Will excessive exercise cause heartache? The latest research in the English Journal of Medicine says

The English Journal of Medicine (NEJM Evidence) published Can the Heart Get an Overuse Sports Injury yesterday (2022-12-27) . The communication author is Jonathan Kim, a doctor at the Department of Sports Cardiology at Emory University.

Readers who have been following my website for a long time should know that I do a lot of exercise every day. So, I myself have always been paying attention to medical reports about excessive exercise. This NEJM article certainly attracted my great interest, but because it required subscription to the journal to download, I wrote a letter to Dr. Jonathan Kim, and he immediately sent the article to me. I am really grateful for his enthusiastic help.

This article was written for sports scientists to read, so I chose some simpler parts to share with you.

Preface

Professor Jeremy Morris, the leader of the London Public Services Research, called sports the “best choice in the public health field”. Several epidemiological studies have proven that this review is justified, which show that the most active people have 40% to 50% fewer cardiovascular events than the least active people. The biggest reduction in cardiovascular risk occurs between the group with minimal activity and slightly more activity. The additional increase in movement is associated with an additional decrease in risk (but gradually decreases) and some studies show that the risk of the highest movement is flat or slightly increased. The author of the latest guide to American sports activities emphasizes the benefits of a small amount of increased activity. These guidelines recommend that Americans “move more and sit less”, perform 150 to 300 minutes of suitability (i.e. brisk walking) or 75 to 150 minutes of dramatic (i.e. jogging) aerobic exercises, plus two resistance exercises per week and some balanced training for the elderly.

Since ancient times, there has been a severance of excessive movement. These worries reappeared in England in the Victorian era, when social elite schools and universities began to participate in activities such as running, cycling and boating, which were formerly workers-level and work-related competitions. Strong exercise in adults can cause acute myocardial infarction and sudden cardiac death. Recent studies have also shown that long-term, intense aerobic exercise can lead to acute myocardial injury, myocardial scarring, coronary calcification, atrial atrial and active ventricular expansion. This summary summarizes evidence of connecting to these conditions and proposes a method to manage these conditions.

Myocardial calcin increases after acute endurance exercise

More than 200 papers have measured cardiac troponin after exercise. These studies examined various patients after various endurance exercises. More than 50% of participants had myocardial calcin levels after long-term endurance exercises (such as marathons) that exceeded the diagnosis levels of acute myocardial infarction. A marathon study shows that all runners have at least increased myocardial protein after the competition. Due to many factors, including age, gender, training status, health status and environmental conditions, the increase in myocardial calcin varies greatly between individuals, but exercise strength and sustainability are the most important determining factors.

The increase in myocardial calcin related to movement is considered benign, but static myocardial calcin levels are cardiac risk markers. A review identified 21 prospective studies that measured 64,855 asymptomatic tissues in the general population. Myocardial calcin levels were found to be higher than the 99th percentile in 5% of the population and were related to a triple increase in total and cardiovascular disease mortality. Only detectable myocardial calcin levels were associated with a 30% increase in cardiovascular disease mortality and the risk increased gradually with the increase in myocardial calcin.

To avoid excessive diagnosis of acute myocardial infarction, clinical doctors should know that endurance events increase myocardial calcin, but the long-term effects of these discoveries are not yet clear.

Acute effects of endurance exercise on the right ventricle

Endurance exercise training reduces heart rate and increases the size of all four heart chambers. This exercise-induced heart remodeling helps increase stroke volume to maintain calm heart output and increase heart output at peak exercise because exercise training does not increase maximum heart rate.

Endurance exercise can also cause acute cardiac changes. Ultrasonic cardiac image studies show that left ventricular contraction and sedation function only showed a slight acute decrease, but the right ventricular function decreased significantly after long periods of exercise.

The acute and chronic effects of exercise on the right ventricle have important clinical implications for patients with arrhythmic right ventricular cardiomyopathy. Current guidelines recommend that patients with this cardiomyopathy or suffer from this cardiomyopathy risk are not allowed to exercise vigorously.

Myocardial fibrosis by

Gadolinium and cardiac magnetic resonance imaging (cMRI) can identify myocardial scarring and fibrosis. The normal myocardium does not retain gadolinium due to its linear myocardial structure, while the vitreous tissue retains gadolinium, resulting in late gadolinium enhancement (LGE). The saccharine analysis of the sportsman's cMRI study included 14 studies involving 1,342 participants. LGE was present in 16.6% of the athletes and 2.3% of the control group participants. LGE Insertion point at the right ventricular access point in 7% of athletes and 0.3% of control groups.

Endurance sportsmen's prevalence of LGE at right ventricular insertion site is consistent with the concept that increased right ventricular size and wall stress lead to increased stimulus of the site. However, these discoveries of clinical correlations are not yet certain. Clinical doctors should realize that asymptomatic athletes may have LGE at the right ventricle insertion site. Runners with reports that LGE had worse results, but these participants’ LGE was not limited to insertion points, but 40% of runners had typical LGE patterns of coronary disease scarring.

Endurance athlete's championship calcification

Clarence DeMar won the Boston Marathon championship seven times and participated in the competition until he was 69 years old. He died of kidney cancer at the age of 70. Paul Dudley White, a famous Boston-based cardiologist, reported Clarence DeMar's sterilization results, pointing out that his crown was two to three times larger than normal, but the left dorm showed "a considerable degree of wall aphrodisiac but still had a good lumen."

subsequent reports affirmed the benefits of sports training for crown sizing and vascular response, but recent reports examined the possibility that end-of-life sports training increases the likelihood of coronary calcification and atherosclerosis. A conclusion from the review of endurance exercise training associated with crown calcification and calcification aphrodisiac tests with calcification and calcification aphrodisiac tests is that middle-aged endurance athletes have more severe crown calcification and crown calcification aphrodisiac than those of the control participants and are the highest among the most active athletes. Sportsmen have more often calcified coronary plaques, less decalcified or mixed plaques, which means more stable features of acne-like hardening plaques.

Management of asymptomatic coronary calcification and coronary atherosclerosis sportsmen is based on common suggestions, but should include the management of ischemia and invasive coronary disease risk factors that rule out sports induce ischemia and invasive coronary disease. These people are allowed to continue to participate in sports to decide risks related to sports-related crown disease events and joint decisions with sportsmen.

Atrial Movement

The relationship between exercise and atrial Movement is complex, but it seems to follow a U-shaped pattern, at least in men, meaning that atrial Movement decreases with low to moderate levels of physical activity, but no difference or increase with increased amount of exercise. In contrast, women appear to reduce atrial virility risk at all levels of activity. The mechanism of increased atrial dysfunction in endurance athletes is not yet known. Increased parasympathetic nerve force caused by exercise training and increased sympathetic nerve force caused by acute exercise may increase the risk of atrial fluid. Inflammation caused by the acute effects of exercise is also possible. Sports performance is an indicator of increased output per stroke and due to increased atrial size in the most active and successful sports center, increased atrial size caused by endurance exercise training may be a factor. The management of atrial dysfunction for sportsmen should follow the general population's guidelines for atrial dysfunction.

Active Extended

Screen Scanning Imaging Comparison of the mid-up active gauges of former American football players and participants, and found that the active gauges of former professional players were larger (38 mm vs 34 mm). However, this expansion may have nothing to do with this movement, but rather with other factors, including hypertension, which is common among active American football players. Active expansion is related to the length of the player's career, and active shrinkage is more common among elite players.

The athletes examined by these institutes mainly engage in resistance movements, which will increase the contraction pressure. A super-sounding picture study of 442 61-year-old craft athletes found that 31% of men and 6% of women had active veins larger than 40 mm. Elite athletes more often find active enlargement. With years of exercise training, the size of the active vent has also increased.

The clinical implications of these observations are not yet clear. Excellent sports performance is directly related to the extent of the increase in active veins, which again increases the likelihood of increased exercise training or the increase in the stroke output required to achieve elite performance, resulting in increased active veins. The management of active expansion of the movement should follow guidelines developed for the general population.

Conclusion

Increasing physical activity and exercise volume is related to reducing cardiovascular morbidity and mortality. However, increasing evidence suggests that endurance exercise can increase myocardial injury marks and reduce right ventricular function. Long-term exercise training is also related to mild myocardial intensiveness, coronary aplasia and increased coronary calcification, increased atrial morbidity and active calcification. The clinical implications of these possible impacts of large-scale exercise training are not yet certain, but provide opportunities for further investigation of the long-term health effects of high-strength exercise training. Clinical doctors should be aware of the training effects of these possible sports inducement in order to provide appropriate management for these unusual middle-aged athletes.

Original text: Will excessive exercise cause pain?