# Exercise as it relates to Disease/The effects of exercise on low-density lipoprotein (LDL) and cardiovascular disease

This article critiques and analyses the paper: "Exercise and Cardiovascular Disease: A New Perspective"

## What is the background to this research?

Cardiovascular Disease is one of the largest causes of disability and premature death around the world, where the underlying cause comes from atherosclerosis (a build up of fats and cholesterol on the walls of the arteries that restricts blood flow).
Low-Density Lipoproteins are the physical form in which lipids are transported around the body via the bloodstream, and it is believed that they are also a key event in atherogenesis (the formation of fatty deposits in the arteries). Exercise puts the body through an oxidative state of stress which is an important deterrent for any development of cardiovascular disease, although LDL production is enhanced under this stress, therefore, creating a paradox.
Further research must be done in order to fully understand the events that occur within the body in relation to LDL production when it undergoes oxidative stress during exercise. This will allow researchers to gain additional information on how other health professionals should prescribe exercise as an intervention to decrease the risk of developing cardiovascular disease.

## Where is the research from?

The research paper that I have chosen was published in the Journal of the American Heart Association, which is acknowledged as one of the most reliable medical journals for Cardiovascular and Cerebrovascular Disease studies.
The lead author of this paper, Robin Shern-Brewer, has acquired a PhD and is a licensed and registered dietitian who has been involved in several studies around exercise and how it impacts health and its relationship with cardiovascular disease.
Shern-Brewer worked on this study with four other researchers who each have a varied background in health science studies and past research. This worked to their advantage for creating a method that is valid, reliable and successful in what they were trying to measure in such a complicated and invasive study. There is no reason to suggest or believe that any bias has been incorporated into the study.

## What kind of research was this?

This research can be considered as both basic research and applied research because of what the study tried to achieve in its results. In basic research, it is about investigating the occurrence of events, processes or phenomenon based off basic principles and reasoning, while applied research focuses on what changes would need to be made and how to correct any issues that may seem problematic to the study.
Both types of research provide valuable insights into any problems that may arise and can provide conclusions and logical explanations for any findings that relate directly to the study. Although it is important to remember that human error can occur at any stage, and an unknown bias from any of the researchers can also affect the conclusions made at the end of the study.

## What did the research involve?

Study 1 consisted of 8 Exercisers (6 Males, 2 Females) and 9 Sedentary Controls (1 Male, 8 Females) and was conducted to examine the ability of LDL to oxidise between exercisers versus sedentary subjects. Oxidation levels during exercise were measured by the use of a 2.5 μmol/L copper system, and other measures such as biochemical markers, plasma lipid levels, plasma and LDL vitamin E levels, plasma TBARS, and plasma and LDL electrophoretic mobility were recorded.
Study 2 consisted of 30 Exercisers (15 Females, 15 Males) and 33 Sedentary Controls (21 Females, 12 Males) and was conducted to evaluate any confounders in Study 1. Oxidation levels during exercise were measured by the use of a 5 μmol/L copper oxidation system, and all the measures described in Study 1 were also used for Study 2, along with a few additional measurements. These include: LDL fatty acid composition (linoleic, linolenic, and arachidonic), and MPO protein levels.
The exercisers in the Study 1 group had been in regular bouts of training for less time (<1 year) than compared to exercisers in the Study 2 group (>2 years).
Exercise testing measured Vo2 Peak on a Marquette treadmill where the intensity of the exercise was monitored every minute by heart rate monitors and self-reported ratings of perceived exertion. The test was to be ceased immediately if the subject asked to stop, if they reached 95% of their age-predicted maximal heart rate (APMHR), or if they reached a respiratory exchange ratio ≥1.1. Blood samples of 15mL were taken from the subjects' forearm vein after an overnight fast but immediately before and after each exercise intervention on the treadmill.
Lipid analysis, isolation, and oxidation of LDL were measured using a Cholestech L*D*X analyser, where TBARS were also measured within the plasma. The fatty acid determinations were analysed by a high-performance liquid chromatography system called Rainin and monitored at 192 nm on a UV detector. An Enzyme-Linked Immunosorbent Assays (ELISA) laboratory technique was used to measure the plasma MPO levels.

## What were the basic results?

* In the findings of Study 1, it is suggested that the exercisers had increased amounts of preformed lipid peroxides, which could potentially increase their susceptibility to LDL oxidation. In Study 2, the findings suggest that chronic exercisers are always going through increased levels of oxidative stress, based off the higher level of MPO protein found in their plasma in comparison to the sedentary subjects.
| | BMI, kg/m2 | Vo2 peak, (mL/min)/kg | LDL, mmol/L | HDL, mmol/L | Total cholesterol, mmol/L |
| Study 1 (Exercisers) | 20.95±1.4 | 58.63 ±11 | 2.37±0.39 | 1.28±0.27 | 4.47±0.98 |
| Study 1 (Sedentary Controls) | 24.3±1.5 | 36.13±6 | 3.0±0.67 | 1.33±0.40 | 5.23±0.80 |
| Study 2 (Exercisers) | 21.69 ±2.1 | 58.64±7.0 | 1.96±0.55 | 1.51±0.35 | 3.91±0.65 |
| Study 2 (Sedentary Controls) | 24.57±4.2 | 34.37±5.1 | 2.59±0.75 | 1.32±0.34 | 4.44±0.83 |

## What conclusions can we take from this research?

Men that engage in regular "chronic" exercise over months at a time can reap the benefits of decreasing their susceptibility of the oxidation of LDL throughout the body. In saying this, regular aerobic stress can also create a higher oxidative environment throughout the body when done over a smaller time span, which would therefore increase LDL oxidation susceptibility. In women, when aerobic exercise creates an oxidative stress in the body, there is no evidence to suggest any effects on the oxidizability of LDL.
Therefore, the paradox addressed in the study has been supported through this research.

## Practical advice?

A number of factors such as dietary, exercise, and lifestyle habits all play a part in potential health implications associated with obesity, cardiovascular disease, and coronary heart disease. Clinical practice guidelines about diet and exercise have been implemented in order to decrease the risk of developing the mentioned risks, and these include: consuming 2 or more servings of fruit, 3 or more servings of vegetables, in conjunction with 30 minutes of physical activity or more each day.
Although exercise has been renowned worldwide as the leading recommendation for decreasing the risk of cardiovascular disease, it also increases total oxygen consumption and enhances the depletion of plasma antioxidants, due to the oxidative environment created by exercise.
To fully understand this paradox, more intensive and extensive research must be carried out in order to gain further knowledge about the oxidative environment in the body and what effects (both positive and negative) it may have on the body in short and long term.

## Further information/resources

Below are a few extra resources for additional learning if anything in this article was of interest to you:
* Heart Foundation
* American Heart Association
* Heart Research Institute
* Heart Foundation
* WebMD: LDL Cholesterol

## References

* 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 Shern-Brewer R, Santanam N, Wetzstein C, White-Welkley J, Parthasarathy S. Exercise and Cardiovascular Disease. Arteriosclerosis, Thrombosis, and Vascular Biology. 1998;18(7):1181-1187.
* ↑ Prevention of Cardiovascular Disease. Pocket Guidelines for Assessment and Management of Cardiovascular Risk. Africa: Who/Ish Cardiovascular Risk Prediction Charts for the African Region. World Health Organization [Internet]. 2007 [cited 1 October 2020];:1. Available from: https://books.google.com.au/books?hl=en&lr=&id=AS2RmtQVuLwC&oi=fnd&pg=PT5&dq=cardiovascular+disease&ots=AKIge33cFJ&sig=ON2cvMGs7iIXY57yMxy8dKB_0Hk&redir_esc=y#v=onepage&q=cardiovascular%20disease&f=false
* ↑ Home | AHA/ASA Journals [Internet]. Ahajournals.org. 2020 [cited 6 October 2020]. Available from: https://www.ahajournals.org/
* ↑ Types of scientific research [Internet]. International network for natural sciences - research journal. 2020 [cited 6 October 2020]. Available from: https://innspub.net/types-of-scientific-research/
* ↑ Thomas R, Kottke T, Brekke M, Brekke L, Brandel C, Aase L et al. Attempts at Changing Dietary and Exercise Habits to Reduce Risk of Cardiovascular Disease: Who's Doing What in the Community?. Preventive Cardiology [Internet]. 2002 [cited 7 October 2020];5(3):102-108. Available from: https://onlinelibrary.wiley.com/doi/full/10.1111/j.1520-037X.2002.00565.x