Not All Of Us Have The Same Response To Exercise. Here’s Why!

Individual responsiveness to exercise with regard to endurance or metabolic health differs markedly.

Highlights

Some people derive little benefit from the health promoting effects of regular exercise.
Selenoprotein P causes 'exercise resistance’ by affecting muscles through the receptor LRP1.
Individual persons could be diagnosed to be exercise-effective or exercise-ineffective by measuring selenoprotein P level in the blood.

Regular physical exercise is recommended as 'exercise therapy' to prevent lifestyle diseases like metabolic syndromes, type-2 diabetes and hypertension.

However, individual responsiveness to exercise is known to differ markedly. Some people derive little benefit from the health promoting effects of regular exercise.

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‘Deficiency of the hepatokine selenoprotein P increases responsiveness to exercise through upregulation of reactive oxygen species and AMP-activated protein kinase in muscle.’

The researchers of Kanazawa University reported that selenoprotein P, a protein produced in and secreted from the liver, was high in terms of its concentration in the blood in type-2 diabetes patients and that selenoprotein P augmented the insulin resistance to induce elevation of blood glucose level.

They proposed to call the hormone 'hepatokine' that was secreted from the liver, was delivered to various organs and tissues of the body by the blood, and would exert diverse effects. However, the effects of selenoprotein P, a hepatokine, on health promotion by physical exercise was unclear.

Selenoprotein P Influences Effect of Exercise in the Body

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The present research team of Kanazawa University, investigated the effects of selenoprotein P on the results of physical exercise by the experiments with mice and cultured muscle cells and by clinical studies.

Mice were subjected to exercise training on a treadmill for 30 min per day during one month. The team has found that after the one month exercise, the selenoprotein P-deficient mice showed twice higher exercise capacity than the wild type (WT) mice. After the training, the selenoprotein P-deficient mice also showed larger reduction in the blood glucose level upon insulin injection than the WT mice.

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It was shown that with the WT mice administered with selenoprotein P, muscles after the one month training exhibited reduced level of AMPK phosphorylation; AMPK phosphorylation is considered to be related with a variety of favorable training effects.

Furthermore, it was shown that the mice deficient of LRP1, the receptor of selenoprotein P in muscles, did not incorporate administered selenoprotein P into muscles and that AMPK phosphorylation upon training was not affected.

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A total of 31 healthy but sedentary women without obesity or type-2 diabetes underwent aerobic training for 8 weeks, and maximal oxygen consumption was measured as exercise capacity.

In general, the maximal oxygen consumption was elevated after the training, whereas some women did not show much elevation. Those women had high level of selenoprotein P in the blood before the training. These results demonstrate that selenoprotein P causes 'exercise resistance’ by affecting muscles through the receptor LRP1, hence cancelling the effects of exercise.

About Selenoprotein P

Selenoprotein P is a secretory protein, produced mainly in the liver and contains high levels of selenium, a mineral.
Concentration of selenoprotein P in the blood is elevated in type-2 diabetes patients and functioned as a hormone to increase the blood glucose level.
The blood level of selenoprotein P is elevated in patients with fatty liver and in persons at high age.
Selenoprotein P causes 'exercise resistance’ by affecting muscles through the receptor LRP1.

The results of the present research are expected to lead to discovery of 'drugs to promote exercise effects' through the search for drugs reducing selenoprotein P production in the liver and for others competing with LRP1, the selenoprotein P receptor of muscles. It is also expected that individual persons could be diagnosed to be exercise-effective or exercise-ineffective by measuring selenoprotein P level in the blood.

Reference

Hirofumi Misu et al., Deficiency of the hepatokine selenoprotein P increases responsiveness to exercise in mice through upregulation of reactive oxygen species and AMP-activated protein kinase in muscle, Nature Medicine (2017) http://dx.doi.org/10.1038/nm.4295.

Source-Medindia