as basketball, volleyball, soccer, football, tennis and others, in which bursts of anaerobic activity (jumping, sprinting) alternate with aerobic exercise (running, walking). In these athletes, some degree of concentric (pressure overload) and eccentric type (volume overload) left ventricle hypertrophy is the heart’s usual adaptive. However, since the ratio of the static versus the dynamic component in their training can differ widely, the ratio of concentric to eccentric ventricle hypertrophy is oriented in the same way.
Thus the greater the strength engagement during their training, the more the left ventricle wall thickness-to-radius ratio approaches the SV response to acute exercise of strength athletes. In this sense, we can consider volleyball players, since their situational game is characterized by explosive movements during which energy is almost all supplied by muscle phosphagen reserve (i.e. anaerobic alactacid source) which is an exercising condition not requiring oxygen supply. These athletes’ training schedules mainly consist of physical exercises during which higher arterial blood pressure and heart rate predominate, which is to say exercise of the strength type.
On the contrary, the greater the endurance engagement during their training the lower the left ventricle wall thickness-to-radius ratio, and this in turn brings the resulting SV response to acute exercise closer to that of endurance training. Basket¬ball players well represent athletes with these characteristics. In fact, during their games these athletes spend almost all their energy in running up and down the court, that is, performing a physical exercise which is mainly aerobic. In the training schedules of basketball players endurance exercises obviously predominate in such a way as to induce the cardiovascular adaptations suitable for playing at their best.


While heart rate shows a response to acute exercise which is quite common in most people, stroke volume response to acute exercise may differ radically between one subject and another. In fact, stroke volume behavior during exercise results not only from the subject’s innate physical characteristics but also from the morpho-functional adaptations occurring in the cardiovascular structures controlling ventricular preload, contractility and afterload, as the consequence of the habitual physical activity performed by the subject, if any. In this sense, the stroke volume response to an acute exercise represents a strictly individual characteristic and, in the same subject, it is susceptible to change greatly in relation to the physical exercise schedule which, in a given period of time, dominates the subject’s daily activities. This is to say that, both at rest and during acute exercise, stroke volume depends on the quantity and quality of physical exercises which are chronically performed. Obviously, in the case of untrained subjects, the stroke volume response to an acute exercise is that resulting from the subject’s innate physical characteristics alone.


1. Åstrand, P.O. and K. Rodahl. Textbook of Work Physiology, New York: McGraw-Hill, Inc., 1970.
2. Blomqvist, C.G. and B. Saltin. Cardiovascular adaptations to physical training. Ann. Rev. Physiol., 45: 169-189, 1983.
3. Burton, A.C. Physiology and Biophysics of the Circulation. Chicago: Year Book Medical Publishers, Inc., 1969.
4. Concu, A. and C. Marcello.- Stroke volume response to progressive exercise in athletes engaged in different types of training. Eur. J. Appl. Physiol., 66: 11-17, 1993.
5. Higginbotham, M.B, K.G. Morris, R.S. Williams, P.A. McHale, R.E. Coleman, and F.R. Cobb. Regulation of stroke volume during submaximal and maximal upright exercise in normal man. Circ. Res., 58: 281-291, 1986.
6. Mirski, I., D.N. Ghista, and H. Sandler. Cardiac Mechanics.. New York: John Wiley & Sons. Inc., 1974.
7. Paulsen, W.J., D.R. Boughner, A. Friesien, J.A. Persaud- Ventricular response to isometric and isotonic exercise, echocardiographic assessment. British Heart Journal 42: 521-527, 1979.
8. Peachey, L.D. Handbook of Physiology, section 10: Skeletal Muscle. Bethesda, Maryland: American Physiological Society, , 1983.
9. Shepherd, J.T. and F.M. Abbond. Handbook of Physiology, section 2: The cardiovascular system, volume III, part 2. Bethesda, MD: American Physiological Society, 1983.


1 Comment »

  1. This is great news,well prepared information it was an eye opener for me.

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out /  Change )

Google+ photo

You are commenting using your Google+ account. Log Out /  Change )

Twitter picture

You are commenting using your Twitter account. Log Out /  Change )

Facebook photo

You are commenting using your Facebook account. Log Out /  Change )


Connecting to %s

%d bloggers like this: