Cardiac output limits maximal oxygen consumption, but what limits maximal cardiac output?

IF 2.6 4区 医学 Q2 PHYSIOLOGY
Ilkka Heinonen
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引用次数: 0

Abstract

Maximal oxygen uptake/consumption is an important variable determining exercise performance. It is generally considered to be limited largely, but not exclusively, by maximal cardiac output (CO), which limits the ability of heart to pump oxygen-rich arterial blood to working muscles. Cardiac output is a product of heart rate and stroke volume, which is the amount of blood ejected from the heart by one heart beat. Exercise training, especially of the endurance type, can increase maximal CO substantially. A straightforward way for the heart to increase maximal CO would be to increase maximal heart rate, but this does not happen; instead, maximal heart rate tends to be reduced after training. This is because heart rate is the most important determinant of myocardial oxygen consumption, and ventricular filling and myocardial blood flow (MBF) would be compromised by further increases in heart rate, given that MBF is blunted by contractions and occurs principally during diastole. Myocardial oxygen extraction is already high at rest and is increased further in endurance-trained athletes, making their hearts even more dependent on increases in MBF. The trained heart therefore also shows reduced MBF, enhanced blood mean transit time and higher myocardial vascular resistance at rest and during submaximal exercise, although MBF reserve is not improved. It follows logically that MBF is an important determinant of myocardial performance, and it is proposed in this review that cardiac afferent sensory nerves might contribute to controlling and limiting heart rate, hence maximal CO, in order to protect the heart from ischaemia.

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来源期刊
Experimental Physiology
Experimental Physiology 医学-生理学
CiteScore
5.10
自引率
3.70%
发文量
262
审稿时长
1 months
期刊介绍: Experimental Physiology publishes research papers that report novel insights into homeostatic and adaptive responses in health, as well as those that further our understanding of pathophysiological mechanisms in disease. We encourage papers that embrace the journal’s orientation of translation and integration, including studies of the adaptive responses to exercise, acute and chronic environmental stressors, growth and aging, and diseases where integrative homeostatic mechanisms play a key role in the response to and evolution of the disease process. Examples of such diseases include hypertension, heart failure, hypoxic lung disease, endocrine and neurological disorders. We are also keen to publish research that has a translational aspect or clinical application. Comparative physiology work that can be applied to aid the understanding human physiology is also encouraged. Manuscripts that report the use of bioinformatic, genomic, molecular, proteomic and cellular techniques to provide novel insights into integrative physiological and pathophysiological mechanisms are welcomed.
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