Chapter 8:Acute and Chronic Cardiorespiratory Responses to Exercise Flashcards
Cardiorespiratory Changes and Responses to Exercise and Recovery
The immediate changes that occur at the onset of exercise are governed by:
–increased output from the motor cortex in the brain that directs the cardiovascular control
–respiratory control centers located in the medulla
Heart Rate
SA Node- “Pacemaker” of the heart
Parasympathetic Activity: Keeps heart rate below 100 bpm
When exercise starts:
The parasympathetic system is decreased allowing HR to rise.
Activity of the sympathetic nervous system gradually increases.
Initial rise in HR is abrupt and occurs within the first few minutes of activity.
Steady state: HR reaches a plateau and remain stable when exercise intensity is constant and lactate threshold is not reached
Increasing Intensity=Increased HR and demand for oxygen
Stroke Volume & Cardiac Output
Stroke Volume: Amount of blood ejected by the heart in one beat
Increased SV at the start of exercise is caused by the release of norepinephrine (also increases ventricular contractility).
SV increases in proportion to exercise intensity but reaches a maximum value at approximately 40%-60% VO2max
Stroke Volume & Cardiac Output
Notice that “Q” or cardiac output remains stable.
Increases inHR and SV combine to increase Q during prolonged exercise.
Blood Pressure and Total Peripheral Resistance
Systolic blood pressure (SBP), mean arterial pressure (MAP), and pulse pressure (PP) rise at the onset of cardiorespiratory exercise, whereas DBP remains stable (~70–80 mm Hg).
–Typical maximal values for SBP range from 160 to 220 mm Hg.
–Further increase is a hypertensive response, and a failure to increase normally is a hypotensive response.
How does BP increase at the start of exercise?
Increased sympathetic vasoconstriction of veins and arterioles
Reduced parasympathetic activity to heart and blood vessels
Abrupt increase in cardiac output
Total Peripheral Resistance (TPR) decreases to enhance delivery of blood and oxygen to the working muscle, a process known as Blood Flow Redistribution.
Blood is pushed where it needs go, our muscle will open up to allow more blood flow in an area
EX
Digestion system may be vasoconstricted when we run
Skeletal muscle will vasodilate when we run
Pulmonary Ventilation
Increase in ventilation at the onset of exercise happens because of increased tidal volume and respiratory rate (RR)
Change if we rest and trying to recover back to ocygenlevels- EPOC
Ventilation will continue to rise during prolonged exercise and can reach even greater levels during incremental exercise to maximum intensity.
PO2 & PCO2
Arterial partial pressure of oxygen (PO2) and carbon dioxide (PCO2) deviate very little from rest to steady-state exercise.
Generally, PO2 remains constant up to maximal exercise levels in most people.
In some cases, however, PO2 may decrease significantly, a phenomenon known as exercise-induced hypoxemia.
Ventilatory Drift
During long duration sub-maximal exercise of high intensity (e.g., >75% V̇O2max) and exercise in a hot environment, V̇E drifts progressively upward (increase in V̇E/V̇O2 ratio), despite no change in exercise workload.
Start to breathe a lot faster
Drifting of V̇E is due primarily to the increased respiratory rates that accompany high intensity exercise.
Main stimuli for increased ventilation:
Increased epinephrine/norpinephrine
Increased body temperature
Ventilatory Threshold
Ventilatory Threshold 1:The point (or exercise intensity) at which V̇E first breaks from linearity with respect to oxygen uptake (expressed as %V̇O2 max)
Ventilatory Threshold 2: When ventilation continues to increase and reaches second deviation- AKA respiratory compensation point
Blood Flow and Oxygen Delivery to Skeletal Muscle
Metabolic demand can rise 15-20 times during exercise
Oxygen is used to regenerate mitochondrial ATP
Blood flow must increase proportionally with exercise demand
A limitation of the cardiovascular system is that it contains a finite amount of blood volume (5–6 L) to be circulated.
3 ways the cardiovascular system can overcome this:
1.Recirculate blood at a higher rate above resting levels
2.Shunt more blood away from non-active tissues to active tissues through targeted vasoconstriction
3.Extract more oxygen from the blood
Cardiac Output Responses
Q increases as a function of increases in HR and SV.
Q can increase five to eight times above resting values (25–40 L/min at maximal exercise)
Increases in Q provide the exercising muscle with the blood flow it needs to match its energy demand.
Redistribution of Systemic Blood Flow
During maximal exercise, up to 80% to 85% of total Q is delivered to skeletal muscle. Along these lines, if maximal Q is measured at 30 L/min, then roughly 25 L of blood are perfusing skeletal muscle every minute.
How does this happen?
The sympathetic nervous system and local vasodilators work in concert to redistribute blood flow to where it is needed most: working muscles, heart, and skin.
Vasoconstriction occurs at areasthat do not need as much blood supply (digestive system)
Arterial-Venous Oxygen Difference
Increases in a nonlinear fashion with incremental exercise
Cardiorespiratory Control During Exercise
The cerebral cortex provides the initial drive to increase Q and V̇E at the start of exercise.
Cardiovascular sensory information (e.g., HR, SV, blood pressure, etc.) and respiratory sensory information (e.g., V̇E, PO2, PCO2, blood pH level, respiratory muscle activity, etc.) is detected by various peripheral and central chemoreceptors located throughout the body and brain.
The receptors provide beat-by-beat and breath-by-breath information that is relayed back to the control centers in the brain, whereby adjustments are made in cardiovascular and respiratory function so that homeostasis is maintained during exercise.
Mechanoreceptors
Mechanoreceptors in the muscles (e.g., muscle spindle and Golgi tendon organ) and joints send output signals to the cardiorespiratory control centers with regard to the intensity of movement, changes in joint movement, pressure, and position.
When stimulated during exercise, impulses are relayed to the medulla to modify activity of the cardiovascular and respiratory control centers so that Q and V̇E can be regulated during exercise.
Some evidence suggests that the right atrium and ventricle contain mechanoreceptors that sense changes in the size (or volume) of the chamber.
–When Q rises, these receptors send impulses to the respiratory control center to stimulate an increase in V̇E and HR.
Chemoreceptors
The primary chemoreceptors that fine-tune activity of the cardiorespiratory system are the aortic and carotid bodies and the central chemoreceptors located in the medulla.
–Modulate V̇E by supplying the respiratory control center with continuous breath-by-breath information on arterial PCO2, PO2, and blood pH
Baroreceptors
Sense pressure or stretch in the heart, carotid sinus, aortic arch, and other major arteries
Baroreflex: At the onset of exercise, the blood pressure set point at which the baroreceptors have been established is raised from its resting state, allowing blood pressure and HR to rise abruptly.
Thermoreceptors
When body temperature rises during exercise, blood flow through the hypothalamus stimulates thermoreceptors that modify the cardiovascular control center, which causes vasodilation of skin blood vessels to dissipate heat from the body.
The hypothalamus also sends output signals to sweat glands in the skin to increase sweat production.
Summary
Increased sympathetic nervous system activity causes HR and SV (due to increased myocardial contractility) to rise.
Local factors within the working muscle (and sympathetic activity) stimulate vasodilation, which lowers TPR (decreases afterload), facilitating a greater Q.
Respiratory pump, skeletal muscle pump, and venoconstriction help to increase venous return.
Venous return enhances end-diastolic volume, which helps to increase SV as exercise intensity increases.
Vasoconstriction of vessels of less active tissues helps to redistribute blood flow to the working muscle.
Cardiac Output and HR
Consistent participation in aerobic exercise lowers resting HR, often below 60 bpm.(ex runner)
Resting HR is reduced with training; resting SV is increased to maintain Q.
–More ventricular filling time
–Larger ventricular chamber size
Q will be higher in a trained person compared with an untrained person. Bc have a high SV
Stroke Volume
SV is substantially increased following training.
–Left ventricular chamber enlargement and increased plasma volume combine to significantly increase end-diastolic volume.
–Increased end-diastolic volume enhances preload, which increases myocardial contractility.
–Training helps to lower TPR (afterload), which facilitates ventricular emptying.
–Endurance training improves diastolic filling.
Cardiac Hypertrophy
Endurance training increases the size of the heart, primarily by enlarging the left ventricular chamber volume and mild-to-moderate hypertrophy of the left ventricular myocardium.
Greater left ventricular filling volumes combined with more muscle mass will produce a greater SV and maximal Q.
Ventilation
Resting V̇E is unchanged following training; although, RR may be lower and VT higher at rest due to increased parasympathetic control.
Reduced V̇E during exercise is partly attributed to lower respiratory rates during exercise and increased VT.
Improved ventilatory efficiency is attributed to increased strength and endurance of the respiratory muscles and improved regulation of blood pH.
Blood: Plasma and Other Factors
Plasma volume can be increased up to 500 mL or more by training.
Increases the force of contraction, enhancing SV, allowing for a decrease in HR, and permitting the heart to be more efficient at maintaining Q at rest
Better capacity to extract oxygen from blood during exercise (increased a-Vo2 difference)
Vasodilation lowersvascular resistance to exercising muscle, improving delivery of oxygen
Post training can increase plasma increase and cause heart to be more efficent
