Control of Blood Flow to Cardiac and Skeletal Muscle During Exercise

Laughlin, M. Harold; Korthuis, Ronald J.; Duncker, Dirk J.; Bache, Robert J.

doi:10.1002/cphy.cp120116

Cited by 134 publications

(220 citation statements)

References 428 publications

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“…A recent study showed a prolonged unfavourable effect of mental stress on indices of aortic stiffness and wave reflection. 15 Activation of the sympathetic nervous system has been documented during both mental stress 16 and exercise (static 17 or dynamic 18 ).…”

Section: Introductionmentioning

confidence: 99%

Changes of central haemodynamic parameters during mental stress and acute bouts of static and dynamic exercise

et al. 2008

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Chronic dynamic (aerobic) exercise decreases central arterial stiffness, whereas chronic resistance exercise evokes the opposite effect. Nevertheless, there is little information available on the effects of acute bouts of exercise. Also, there is limited data showing an increase of central arterial stiffness during acute mental stress. This study aimed to determine the effect of acute mental and physical (static and dynamic exercise) stress on indices of central arterial stiffness. Fifteen young healthy volunteers were studied. The following paradigms were performed: (1) 2 min of mental arithmetic, (2) short bouts (20 s) of static handgrip at 20 and 70% of maximal voluntary contraction (MVC), (3) fatiguing handgrip at 40% MVC and (4) incremental dynamic knee extensor exercise. Central aortic waveforms were assessed using SphygmoCor software. As compared to baseline, pulse wave transit time decreased significantly for all four interventions indicating that central arterial stiffness increased. During fatiguing handgrip there was a fall in the ratio of peripheral to central pulse pressure from 1.69 ± 0.02 at baseline to 1.56±0.05 (Po0.05). In the knee extensor protocol a nonsignificant trend for the opposite effect was noted. The augmentation index increased significantly during the arithmetic, short static and fatiguing handgrip protocols, whereas there was no change in the knee extensor protocol. We conclude that (1) during all types of acute stress tested in this study (including dynamic exercise) estimated central stiffness increased, (2) during static exercise the workload posed on the left ventricle (expressed as change in central pulse pressure) is relatively higher than that posed during dynamic exercise (given the same pulse pressure change in the periphery).

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Section: Introductionmentioning

confidence: 99%

Changes of central haemodynamic parameters during mental stress and acute bouts of static and dynamic exercise

et al. 2008

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“…SKELETAL MUSCLE BLOOD FLOW has long been known to exhibit a rapid increase at the onset of exercise (1,9,12,22,27). The mechanisms behind this phenomenon are still a matter of debate despite the many new insights provided by different research groups in recent years.…”

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confidence: 99%

Evidence that the contraction-induced rapid hyperemia in rabbit masseter muscle is based on a mechanosensitive mechanism, not shared by cutaneous vascular beds

Turturici

Mohammed

Roatta

2012

Journal of Applied Physiology

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Turturici M, Mohammed M, Roatta S. Evidence that the contraction-induced rapid hyperemia in rabbit masseter muscle is based on a mechanosensitive mechanism, not shared by cutaneous vascular beds. J Appl Physiol 113: 524 -531, 2012. First published June 7, 2012 doi:10.1152/japplphysiol.00237.2012.-Several mechanisms have been hypothesized to contribute to the rapid hyperemia at the onset of exercise. The aim of the present study was to investigate the role played by the mechanosensitivity of the vascular network. In 12 anesthetized rabbits blood flow was recorded from the exclusively muscular masseteric artery in response to brief spontaneous contractions (BSC) of the masseter muscle, artery occlusion (AO), muscle compression (MC), and muscle stretch (MS). Activation of masseter muscle was monitored by electromyography (EMG). Responses to AO were also recorded from the mostly cutaneous facial and the central ear arteries. Five animals were also tested in the awake condition. The hyperemic response to BSC (peak amplitude of 394 Ϯ 82%; time to peak of 1.8 Ϯ 0.8 s) developed with a latency of 300 -400 ms from the beginning of the EMG burst and 200 -300 ms from the contractioninduced transient flow reduction. This response was neither different from the response to AO (peak amplitude ϭ 426 Ϯ 158%), MC, and MS (P ϭ 0.23), nor from the BSC response in the awake condition. Compared with the masseteric artery, the response to AO was markedly smaller both in the facial (83 Ϯ 18%,) and in the central ear artery (68 Ϯ 20%) (P Ͻ 0.01). In conclusion, the rapid contractioninduced hyperemia can be replicated by a variety of stimuli affecting transmural pressure in muscle blood vessels and is thus compatible with the Bayliss effect. This prominent mechanosensitivity appears to be a characteristic of muscle and not cutaneous vascular beds. muscle stretch; myogenic response; rapid dilatation; reactive hyperemia; muscle compression SKELETAL MUSCLE BLOOD FLOW has long been known to exhibit a rapid increase at the onset of exercise (1,9,12,22,27). The mechanisms behind this phenomenon are still a matter of debate despite the many new insights provided by different research groups in recent years. In particular it has been shown that the contraction-induced compression of venous compartments (muscle pump) cannot fully account for the blood flow increase and that the additional occurrence of a rapid active dilatation is required (18,33,45,46). Other studies have shown that this rapid dilatation is mediated neither by changes in sympathetic neural drive (7, 41), nor by ACh spillover from the motor endplate (6, 33), nor by endothelium-released NO (6), although this last assertion is debated (see DISCUSSION). As early as 1974, Mohrman and Sparks (31) hypothesized that the rapid dilatation could result from the myogenic response of muscle blood vessels to decreased transmural pressure, which in turn results from the increase in intramuscular (extravascular) pressure produced by the contraction. They showed, in fact, that the rapid hypere...

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“…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). Elevated sympathetic activity has also been reported in patients with chronic hypoxaemia (defined as a low arterial pressure of O 2 (P a, J)) (Heindl et al 2001), as well as in patients with sleep apnoea who are intermittently hypoxaemic (Imadojemu et al 2002).…”

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confidence: 99%

Chronic hypoxia increases blood pressure and noradrenaline spillover in healthy humans

Calbet¹

2003

J Physiology

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Control of Blood Flow to Cardiac and Skeletal Muscle During Exercise

Cited by 134 publications

References 428 publications

Changes of central haemodynamic parameters during mental stress and acute bouts of static and dynamic exercise

Changes of central haemodynamic parameters during mental stress and acute bouts of static and dynamic exercise

Evidence that the contraction-induced rapid hyperemia in rabbit masseter muscle is based on a mechanosensitive mechanism, not shared by cutaneous vascular beds

Chronic hypoxia increases blood pressure and noradrenaline spillover in healthy humans

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