Oxygen tension and content in the regulation of limb blood flow

Abstract

During submaximal exercise, muscle blood flow increases when arterial oxygen content (CaO2) is reduced. The increase in blood flow is brought about by elevating cardiac output (CO) and enhancing leg vascular conductance. Conversely, increased CaO2 elicits lower limb blood flow (LBF) and CO. During maximal exercise, the influence of CaO2 on muscle blood flow is modulated depending on the amount of muscle mass recruited. When a small muscle mass is activated and the pumping capacity of the heart is not limited, changes in CaO2 barely influence the level of blood flow attained at peak exercise. However, when a large muscle mass is engaged in the exercise, as occurs for example during cycling and running, muscle blood flow is decreased if maximal CO is reduced, as happens during exercise in severe hypoxia. In contrast, maximal muscle blood flow and CO are maintained at peak exercise when CaO2 is increased. As such, exercise intensity, muscle mass and CaO2 appear to be the critical factors determining muscle blood flow during exercise.

Effect of exercise-induced arterial hypoxemia on quadriceps muscle fatigue in healthy humans

“…Second, locomotor muscle fatigue resulting from near-maximal, sustained exercise cannot be extrapolated necessarily to lower intensities of exercise. During submaximal exercise, cardiac output and muscle blood flow are capable of increasing to compensate for acute reductions in Ca O 2 (5,28,48), and O 2 extraction will increase across the working limb when cardiac output is reduced experimentally (48). At near-maximum exercise intensities, however, cardiac output, limb blood flow, and arteriovenous O 2 difference may not be able to compensate for reduced O 2 delivery.…”

Why do arms extract less oxygen than legs during exercise?

“…During exercise with a large muscle mass, the V O 2 peak of the lower extremities appears to be O 2 delivery dependent (6,7,16,33,35,57). O 2 extraction across the lower extremities may reach maximal values between 90 and 92% of the arterial O 2 content (Ca O 2 ), and the PO 2 in the femoral vein may be close to 10 mmHg in active subjects (6,7,16), leaving little room for further extraction. However, in sedentary subjects, the maximal O 2 extraction across the legs lies close to 70% of the Ca O 2 (59), implying that their peak muscular V O 2 also may be limited by intrinsic factors (20).…”

“…It is currently assumed that during exercise with a small muscle mass, intrinsic factors are the main determinants of peak local muscular V O 2 , because the O 2 delivery is extraordinary high (3,44,61). During exercise with a large muscle mass, the V O 2 peak of the lower extremities appears to be O 2 delivery dependent (6,7,16,33,35,57). O 2 extraction across the lower extremities may reach maximal values between 90 and 92% of the arterial O 2 content (Ca O 2 ), and the PO 2 in the femoral vein may be close to 10 mmHg in active subjects (6,7,16), leaving little room for further extraction.…”

Chronic hypoxia increases blood pressure and noradrenaline spillover in healthy humans

“…Hypoxia-mediated sympathetic activation is currently envisaged as a defence mechanism to assure O 2 supply to critical organs by means of raising cardiac output and regulating regional conductances (Rowell et al 1989;Leuenberger et al 1991;Duplain et al 1999;Calbet, 2000). In contrast, hypoxia either directly, or through its metabolic effects, causes vasodilatation in most vascular beds, such that sympathetic tone should be increased to avoid exaggerated vasodilatation and hypotension (Hilton & Eichholtz, 1925;Rowell et al 1989;Laughlin et al 1996).…”