What are the 3 factors that determine stroke volume?

Cardiac Reserve and Stroke Volume

Stroke volume is variable and depends on the amount of shortening that the myocardial fibers can attain when working against arterial pressure. It is determined by the interplay of four factors:

Ventricular distending or filling pressure (preload)

Contractility of the myocardium (inotropic state)

The tension that the ventricular myocardium must develop during contraction and early ejection (afterload)

The sequence of atrial and ventricular depolarization

An increase in ventricular distending pressure (end-diastolic pressure or volume) will increase ventricular end-diastolic fiber length, which, by the Frank–Starling mechanism and stretch-dependent calcium sensitization, will result in increased stroke work and a larger stroke volume. Ventricular distending pressure is influenced by atrial contraction and is greatly augmented by increased venous return associated with exercise and increased sympathetic activity. Contractility is most influenced by adrenergic activity and circulating catecholamines. An increase in stroke volume is achieved primarily by an increase in the ejection fraction and a reduction in the end-systolic volume but can also be achieved by a decrease in afterload, which is primarily a function of aortic or pulmonary impedance (the resistance and reactance of the vasculature to ejection).

Stroke volume and cardiac output

Stroke volume in the resting horse is approximately 800–900 mL, or about 2–2.5 mL/kg.42,43 Stroke volume increases by about 20–50% in the transition from rest to submaximal exercise.7,46,52,53 It does not change as intensity of exercise increases from approximately 40%

Values reported for cardiac output in fit Thoroughbreds during treadmill exercise at

During tethered swimming at low work loads, stroke volume decreased from 2.06 mL/kg at rest to about 1.5 mL/kg. This response may be related to decreased venous return secondary to the alterations to breathing pattern during swimming.6

During prolonged exercise cardiac output is decreased in dehydrated horses, and this limits thermoregulation.22 In an experiment in which horses were exercised for 40 minutes while euhydrated, or dehydrated by either withdrawal of water (DDH) or administration of furosemide (FDH), cardiac output was significantly lower in FDH (144.1 ± 8.0 L/minute) and in DDH (156.6 ± 6.9 L/minute) than in euhydrated horses (173.1 ± 6.2 L/minute) after 30 minutes of exercise (see Fig. 3.5). Dehydration resulted in higher temperatures in the middle gluteal muscle and pulmonary artery during exercise, but temperatures in the superficial thoracic vein and at subcutaneous sites on the neck and back were not significantly different. Sweating rates were also similar in control and dehydrated horses, and it was concluded that the impairment of thermoregulation was primarily due to decreased transfer of heat from core to periphery.

Stroke Volume

Although SV increases during upright dynamic exercise (it changes minimally if at all during swimming), its contribution to increases in CO at peak effort is relatively small. Table 1 illustrates that most of the increases in CO stems from a 2.4-fold increase in HR, with a relatively small increase (1.3-fold) in SV. It is difficult to measure SV directly in human subjects at rest, and even harder during exercise, so typically this is a calculated measure, based on CO and HR. Although HR can be precisely measured, measures of CO typically have coefficients of variation of 15% in healthy subjects, so value shown for basal SV in Table 1 (73 ml) translates to a range from 64 to 84 ml. Alterations in SV of 24 ml, the difference between basal and peak exercise in Table 1, are barely outside experimental error. To determine rigorously whether such a small change predominantly reflects in increased left ventricular (LV) end-diastolic volume (EDV) (Starling effect) or a reduction in LV end-systolic volume (ESV) (an inotropic effect) is an irresolvable matter in humans. Although magnetic resonance imaging and computed tomography have enabled resolution of relatively small changes in LV volume in human subjects, their application to upright dynamic exercise is limited. Suffice it to say that during peak exercise, increased HR is the primary means by which CO increases, and HR increases in SV are less important.

Studies using ultrasonic micrometers to measure LV volumes during maximal upright dynamic exercise in dogs confirm that increases in LV EDV during dynamic exercise are a minor contributor to increasing CO during peak effort (Vatner et al., 1972). The difficulty in demonstrating that the Starling effect is a dominant factor in the exercise response is also reported in clinical studies (Stratton et al., 1994).

HR also rises linearly with work rate and plateaus briefly right before exhaustion. Therefore, it can be used as an objective assessment of effort intensity. There is a decline in maximal HR with age, i.e., it falls about 10 beats min−1 per decade. A useful formula provides an estimate of maximal HR:

Maximal HR = 220−age

For example, a 40-year-old subject would be predicted to attain a maximal exercise HR of 180 beats min−1. Although more complex formulas may provide somewhat better estimates, the standard error of the estimate of these formulas is ±15 beats min−1, providing rough but useful guidelines. Barring primary abnormalities in cardiac conduction system function or pharmacological agents that influence HR, the value of HR at maximal effort should be close to the one predicted by formula. The individual also provides a subjective assessment of whether they feel they are approaching maximal effort.

HR alone, however, is an inadequate means to increase CO. For example, a doubling of HR by atrial pacing in a supine nonexercising subject results in a halving of SV and no change in CO. A case can be made that the force–frequency effect may provide a small increase in CO in this setting, but it would be small, of the order of a 10% increase. While it is true that patients with third degree AV block with extremely low HR (<40 beats min−1) may have increased CO with increased HR, this does not apply when basal HR is in the physiologically normal range and is then doubled by pacing. The dependence of CO on venous return is at play here, and doubling the HR by atrial pacing does not provide a means of increasing venous return, hence the fall in SV (Figure 3). In contrast, having a subject double his/her resting HR by running on a treadmill would more than double CO – SV would be maintained and likely increased somewhat (Table 1) due to increased inotropy associated with increased sympathetic activation.

Oxygen consumption. Oxygen consumption (VO2) is measured in ml kg−1 min−1. The normal basal VO2 is 3.5 ml kg−1 min−1, and is referred to as 1 MET (metabolic equivalent of task) in many exercise laboratories. This is a useful index that enables one to refer to multiples of basal VO2. The VO2 at peak effort (VO2max) is a reliable and reproducible measure of aerobic fitness.

There is a 10 ml kg−1 min−1 decay in VO2max with each decade in life. A useful formula to predict VO2max (in METS) is

Maximal METS = 15−(age/10).

For example, a sedentary but otherwise healthy 40-year-old should be able to achieve 15−(40/10) = 11 METS at peak dynamic effort. Since 1 MET = 3.5 ml kg−1 min−1, this would be 11 (3.5) = 39 ml kg−1 min−1. By comparison, a 20-year-old sedentary subject would be anticipated to attain 2 METS more (two decades younger) or an additional 7 ml kg−1 min−1 for a total of 46 ml kg−1 min−1. If one would collect expired air on such an individual, the actual measure of VO2 would be near this value, and, for research purposes actual measurement of VO2 is preferred. However, in clinical settings, one can calculate METS based on treadmill grade and speed and estimate a subject's aerobic fitness on the basis of maximal work rate achieved. We will later examine the effects of chronic sustained dynamic exercise (training), where the hallmark of a training effect is increased VO2max. A normal (not genetically gifted) subject should be able to increase his/her VO2max by about 25% – for our 40-year-old subject with a pretraining VO2max of 39 ml kg−1 min−1, this would mean attaining a VO2max after training of 49 ml kg−1 min−1 – superior to a sedentary subject who is 20 years younger.

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