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Exercise and Vascular Function

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Textbook of Sports and Exercise Cardiology

Abstract

The vascular system does not only supply organs with oxygen and nutrients, but also adjusts blood flow to each organ and blood pressure. The endothelium furthermore controls haemostasis and passage of cells and molecules between blood and tissues. Hence, there is a strong association between loss of vascular function and increased cardiovascular risk. Regular physical activity effectively counteracts and delays the development of vascular dysfunction by exerting shear forces, regulating energy expenditure and thus metabolic function and furthermore by initiating the release of circulating anti-inflammatory and anabolic mediators. This is initiated by a systemic adaptation to the altered muscular energy demands, by anabolic and vasodilative signalling, which allows adaptation of the local and systemic vasculature to increased perfusion demands, as well as by engagement of neuro-humoral and metabolic mechanisms. Exercise parameters such as intensity, type and frequency, differentially address these mechanisms, resulting in heterogeneous effects on metabolic, inflammatory and structural outcomes. In addition, patients’ underlying pathology, fitness level, age and sex modulate the effect of exercise on cardiovascular risk. A number of methods have been developed to study micro- and macrovascular functions as well as overall perfusion, with variance as to their suitability for study purposes and clinical routine. This chapter provides an overview over bio-chemical and cellular mechanisms of vascular dysfunction in cardiovascular diseases and mechanisms by which exercise can prevent the deterioration of vascular function. We also introduce methods to study vascular function in human subjects and discuss their utility in experimental and routine clinical settings.

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Correspondence to Nicolle Kränkel .

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1.1 Questions

  1. 1.

    Which is the most prominent factor regulating vasodilation?

  2. (a)

    Bioavailability of nitric oxide (NO)

  3. (b)

    Degradation of extracellular matrix by matrix metalloproteases

  4. (c)

    Expression of ROS generating enzymes and subsequently the concentration of ROS.

  5. (d)

    The level of ATP generated by the mitochondria

  6. 2.

    Increased plasma levels of LDL cholesterol and low plasma levels of HDL cholesterol are associated with increased cardiovascular risk. How can regular exercise training affect HDL and LDL levels? Which exercise parameters (type, duration, intensity, frequency) impact on the outcome? Which patients benefit most?

  7. (a)

    HDL levels are increased by endurance exercise with longer exercise durations improving the effect.

  8. (b)

    Lipoprotein(a) is decreased by high-intensity training in non-diabetic individuals.

  9. (c)

    LDL is increased by combined endurance/resistance exercise.

  10. (d)

    LDL levels are reduced by high-intensity interval endurance exercise in MetS.

  11. (e)

    HDL levels are only increased in exercise interventions when the weight remains stable.

  12. 3.

    What is the underlying mechanism for vasodilation in response to cuff occlusion/release in healthy arteries?

  13. (a)

    Shear stress-induced NO production through mechanosensors in the endothelial cell

  14. (b)

    Accumulated ROS, generated during occlusion, suddenly flood the artery.

  15. (c)

    Temperature increase due to restored blood flow.

  16. (d)

    Hypoxia-induced signalling from the occluded region.

  17. (e)

    Oxygen-induced spike in NO production after the cuff has been released.

1.2 Answers

  1. 1.
    1. (a)

      Bioavailability of nitric oxide (NO)

  2. 2.
    1. (a)

      HDL levels are increased by endurance exercise with longer exercise durations improving the effect.

  3. 3.
    1. (a)

      Shear stress-induced NO production through mechanosensors in the endothelial cell

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Kränkel, N., van Craenenbroeck, E., Adams, V. (2020). Exercise and Vascular Function. In: Pressler, A., Niebauer, J. (eds) Textbook of Sports and Exercise Cardiology. Springer, Cham. https://doi.org/10.1007/978-3-030-35374-2_40

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