Skeletal Muscle-Cardiovascular System Interaction
The skeletal muscular system and cardiovascular system function as an integrated unit during exercise, where contracting muscles drive dramatic increases in cardiac output (up to 4-6 fold above baseline) primarily through metabolic vasodilation that redistributes up to 90% of total cardiac output to working muscles, while the muscle pump facilitates venous return and the heart responds with coordinated increases in both heart rate and stroke volume. 1
Primary Mechanisms of Interaction
Cardiac Output Response to Muscle Demand
During exercise, maximal cardiac output correlates directly with peak oxygen consumption (VO2), and inadequate cardiac output reserve is the primary determinant of impaired aerobic capacity. 1
As exercise intensity increases, cardiac output rises through augmentation of both stroke volume (via the Frank-Starling mechanism) and heart rate, though stroke volume typically plateaus at 50-60% of maximal oxygen uptake except in elite athletes. 1
The heart rate increases linearly with workload and oxygen demand during dynamic exercise, rising approximately 10 beats per minute per metabolic equivalent (MET). 1
Blood Flow Redistribution to Working Muscle
In normal subjects, approximately 90% of total cardiac output is distributed to exercising skeletal muscle during maximal lower extremity exercise, compared to only 50-60% in patients with heart failure. 1
This redistribution occurs through sympathetic-mediated vasoconstriction in most circulatory systems (except exercising muscle, cerebral, and coronary circulations), while metabolic vasodilation dominates in working muscles. 1
Skeletal muscle blood flow and oxygen extraction increase dramatically during exercise, with oxygen extraction increasing as much as 3-fold, while total peripheral resistance decreases. 1
Metabolic Vasodilation as the Primary Driver
The primary determinant of sustained exercise hyperemia in skeletal muscle is metabolic vasodilation, not the mechanical muscle pump. 2
Metabolites from contracting muscle diffuse to resistance arterioles and induce vasodilation directly, or indirectly inhibit noradrenaline release from sympathetic nerve endings to oppose vasoconstriction. 2
Capillaries play an active role by responding to skeletal muscle contraction and transmitting dilatory signals to at least three branch orders of upstream arterioles, directing increased blood flow specifically to contracting muscle fibers. 3
The Muscle Pump Mechanism
Limited Role in Flow Generation
The skeletal muscle pump is not obligatory for sustaining venous return, central venous pressure, stroke volume, or cardiac output during exercise, and its contribution to peak exercise hyperemia is minimal compared to metabolic vasodilation. 4
Passive exercise and thigh compressions increase blood flow by only 0.5-0.7 L/min without altering cardiac output, mean arterial pressure, or oxygen consumption, accounting for only approximately 5% of peak exercise hyperemia. 4
However, the muscle pump does facilitate venous return through rhythmic propulsion of blood from skeletal muscle veins back to the heart. 2, 5
Mechanical Flow-Generating Capacity
- The isolated skeletal muscle pump can generate significant blood flow (87 ml/min increase) through mechanical forces alone during contraction and relaxation, even without an arterial-venous pressure gradient. 5
Pressure Responses During Exercise
Dynamic (Aerobic) Exercise
Dynamic exercise imposes primarily a volume load on the cardiovascular system, with progressive increases in systolic blood pressure while diastolic blood pressure remains unchanged or slightly decreases, resulting in widened pulse pressure. 1
Mean arterial pressure increases modestly during dynamic exercise, with decreased peripheral vascular resistance as blood is shunted to active skeletal muscle. 1
Isometric (Resistance) Exercise
Isometric exercise imposes a significant pressure load, with disproportionate rises in both systolic and diastolic blood pressure, mean blood pressure, and peripheral vascular resistance. 1
At 20-30% maximum voluntary contraction, intramuscular pressure exceeds intravascular pressure, significantly reducing localized blood flow and causing muscle ischemia. 1
Neurohormonal Integration
Sympathetic Control
As exercise intensity surpasses anaerobic threshold, sympathetic discharge becomes maximal and parasympathetic stimulation is inhibited, resulting in vasoconstriction in non-exercising tissues. 1
Complex interactions between the sympathetic nervous system and the microcirculation permit just enough sympathetic control of blood flow to contracting muscles to regulate blood pressure during large muscle mass exercise. 6
Baroreceptor Regulation
Baroreceptor stimulation triggers reflex vasodilation in skeletal muscle through withdrawal of sympathetic vasoconstrictor tone, while decreased carotid sinus pressure causes compensatory vasoconstriction to maintain blood pressure. 7
Control of vasomotor function by the arterial baroreflex is the key mechanism for rapid hemodynamic adjustments, particularly during postural changes. 7
Clinical Implications in Heart Failure
In moderate to severe chronic heart failure, decreased skeletal muscle vasodilation in response to exercise is an important determinant of decreased peak VO2, caused by increased vascular resistance and endothelial dysfunction. 1
Skeletal muscle atrophy is frequent in heart failure patients, linked to under-perfusion, malnutrition, and cytokine effects, resulting in decreased strength and muscle endurance capacity. 1
The main mechanisms responsible for functional abnormalities of peripheral perfusion include systemic neurohormonal hyperactivity with predominance of vasoconstrictor systems (sympathetic nervous system, renin-angiotensin-aldosterone system, endothelin, vasopressin). 1