Dr. James Manos (MD)
January 22, 2016
Heart attack prevention
‘Prevention is better than cure’ (Hippocrates, ancient Greek doctor – the father of Western medicine, 460 – 370 B.C.)
Note: in this text, the writer expresses his point of view. Some advice is empirical, so you should consult your family doctor beforehand.
Prevention & treatment of coronary artery disease/ ischemic heart disease (CAD/ IHD) & myocardial infarction (MI; heart attack)
Coronary artery disease (CAD) is the most frequent reason people die (1: 4 deaths in the UK). CHD is the result of atheromatosis (building up of plaque inside the arteries), which, in simple words, is the obstruction of the coronary (heart) vessels from clots (thrombus), which are the branches of the coronary artery that supply the heart with blood (and itself is a branch of the aorta).
When the blockage of the coronary vessels is complete, the patients suffer from myocardial infarction (MI), namely necrosis (death) of the heart muscle. When the obstruction is not complete, it can appear as angina pectoris (chest pain) caused by heart ischemia (restriction in blood supply to the heart, causing a shortage of oxygen and glucose needed for the metabolism of the cells). Still, sometimes it may not, especially in diabetics. Then we call it ‘silent angina.’ The last one is why some patients die from MI without having any history of chest pain.
The procedure of CHD begins with creating plaque in the tunica intima (the inner layer) of artery walls, a degenerative, inflammatory, and oxidative process. Plaque consists of debris made by the progressive deposit of cholesterol and other lipids (fats; cholesterol & fatty acids), macrophage cells [that ‘eat’ fats, specifically the oxidized – LDL (low-density lipoprotein), and become ‘foam cells’], fibrous connective tissue and calcium. Eventually, calcium causes calcification on the inner wall (layer) of the vessels (coronary arteries in the case of heart vessel atheromatosis). This calcification makes what we call atherosclerosis (hardening of the arteries). Calcified arteries or aorta may be noticed on X–rays.
These deposits that form the plaque induce the activation of the inflammatory process by releasing chemicals called cytokines that worsen the problem. The accumulated material forms a swelling in the artery wall and creates a ball called a thrombus (clot) that, when unstable, can break and obstruct a coronary artery branch. Thrombus may intrude into the channel of the artery, narrowing it and restricting blood flow, causing heart ischemia (restriction in blood supply to the heart, causing a shortage of oxygen and glucose needed for the metabolism of the cells), that manifests as angina pectoris (chest pain from heart ischemia; usually after exertion (work, effort), such as stair climbing).
When angina lasts more than 30 minutes, we must investigate for myocardial infarction (MI; heart attack). Unstable angina (UA) is refractory angina that may also appear at rest. Another variety is 'angina Prinzmetal’s' from coronary artery spasm.
ACS (acute coronary syndrome) (myocardial infarction (MI); heart attack) is classified with electrocardiography (ECG) to STEMI (ST-elevation MI) or NSTEMI (non-STEMI)/ UA (unstable angina). STEMI is treated with thrombolysis (e.g., rTPA (alteplase)) or primary PCI (percutaneous coronary angioplasty). Today PCI is the treatment of choice. Antiarrhythmic drugs such as beta-blockers may be given (however, they do not seem to prevent mortality during the first 24 – 72 hours). Patients can be treated with thrombolytic drugs such as r–TPA only if there aren’t any contraindications for it (e.g., bleeding disease, recent major surgery, recent anticoagulation, history of hemorrhagic stroke, and so on).
Thrombolysis may cause bleeding as an adverse effect, including brain bleeding. Additional treatment includes aspirin, morphine, oxygen, nitrates (the last 4 are called ‘OANM’ and used for emergencies), beta-blockers, statins (to lower cholesterol levels), stool softeners (if the patient has constipation), mild sedation (e.g., diazepam), anticoagulation (heparin as unfractionated or LMWH (low molecular weight heparin) that has fewer side effects), antiplatelet (aspirin and/or clopidogrel) and ACE inhibitors. Chronic stable angina is treated with PCI or bypass (CABG) surgery. NSTEMI is treated with antiplatelet aspirin +_ clopidogrel. Depending on whether early PCI is planned, a factor Xa inhibitor or a potentiator of antithrombin (fondaparinux or LMWH (low molecular weight heparin), respectively) may be added. In very high-risk patients, inhibitors of the platelet glycoprotein IIb/ IIIa, such as eptifibatide or tirofiban, may be used.
Thrombolysis may cause bleeding as an adverse effect, including brain bleeding. Additional treatment includes aspirin, morphine, oxygen, nitrates (the last 4 are called ‘OANM’ and used for emergencies), beta-blockers, statins (to lower cholesterol levels), stool softeners (if the patient has constipation), mild sedation (e.g., diazepam), anticoagulation (heparin as unfractionated or LMWH (low molecular weight heparin) that has fewer side effects), antiplatelet (aspirin and/or clopidogrel) and ACE inhibitors. Chronic stable angina is treated with PCI or bypass (CABG) surgery. NSTEMI is treated with antiplatelet aspirin +_ clopidogrel. Depending on whether early PCI is planned, a factor Xa inhibitor or a potentiator of antithrombin (fondaparinux or LMWH (low molecular weight heparin), respectively) may be added. In very high-risk patients, inhibitors of the platelet glycoprotein IIb/ IIIa, such as eptifibatide or tirofiban, may be used.
A diagnostic lab marker for ACS (acute coronary syndrome) that increases early is Troponin I & T (in the last years, labs measure the high-sensitive cardiac troponin). Another biomarker that increases early is Copeptin (a long peptide), and some combine its increased values with increased Troponin levels to diagnose early myocardial infarction (heart attack). Other markers that are less used today are CK – MB, sGOT (AST), and LDH. Some labs also test serum myoglobin. These biomarkers, as well as Troponin, may also increase for other reasons apart from heart problems.
The ECG (electrocardiogram) on ACS will show ST elevation (then we have STEMI) in 2 or more adjustment ECG leads. But it may not show ST elevation in the case of NSTEMI. Other ECG signs may include ST depression (angina or MI), T inversions, Q wave (however, it may indicate an old MI), and/or a new (or presumably new) LBBB (left bundle branch block).
Imaging tests for angina include coronary angiography, ambulatory 24h ECG monitoring/Holter, exercise stress test (treadmill or bicycle or arm ergometry) alone or combined with echocardiography (Echo) or perfusion scintigraphy (with thallium 201 or Tc 99m – sestamibi) or pharmacological stress test (with dobutamine or dipyridamole or adenosine) combined with Echo or perfusion scintigraphy. A new imaging test is CT coronary arteriography.
Cardiovascular disease (CVD, including coronary artery disease (CAD), stroke, and peripheral vascular disease (PVD)) risk factors
The cardiovascular disease (CVD) risk factors related to coronary artery disease (CAD) & stroke are classified into:
Modifiable: these include tobacco use/ smoking, hypertension (high blood pressure), dyslipidemia [increased blood lipids (fats), such as cholesterol and triglycerides], diabetes mellitus (elevated blood sugar), diet (rich in saturated fats and carbohydrates), overweight/ obesity, heart failure and left ventricular dysfunction, specific behavior (being competitive, combative, or feeling overly stressful) and sedentary lifestyle (lack of physical activity). Other modifiable risk factors include depression, increased blood fibrinogen (which is a factor of blood clotting), and increased blood homocysteine (congenital with premature atheromatosis or from decreased intake of vitamin B12, B6, and folic acid).
Hypertension is the single most significant risk factor for stroke. It also plays a vital role in heart attacks. It can be prevented and successfully treated only if it has been diagnosed and the patient complies with his/her doctor’s recommended management plan.
Abnormal blood lipid levels include high total cholesterol, elevated levels of triglycerides, elevated levels of low-density lipoprotein (LDL-cholesterol; also known as ‘bad’ cholesterol), or low levels of high-density lipoprotein (HDL-cholesterol; also known as ‘good’ cholesterol) all increase the risk of heart disease and stroke. Changing to a healthy diet, exercise, and medication (such as the ‘statins’ cholesterol-lowering drugs) can modify the blood lipid profile.
Tobacco use, whether it is smoking or chewing tobacco, increases the risks of cardiovascular disease. The risk is especially high if someone has started smoking when young, smokes heavily or is a woman. Passive smoking is also a risk factor for cardiovascular disease. Stopping tobacco use can significantly reduce the risk of cardiovascular disease, no matter how long someone has smoked.
Physical inactivity increases the risk of heart disease and stroke by 50%. Obesity is a significant risk for cardiovascular disease and predisposes to diabetes.
Diabetes is a risk factor for cardiovascular disease. Type 2 diabetes mellitus is a major risk factor for coronary artery disease (CAD) and stroke. Having diabetes makes a person twice as likely as someone who does not develop cardiovascular disease. If diabetes is uncontrolled, the person is more likely to develop cardiovascular disease earlier than others, and it will be more devastating. In pre-menopausal (before menopause) women, diabetes cancels out the protective effect of estrogen, and the risk of heart disease rises significantly.
A diet high in saturated fat increases the risk of heart disease and stroke. It is estimated to cause about 31% of coronary heart disease and 11% of strokes worldwide.
Being poor, no matter where in the globe, increases the risk of heart disease and stroke. A chronically stressful life, social isolation, anxiety, and depression increase the risk of heart disease and stroke.
Having one to two alcoholic drinks a day may lead to a 30% reduction in heart disease, but above this level, alcohol consumption will damage the heart muscle.
Certain medicines such as contraceptive pills and hormone replacement therapy (HRT) may increase the risk of heart disease.
Left ventricular hypertrophy (LVH) is a risk factor for cardiovascular mortality.
Non-modifiable: age, men (if less than 65 years old, because of the protective role of estrogens on women; after menopause, women have a similar risk to men. Risk of stroke, however, is similar for men and women), race (e.g., from India), low socioeconomic status, personal or family medical history of CHD, and low birth weight [IUGR (intrauterine growth restriction), SGA (small for gestational age)].
Getting old is a risk factor for cardiovascular disease; the risk of stroke doubles every decade after age 55.
A family’s history of cardiovascular disease indicates the risk. If a first-degree blood relative has had coronary artery disease (CAD) or stroke before the age of 55 years (for a male relative) or 65 years (for a female relative), the risk increases.
Gender is significant: men are at higher risk of heart disease than pre-menopausal (before menopause) women. But after menopause, women have a similar risk to men. The risk of stroke is the same for men and women.
Ethnic origin also plays a role. People with African or Asian ancestry risk developing cardiovascular disease more than other racial groups.
Management of the modifiable risk factors for coronary artery disease (CAD)
Modifiable risk factors can be managed by stopping smoking (and avoiding passive smoking) and also by controlling diabetes mellitus (DM) and hypertension with medication, exercise, and diet (avoiding sugar and salt, respectively), reducing the risk for CHD by controlling obesity (with diet, exercise, medication, and surgery –if morbid), by treating heart failure and by taking adequate folic acid and vitamins B12 and B6 (e.g., from diet or taking a dietary supplement) that lower homocysteine levels.
An annual medical checkup is helpful, including a blood test for cholesterol [total, LDL (‘bad’) and HDL (‘good’) cholesterol] & triglyceride levels. Also, an oral glucose tolerance test (OGTT) and glycosylated hemoglobin (glycated hemoglobin ((HbA1C)) levels may be needed (HbA1C reflects the glucose levels control during the last 3 months), especially if high glucose levels, insulin resistance, metabolic syndrome, and prediabetes is suspected and on pregnant women (the protocol on the OGTT is different here). Other specialized tests include lipoprotein (a) levels, clotting tests (including fibrinogen), and blood homocysteine. A specific CRP (C – Reactive Protein) fraction shows an increased risk for heart attack. However, other causes for increased CRP (such as infection and collagen diseases) should be excluded.
The check-up on patients aged more than 35 – 40 years old should also include an electrocardiogram (ECG) and – if indicated – a standard exercise stress test (such as the treadmill).
Regarding CHD-prone behavior, people who are combative, aggressive, and competitive may be helped by anger control schools, counseling, psychotherapy, and relaxing techniques. There are many relaxing techniques such as yoga, exercising, massage/ shiatsu, hobbies/sports (e.g., swimming, jogging, cycling), biofeedback, aromatherapy, relaxing music, Tai Chi, etc.
Some drugs help the prevention of CHD and stroke, such as aspirin (e.g., 75 mg od (once daily)) and statins (cholesterol-lowering agents such as simvastatin). Aspirin should not be taken concomitantly with other anticoagulants (such as warfarin); an enteric-coated preparation is also preferred. Also, to prevent peptic ulcer disease (PUD) induced by aspirin, the patient may need to take (with an empty stomach) a drug that decreases the acid of the stomach, such as a PPI (proton–pump inhibitor), such as pantoprazole or an H2R (histamine H2 receptor antagonist), such as ranitidine. Aspirin has many contraindications (especially bleeding diseases and surgery) and many side effects (such as gastric ulcer, asthma exacerbation, renal problems in overdose, etc.), and clopidogrel is an alternative if aspirin cannot be tolerated. However, the above and all the drugs mentioned in this text should be prescribed only by a doctor such as a GP.
Other preventive drugs are the statins used for hyperlipidemia (increased cholesterol or triglycerides), which also have side effects such as increasing the liver enzymes and causing myopathy that sometimes may be severe (rhabdomyolysis) and cause kidney failure.
Evidence shows that all patients with CHD benefit from reducing their blood cholesterol and LDL – cholesterol (‘bad’ cholesterol) by using a statin, regardless of their initial cholesterol concentration!
Diet & dietary supplements that may prevent CHD include red wine in moderate amounts that has many antioxidants such as phenols and other antioxidant foods, such as Vitamins A, vitamin C (in oranges and in wild roses & acerola), vitamin E, black chocolate, olive oil (vitamin E & polyphenols), green tea, garlic, beetroots, cauliflower, etc. Antioxidants help us prevent vascular diseases and general diseases of oxidative stress, including cancer and even dementia, all connected with oxidative stress from free radicals that ‘attack’ the cells and derange the DNA inside their nucleus.
Another dietary substance that may prevent CHD is fish oil containing omega-3 fatty acids, which decrease triglycerides and are contained in fish oil in fatty fish such as mackerel. Traditionally, CHD rates are low in Japan, but not in Japanese immigrants living in the US who follow traditional American junk food! However, for unknown reasons, Japan has a higher gastric (stomach) cancer rate.
Dyslipidemia (high blood fats such as cholesterol & triglycerides) may be familiar, so people with a family history of CHD or hyperlipidemia and/or relatives who died young (< 50) from a heart attack should check their blood lipids (fats) with blood tests to exclude familial hyperlipidemia. This also applies to children who may have premature atherosclerosis and suffer from a heart attack at an early age in the case of familial dyslipidemia.
Many drugs induce dyslipidemia, including steroids, beta-blockers (!), thiazide (a diuretic), COC (for contraception, ‘the Pill’), and isotretinoin (for skin problems such as acme).
Also, many diseases may increase atherosclerosis and atheromatosis risk, including DM (diabetes mellitus), hypothyroidism, renal failure, nephrotic syndrome, Cushing syndrome, myeloma, porphyrias, cholestasis, PCOs (polycystic ovaries syndrome), glycogen storage disease, and lipodystrophies. Also, pregnancy and excess alcohol increase lipids. Pregnancy also increases the risk for DVT (Deep Vein Thrombosis) and Pulmonary Embolism. High-risk patients should take anticoagulation therapy and avoid lengthy trips by car or long air flights.
Patients with dyslipidemia are usually treated with a statin (cholesterol-lowering agent). However, they need a special diet (they may consult a dietician) with decreased intake of saturated fats and cholesterol/ triglycerides (butter, snacks, red meat, full-fat dairy products) and reduced sugar intake (sweets, refreshments, snacks, drinks with alcohol). They need to lose weight if they have a BMI of over 25. They should also stop smoking, start regular exercise, avoid excess alcohol, and prefer products (usually dairy) enriched with plant sterols and stanol esters that decrease the LDL cholesterol (‘bad’ cholesterol).
People taking drugs for their circulation and heart problems should be aware that a drug may cost their life if they stop it abruptly (such as beta-blockers and other antiarrhythmic drugs) or take the wrong dose or take them concomitantly with other drugs. For example, diuretic drugs (e.g., for heart problems such as heart failure CHF) can increase or decrease potassium or magnesium levels, causing severe cardiac dysrhythmias (irregular rate).
Prevention & treatment of cardiovascular disease
-Motivational therapy; Cognitive - Behavioral Therapy (CBT); Tai Chi
-Weight reduction: increased physical activity/Exercise, caloric restriction, medications (e.g., orlistat), bariatric surgery on morbid obesity
-Statins for lipid abnormalities. In some cases, fibrates, or niacin.
-Omega – 3 fatty acids (fish oil) for increased triacylglycerols
-Mediterranean diet (? ketogenic)
-Antihypertensive drugs, including ACE inhibitors or ARBs, when possible
-Hypoglycemic drugs, e.g., metformin and thiazolidinediones (glitazones) for reducing insulin resistance
Herbs & dietary supplements used for the prevention & treatment of cardiovascular disease
-Lecithin (cholesterol-lowering effects)
-Plant sterol (phytosterols) & stanol esters; including beta-sitosterol (they are famous for their cholesterol-lowering effects)
-Red Yeast Rice (cholesterol-lowering effects; however, it may be adulterated with a statin drug!)
-Garlic & Kyolic™ (aged garlic extract) (blood-pressure-lowering effects & prevention of atherosclerosis)
-Pomegranate (blood-pressure-lowering effects)
-Cinnamon (sugar-lowering effects)
-Blueberry (excellent antioxidant)
-Valerian, Rhodiola, St John's wort, lemon balm (Melissa) & passionflower (relaxing and antidepressant effects, decrease of the overstimulated sympathetic system)
-Hawthorn [blood pressure–lowering effects; cardioprotective (protective for the heart), used for heart failure]
-Milk thistle/ silymarin and also NAC (N- acetylcysteine) (liver detoxification) (liver detoxification on metabolic syndrome & perhaps on statin drugs that may increase the transaminases (liver function enzymes))
-Astaxanthin (from microalgae, krill, and other sea sources; a keto-carotenoid; many benefits for the circulation)
-Coenzyme Q10 (CoQ10) (myriads benefits, including blood pressure–lowering effects)
-Soy protein (cholesterol-lowering effects)
-Red wine (beneficial to the heart) & resveratrol (a substance in red wine; has metabolic effects; may increase longevity!)
-Quercetin
-Pterostilbene
-Artichoke (cholesterol-lowering effects)
-Flavonoids & polyphenols
-OPCs (Oligomeric Proanthocyanidins) from grape seed extract & French maritime pine bark extract (also known as ‘pycnogenol’) is excellent for vein problems
-Coffee (it contains chlorogenic & caffeic acid, has sugar-lowering effects; green bean coffee is rich in antioxidants)
-Grapefruit
-Black & green tea (has many antioxidants such as tannins and EGCG)
-Alpha-lipoic acid
-Strawberries (contains the antioxidant fisetin)
-Cranberries (high in antioxidants)
-Beta-glucan (e.g., from oat) (cholesterol-lowering effects)
-Black chokeberry
-Bilberry
-Beta-carotene (an antioxidant)
-Acai berry (a great antioxidant)
-Lycopene (a carotene contained in tomato juice that gives the red color to tomatoes; it is an antioxidant that has many benefits for the cardiovascular system.
-Tart cherry (has antioxidant polyphenols)
-Spirulina & Chlorella (green algae) (excellent multi-nutrients; spirulina is called ‘the astronauts’ food’)
-Wheatgrass
Dietary advice for preventing coronary artery disease (CAD) & heart attack
In atheromatosis, the heart's coronary arteries are blocked with atheroma plaque with a deposit of fat – such as cholesterol – calcium and immune cells, such as macrophages, called foam cells, as they ingest fat! Plaque, when raptures cause blockage of the artery, and if this a coronary artery of the heart, then it may manifest as heart ischemia (deprivation of tissues from blood in which the red blood cells (RBCs) carry oxygen essential for metabolism) that may cause angina pectoris (chest pain from ischemic heart disease) and even may manifest as a myocardial infarction (heart attack). These belong to the ischemic heart disease (IHD) & coronary artery disease (CAD) spectrum.
· People aged more than 40 – 45 years old may also do an exercise tolerance test (Bruce protocol treadmill stress test), as the electrocardiogram (ECG) performed by a cardiologist usually does not show evidence of atherosclerosis (hardening of the arteries), unless the ischemic heart disease is moderate to severe. Then, the patient exhibits heart ischemia, i.e., deprivation of tissues from blood in which the red blood cells (RBCs) carry oxygen essential for metabolism. That will manifest with symptoms (such as chest pain) and ECG changes (e.g., on ST-segment & T waves). However, these usually may appear only on exertion (e.g., on climbing stairs) rather than resting. The latter shows an advanced disease. That’s why an exercise tolerance test may help, as it may uncover ischemic heart disease at exertion. ECG may also show if someone has suffered a heart attack in the past (with old Q waves in ECG) that may have occurred unnoticed! CT coronary angiogram is less invasive than the standard coronary angiography (the gold standard for diagnosing ischemic heart disease) method but with less sensitivity & specificity.
· The cholesterol-lowering drugs ‘statins’ (such as simvastatin & atorvastatin) have been found to prevent heart attack. Talk to your general practitioner (GP) about taking this drug if you have hyperlipidemia (high blood lipids such as cholesterol and/or triglycerides), coronary artery disease, hypertension, and diabetes. These drugs may irritate the liver, as shown on liver function tests with the increased enzymes called transaminases. They may also cause myopathy (muscle disease; it may be severe with the form of rhabdomyolysis that may even cause kidney failure). They may also predispose to diabetes mellitus!
· Most doctors are unaware that Coenzyme Q10, as a dietary supplement, is needed on patients taking a cholesterol-lowering ‘statin’ drug, as these drugs lower this enzyme, and its supplementation may even prevent myopathy (muscle disease)!
· Herbs & dietary supplest that may help cardiovascular system and protect the heart include Hawthorn (used for chronic heart failure!), lycopene (an antioxidant in tomato juice), fish oil in fat fish such as sardines & mackerel (contains omega – 3 fatty acids that decrease the triglycerides), red yeast rice (decreases blood cholesterol similar to the ‘statin’ drugs, however often it may be adulterated with a ‘statin’!), phytosterols & stanol esters (they both decrease cholesterol levels), astaxanthin (an excellent carotenoid antioxidant from the green algae Heamatococcus pluvialis), folic acid & vitamin B12 & B6 (they decrease homocysteine), oat (contains beta glucans) & soybean – soy protein (contains phytoestrogens) (they both decrease cholesterol), pomegranate & garlic (including the aged garlic extract ‘kyolic (TM)) (both decrease blood pressure), chicory root & chromium (both decrease blood sugar) , lecithin (decreased blood cholesterol), blueberry, beta - carotene, astaxanthin, selenium (a potent antioxidant) etc.
· Regular exercise & a healthy diet are essential in preventing cardiovascular disease. They are both described above.
· Avoid hard (yellow) cheese with an extremely high percentage of saturated fatty acids (about 20 – 30% fats) that damage the heart. Prefer only cottage cheese but in moderate amounts. Cheese is not desirable for osteoporosis prevention, as it contains considerable amounts of fat. Even the ‘light’ cheese is very fatty, as it may provide even 10% fat. Philadelphia cheese is not healthy, either.
· Avoid sweets, dressings, fried / sautéed, and generally foods with saturated fats that block the arteries and cause heart attacks and stroke.
· Avoid hydrogenated saturated / ‘trans’ fat that is added in most processed food such as pasta, fried food, sautéed food, snacks, pizza, fried potatoes (French fries), toast, hamburgers, pie, cheese, sweets, etc. They are even contained in some creams for babies in which they use, e.g., palm oil!
· Prefer low-fat ‘light’ foods, e.g., skimmed milk, rather than full-fat foods.
· Avoid butter and margarine. They are high in fat. In the past, they contained ‘trans’ saturated fats that cause atherosclerosis (hardening of the arteries) & ischemic heart disease (IHD).
· Avoid dressings. Most are unhealthy, with high fats, salt & sugar.
· Prefer fresh milk (not evaporated that may have preservatives) with low fat (skimmed).
· Eat only boiled eggs and not fried or omelet that contains saturated fatty acids (boil them hard to kill bacteria such as Salmonella) 2 – 3 times weekly. Don’t exclude eggs entirely from your diet because their white part contains all the required protein. The white of the egg, contrary to the yolk, has no cholesterol, and many bodybuilders consume it as an excellent protein source (used to compare other proteins). There are no guidelines for the total amount of eggs that can be consumed daily or weekly. Some medical sites say that healthy people can eat one egg daily. The number of eggs people with high blood cholesterol and/or high disease can eat daily relates to total cholesterol consumption. Some medical sites agree with the old instructions for people with high cholesterol and/or heart disease to not consume more than 3 eggs weekly, including those used in food.
· In some dairy products and toast bread, manufacturers add plant sterols (phytosterols), stanol esters, or beta-glucans to reduce cholesterol. However, avoid dressings and butter, which give extra calories and fat. A better choice is yogurt or other dairy products (such as milk) enriched with the above elements. Beta-glucans are also contained in oats. Soybean also decreases cholesterol with their phytoestrogens (plant estrogens), the isoflavones genistein & daidzein. Plant sterol (also known as phytosterols) & stanol esters decrease LDL cholesterol (also known as ‘bad’ cholesterol) that is responsible for coronary (coronary heart arteries) heart disease. Studies show that eating spreads enriched with phytosterols daily reduced total cholesterol by up to 11% and LDL cholesterol (bad) cholesterol by up to 15%. The dose is important. The National Cholesterol Education Program recommends consuming 2 grams of plant sterols/stanols daily as part of an overall heart-healthy diet.
· On cooking, prefer steaming and baking foods rather than frying. There are special steamers that steam food without boiling it, so most of the nutrients, including vitamins, are not destroyed by heat. Frying is unhealthy, so fish/chicken & chips are just junk food. Do not sauté food, as it is unhealthy. If you definitely want to eat fried food (although it is unhealthy), fry it with a few oils in a non-stick pan (such as ‘Tefal (TM)’).
· Olive oil is essential for the heart with its vitamin E (tocopherol), an excellent antioxidant. Prefer extra–virgin olive oil (the Greek ones are of outstanding quality) but avoid excessive amounts (like the Greeks who eat their Greek salad in a bowl of olive oil), as it is rich in calories (1 tablespoon has 131 calories, almost the half amount of a cheese pie). The daily upper limit is 2 tablespoons.
· Omega-3 fatty acids (EPA & DHA) benefit the heart. Positive effects include anti-inflammatory and anti-blood clotting actions, lowering cholesterol and triglyceride levels, and reducing blood pressure. They may also reduce the risks and symptoms of other disorders, including diabetes, stroke, some cancers, and age-related cognitive decline. Omega-3 fatty acids are contained in fish oil. -The linseed oil contains another omega-3 fatty acid: alpha-linolenic acid (ALA). The value of ALA has recently emerged, although most companies that sell supplements of omega-3 use fish oil EPA and DHA as sources for omega-3 polyunsaturated fatty acids and do not include ALA. Omega 3 fatty acids are useful in lowering triglycerides (blood fats) in the blood (the only FDA indication). They are used in Europe as secondary prevention after cardiovascular events.
· Eating fatty fish such as mackerel, herring, and salmon offers omega-3 fatty acids that reduce triglycerides and protect the heart.
· Fish are fished, especially in developed countries (such as Tunisia & Morocco), often in waters contaminated with heavy metals such as mercury, arsenic & lead. The Mediterranean Sea is a closed sea, and seawater is not refreshed, so pollution is greater than in the Ocean.
· Very healthy is the juice of pomegranate, blueberry, and grapes.
· Eat plenty of fruits, legumes, and vegetables.
· Eating at least 5 servings of fruits and vegetables daily is essential for our health and is recommended by doctors and WHO. You can eat steamed vegetables, e.g., zucchini with oregano, vinegar, and 2 tablespoons of olive oil.
· About fruits and vegetables prefer organics because they have no pesticides, fertilizers (such as nitrogen and phosphorus), and chemicals. However, if cultivated beside a non–organic farm, they may be contaminated with pesticides and fertilizers.
· Prefer (better homemade) with all bran flour bread, with seeds. It is rich in fibers, vitamins, and minerals.
· Fibers protect against colon cancer (a diet rich in fat predisposes to it) and help the cardiovascular system. Fiber-rich foods include oats, fruit & vegetables, all bran bread & cereals, etc. Fiber helps the heart, lowers cholesterol, and prevents constipation. Psyllium and inulin have the same benefits.
· Antioxidant, cancer-preventive foods include cauliflower, broccoli, beetroots, mashed tomatoes, garlic, dark chocolate, green tea, berries, grapes, pomegranate, red wine (e.g., from the Bordeaux region of France), etc.
· Avoid sugar. Remember that salt & sugar are added to many processed goods (e.g., cereals, snacks, etc.), so always check the ingredients. Instead, prefer fructose sugar (it has only 12 calories a teaspoon; sugar has 20; it is not natural, and its benefits are debated) or honey as sweeteners. Avoid, however, sweeteners saccharin, cyclamate acid, aspartame, and other artificial sweeteners that have been suspicious for cancer. Stevia is an herb that is a natural sweetener, but I don’t prefer it as it is bitter.
· Do not add sugar or honey to fresh fruit juices, as they already have many carbohydrates.
· Eating less than 1 teaspoon of salt daily is important, keeping in mind that salt (and sugar) is added in all processed foods. However, during a hot day in summer or strenuous physical exercise, we need extra salt, water, and carbohydrates to avoid dehydration and electrolyte imbalance that may be life-threatening. Some years ago, thousands of elderly people died in a heatwave in France, as they avoided replacing salt and other electrolytes, as well as water, during the heat, and died from heatstroke and dehydration, as well as thrombosis that was predisposed by dehydration.
· Doctors recommend avoiding excess salt, which increases blood pressure (hypertension). Salt is a combination of sodium and chloride. According to Mayo Clinic, the Dietary Guidelines for Americans recommend limiting sodium to less than 2,300 mg a day or 1,500 mg for people who are age 51 or older, are black, or have high blood pressure, diabetes, or chronic kidney disease. A single teaspoon of table salt has 2,325 milligrams (mg) of sodium, a bit more than healthy people's upper limit. However, many processed and prepared foods contain sodium.
· L – carnitine is an amino acid that has many benefits for the heart (and the kidneys as well).
· Avoid sugar. Remember that salt & sugar are added to many processed foods (e.g., cereals, snacks, etc.), so always check the ingredients.
Other dietary advice
· High carbohydrate diets are not healthy, as they predispose to diabetes and coronary heart disease that is accelerated by hyperglycemia (high blood sugar) and the advance-glycation end products (AGEs) that are responsible for the vascular complications of diabetes mellitus. AGEs are the products of non-enzymatic glycation and oxidation of proteins and lipids. AGEs, by stimulating processes linked to inflammation, are implicated in many diseases, such as diabetes, inflammation, neurodegeneration (including dementia), and aging.
· Dietary AGEs can be present in foods such as meat and butter and can form during frying, roasting, and baking, but less in boiling, stewing, steaming, and microwaving.
· Barbecue foods are high in AGEs. They are also carcinogenic because cold cuts & cured meat contain nitrates, carcinogenic preservatives that may cause cancer, e.g., stomach cancer. When cooked in carbon smoke, the food becomes immediately carcinogenic.
· Excess dietary carbohydrates (‘carbs’) and fat are the major causes of obesity and its related diseases.
· Glycemic index. Foods with a low glycemic index should be preferred. The glycaemic index (GI) is associated with a particular type of food that indicates the food’s effect on a person’s blood glucose. The number typically ranges between 50 and 100, where 100 represents the standard, an equivalent amount of pure glucose. We all need to choose foods with a low glycemic index (GI), as foods with a high glycaemic index may predispose us to diabetes and cardiovascular disease. Common foods like bananas have a high glycaemic index, so we should eat them moderately or less. For a calculator of the glycaemic index on foods, see http://www.glycemicindex.com/foodSearch.php
· Do not add sugar or honey to fresh fruit juices, as they already have many carbohydrates.
· Many people prefer fructose as a sweetener (it has only 12 calories a teaspoon; sugar has 20). But its benefits are debated. Others prefer honey.
· Avoid artificial sweeteners, such as saccharin, cyclamate acid, and aspartame, which have been suspicious for cancer.
· Stevia is a herb that is a natural sweetener, but I don’t prefer it as it is bitter.
· In a study in 1990, 33 upper-trimester chiropractic students volunteered for oral glucose tolerance testing comparing sucrose, fructose, and honey during successive weeks. A 75-gm carbohydrate load in 250 ml of water was ingested, and blood sugar readings were taken at 0, 30, 60, 90, 120, and 240 minutes. Fructose showed minimal changes in blood sugar levels, consistent with other studies. Sucrose gave higher blood sugar readings than honey at every measurement, producing significantly (p less than .05) greater glucose intolerance. Honey provided the fewest subjective symptoms of discomfort. Since honey has a gentler effect on blood sugar levels per-gram basis and tastes sweeter than sucrose so that fewer grams would be consumed, it would seem prudent to recommend honey over sucrose (Reference: http://www.ncbi.nlm.nih.gov/pubmed/2394949 ).
· Commercially, fructose is frequently derived from sugar cane, sugar beets, and corn. Fructose is often recommended for diabetics because it does not trigger insulin production by pancreatic beta–cells. However, the net effect for both diabetics and non-diabetics is debated. Fructose has a very low glycemic index of 19 ± 2, compared with 100 for glucose and 68 ± 5 for sucrose (refined sucrose is the table sugar). Fructose is also 73% sweeter than sucrose. Studies show that fructose consumed before a meal may even lessen the glycemic response of the meal. Excessive fructose consumption may contribute to the development of fatty liver (liver steatosis). A 2008 study found a substantial risk of gout associated with fructose consumption. A meta-analysis in 2012 concluded that the isocaloric exchange of fructose for another carbohydrate improves long-term glycemic control, as assessed by glycated blood proteins, without affecting insulin in people with diabetes (Reference: http://care.diabetesjournals.org/content/35/7/1611.abstract ).
· High-heat food cooking induces the formation of advanced glycation end products (AGEs), which are thought to impair glucose metabolism in type 2 diabetic patients. High intake of fructose might additionally affect the endogenous formation of AGEs. A study in 2014 investigated whether adding fructose or cooking methods influencing the AGE content of food affects insulin sensitivity in overweight individuals. Seventy-four overweight women were randomized to follow either a high- or low-AGE diet for 4 weeks and consume either fructose or glucose drinks. Glucose and insulin concentrations after fasting and 2 hours after an oral glucose tolerance test were measured before and after the intervention. The results showed that the low-AGE diet decreased urinary AGEs, fasting insulin concentrations, and homeostasis (regulation) model assessment of insulin resistance (HOMA-IR), compared with the high-AGE diet. The addition of fructose did not affect any outcomes. The study concluded that diets with high AGE content may increase the development of insulin resistance. AGEs can be reduced by modulation of cooking methods but are unaffected by moderate fructose intake (Reference: http://www.ncbi.nlm.nih.gov/pubmed/23959566 ). A study in rabbits in 2005 concluded that fructose worsened the atheromatous lesions caused by cholesterol feeding. The mechanism is most likely through lipid peroxidation, which was increased by cholesterol-feeding-induced hyperlipidemia and the formation of AGEs (Reference: http://www.ncbi.nlm.nih.gov/pubmed/16205022 ).
· People should eat daily less than half a teaspoon of salt. However, they should keep in mind that in all processed & restaurant foods, salt (and sugar as well) is added.
· The American Heart Association recommends consuming less than 1,500 mg of sodium daily. 1/4 teaspoon of salt has 575 mg sodium; 1/2 teaspoon salt contains 1,150 mg sodium; 3/4 teaspoon salt contains 1,725 mg sodium, and 1 teaspoon has 2,300 mg sodium.
· Table salt combines two minerals: sodium (Na+) and chloride (Cl-). Table salt is approximately 40% sodium and 60% chloride by weight. About 90% of Americans’ sodium intake comes from sodium chloride.
· You can find the amount of sodium in packaged food sold in stores by looking at the Nutrition Facts label. The amount of sodium per serving is listed in milligrams (mg). The sodium content of packaged and prepared foods can vary widely. Check the labels to help you achieve the American Heart Association’s recommendation of 1,500 mg a day.
· Ninety percent of American adults are expected to develop high blood pressure in their lifetimes, and overeating sodium is strongly linked to the development of high blood pressure. If the U.S. population moved to an average intake of 1,500 mg/day sodium from its current level, it could result in a 25.6% overall decrease in blood pressure and an estimated $26.2 billion in health care savings. Achieving this goal would reduce deaths from CVD by anywhere from 500,000 to nearly 1.2 million over the next 10 years (Reference: http://www.heart.org/HEARTORG/GettingHealthy/NutritionCenter/HealthyEating/About-Sodium-Salt_UCM_463416_Article.jsp and http://www.heart.org/HEARTORG/GettingHealthy/NutritionCenter/HealthyEating/Frequently-Asked-Questions-FAQs-About-Sodium_UCM_306840_Article.jsp ).
· For tracking the sodium in the food, you may check the articles of the American Heart Association (AHA): http://www.heart.org/HEARTORG/GettingHealthy/NutritionCenter/HealthyEating/How-to-Track-Your-Sodium_UCM_449547_Article.jsp and http://www.heart.org/HEARTORG/GettingHealthy/NutritionCenter/HealthyEating/About-Sodium-Salt_UCM_463416_Article.jsp
· The recommendation for less than 1,500 mg of sodium daily does not apply to people who lose substantial amounts of sodium in sweat, such as competitive athletes and workers exposed to extreme heat stress (for example, foundry workers and firefighters), or to those directed otherwise by their healthcare provider (Reference: http://www.heart.org/HEARTORG/GettingHealthy/NutritionCenter/HealthyEating/Frequently-Asked-Questions-FAQs-About-Sodium_UCM_306840_Article.jsp ).
· During a hot day in summer or strenuous physical exercise, we need extra salt, water, and carbohydrates (sugar) to avoid dehydration and electrolyte imbalance that may be life-threatening. In 2003, 14,802 people – most of them elderly – died in a heatwave in France, as they avoided replacing salt and other electrolytes and water during the heat, and died from heatstroke and dehydration, as well as thrombosis that was predisposed by dehydration.
· Salt also has iodine as an additive necessary for the thyroid gland. Its deficiency in children may cause cretinism, a serious mental disease. We can’t live with zero salt. However, as mentioned above, salt is added to almost all processed food.
Arterial compliance & cardiovascular risk
· -Arterial compliance, an index of the elasticity of large arteries such as the thoracic aorta. Arterial compliance is an important cardiovascular risk factor. Compliance diminishes with age and menopause. Arterial compliance is measured by ultrasound as a pressure (carotid artery) and volume (outflow into the aorta) relationship.
· -Arterial Compliance is an action in which an artery yields to pressure or force without disruption. A measure of arterial compliance is used as an indication of arterial stiffening. An increase in age and systolic pressure is accompanied by decreased arterial compliance.
· -Protecting the endothelium is key to reducing cardiovascular (CV) disease risk. Endothelial dysfunction reduces compliance or increases arterial stiffness, particularly in the smaller arteries. This abnormality is characteristic of patients with hypertension but may also be seen in normotensive (with normal blood pressure) patients before the appearance of clinical disease. Reduced arterial compliance is also seen in patients with diabetes and smokers and is part of a vicious cycle that further elevates blood pressure, aggravates atherosclerosis (hardening of the arteries) and leads to increased CV risk.
· -Arterial compliance can be measured by several techniques, most invasive or otherwise not clinically appropriate. Pulse contour analysis is a newly developed noninvasive method that allows for easy, in-office measurement of arterial elasticity to identify patients at risk for CV events before the disease becomes clinically apparent.
· The peripheral resistance of the arteries rises with age. Thus, older people tend to have higher BP than younger people. The elderly, because of arteriosclerosis (hardening of the arteries), tend to have higher BP than younger people. They have increased arterial stiffness, reduced arterial compliance, and decreased elasticity.
· Arterial compliance, an index of the elasticity of large arteries such as the thoracic aorta. Arterial compliance is an important cardiovascular risk factor. Compliance diminishes with age and menopause. Arterial compliance is measured by ultrasound as a pressure (carotid artery) and volume (outflow into the aorta) relationship. Arterial Compliance is an action in which an artery yields to pressure or force without disruption. A measure of arterial compliance is used as an indication of arterial stiffening. An increase in age and systolic pressure is accompanied by decreased arterial compliance.
· Arterial compliance mostly depends on arterial intrinsic elastic properties and is a determinant of the propagation speed of the pulse pressure wave. Decreased arterial compliance is responsible for increased incident pressure waves and the higher effect of reflected pressure waves. This increases systolic pressure and ventricular afterload and generates left ventricular hypertrophy (heart muscle enlargement associated with heart failure). Arterial structural changes that accompany the aging process result in a loss of distensibility and compliance. In primary (essential) and secondary hypertension, arterial compliance is reduced, and age-related structural changes of the arterial wall are accelerated (Reference: http://www.ncbi.nlm.nih.gov/pubmed/7512488 ).
· Reference:
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Methods of attenuation of the reduction of arterial compliance
· Natural ways
· Exercise (aerobic training) such as swimming
· Tai Chi (Chinese)
· Medications
· Rosiglitazone (a drug for diabetes mellitus type 2)
· Combination of amlodipine (a drug for hypertension) & atorvastatin (a statin; a cholesterol-lowering agent)
· Combination of Angiotensin-Converting Enzyme inhibitor (ACEI) and the diuretics hydrochlorothiazide and amiloride (ACEI & the diuretics are used for hypertension and heart failure)
· Pravastatin (a statin; a cholesterol-lowering agent)
· ALT-711 (a novel non-enzymatic breaker of advanced glycation end-product crosslinks)
· The vitamins folic acid (folate), vitamin B6 (pyridoxine) & vitamin B12 decrease homocysteine levels that harm the heart.
· Calcium antagonists, as antihypertensive drugs, improve the distensibility and compliance of large and small arteries, contributing significantly to the improvement in managing essential and secondary hypertension (Reference: http://www.ncbi.nlm.nih.gov/pubmed/7512488 ).
Regular aerobic exercise & its benefits for the cardiovascular system
· Before starting any exercise, you need to first consult your general practitioner (GP)/ family physical (doctor) and a cardiologist for a cardiological exam with an ECG (electrocardiogram) and an Echo (echocardiography; cardiac ultrasound). You may also have a chest X-ray (CXR) to exclude lung problems and heart enlargement (although a cardiac Echo will show it). A physical examination and ECG and echo tests by a cardiologist are essential for excluding cardiac pathology (medical problems) that may be silent, i.e., without or with minor symptoms.
· People aged more than 40 – 45 years old may also do an exercise tolerance test (Bruce protocol treadmill stress test), as the electrocardiogram (ECG) performed by a cardiologist.
· In young people excluding cardiomyopathy (muscle heart disease; in imaging tests, it may appear as megalocardia, i.e., heart enlargement, because of the heart hypertrophy) such as dilated cardiomyopathy is important, as it may be silent (without or with minor symptoms) and is a common reason of sudden death in young people who exercise. Another reason for sudden death that we should consider is supplementation with dangerous unlicensed substances (taken without a doctor's consultation; some consult a gymnast or a personal trainer, but they have no medical knowledge) that many athletes take to improve their performance. These substances may be life-threatening, such as ephedra, thyroxine, ephedrine, diuretics (‘water pills,’ e.g., taken from boxers to lose weight before the match), excess caffeine (also contained in the herb Guarana), iodine, anabolic steroids, and other hormones (such as erythropoietin (EPO) used by cyclists for increasing blood hematocrit), etc. Even creatinine has adverse effects, e.g., on the kidneys. Also, some athletes may take illicit drugs. All of the above may be a cause of sudden death.
· For years, the myocardial (heart muscle) hypertrophy (enlargement; especially left ventricular hypertrophy (LVH)) (called cardiomegaly) on long-distance runners (such as marathon runners) was considered an adjustment to the increased demands of this exercise that is benign and harmless, however, lately there is a debate about its long-term consequences. The author of this text believes that even if this hypertrophy is benign, there is a consideration about the athletes who continue having a large heart after completing their career, and this is complicated by increasing age, when risk factors for coronary artery disease (CAD) accumulate, including hypertension (high blood pressure), especially on people who stop exercising, so that a large heart does not need to support enhanced demands of the periphery.
· LVH (left ventricular hypertrophy) is also characteristic of chronic heart failure (CHF); in this case, the BNP (brain natriuretic peptide) polypeptide (protein) levels in blood appear to increase.
· Long-distance runners also usually have bradycardia (low heart rate).
· A study assessed the left ventricular hypertrophy (LVH), diastolic dysfunction of the heart, pulse pressure (PP; the difference between systolic and diastolic blood pressure), and plasma endothelin (ET)-1 level in amateur marathon runners with an exaggerated blood pressure response (EBPR) to exercise. The participants in the study included normotensive (with normal blood pressure) marathon runners (NM, n = 15 subjects), EBPR marathon runners (EBPR, n = 17 subjects), normotensive sedentary individuals (CON, n = 13 subjects), and hypertensive (with high blood pressure) patients (HTN, n = 14 subjects). An integrated M-mode/2-dimensional echocardiographic analysis was performed. The results showed that LV wall thickness, end-diastolic dimensions, and LV mass index (LVMI) were higher in EBPR than in CON. There were no differences in systolic function among the groups. Analysis of diastolic function, such as lower Em and higher E/Em ratio on TDI, showed a worse relaxation pattern in EBPR. Despite LVH, NM subjects showed no abnormality of LV diastolic dysfunction. HTN subjects in the early stage of their disease showed a slightly modified LV structural and diastolic function, but there was no statistical difference compared with CON. The E/Em ratio was significantly correlated with PP and LVMI. LVMI was significantly correlated with PP. There was a significant difference in plasma ET-1 concentration between marathon runners and hypertensive subjects. In conclusion, the study demonstrated that marathon runners with an exaggerated blood pressure response (EBPR) to exercise had an increase in the left ventricular mass index (LVMI) and diastolic dysfunction (of the heart) more than hypertensive (HTN) subjects in the early stage. Pulse pressure (PP; the difference between systolic and diastolic blood pressure) was significantly related to these two variables. Caution should be exercised when connecting left ventricular hypertrophy (LVH) and diastolic dysfunction of the heart with plasma endothelin (ET-1) concentration in all marathon runners (Reference: http://www.ncbi.nlm.nih.gov/pubmed/23676367 ).
· Professional, long-term physical training is often associated with morphological and metabolic changes in the heart. A study assessed the left ventricular (LV) and right ventricular (RV) heart morphology and function and the LV high-energy phosphates of athletes trained in sustained power or aerobic exercise. Magnetic resonance imaging (MRI) of the LV and RV and phosphorous 31 magnetic resonance spectroscopy of the LV were performed in twenty-three elite track sprinters (sustained power or anaerobic power sprint training, 100-400 m) or marathon runners (sustained aerobic endurance training) and in 10 sedentary, young, lean men. The results showed that athletes had LV hypertrophy, unaffected chamber size, systolic and diastolic functions, and high-energy phosphates metabolism. Also, the RV of the athletes was hypertrophied in comparison with that of the nonathletic controls, and the systolic and diastolic functions were unaffected; the chamber volume was higher in the sprinters (end-diastolic volume 190 +/- 15 mL) in comparison with that of the marathon runners (174 +/- 19 mL) and controls (168 +/- 19 mL) even if this difference, when adjusted for body surface area, was maintained only when compared with that of controls. The study concluded that athletes' left ventricular (LV) and right ventricular (RV) hypertrophy is associated with normal systolic and diastolic functions and resting cardiac energy metabolism, supporting its benign nature. A more pronounced RV dilatation was found in the anaerobic power athletes, and further investigation is warranted to establish the clinical significance of this training effect (Reference: http://www.ncbi.nlm.nih.gov/pubmed/17967601 ).
· Data from the London Marathon, with 650,000 completed runs, shows cardiac arrests occur even among the most experienced runners. Although coronary artery disease (CAD) of the heart was the commonest cause of sudden cardiac arrest (SCA) with five deaths and six resuscitations, hypertrophic cardiomyopathy, or idiopathic left ventricular hypertrophy (HCM), was diagnosed at autopsy on three occasions. HCM deaths were the same average age as runners with ischemic heart disease who had SCA or sudden cardiac death. The cardiac arrests were at the finish in less than one-third of cases, and the remainder occurred between 6 and 26 miles on the course. Only one of the eight runners who died had reported symptoms to his family or physician suggestive of cardiac disease. The runner who had reported pre-race (before the marathon) angina pectoris (chest pain from heart ischemia, i.e., restriction in blood supply to the heart muscle) pain was investigated with a negative exercise stress test before the marathon and, despite this, died with a left anterior descending coronary artery (of the heart) stenosis (narrowing). The cardiac death rate for the London Marathon is 1 in 80,000 finishers (Reference: http://www.ncbi.nlm.nih.gov/pubmed/17465632 )
· Long-distance running results in considerable stress. Little evidence exists about the role of the atrial and brain natriuretic peptides, ANP and BNP, deriving from the myocardium. A study investigated the influence of running 42.195 km on changes in circulating natriuretic pro-peptides and adrenocortical steroids. The subjects were 17 male and 2 female runners (28-62 years old) participating in a marathon. Blood samples were obtained before and immediately after the competition. proANP(1-98) and proANP(1-30), as well as Nt-proBNP(8-29), were determined by enzyme immunoassays. The result showed that runners finished the competition between 2 hours & 58 min and 4 hours & 25 min. The researchers observed a more pronounced increase in proANP(1-98) (+58%) and proANP(1-30) (+99%) compared with Nt-proBNP(8-29) (+6%). Increases in proANP(1-30) positively correlated with runners' age. The scientists also observed a marked increase in cortisol (+73%), especially in aldosterone (+431%). The study concluded that cardiac strain during long-distance running may explain the pronounced increase in the pro-atrial natriuretic peptide (proANP). Other explanations for the observed rise in plasma levels might be a change in myocardial (heart muscle) cell permeability and impaired clearance. A rise in adrenocortical steroids may compensate for the negative influence of ANP on natriuresis (salt excretion with urine) and blood pressure. Positive effects of ANP during a marathon could be regulating body temperature by influencing sweat glands and stimulating lipolysis (fat burning), compensating for the enormous energy demand (Reference: http://www.ncbi.nlm.nih.gov/pubmed/14640997 ).
· Many studies have demonstrated a rise in troponin (a cardiac biomarker used to diagnose a heart attack) and brain natriuretic peptide (BNP) levels following prolonged and/or strenuous exercise. A study assessed the changes in troponin and BNP in three groups of non-elite runners at the 2009 London marathon: those with and without known structural heart disease (SHD) and those who collapsed on completion. The first group (recruited group, RG) was recruited at the prerace exhibition. This group had two subsets, runners with SHD and without (non-SHD). A second group was recruited from those who collapsed (collapsed group, CG). Blood was taken for troponin I (TnI), troponin T (TnT), high sensitivity TnT (HSTnT; as a cardiac biomarker, it increases earlier in a heart attack), and BNP. The results showed that cardiac (heart) biomarker levels increased in all groups following the marathon. No statistically significant difference was seen between the SHD and non-SHD subgroups. When comparing the RG and CG, the number and degree of rise were greater in those who collapsed. A trend for the degree of rising of HSTnT was demonstrated. The study identified runners with troponin levels that, in other circumstances, would raise concern for myocardial necrosis (heart attack). However, the absence of adverse clinical sequelae would suggest this rise is physiological. The cause and clinical significance of the increased high–sensitivity troponin (HSTnT) levels seen in those that collapsed are yet to be fully elucidated (Reference: http://www.ncbi.nlm.nih.gov/pubmed/23513235 ).
· Exercise-induced arterial hypertension (EIAH) leads to myocardial (heart muscle) hypertrophy and is associated with a poor prognosis. EIAH might be related to the "cardiac fatigue" caused by endurance training. A study examined whether there is any relationship between EIAH and left ventricular hypertrophy in Ironman triathletes. Scientists used echocardiography and spiroergometry to determine the left ventricular mass (LVM), the aerobic/anaerobic thresholds, and the steady-state blood pressure of 51 healthy male triathletes. The main inclusion criterion was participation in at least one middle or long-distance triathlon. When comparing triathletes with LVM <220g and athletes with LVM >220g, there was a significant difference between blood pressure values (BP) at the anaerobic threshold (185.2± 21.5 mmHg vs. 198.8 ±22.3 mmHg). The spiroergometric results showed maximum oxygen uptake (relative VO 2max) of 57.3 ±7.5ml/min/kg vs. 59.8±9.5ml/min/kg. Cut-point analysis for the relationship of BP >170 mmHg at the aerobic threshold and the probability of LVM >220g showed a sensitivity of 95.8%, a specificity of 33.3%, with a positive predictive value of 56.8 %, a good negative predictive value of 90%. The probability of LVM >220g increased with higher BP during exercise or with higher training volume. Echocardiography showed predominantly concentric remodeling, followed by concentric hypertrophy. The study concluded that significant left ventricular hypertrophy with left ventricular mass (LVM) >220g is associated with higher arterial blood pressure at the aerobic or anaerobic threshold. Endurance athletes with exercise-induced arterial hypertension (EIAH) may require therapeutic intervention to at least prevent extensive stiffening of the heart muscle and exercise-induced cardiac fatigue (Reference: http://www.ncbi.nlm.nih.gov/pubmed/25132960 ).
· Besides having health-promoting effects, exercise is considered to induce oxidative stress. A study investigated the effects of aerobic and anaerobic exercise on a series of oxidative damage markers. One group of subjects performed aerobic exercise, while another performed anaerobic exercise with similar workloads but with different oxygen consumption levels. Blood and urine samples were collected before, immediately after, and 3, 9, and 24 hours after exercise. Serum uric acid (UA) and creatine phosphokinase were evaluated. As markers of oxidative damage to lipids, proteins, and DNA, we evaluated serum 4-hydroxy-2-nonenal, urinary F2-isoprostanes, serum protein carbonyls, and leukocyte 8-hydroxydeoxyguanosine. The results showed that oxygen consumption was significantly greater during aerobic exercise. Although UA level increased immediately after aerobic exercise and decreased thereafter, UA level did not change after anaerobic exercise. The two types of exercise had significantly different effects on the change in UA level. After anaerobic exercise, the levels of 8-hydroxydeoxyguanosine and 4-hydroxy-2-nonenal significantly increased at 24 h and 3 h, respectively. The levels of creatine phosphokinase and F2-isoprostanes decreased after exercise. The two types of exercise caused no apparent significant differences in the levels of these biomarkers. In conclusion, these findings suggest that similar workloads of anaerobic exercise and aerobic exercise induce reactive oxygen species (ROS) differently: aerobic exercise seems to initially generate more ROS, whereas anaerobic exercise may induce prolonged ROS generation. Although more oxygen was consumed during aerobic exercise, ROS generated did not induce significant oxidative damage. Oxygen consumption per se may not be the major cause of exercise-induced oxidative damage (Reference: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2723376/ ).
· A common (usually post-mortem discovered) cause of sudden death in people exercising is hypertrophic cardiomyopathy (HCM) or idiopathic left ventricular hypertrophy.
· A more common cause of sudden death in people exercising beyond the age of thirty-five is ischemic heart disease (that causes a heart attack) that may worsen by hyperlipidemia (high blood lipids, i.e., fats, such as cholesterol & triglycerides), hypertension (high blood pressure) and diabetes mellitus.
· Another common cause of sudden death during exercises is heart arrhythmias, specifically tachyarrhythmias caused by an athlete who over exaggerates by doing exhausting exercises. This is common in athletes such as marathon / long-distance runners. Ordinary people who are not athletes should exercise mildly to moderately. Strenuous exercise is discouraged as it not only may cause myoskeletal injuries (on bones, muscles, and ligaments) but also may cause dehydration and heart arrhythmias that may be life-threatening.
· A dermatologist (skin doctor) examination is needed on people who want to exercise in a swimming pool, such as swimmers. In these athletes, ear problems (‘swimmer’s ear’) are common.
· Unfortunately, most people, including the young, rarely or never exercise. Children today are more obese than in the past. The most obese children are American and Greek. Young people prefer other ‘sports’ such as TV zapping, computer video games, internet surfing & socializing on social media, hanging out clubbing or drinking coffee at the cafeteria or alcohol at the pub, etc.
· Competitive team sports like football and rugby predispose to injuries. Rugby is an aggressive sport where injuries are common. The Aussie (Australian) football (it is like American rugby but has many differences; the ball is the same) is very dangerous, as the athletes don’t wear protective equipment.
· For working out, you may register at a gym or a sports center.
· The cardiologists recommend, for healthy circulation, mild to moderate AEROBIC exercise at least 30 min daily, at least 5 days weekly. I recommend at least 1 day of abstention from aerobic exercises (e.g., on Sunday) to give the muscles and ligaments a chance to recover & self-heal from minor injuries. However, for weightlifting and weight exercises with machines, I recommend 2 days of absence, one in the middle of the week (e.g., on Wednesday) and one on Sunday, to give the opportunity for self-healing of minor soft tissue (muscles & ligaments) injuries.
· A prospective follow–up of a large study (‘the Copenhagen City Heart Study’) in 1,098 healthy joggers in Copenhagen, Denmark, that was published in February 2015 showed that aerobic exercise such as jogging for at least 2 – 3 days weekly in a total of 1 – 2.4 hours weekly is sufficient for being beneficial for our health, compared with people who follow a sedentary life and don’t exercise with jogging. According to the study, the optimal pace was slow to average. The lowest hazard ratio (HZ) for mortality was found in light joggers, followed by moderate and strenuous joggers! The study concluded that its findings suggest a U-shaped association between all-cause mortality and dose of jogging as calibrated by pace, quantity, and frequency of jogging. Light and moderate joggers have lower mortality than sedentary non-joggers, whereas strenuous joggers have a mortality rate not statistically different from that of the sedentary group (Reference: http://www.ncbi.nlm.nih.gov/pubmed/25660917 ).
· The concept of the above study is that instead of not exercising at all, you can exercise, such as jogging, 2 – 3 days weekly for a total of 1 – 2,4 hours weekly, and you should prefer mild to moderate exercise. Thus, strenuous exercise is discouraged! My personal lower limit is 3 times weekly for aerobic exercises & for anaerobic exercises as well. Anaerobic exercises, like weightlifting, may predispose to injuries.
· Aerobic exercise is beneficial for circulation, as it decreases blood lipids such as cholesterol & triglycerides, increases HDL cholesterol (also known as ‘good’ cholesterol), makes muscle pump of the gastrocnemius (a muscle in our shin) work, helps the return of the blood from the legs to the heart (only when the exercises involve the legs), lower blood pressure and blood sugar (thus are essential for people with diabetes & hypertension) and protect the heart by decreasing the stiffness of the arteries and improving arterial compliance, preventing coronary artery disease (CAD) that may cause a heart attack.
· Physical activity practices benefit obesity and related disorders such as hypertension (high blood pressure) and dyslipidemia (increased blood fats). A study investigated the effects of 6 and 12 months of moderate physical training on the levels of adipokines and cardiovascular disease (CVD) markers in normal-weight, overweight and obese volunteers. The 143 participants were followed up at baseline and after six and twelfth months of moderate regular exercise, 2 times a week, for 12 months. The volunteers were distributed into 3 groups: Normal Weight Group (NWG,), Overweight Group (OVG), and Obese Group (OBG). No significant changes in anthropometric parameters and body composition were observed in any groups following 6 and 12 months of exercise training. Before the training, Leptin, IL-6 levels, and systolic blood pressure were significantly elevated in OBG. Regular exercise decreased HDL-c (‘good’ cholesterol), leptin, adiponectin, resistin levels, and diastolic blood pressure in OVG. In OBG, exercise diminished HDL-c, homocysteine, leptin, resistin, IL-6, adiponectin. Moderate exercise had no effect on the body composition; however, exercise did promote beneficial effects on the low-grade inflammatory state and cardiovascular disease (CVD) clinical markers in overweight and obese individuals (Reference: http://www.ncbi.nlm.nih.gov/pubmed/26474157 ).
· It has been conclusively shown that a single episode of aerobic exercise reduces ambulatory blood pressure in hypertensive patients. Similarly, regular aerobic training also decreases ambulatory blood pressure in hypertensive individuals. Based on current knowledge, aerobic training should be recommended to decrease ambulatory blood pressure in hypertensive (with high blood pressure) individuals. At the same time, resistance exercise could be prescribed as a complementary strategy (Reference: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2845774/ ).
· Exercise-induced increases in the peripheral beta-endorphin (a natural painkiller similar to morphine that fights pain & depression) concentration is mainly associated with changes in pain perception and mood state and possibly substrate metabolism. In endurance exercise performed at a steady state between lactate production and elimination, blood beta-endorphin levels do not increase until exercise duration exceeds approximately 1 hour, with the increase being exponential thereafter. Beta-endorphin and ACTH are secreted simultaneously during exercise, followed by a delayed release of cortisol. These results support a possible role of beta-endorphin in changes in mood state and pain perception during endurance sports (Reference: http://www.ncbi.nlm.nih.gov/pubmed/1553453).
· The endocannabinoid system is known to have positive effects on depression partly through its actions on neurotrophins, such as Brain-Derived Neurotrophic Factor (BDNF). As BDNF is also considered the major candidate molecule for exercise-induced brain plasticity, the study's authors hypothesized that the endocannabinoid system represents a crucial signaling system mediating the beneficial antidepressant effects of exercise. A study investigated, in 11 healthy trained male cyclists, the effects of an intense exercise (60 min at 55% followed by 30 min at 75% W(max)) on plasma levels of endocannabinoids (cannabinoids in the body that bind to cannabinoid receptors and have painkilling and mood-stabilizing effects) (anandamide, AEA and 2-arachidonoylglycerol, 2-AG) and their possible link with serum BDNF. AEA levels increased during exercise and the 15-minute recovery, whereas 2-AG concentrations remained stable. BDNF levels increased significantly during exercise and decreased during the 15 min of recovery. AEA and BDNF concentrations were positively correlated at the end of exercise and after the 15 min recovery, suggesting that AEA increment during exercise might be one of the factors involved in the exercise-induced increase in peripheral BDNF levels and that AEA elevated levels during recovery might delay the return of BDNF to basal levels. AEA production during exercise might be triggered by cortisol since the scientists found positive correlations between these two compounds and because corticosteroids are known to stimulate endocannabinoid biosynthesis. These findings provide evidence in humans that acute exercise represents a physiological stressor able to increase peripheral levels of the endocannabinoid anandamide (AEA) and that Brain-Derived Neurotrophic Factor (BDNF) might be a mechanism by which AEA influences the neuroplastic and antidepressant effects of exercise (Reference: http://www.ncbi.nlm.nih.gov/pubmed/22029953 ).
· Regular aerobic exercise helps in losing weight.
· About how many calories you can lose with exercise, you can visit the online calculator on http://www.cancer.org/healthy/toolsandcalculators/calculators/app/exercise-counts-calculator
· Right after you stop exercising, take your pulse: place the tips of your first two fingers lightly over one of the blood vessels on your neck, just to the left or right of your Adam's apple. You may also try the pulse spot inside your wrist just below the base of your thumb. For calculating the pulses per minute, count your pulse for 10 seconds and multiply the number by 6 (as 1 minute is 60 sec). Check your pulse periodically to see if you exercise within your target zone. As you get in better shape, try exercising within the upper range of your target zone.
· During exercise, the heart rate (HR) should not reach the maximum (220 – age) but within the target zone of 50 – 85% of the average (related to age) maximum heart rate. During the first few weeks of working out, aim for the lower range of your target zone (50%) and gradually build up to the higher range (85%). After six months or more, you may be able to exercise comfortably at up to 85 percent of your maximum heart rate (Reference (Retrieved October 7, 2015): http://www.heart.org/HEARTORG/GettingHealthy/PhysicalActivity/FitnessBasics/Target-Heart-Rates_UCM_434341_Article.jsp and http://www.cancer.org/healthy/toolsandcalculators/calculators/app/target-heart-rate-calculator ).
· For an online calculator of the target heart rate on the exercise, you may visit the site http://www.cancer.org/healthy/toolsandcalculators/calculators/app/target-heart-rate-calculator
· Running on the treadmill is excellent ‘cardio’ training, i.e., it is excellent for a healthy cardiovascular system and helps lose weight.
· Other particularly good ‘cardio’ exercises that benefit the heart are the elliptical machine or jumping rope (as boxers do). One professor of mine also added ‘rowing’ as an excellent ‘cardio’ exercise. However, to my mind, it may harm the lower back.
· Step and cycling are good only for the legs, as the upper body does not work. I personally recommend cycling only to the elderly! The elderly can go jogging, but if they find it difficult (e.g., because of arthritis), they may walk fast.
· People who like jogging should never do it on a firm surface, e.g., on the cement of the street or the marble of the pavement, as many people do by jogging on the pavement instead of jogging in a park. They also breathe polluted air! The surface may be soil but without stones that may cause injuries. A hard running surface, such as cement, may cause injuries to the ligaments and tendons of the knees and predispose them to osteoarthritis. The ideal surface is the special running track surface/ flooring that many gyms and sports centers/ stadiums are equipped with.
· Treadmill is an important ‘cardio’ exercise. As a doctor & physical therapist, the program I recommend is the following: Start with 5 min of pacing (I start with 4 mph) with zero inclines, and every minute, increase velocity until 6 – 6.5 mph (miles per hour). When you reach this level, you will be forced to run. Increase incline to 1%. Then gradually – every 1 – 2 min – increase speed and incline until a maximum speed of 8 mph and a maximum incline of 3%. Stay for some min (e.g., 2 – 5 min) at this speed & incline, then gradually decrease speed & incline every 1 – 2 min. When you reach 6 mph, you can continue pacing with zero inclines. You will complete with pacing for 3 – 5 min, decreasing speed & incline every 1 – 2 min until the level of 4 mph. Then you will continue pacing with increasing speed & incline until 6 – 6.5 mph, and you will continue jogging with increasing speed & incline every 1 – 2 min until the above limit (speed 8 mph, incline 3%) in which you will continue for some min (e.g., 2 – 5 min) and then every 1 – 2 min you will decrease speed & incline, continue with pacing with zero inclines when you reach the level of 6 mph and eventually you will finish with cool down with pacing with decreasing speed every 1 – 2 min. This scheme is the double pyramid that, to my mind, is ideal as it gradually increases energy and heart rate to a maximum level. After this, the energy gradually decreases until pacing. The pyramid is repeated by gradually increasing and then decreasing speed & incline. The scheme finishes with a 5-minute cooldown with pacing with zero inclines and a gradual decrease in velocity. If you exercise for longer than 30 min, you may do a triple pyramid.
· High incline (more than 3 – 4%) on the treadmill and jogging on a hard surface (e.g., the cement of a street or the marble) burdens the knee joint, may cause injuries to the tendons & ligament of the knee and hip, and may predispose to knee osteoarthritis. It also may cause injuries in tendons, ligaments, and muscles in the body, stress fracture in the shin bones and foot, and may cause back pain, foot pain from disturbance of plantar muscles, and injury to muscles such as the hamstrings and the quadriceps.
· There is no consensus about which incline slope is safer on treadmills. In any case, we should prefer a low incline. I recommend a maximum 3% incline, but a study below showed that 4% is OK. A study in well–trained distance runners concluded that incline treadmill training is effective for improving the components of RE, but insufficient as a resistance-to-movement exercise for enhancing muscle power output (Reference: http://www.ncbi.nlm.nih.gov/pubmed/24172721 ). A crossover study in 2010 with 3 D –k motion analysis examined nineteen healthy young runners/joggers (age = 25.3 +/- 2.5 years). Participants ran at 3.13 m/s on a treadmill under 3 different running surface slope conditions: 4 degrees decline, level, and 4 degrees incline. The study showed that moderate changes in running surface slope had a minimal effect on the ankle, knee, and hip joint kinetics when velocity was held constant. Only changes in knee power absorption (increased with decline-slope running) and hip power (increased generation on incline-slope running and increased absorption on decline-slope running in early stance) were noted. The scientists observed an increase only in the impact peak of the vertical ground reaction force component during decline-slope running, whereas the non-vertical components displayed no differences. The study concluded that running style modifications associated with running on moderate slopes did not manifest as changes in 3-dimensional joint moments or in the active peaks of the ground reaction force. The data indicate that running on level and moderately inclined slopes appears to be a safe component of training regimens and return-to-run protocols after injury (Reference: http://www.ncbi.nlm.nih.gov/pubmed/20064043 ).
· Sneakers with full–length air – cushions are very good for jogging/ running and daily use, as the foot is supported by the cushion.
· Warming up before exercise is essential to avoid muscle & ligament injury and to give the heart a chance to gradually increase its beat rate. The warm-up should include a physical activity where all muscles work, e.g., fast walking or running on the treadmill, the elliptical machine, or jumping rope (as boxers do). Warming up should be done for at least 5 minutes.
· After warming up, muscle stretching is essential for preventing ligament and muscle injuries. It should be done for 10 – 15 min and should include the muscles of the arms and legs. You may consult a physiotherapist who can show you these techniques.
· After stretching, a brief warm-up is needed, e.g., jogging for 5 minutes. Then you can start exercise, e.g., weightlifting.
· After completing the exercises (such as weightlifting), a brief cool down (e.g., with slow jogging) and stretching are also important.
· Most people do exercises, especially weight exercises & abdominal working out, wrong.
· Many people in the gym cheat during exercises, e.g., making an exercise fast, not completing the full range of motion, using other auxiliary muscles, etc.
· Classically, most people do the abdominal crunches wrong. They do the exercise in a supine position. With the knees bent, they bend the trunk more than 45 degrees, so they mostly do the exercise by working the muscles of the legs (quadriceps) instead of the abdominals (abs)! The abdominal muscles work only when we bring our chin to our chest and bend our trunk less than 45 degrees so that we just raise the inferior angles (the angles on the lower part) of our scapulae (shoulder blades) from the floor. That is what I was taught in physical therapy school.
· The abdominal exercise with leg lifting in the supine position may harm the back, causing back pain.
· In excess sweating, water, sugar (also called dextrose) & electrolyte (especially sodium & potassium) replacement may be needed to avoid dehydration. Special electrolyte replacement solutions can be found in chemists or supermarkets (energy drinks). However, self–treatment is not recommended, as severe dehydration needs emergency hospital care. Sports drinks may cover the loss of electrolytes & sugar. Plenty of water is also needed. In the market, someone may buy an energy sports drink that contains dextrose (sugar) and electrolytes (e.g., Lucozade (TM) is a famous brand). However, avoid drinks with caffeine & taurine, as they may increase heartbeat (taurine may also lower blood pressure).
· In anaerobic exercise, few repetitions (e.g., less than 8) offer muscle hypertrophy (enlargement); more repetitions (e.g., more than 8) offer a leaner muscle body without muscle hypertrophy. On weight exercise, the muscle cells do not increase in number but in size as they sustain hypertrophy (enlargement). It is the connective tissue that enlarges, not the muscle fiber.
· The disadvantages of anaerobic exercise include the increase in blood pressure during exercise and its consequences in the heart on high risk for coronary artery disease (CAD) people (especially in those with stenosed (narrowed) coronary arteries of the heart), as well as the risk of severe arrhythmias and the risk of aneurysm rupture on people with brain or aorta (chest or abdominal) aneurysm; the increased risk for injuries on muscles, tendons, ligaments, and joints; the increased oxidative stress; the increased lactate levels (that cause exhaustion); and the absence of benefits to the heart and generally the cardiovascular system. However, recent studies have shown that resistance and isometric training may, in fact, decrease blood pressure. Another benefit is that they may prevent osteoporosis in post-menopausal (after menopause) women.
· Anaerobic exercise is contraindicated in people with medical problems such as hypertension, hernia, aneurysm (in the brain or abdominal or chest), back pain, etc. Weightlifting, especially when done wrong, may cause severe back pain and induce disc problems (discopathy with disc – the cushion between the vertebra of the spine that acts as a shock absorber for the pressure forces tension – prolapse that may pressure spinal nerves causing back pain that may be radiated to the leg – called sciatica) that may cause permanent back pain. The worst weight exercise for causing back pain, although many men like it to have strong buttocks, is squatting. Also, abdominal muscle exercise by leg lifting (with the knees extended) in a supine position may also cause back pain.
· Professional, long-term physical training is often associated with morphological and metabolic changes in the heart. A study assessed the left ventricular (LV) and right ventricular (RV) heart morphology and function and the LV high-energy phosphates of athletes trained in sustained power or aerobic exercise. The study concluded that athletes' left ventricular (LV) and right ventricular (RV) hypertrophy is associated with normal systolic and diastolic functions and resting cardiac energy metabolism, supporting its benign nature. A more pronounced RV dilatation was found in the anaerobic power athletes, and further investigation is warranted to establish the clinical significance of this training effect (Reference: http://www.ncbi.nlm.nih.gov/pubmed/17967601 ).
· Exercise-induced arterial hypertension (EIAH) leads to myocardial (heart muscle) hypertrophy and is associated with a poor prognosis. EIAH might be related to the "cardiac fatigue" caused by endurance training. A study examined whether there is any relationship between EIAH and left ventricular hypertrophy in Ironman triathletes. Scientists used echocardiography and spiroergometry to determine the left ventricular mass (LVM), the aerobic/anaerobic thresholds, and the steady-state blood pressure of 51 healthy male triathletes. The study concluded that significant left ventricular hypertrophy with left ventricular mass (LVM) >220g is associated with higher arterial blood pressure at the aerobic or anaerobic threshold. Endurance athletes with exercise-induced arterial hypertension (EIAH) may require therapeutic intervention to at least prevent extensive stiffening of the heart muscle and exercise-induced cardiac fatigue (Reference: http://www.ncbi.nlm.nih.gov/pubmed/25132960 ).
· Besides having health-promoting effects, exercise is considered to induce oxidative stress. A study investigated the effects of aerobic and anaerobic exercise on a series of oxidative damage markers. The study's findings suggest that similar workloads of anaerobic exercise and aerobic exercise induce reactive oxygen species (ROS) differently: aerobic exercise initially generates more ROS, whereas anaerobic exercise may induce prolonged ROS generation. Although more oxygen was consumed during aerobic exercise, ROS generated did not induce significant oxidative damage. Oxygen consumption per se may not be the major cause of exercise-induced oxidative damage
Reference
Bibliography & External Links
Bibliography
· Simon C., Everitt H., Kendrick T., Oxford Handbook of General Practice, Oxford Medical Publications, 2nd edition, 2005.
· Longmore M., Wilkinson I., Turmezei T., Kay Cheung C., Oxford Handbook of Clinical Medicine, Oxford Medical Publications, 7th edition, 2008.
· Collier J., Longmore M., Brinsden M., Oxford Handbook of Clinical Specialties, Oxford Medical Publications, 7th edition, 2006.
· Stone C.K., Humphries R.L., Current Diagnosis and Treatment in Emergency Medicine, McGraw–Hill LANGE, 6th edition, 2008.
· Disease prevention & health maintenance, p. 1103 – 1130, Harrison’s Manual of Medicine, Fauci A.S., Braunwald E.B., Kasper D.L., Hauser S.L., Longo D.L., Jameson J.L., Loscalzo J., 17th edition, Mc Graw Hill Medical, 2009.
mcgraw-hillmedical.com
mcgraw-hillmedical.com
· Screening in the future, p. 160 – 161, Oxford Handbook of General Practice, C. Simon, H. Everitt, T. Kendrick, 2nd edition, Oxford University Press,2005.
Longo D.L., Fauci A.S., Kasper D.L., Hauser S.L., Jameson J.L., Loscalzo J.L., Harrison’s Manual of Medicine, 18th edition, McGraw–Hill, 2013.
Longmore M., Wilkinson I.B., Davidson E.H., Foulkes A., Mafi A.R., Oxford Handbook of Clinical Medicine, 8th edition, Oxford University Press, 2010.
Ahmed N., Clinical Biochemistry, Oxford University Press, 2010.
Reference – Links
(Retrieved January 16, 201
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(Retrieved January 18, 2015)
• http://www.ncbi.nlm.nih.gov/pubmed/18672019
• http://www.ncbi.nlm.nih.gov/pubmed/18003755
• http://www.ncbi.nlm.nih.gov/pubmed/16531786
• http://www.ncbi.nlm.nih.gov/pubmed/25375075
Reference (Retrieved: January 16, 2016):