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Review
. 2023 Aug 14;12(8):1609.
doi: 10.3390/antiox12081609.

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

Cristina Barale  1 , Elena Melchionda  1 , Giulia Tempesta  1 , Alessandro Morotti  1 , Isabella Russo  1
Affiliations
Review

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

Cristina Barale et al. Antioxidants (Basel). .

Abstract

Chronic disorders are strongly linked to cardiovascular (CV) diseases, and it is unanimously accepted that regular exercise training is a key tool to improving CV risk factors, including diabetes, dyslipidemia, and obesity. Increased oxidative stress due to an imbalance between reactive oxygen species production and their scavenging by endogenous antioxidant capacity is the common ground among these metabolic disorders, and each of them affects platelet function. However, the correction of hyperglycemia in diabetes and lipid profile in dyslipidemia as well as the lowering of body weight in obesity all correlate with amelioration of platelet function. Habitual physical exercise triggers important mechanisms related to the exercise benefits for health improvement and protects against CV events. Platelets play an important role in many physiological and pathophysiological processes, including the development of arterial thrombosis, and physical (in)activity has been shown to interfere with platelet function. Although data reported by studies carried out on this topic show discrepancies, the current knowledge on platelet function affected by exercise mainly depends on the type of applied exercise intensity and whether acute or habitual, strenuous or moderate, thus suggesting that physical activity and exercise intensity may interfere with platelet function differently. Thus, this review is designed to cover the aspects of the relationship between physical exercise and vascular benefits, with an emphasis on the modulation of platelet function, especially in some metabolic diseases.

Keywords: diabetes; dyslipidemia; exercise; obesity; platelets.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
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).
Figure 2
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].
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Grants and funding

This study was supported by a grant from the Department of Clinical and Biological Sciences of Turin University (RUSI_RILO_22) to I.R.
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