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      Enhanced muscle blood flow with intermittent pneumatic compression of the lower leg during plantar flexion exercise and recovery

      Author(s): 1 , 2 , 1 , 3 , 2
      Publication date Created:
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      Journal: Journal of Applied Physiology
      Publisher: American Physiological Society

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          Abstract

          This study tested the hypothesis that intermittent compression of the lower limb would increase blood flow during exercise and postexercise recovery. Data were collected from 12 healthy individuals (8 men) who performed 3 min of standing plantar flexion exercise. The following three conditions were tested: no applied compression (NoComp), compression during the exercise period only (ExComp), and compression during 2 min of standing postexercise recovery. Doppler ultrasound was used to determine superficial femoral artery (SFA) blood flow responses. Mean arterial pressure (MAP) and cardiac stroke volume (SV) were assessed using finger photoplethysmography, with vascular conductance (VC) calculated as VC = SFA flow/MAP. Compared with the NoComp condition, compression resulted in increased MAP during exercise [+3.5 ± 4.1 mmHg (mean ± SD)] but not during postexercise recovery (+1.6 ± 5.9 mmHg). SV increased with compression during both exercise (+4.8 ± 5.1 ml) and recovery (+8.0 ± 6.6 ml) compared with NoComp. There was a greater increase in SFA flow with compression during exercise (+52.1 ± 57.2 ml/min) and during recovery (+58.6 ± 56.7 ml/min). VC immediately following exercise was also significantly greater in the ExComp condition compared with the NoComp condition (+0.57 ± 0.42 ml·min −1·mmHg −1), suggesting the observed increase in blood flow during exercise was in part because of changes in VC. Results from this study support the hypothesis that intermittent compression applied during exercise and recovery from exercise results in increased limb blood flow, potentially contributing to changes in exercise performance and recovery.

          NEW & NOTEWORTHY Blood flow to working skeletal muscle is achieved in part through the rhythmic actions of the skeletal muscle pump. This study demonstrated that the application of intermittent pneumatic compression during the diastolic phase of the cardiac cycle, to mimic the mechanical actions of the muscle pump, accentuates muscle blood flow during exercise and elevates blood flow during the postexercise recovery period. Intermittent compression during and after exercise might have implications for exercise performance and recovery.

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          Vasodilatory mechanisms in contracting skeletal muscle.

          Philip S. Clifford, Ylva Hellsten (2004)
          Skeletal muscle blood flow is closely coupled to metabolic demand, and its regulation is believed to be mainly the result of the interplay of neural vasoconstrictor activity and locally derived vasoactive substances. Muscle blood flow is increased within the first second after a single contraction and stabilizes within approximately 30 s during dynamic exercise under normal conditions. Vasodilator substances may be released from contracting skeletal muscle, vascular endothelium, or red blood cells. The importance of specific vasodilators is likely to vary over the time course of flow, from the initial rapid rise to the sustained elevation during steady-state exercise. Exercise hyperemia is therefore thought to be the result of an integrated response of more than one vasodilator mechanism. To date, the identity of vasoactive substances involved in the regulation of exercise hyperemia remains uncertain. Numerous vasodilators such as adenosine, ATP, potassium, hypoxia, hydrogen ion, nitric oxide, prostanoids, and endothelium-derived hyperpolarizing factor have been proposed to be of importance; however, there is little support for any single vasodilator being essential for exercise hyperemia. Because elevated blood flow cannot be explained by the failure of any single vasodilator, a consensus is beginning to emerge for redundancy among vasodilators, where one vasoactive compound may take over when the formation of another is compromised. Conducted vasodilation or flow-mediated vasodilation may explain dilation in vessels (i.e., feed arteries) not directly exposed to vasodilator substances in the interstitium. Future investigations should focus on identifying novel vasodilators and the interaction between vasodilators by simultaneous inhibition of multiple vasodilator pathways.
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            Regulation of the skeletal muscle blood flow in humans.

            Stefan P Mortensen, Bengt Saltin (2014)
            In humans, skeletal muscle blood flow is regulated by an interaction between several locally formed vasodilators, including NO and prostaglandins. In plasma, ATP is a potent vasodilator that stimulates the formation of NO and prostaglandins and, very importantly, can offset local sympathetic vasoconstriction. Adenosine triphosphate is released into plasma from erythrocytes and endothelial cells, and the plasma concentration increases in both the feed artery and the vein draining the contracting skeletal muscle. Adenosine also stimulates the formation of NO and prostaglandins, but the plasma adenosine concentration does not increase during exercise. In the skeletal muscle interstitium, there is a marked increase in the concentration of ATP and adenosine, and this increase is tightly coupled to the increase in blood flow. The sources of interstitial ATP and adenosine are thought to be skeletal muscle cells and endothelial cells. In the interstitium, both ATP and adenosine stimulate the formation of NO and prostaglandins, but ATP has also been suggested to induce vasoconstriction and stimulate afferent nerves that signal to increase sympathetic nerve activity. Adenosine has been shown to contribute to exercise hyperaemia, whereas the role of ATP remains uncertain due to lack of specific purinergic receptor blockers for human use. The purpose of this review is to address the interaction between vasodilator systems and to discuss the multiple proposed roles of ATP in human skeletal muscle blood flow regulation.
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              Mechanical influences on skeletal muscle vascular tone in humans: insight into contraction-induced rapid vasodilatation.

              Frank Dinenno, Wyatt F Voyles, Roger Markwald … (2007)
              We tested the hypothesis that mechanical deformation of forearm blood vessels via acute increases in extravascular pressure elicits rapid vasodilatation in humans. In healthy adults, we measured forearm blood flow (Doppler ultrasound) and calculated forearm vascular conductance (FVC) responses to whole forearm compressions and isometric muscle contractions with the arm above heart level. We used several experimental protocols to gain insight into how mechanical factors contribute to contraction-induced rapid vasodilatation. The findings from the present study clearly indicate that acute increases in extravascular pressure (200 mmHg for 2 s) elicit a significant rapid vasodilatation in the human forearm (peak DeltaFVC approximately 155%). Brief, 6 s sustained compressions evoked the greatest vasodilatation (DeltaFVC approximately 260%), whereas the responses to single (2 s) and repeated compressions (five repeated 2 s compressions) were not significantly different (DeltaFVC approximately 155% versus approximately 115%, respectively). This mechanically induced vasodilatation peaks within 1-2 cardiac cycles, and thus is dissociated from the temporal pattern normally observed in response to brief muscle contractions ( approximately 4-7 cardiac cycles). A non-linear relation was found between graded increases in extravascular pressure and both the immediate and peak rapid vasodilatory response, such that the responses increased sharply from 25 to 100 mmHg, with no significant further dilatation until 300 mmHg (maximal DeltaFVC approximately 185%). This was in contrast to the linear intensity-dependent relation observed with muscle contractions. Our collective findings indicate that mechanical influences contribute largely to the immediate vasodilatation (first cardiac cycle) observed in response to a brief, single contraction. However, it is clear that there are additional mechanisms related to muscle activation that continue to cause and sustain vasodilatation for several more cardiac cycles after contraction. Additionally, the potential contribution of mechanical influences to the total contraction-induced hyperaemia appears greatest for low to moderate intensity single muscle contractions, and this contribution becomes less significant for sustained and repeated contractions. Nevertheless, this mechanically induced vasodilatation could serve as a feedforward mechanism to increase muscle blood flow at the onset of exercise, as well as in response to changes in contraction intensity, prior to alterations in local vasodilating substances that influence vascular tone.
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                Author and article information

                Journal
                Title: Journal of Applied Physiology
                Abbreviated Title: Journal of Applied Physiology
                Publisher: American Physiological Society
                ISSN (Print): 8750-7587
                ISSN (Electronic): 1522-1601
                Publication date Created: February 01 2018
                Publication date (Print): February 01 2018
                Volume: 124
                Issue: 2
                Pages: 302-311
                Affiliations
                [1 ]University of Waterloo, Department of Kinesiology, Waterloo, Ontario, Canada
                [2 ]University of Waterloo, Department of Mechanical and Mechatronics Engineering, Waterloo, Ontario, Canada
                [3 ]Schlegel-University of Waterloo Research Institute for Aging, Waterloo, Ontario, Canada
                Article
                DOI: 10.1152/japplphysiol.00784.2017
                PMC ID: 5867371
                PubMed ID: 29122964
                SO-VID: 1a218bfc-4926-4d36-a1fb-6371c2fbb32d
                Copyright © © 2018
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