Protein might explain why exercise is more difficult after time of idleness

by Medically Speaking Team March 11, 2022

Physical inactivity caused by a sedentary lifestyle, sickness, or injury is linked to a decreased ability to exercise, or detraining.

According to a recent mouse research, the Piezo1 protein, which is produced by endothelial cells that line the inner surface of blood arteries, may mediate these effects of physical inactivity on exercise capacity.

Earlier research

The endothelium Piezo1 protein may detect variations in blood flow during physical exercise, according to Trusted Source. The deactivation of Piezo1 led in a decrease in the density of capillaries in the muscle and a decrease in physical activity capacity, according to the findings.

These findings imply that Piezo1 can regulate local blood supply to muscles and consequently physical performance capability in response to levels of physical activity.

Physical activity and Piezo1

Scientists have speculated for some time now that certain molecules in the body may be able to detect physical activity levels and help the body adapt as the levels of physical activity change.

Physical activity is associated with an increase in blood flow to the muscles. Thus, molecules capable of detecting changes in blood flow to the muscles could serve as exercise sensors.

The endotheliumTrusted Source is a layer of cells that forms the innermost surface of blood vessels and can detect changes in blood flow.

Recent studies have shown that the Piezo1 protein expressed by endothelial cells can sense the increase in blood flow during physical activity. Moreover, the Piezo1 protein is also essentialTrusted Source for enhancing blood flow to the muscles during physical activity.

However, the impact of Piezo1 on physical activity levels remains unclear. Researchers undertook the present study to examine the ability of Piezo1 to modulate physical activity levels.

Reduced physical activity

In the present study, the researchers used adult mice that they had genetically engineered by disrupting the expression of the Piezo1 gene in their endothelial cells. Deactivating Piezo1 in adult mice helped the researchers avoid any potentially harmful effects that disrupting this protein might have had in developing mice.

They compared the effects of Piezo1 deactivation on physical activity with a control group consisting of adult mice with intact endothelial Piezo1 expression.

The researchers found that mice in the Piezo1 deactivation group showed lower running, climbing, and walking levels at 10 weeks than the control group.

Underlying mechanisms

Changes in respiration, metabolism, heart function, or muscle composition could potentially explain the decline in physical performance after Piezo1 deactivation.

The researchers found that Piezo1 deactivation did not alter energy metabolism, respiratory or cardiac function. Similarly, animals in the experimental and control groups did not differ in skeletal muscleTrusted Source mass or the composition of muscle fibers, both of which can influence physical performance.

Subsequently, the researchers examined the impact of Piezo1 disruption on the density of capillaries in the skeletal muscle. They found that Piezo1 deactivation reduced capillary density in muscles by 20%. Moreover, such a reduction in capillary density was absent in cardiac tissue, suggesting that the effects of Piezo1 deactivation were specific to the skeletal muscle tissue.

The researchers then examined if the reduced capillary density in skeletal muscle tissue after Piezo1 deactivation was due to the regression of previously existing blood vessels. The endothelial cells in the blood vessels are supported by a matrix called the vascular basement membrane.

After deactivation of Piezo1, the researchers found remnants of previously existing capillaries in the form of the vascular basement membrane without attached endothelial cells in skeletal muscle.

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