Impact of Physical Exercise on Platelets: Focus on Its Effects in Metabolic Chronic Diseases

Figures

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  Figure 1. Effects of different types of physical activity on the increased risk of thrombus formation and cardiovascular (CV) events. Sedentary habits induce vascular inflammation that can lead to metabolic diseases. In the same way, prolonged intense training can promote an inflammatory milieu in blood vessels. Reactive oxygen species (ROS) production increases during both types of exercise, reducing nitric oxide (NO) availability and leading to platelet activation, which can contribute to CV events in the long term. Moderate and constant physical activity over time increases the bioavailability of NO, a potent platelet inhibitor, lowering the CV risk. Abbreviations: cyclooxygenase (COX); nicotinamide adenine dinucleotide phosphate (NADPH).

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  Figure 2. Pathways implicated in platelet activation; molecules involved in platelet granule release and ROS production. Fibrinogen binds to GPIIbIIIa, leading to an increase in cytosolic Ca2+ via PI3K; this leads to activation of integrin αIIbβ, granule release and PS externalization. Collagen binds to GPVI, enhancing the downstream FcR γ-chain ITAM domain-SYK pathway. This leads to Ca2+ mobilization and increased ROS production through Nox2 activation. The p38-PLA2 pathway leads to TxA2 formation via COX-1; the increase in COX-1 activity leads to ROS formation. Thrombin interacts with PAR1 and PAR4 on the platelet surface. PARs activate the Rho family GTPases RhoA, Rac1, and Cdc42, which are involved in platelet shape changes during platelet activation. This pathway also contributes to ROS generation. PCSK9 binds to the scavenger receptor CD36 on the platelet surface, enhancing ROS production through the GPVI-ITAM-SYK, the ERK5, and the JNK pathways. Other sources of ROS generation are mitochondria and endothelial and vascular smooth muscle cells. The imbalance between ROS production and ROS clearance causes oxidative stress [16].