Athletic Training On The Introphysiology Of The Heart

Introduction

The heart is a complex yet well-studied organ that is key for life in all mammals. It is responsible for pumping blood around the body, transporting essential oxygen to all living cells whilst moving deoxygenated blood to the lungs. It is part of the autonomous nervous system, acting below the level of consciousness to keep the host well regulated and to maintain life. Failure to do so can lead to cardiac arrest, stroke and ventricular defibrillation. In 2008 cardiovascular diseases (CVDs) were responsible for 30% of all deaths, and CVDs are currently the number one cause of death globally . There are many proposed methods of reducing the risk of heart disease, with lifestyle and behaviour risk factors such as smoking, bad nutrition, alcohol and lack of physical activity noted as the main contributors . It is important to study the effects of physical activity, and the aim of this report is to study the affect of athletic training on the electrophysiology of the heart.

Throughout history animal testing has been conducted and plays a great role in our understanding of anatomy and bodily functions. Whilst ethically questionable, there is no denying the historical significance of animal experimentation. From third century BC animal dissections conducted by Aristotle , to Louis Pasteur’s work on sheep to discover vaccination , to modern day stem cell research, all have produced profound medical advances that have helped increase human understanding and saved innumerable lives. This report will use data collected from the athletic training of rats and mice to study pacing rate of the heart and arrhythmias. Rats and mice are commonly used due to their convenience: they are easily housed and maintained, are adaptable and...

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...by the values in the excel spreadsheet shown above.

Using the literature we find that the athletic heart rate should be around 80-90% of the control rate, so we can tailor the decrease in both INaCa and ICaL13 in order to observe this effect.

By observing the above plot we find that the peaks of two consecutive control cycles have x coordinates 1387.66 and 1600.38 respectively. This corresponds to a cycle length of 212.72ms, or 282.06bpm.

Using this data we therefore require the athletic mouse to have a heart rate of between 225 and 253bpm.

The above athletic plot, which has no decreasing INaCa or ICaL13, has consecutive peaks at coordinates 1362.28 and 1638.46. This corresponds to a cycle length of 276.18ms or 217bpm. We see that this is near to the target range. We will not change the multiplication factors for both INaCa and ICaL13 and observe the effects.