Exercising has many physical and emotional benefits. It can manage blood sugar levels, improve your mood, assist with weight loss, or even strengthen your memory. Endurance training, specifically, benefits tissue health. But could this form of exercise be beneficial for patients with neurological and movement-affected conditions like Friedreich’s ataxia? According to Friedreich’s Ataxia News, yes.
In fact, a study of mice models shows that endurance training could even prevent symptom onset. Read the full study results in Nature Scientific Reports.
Friedreich’s ataxia (FDRA) is a rare genetic disease. Resulting from FXN gene mutations, people with Friedreich’s ataxia don’t produce enough of the fraxatin protein, which plays a role with energy and movement. It also plays a role in mitochondrial function. As a result, many patients experience issues with movement or neurological development.
Generally, symptom onset appears between ages 5 and 15. In rarer cases, symptom onset occurs after age 25 or age 40. Symptoms include:
- Hearing loss
- Foot abnormalities
- Irregular heartbeats
- Involuntary eye movements
- Heart disease
- Diabetes mellitus
- Slurred speech
- Loss of movement and coordination
- Chest pain and shortness of breath
Learn more about Friedreich’s ataxia.
Endurance Exercise: Study Findings
Generally, faulty mitochondria – such as those in patients with Friedreich’s ataxia – cause exercise intolerance. However, researchers wanted to determine if partaking in endurance training could still benefit these patients through stopping disease progression. Ideally, this training would also reverse some symptoms.
So, a study began to test the efficacy of endurance training in mice models of Friedreich’s ataxia. The study wanted to look at exercise’s impact, efficacy, and timeline (when training is needed / when it benefits someone). Genetically modified KIKO mice were used, with reduced fraxatin in the liver, heart, and skeletal muscles.
Results of the Friedreich’s Ataxia Study
Keep in mind that 2 month old mice roughly correlate to a 7 year old human child:
- 2 months old: KIKO and control mice were running similar distances. They also had similar levels of lactate in their blood. According to Lab Tests Online, high levels of lactate suggest either a lack of oxygen in the blood, or mitochondrial dysfunction causing lactate to not properly be removed from the blood.
- 4 months old: At 4 months old, both groups saw similar results.
- 6 months old: By 6 months old, KIKO mice could not run for distances as far as control mice. KIKO mice had higher lactate levels, glucose intolerance (symptomatic of diabetes), and diminished cardiac function.
Next, researchers wanted to see if voluntary endurance exercise could stop symptom onset from occurring. So, they provided running wheels to 2-month old mice. Results showed:
- Sedentary KIKO mice ran 2x shorter distances than KIKO mice who willingly trained on the wheel.
- Endurance-trained KIKO mice ran farther distances than healthy mice who did not exercise on the wheel.
- Endurance training improved blood lactate levels and cardiac function. It also inhibited glucose intolerance and regulated collagen I and Mmp9, both of which could lead to fibrosis of the heart.
But how did this happen? Stimulating the production of fraxatin? Nope! Instead, endurance exercise strengthened mitochondrial function and lowered oxidative stress, defined as:
an imbalance between free radicals and antioxidants in your body.
Ultimately, researchers determined that Friedreich’s ataxia symptoms could be prevented by increased endurance training. However, these results now need to be replicated in humans.