The causes of bradycardia in athletes

The effects of ivabradine under autonomic blockade in endurance athletes.

Status

Recruiting

Phases

Phase 4

Study type

Interventional

Source

ANZCTR

Registry ID

ACTRN12617000983303

Enrollment

Registered

2017-07-10

Start date

2017-07-18

Completion date

2019-09-23

Last updated

2019-08-26

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

None listed

Brief summary

It is well known that athletes have lower heart rates (bradycardia) than non-athletes. This is generally considered a healthy adaptation. However, bradycardia has been associated with the subsequent development of atrial fibrillation (AF), an arrhythmia known to increase the risk of heart failure, stroke and even death. Consequently, bradycardia could conceivably be associated with significant problems later in life. The reasons athletes have slow heart rates are not well understood. Traditionally changes in neural input (vagal tone) were thought to lead to bradycardia in athletes. However, several studies have demonstrated that even after blocking these inputs(autonomic blockade), athletes continue to have lower heart rates than non-athletes. The reasons for this are not known however recent research using athlete mice models suggests this is due to intrinsic changes within the heart by downregulation of the HCN4 gene. In the mouse model, the medication which blocks this gene, ivabradine, helped to equalize the heart rates in athlete and non-athlete mice. Our aim in this study is to understand the reason for lower heart rates in endurance athletes. Participants will undergo repeat testing under experimental conditions to help determine the causes of low heart rates in athletes. We hypothesize that ivabradine will be less effective in athletes, ie it will lower the heart rate of athletes less than nonathletes. This would suggest that bradycardia in athletes is associated with changes within the heart rather than reversible changes in neural inputs. This may provide some insights into the mechanism of atrial fibrillation in athletes.

Interventions

Intervention: Autonomic blockade with single doses of intravenous metoprolol(0.2mg/kg) + intravenous atropine (0.04mg/kg) plus oral ivabradine 15mg Exposure: endurance sport participation A wash out period of at least 24 hours will occur before crossover to the control arm

Study design

Allocation

Randomised controlled trial

Intervention model

Crossover

Primary purpose

Prevention

Masking

Blinded (masking used) (Subject, Caregiver, Outcomes Assessor)

Eligibility

Sex/Gender

All

Age

18 Years to 50 Years

Healthy volunteers

Yes

Inclusion criteria

Group 1 (Endurance athletes): Competing in endurance sport Group 2 (Healthy Volunteers): Less than three hours of exercise per week Group 3 (Endurance athletes with bradycardia): Endurance athletes with a resting heart rate less than 40

Exclusion criteria

1. Allergy to one of the medications 2. Asthma 3. Glaucoma 4. Urinary Retention/Prostate enlargement 5. Past history of psychosis 6. Ulcerative Colitis 7. Gastrointestinal Obstruction 8. Myasthenia gravis 9. Hypotension(low blood pressure 10. Smoker 11. Preexisting cardiac or lung disease 12. Pregnant or breast feeding 13. Contraindication to MRI

Outcome results