Mechanoreceptor-mediated adaptations to physical exercise: from acute responses to long-term training effects

Figures

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  Fig. 1. According to the set-point theory, mean hemodynamic forces remain within the physiological range at rest. During acute exercise in sedentary individuals, physical activity induces hemodynamic forces that exceed this set point. In trained subjects, repeated elevation of hemodynamic forces by training induces vascular adaptation that promotes a larger set-point window, thereby limiting further adaptations. Acute exercise elicits functional immediate vasodilation, whereas long-term exposure leads to vascular remodeling. Figure created with BioRender

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  Fig. 2. Sensors and signals from hemodynamic forces driving vascular function improvement and remodeling with training. During exercise, the increase in hemodynamic forces is sensed by mechanosensors, which initiate signaling cascades. With repeated bouts of endurance training, these stimuli are associated with improvements in vascular function and structural remodeling. However, the precise mechanistic link between the initial molecular signals and the long-term vascular adaptations remains poorly defined, highlighting a critical gap in our understanding of exercise physiology. VSCM vascular smooth muscle cell, NO nitric oxide, eNOS endothelium nitric oxide synthase, VEGF vascular endothelium growth factor, MMps matrix metalloproteinases, ROS reactive oxygen species, ↑ increase, ↓decrease, = remain stable. Figure created with BioRender