Moritz Lampkemeyer, Jonas Kell, Veit Börß, Tobias Claussen, Fabian Spahiu, Michelle Ottlik, Lars C Helbig, Craig G Crandall, Eric J Stöhr
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引用次数: 0
Abstract
It is widely accepted that cardiac output matches the prevailing peripheral demand in healthy humans. However, it remains unknown whether stroke volume and heart rate are regulated interdependently to arrive at a specific cardiac output. The aim of this study was to determine whether the healthy human heart responds specifically according to the peripheral demands of heat stress and exercise. Eleven healthy humans (women/men n = 3/8; age = 26 ± 2 years; body mass = 73 ± 11 kg) underwent leg heat stress and cycling exercise (60 W), with and without blood flow restriction (pressure set at the prevailing mean arterial pressure of the individual). Cardiac output was measured with triplane echocardiography. Additionally, haemodynamics, oxygen consumption, carbon dioxide production and lactate were assessed. Data were analysed using two-way repeated-measures ANOVA. Despite stable heat and exercise demands, cardiac output decreased significantly with blood flow restriction in both conditions (Δ-0.87 and -1.03 L min-1, 17% and 11%, respectively, p = 0.01), owing to a decline in end-diastolic volume (p < 0.0001) and stroke volume (p < 0.0001) not sufficiently compensated for by an increase in heart rate (p = 0.001). Importantly, these responses were accompanied by an increased rate of skin temperature rise (p = 0.04) during heat stress and a significantly greater rise in circulating lactate (p < 0.0001) during exercise. The cardiac output response to local heat stress and submaximal exercise does not appear to be entirely specific to the peripheral thermal and energetic requirements. This finding supports the theory that even the healthy heart does not coordinate stroke volume and heart rate to arrive at a specific target output.
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.