During exercise, significant changes occur in cardiac output and blood flow distribution.
Cardiac output (Q) at rest is approximately 5 L/min, but increases to 25 L/min during heavy exercise.
Blood flow to skeletal muscles increases dramatically:
20% during rest contributes to 1 L/min in muscles.
80-85% during heavy exercise contributes to ~20 L/min in muscles.
Blood flow to less active organs (liver, kidneys, gastrointestinal tract) decreases significantly.
Key factors influencing cardiac output and blood flow include:
Metabolic vasodilation in muscles increases blood flow.
Increased cardiac stroke volume and heart rate (HR) during exercise.
The sympatho-adrenal system enhances heart rate and improves venous return.
Skeletal muscle activity prompts sympathetic vasoconstriction in viscera.
Deeper breathing also contributes to cardiovascular adjustments.
The equation related to cardiac output and physical activity is:
Q (cardiac output) = SV (stroke volume) x HR (heart rate).
The redistribution of blood flow primarily facilitates the increased oxygen demands by muscles during exercise.
During exercise, there is:
An increase in heart rate (HR) and stroke volume (SV).
In untrained subjects, SV does not increase beyond workloads of 40% VO2max.
Consequently, the rise in cardiac output at higher intensities is mainly due to an increase in HR.
Cardiac output is maintained during prolonged exercise, but:
Stroke volume gradually decreases due to dehydration and reduced plasma volume.
Heart rate gradually increases, termed "cardiovascular drift."
At rest, 15-20% of cardiac output is directed to muscles.
This increases to 80-85% during maximal exercise.
The redistribution of blood flow is dependent on exercise intensity and metabolic rate.
Oxygen demand during exercise is 15-25 times greater than at rest.
This demand is met by:
Increased cardiac output and redistribution of blood flow.
Enhanced extraction/uptake of O2 by muscle tissues.
VO2 is expressed as:
VO2 = Q x (a - vO2Δ)
Where a-vO2Δ is the arteriovenous oxygen difference, representing the difference in oxygen content between arterial and venous blood.
Not all O2 delivered to muscles is consumed, necessitating the efficient extraction of O2 to maximize VO2.
The a-vO2 difference reflects the oxygen extracted from 100 mL of blood during its circulatory journey.
Example:
At rest: 20 mL O2 – 15 mL O2 = 5 mL extracted.
During exercise: 20 mL O2 – 10 mL O2 = 10 mL extracted.
A higher a-vO2 difference during exercise indicates better oxygen utilization.
Endurance training involves continuous, dynamic exercises, such as running or cycling, for 20-60 mins at >50% VO2max, 3 times a week over 2-3 months.
Such training enhances:
Cardiac output delivery (Q) and oxygen extraction (a-vO2Δ).
The VO2max, which indicates the maximum capacity of oxygen utilization during exercise.
Qmax largely increases due to a rapid rise in stroke volume (SV).
An 11% increase in SV can occur within the first 6 days of training.
Following training, it has been observed that resting and submaximal heart rates decrease without affecting HRmax.
Stroke volume increases (SVmax) with:
Increased preload (end-diastolic volume).
Increased plasma volume (fluid retention).
Greater filling time due to a decreased resting heart rate.
There is also an increase in ventricular chamber size allowing for maximal filling and decreased afterload.
Aerobic Training:
Results in eccentric hypertrophy (volume overload), characterized by chamber dilation and elongated myocyte length.
Resistance Training:
Leads to concentric hypertrophy (pressure overload), marked by increased myocyte width without chamber dilation.
The maximum a-vO2Δ improves due to:
Increased mitochondrial size and enzyme activity.
Enhanced capillary density and blood flow in muscles through vessel dilation.