Exercise Plus Hydrogen Water Protects Hearts from Heart Attack Damage

Authors
Journal
Applied Biochemistry and Biotechnology
Year
DOI
10.1007/s12010-018-2841-0
Study Type
Rat
Outcome
Positive
Peer Reviewed
Yes
Country
China
Health Condition
Acute Myocardial Infarction
Body System
Cardiovascular

TL;DR

Combining early aerobic exercise with hydrogen-rich saline water may provide better protection against heart damage from a heart attack.

Key Finding

In rats, combining 3 weeks of early aerobic exercise with hydrogen-rich saline pretreatment significantly reduced heart attack damage, improved heart function measurements, and increased protective antioxidant proteins compared to either treatment alone or no treatment.

Summary

Researchers tested whether combining early aerobic exercise with hydrogen-rich saline (a salt solution containing dissolved hydrogen) could protect rat hearts from damage caused by heart attacks. They gave rats either hydrogen-rich saline, exercise training, both treatments, or neither for 3 weeks, then induced a heart attack. Rats that received both treatments showed better heart function, smaller areas of damaged tissue, and higher levels of protective antioxidant molecules (substances that reduce cellular damage) compared to untreated rats.

Practical Takeaway

This is an animal study in rats, so results cannot be directly applied to humans yet. While the findings suggest that hydrogen-rich saline combined with exercise may have cardioprotective effects, human clinical trials would be needed to determine if similar benefits occur in people. The study provides early evidence that warrants further investigation, but should not be interpreted as a proven preventive strategy for heart disease in humans.

Abstract

It has been reported that hydrogen-rich saline (HRS) water reduces oxidative stress, and early aerobic exercise (eAE) acts an efficient exercise preconditioning (EP) against cardiac I/R injury. However, whether early aerobic exercise combined with hydrogen-rich saline (eAE-HRS) water can more effectively protect myocardial damage induced by acute myocardial infarction (MI) is still unknown. This study was aimed to evaluate the effect of eAE-HRS in preventing MI-induced myocardial damage and explore the possible underlying mechanisms. After Sprague-Dawley (SD) rats were given a intragastric administration of HRS (1.6 ppm) at a dosage of 10 mL/kg weight daily for 3 weeks and/or the SD rats were performed a eAE program with 3 weeks running training, the left anterior descending coronary artery was ligated to induce MI. We assessed the effects of eAE-HRS on myocardial injury and oxidative damage in the MI model of rats and detected the effects of eAE-HRS on the expressions of cardiac OGG1 and Tom40, Tom20, and Tim23. The eAE-HRS increased significantly left ventricular systolic pressure, reduced left ventricular end-diastolic pressure, and potentiated + dp/dtmax, -dp/dtmax, heart coefficient and pH after MI injury. The eAE-HRS reduced MI-induced CK-MB level, c-Tnl level, h-FABP level, infarct size. The eAE-HRS enhanced MI-induced levels of the superoxide dismutase and total antioxidant capacity, attenuated MI-induced levels of malondialdehyde and catalase. The eAE-HRS increased expressions of OGG1, Tom20 and Tim23 proteins after MI injury, but not Tom40. The eAE-HRS has the potential to be a novel precautionary measure to protect myocardial injury after MI via partially regulating expressions of antioxidant-related proteins and mitochondrial-associated proteins.