Blood sugar control may improve response to exercise training


Summary: Reducing glucose levels may attenuate blood sugar-associated blunting of the aerobic response, a new study reports.

Source: Joslin Diabetes Center

Exercise has a long list of benefits for everyone. For people with metabolic diseases such as prediabetes, type 1 diabetes, and type 2 diabetes, physical activity can help control blood sugar levels and ward off diabetes-related nerve damage and heart disease.

However, people with diabetes have a lower aerobic exercise capacity than people without metabolic disease, i.e. their body does not burn oxygen as efficiently and may also resist the improvement in exercise capacity with training.

In a new study, scientists from the Joslin Diabetes Center Research Division set out to determine whether high blood sugar blunts the body’s response to exercise and whether reducing it can restore the ability to improve aerobic capacity with energy. ‘coaching.

The team’s findings, published in the journal Diabetessuggest that a combination of a glucose-lowering drug and exercise may improve exercise capacity in people with hyperglycemia or hyperglycemia.

“As the prevalence of metabolic diseases skyrockets, low exercise capacity associated with high blood sugar has the potential to impact a large and growing proportion of the population,” said Sarah J. Lessard, PhD. , assistant researcher in the Clinical, behavioral section. and Outcomes Research at the Joslin Diabetes Center and Professor of Medicine at Harvard Medical School.

“Determining why some people’s bodies resist increasing exercise capacity even with training will help us design strategies to improve the health and longevity of this population.”

In this two-part study, Lessard and his colleagues first tested a drug called canagliflozin that can lower blood sugar in a mouse model. Mice with induced hyperglycemia were monitored as they voluntarily ran on exercise wheels during the six-week study.

When the scientists assessed the animals’ response to physical training, they found a marked improvement in those who received canagliflozin compared to those who did not receive the drug.

By analyzing the animals’ muscle tissue, the researchers were also able to identify specific molecules in skeletal muscle responsible for low exercise capacity in the context of high blood sugar.

Then, using small samples of muscle taken from human study participants before and after exercise sessions, the researchers were able to confirm that the molecules identified in the preclinical experiments may also be relevant in humans.

“We find that having high blood sugar for long periods changes how muscles respond to exercise at the molecular level,” Lessard said.

The team’s findings, published in the journal Diabetes, suggest that a combination of a blood sugar-lowering drug and exercise can improve exercise capacity in people with high blood sugar or high blood sugar. Image is in public domain

“The good news is that we find that lowering blood sugar in mice with diabetes using the drug canagliflozin can prevent impairments that blunt the improvements in exercise capacity that occur with elevated blood sugar.”

As a next step, Lessard and his colleagues plan to test whether other glucose-lowering treatments — such as dietary strategies — can be as effective as drug therapies in improving exercise response. They are also investigating in more detail the molecular signaling events in muscles that lead to impaired remodeling and poor response to exercise.

“If we can better understand how hyperglycemia drives these muscle changes, we can develop targeted therapies to restore exercise response,” Lessard said.

Co-authors included Tara L. McDonald, Pattarawan Pattamprapanon, Eileen M. Cooney, Roberto C. Nava, Joanna Mitri, and Samar Hafida of the Joslin Diabetes Center.

Funding: This work was supported by the National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK 124258); a pilot price and feasibility; and Diabetes Research Center Central Facilities funded by NIH P30 award number DK036836; an American Heart Association Postdoctoral Fellowship (19POST34381036); a Mary K. Iacocca Senior Fellowship; and a fellowship from the Joslin Diabetes Center NIH Training Fellowship (T32 DK 007260). For the human studies, the authors acknowledge the support of the Joslin Clinical Research Center and thank its philanthropic donors.

The authors declare no conflict of interest.

About this exercise research news

Author: Therese Herbert
Source: Joslin Diabetes Center
Contact: Teresa Herbert – Joslin Diabetes Center
Image: Image is in public domain

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Original research: Free access.
“Canagliflozin prevents muscle extracellular matrix accumulation associated with hyperglycemia and improves the adaptive response to aerobic exercise” by Sarah J. Lessard et al. Diabetes


Canagliflozin prevents the accumulation of muscle extracellular matrix associated with hyperglycemia and improves the adaptive response to aerobic exercise

Chronic hyperglycemia is associated with a poor training response to aerobic exercise in rodent models and in humans, including reduced aerobic exercise capacity and impaired oxidative remodeling in skeletal muscle.

Here, we investigated whether lowering blood glucose with the sodium-glucose cotransporter 2 (SGLT2i) inhibitor canagliflozin (Cana; 30 mg/kg/day) could restore response to exercise training in a hyperglycemia model (low dose streptozotocin). [STZ]).

Cana effectively prevented blood sugar from rising in STZ-treated mice. After 6 weeks of voluntary wheel running, Cana-treated mice showed improvements in aerobic exercise capacity, higher capillary density in striated muscle, and more oxidative fiber type in skeletal muscle. In contrast, these responses were blunted or absent in STZ-treated mice.

Recent work implicates glucose-induced accumulation of skeletal muscle extracellular matrix (ECM) and hyperactivation of c-Jun N-terminal kinase (JNK)/SMAD2 mechanical signaling as potential underlying mechanisms. underlying a poor response to exercise. Consistent with this, muscle ECM accretion was prevented by Cana in STZ-treated mice. JNK/SMAD2 signaling with acute exercise was twice as high in STZ compared to control, but was normalized by Cana.

In human participants, ECM accumulation was associated with increased JNK signaling, low VO2picand impaired metabolic health (insulin sensitivity derived from oral glucose tolerance test).

These data demonstrate that disorders of exercise adaptation associated with hyperglycemia can be improved by cotherapy with SGLT2i.

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