Haemodynamic responses to exercise, ATP infusion and thigh compression in humans: insight into the role of muscle mechanisms on cardiovascular function

Abstract

The muscle pump and muscle vasodilatory mechanims are thought to play important roles in increasing and maintaining muscle perfusion and cardiac output (Q) during exercise, but their actual contributions remain uncertain. To evaluate the role of the skeletal muscle pump and vasodilatation on cardiovascular function during exercise, we determined leg and systemic haemodynamic responses in healthy men during (1) incremental one-legged knee-extensor exercise, (2) step-wise femoral artery ATP infusion at rest, (3) passive exercise (n = 10), (4) femoral vein or artery ATP infusion (n = 6), and (5) cyclic thigh compressions at rest and during passive and voluntary exercise (n = 7). Incremental exercise resulted in progressive increases in leg blood flow (ΔLBF 7.4 ± 0.7 l min −1 ), cardiac output (ΔQ 8.7 ± 0.7 l min −1 ), mean arterial pressure (ΔMAP 51 ± 5 mmHg), and leg and systemic oxygen delivery andV O 2 . Arterial ATP infusion resulted in similar increases inQ, LBF, and systemic and leg oxygen delivery, but central venous pressure and muscle metabolism remained unchanged and MAP was reduced. In contrast, femoral vein ATP infusion did not alter LBF,Q or MAP. Passive exercise also increased blood flow (ΔLBF 0.7 ± 0.1 l min −1 ), yet the increase in muscle and systemic perfusion, unrelated to elevations in aerobic metabolism, accounted only for ∼5% of peak exercise hyperaemia. Likewise, thigh compressions alone or in combination with passive exercise increased blood flow (ΔLBF 0.5-0.7 l min −1 ) without alteringQ, MAP orV O 2 . These findings suggest that the skeletal muscle pump is not obligatory for sustaining venous return, central venous pressure, stroke volume andQ or maintaining muscle blood flow during one-legged exercise in humans. Further, its contribution to muscle and systemic peak exercise hyperaemia appears to be minimal in comparison to the effects of muscle vasodilatation.

Blood temperature and perfusion to exercising and non‐exercising human limbs

“…1954; González‐Alonso et al . 2002, 2008), but also because of its sympatholytic properties in the human limb circulation (Rosenmeier et al . 2004; Kirby et al .…”

A systematic review of exercise as a therapeutic intervention to improve arterial function in persons living with spinal cord injury

“…81 Further, others have shown the muscle pump to play a relatively small but significant role in leg blood flow during passive movement in AB individuals. 82 Also, Ballaz et al 49 provided follow-up literature illustrating that long-term passive exercise interventions lead to significantly improved vascular function. This literature 49,[81][82][83] strongly suggests that passive leg exercise increases femoral artery blood flow in people with SCI.…”

“…82 Also, Ballaz et al 49 provided follow-up literature illustrating that long-term passive exercise interventions lead to significantly improved vascular function. This literature 49,[81][82][83] strongly suggests that passive leg exercise increases femoral artery blood flow in people with SCI. Further research, with concurrent femoral artery flow measurements and isolated passive knee extension/flexion, is required to resolve this disagreement.…”

Effects of Dăoyĭn Qìgōng in postpolio syndrome patients with cold intolerance

“…This process requires the involvement of vasodilators and sympatholytic signals capable of replacing the increased vasoconstriction with neural reflexes in the muscle [36][37][38] . The temperature generated by the triggered muscle activity may activate the release of adenosine triphosphate (ATP) within the vascular lumen of the arterial tree, providing oxygenation to the limb tissue (including skeletal muscle and skin) and an increase in intravascular ATP [38][39][40][41][42][43] . This phenomenon suggests that overheating the thermostatic preoptic area (POA) of the anterior hypothalamus increases the rate of heat loss from the body through two mechanisms: (1) evaporative heat loss by stimulating the sweat glands and (2) inhibition of the sympathetic centers in the posterior hypothalamus, which normally cause constriction of cutaneous vessels; this inhibition triggers vasodilatation and a consequent increase in heat loss.…”