Identify a factor that can increase stroke volume in response to endurance training.

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Cited by (0)
How does Endurance training increase stroke volume?
What increases stroke volume?
What are the mechanisms that could increase the stroke volume during exercise?
Which two factors are increased during exercise which subsequently increases stroke volume?

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Abstract

Prolonged exercise induces cardiovascular drift, which is characterized by decreasing mean arterial pressure (MAP), stroke volume and heart rate increase. Cardiovascular drift has been debated for a long time. Although the exact mechanisms underlying cardiovascular drift are still unknown, two theories have been proposed. The first is that increased skin blood flow displaces blood volume from central circulation to the periphery, which reduces stroke volume. According to this theory, the rise in heart rate is presumably responding to the drop in stroke volume and MAP. The alternative theory is that an increase in heart rate is due to an increase in sympathetic nervous activity causing reducing time at diastole, and therefore stroke volume. It may be difficult to determine a single robust factor accounting for cardiovascular drift, due to the broad range of circumstances. The primary focus of this review is to elucidate our understanding of cardiovascular drift during prolonged exercise through nitric oxide and force-frequency relationship. We highlight for the very first time that cardiovascular drift (in some conditions and within a specific time period) may be considered as a protective strategy against potential damage that could be induced by the intense and prolonged contraction of the myocardium.

Keywords

Cardiac-force

Cardiovascular drift

Heart rate

Oxidative stress

Vasodilation

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Exercise Physiology Laboratory

Cardio/CNS contribution

Many factors contribute to the changes observed during and immediately after exercise. The following will be covered:

Cardio-CNS contribution
Respiratory contribution
Changes at the muscular level
Energy expenditure during exercise

Cardiac output may increase to 35L/min in well-trained athletes. In untrained individuals it can reach 20-25L/min. Most of the increase in cardiac output goes to the exercising muscles. There is an increase in blood flow to skin (dissipation of heat) and to the heart (increased work performed by the heart). Increased flows are the result of local arteriolar vasodilation. In both skeletal and cardiac muscles, vasodilation is mediated by local metabolic factors, and in the skin, it is achieved mainly by a decrease in the firing of sympathetic neurons supplying skin vessels. Simultaneously with vasodilation in these three regions, a vasoconstriction occurs in the kidneys and gastrointestinal organs, due to an increase in activity of sympathetic neurons supplying them.

Distribution of the systemic cardiac output at rest
and during strenuous exercise

Vasodilation of arterioles in the skeletal and heart muscles and skin causes a decrease in total peripheral resistance to blood flow. This decrease is partially offset by vasoconstriction of arterioles in other organs. But the vasodilation in muscle arterioles is not compensated, and the net result is a marked decrease in total peripheral resistance to blood flow.

The mean arterial pressure is the arithmetic product of the cardiac output and the total peripheral resistance (P=COxR). During exercise, the cardiac output increases more than the total resistance decreases, so the mean arterial pressure usually increases by a small amount. Pulse pressure, in contrast, markedly increases because of an increase in both stroke volume and the speed at which the stroke volume is ejected.

The cardiac output increase is due to a large increase in heart rate and a small increase in stroke volume.

The heart rate increases because of a decrease in parasympathetic activity of SA node combined with increased sympathetic activity.

The stroke volume increases because of increased ventricular contractility, manifested by an increased ejection fraction and mediated by sympathetic nerves to the ventricular myocardium.

End-diastolic volume increase slightly. Because of this increased filling, the Frank-Starling mechanism also contributes to the increased stroke volume (stroke volume increases when end-diastolic volume increases).

Cardiac output can be increased to high levels only if the peripheral processes favoring venous return to the heart are simultaneously activated to the same degree. Factor promoting venous return:

increased activity of the skeletal-muscle pump.
increased depth and frequency of respiration; respiratory pump.
sympathetically mediated increase in venous tone
greater ease of blood flow from arteries to veins.

Control of sympathetic outflow

One or more discrete control centers in the brain are activated by output from the cerebral cortex. Descending pathways from these centers transmit these centers� activity to the appropriate autonomic preganglionic neurons eliciting the firing patterns typical for exercise. These centers become activated before the exercise started.

Once exercise is started, local chemical changes in the muscle can develop, particularly during high levels of exercise, because of imperfect matching between blood flow and metabolic demands. These changes activate chemoreceptors in the muscle. Afferent input from these receptors goes to the medullary cardiovascular centers. The result is afurther increase in heart rate, myocardial contractility, and vasoconstriction in the nonactivated organs. Mechanoreceptors of the exercising muscle are also stimulated and provide an excitatory input to the medullary cardiovascular center.

The arterial baroreceptors

As mean and pulsatile pressure increase, baroreceptors should respond to increase parasympathetic and decrease sympathetic outflows, a pattern designed to counter the rise in arterial pressure. During exercise the exact opposite occurs: the arterial baroreceptors increase the arterial pressure during exercise. The reason is that one of neuronal component of the central command output goes to the arterial baroreceptors and �resets� them upwards as exercise begins. The resetting causes a decrease firing frequency in the baroreceptors, signalling for decreased parasympathetic and increase in sympathetic outflow.

To continue with the next section: respiratory contribution, click here

How does Endurance training increase stroke volume?

The increase in size of the heart enables the left ventricle to stretch more and thus fill with more blood. The increase in muscle wall thickness also increases the contractility resulting in increased stroke volume at rest and during exercise, increasing blood supply to the body.

What increases stroke volume?

[2] In summary, stroke volume may be increased by increasing the contractility or preload or decreasing the afterload.

What are the mechanisms that could increase the stroke volume during exercise?

The physiological mechanisms for an enhanced stroke volume during exercise may include enhanced diastolic filling due to increases in blood volume, left ventricular diameter, and ventricular compliance, enhanced systolic emptying due to increases in myocardial contractility and decreases in ventricular afterload, or ...

Which two factors are increased during exercise which subsequently increases stroke volume?

The major causes of increased stroke volume during exercise in humans are in- creased myocardial contractility and increased venous return to the heart.

Identify a factor that can increase stroke volume in response to endurance training.

Abstract

Keywords

Cited by (0)

How does Endurance training increase stroke volume?

What increases stroke volume?

What are the mechanisms that could increase the stroke volume during exercise?

Which two factors are increased during exercise which subsequently increases stroke volume?

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