Therapy of Lipodystrophy Syndrome

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No accepted guidelines for the treatment of lipodystrophy syndrome exist, rather, only anecdotal approaches. There is also no validated drug therapy to ameliorate or correct lipodystrophy-associated abnormalities [99]. Instead, treatment must be directed at reducing fat accumulation in visceral adipose tissue (VAT), and dorsocervical fat (buffalo hump), and/or increasing SAT in conditions of lipoatrophy. Thus, prevention is by far the best approach to reverse lipodystrophy.

Table 3. Anthropometric data of patients treated with rhGH (0.63 mg/m2, sc/day) alone (n = 5) or with rhGH + MA (320 mg, orally/day) (n = 5), means ± SD

Baseline

Baseline

15 days

MA 30 days

W:

55.1 ± 8.6

53.2 ± 7.7

47.7 ± 6.8

48.2 ± 6.7

48.3 ± 7.1

% IBW:

19.4

22.2

23.6

24.6

19.6

BMI :

17.4 ± 1.2

16.8 ± 1.1

15.7 ± 1.9

16.1 ± 2.2

16.7 ±2.4

SUM:

17.5 ± 2.5

16.3 ± 2.0

21.2 ±3.8

21.3 ± 5.2

23.5 ± 6.0

LBM

54.3 ± 6.7

52.0 ± 8.4

45.1 ± 10.3

45.2 ± 9.0

44.8 ± 9.8

FBM:

0.77 ± 1.0

1.3 ± 2.2

1.9 ±2.8

2.6 ± 4.1

4.2 ± 4.8

BIA:

482 ± 110

536+-129

643 ± 116

638 ± 92

656+-87

TBW:

72.7 ± 2

72.4 ± 0.5

73.6 ± 2.3

73.7 ± 1.2

73.4 ± 1.3

Caloric intake:

2194 ± 600

2768 ± 1611

1848 ± 480

3605 ±915

3898 ± 634

W, body weight (kg); % IBW, percentage of W loss with respect to ideal body weight; BMI, body mass index [weight (kg)/height (m2)]; SUM, sum (mm) of four skinfold thicknesses (biceps; triceps; subscapular; iliac); LBM, lean body mass (kg). FBM, fat body mass (kg); BIA, bioelectrical impedance analysis (ohms); TBW, total body water (%); caloric intake, Kcal/day

Table 4. Hormonal profile of patients treated with rhGH (0.63 mg/m2/day) alone (n = 5) or with rhGH + MA (320 mg/oral-ly/day; n = 5), means ± SD

Baseline

30 days

Baseline

15 days

30 days

W

55.1 ± 8.6

53.2 ± 7.7

48.2 ± 6.7

47.7 ± 6.8

48.3 ± 7.1

% IBW

19.4

22.2

23.6

24.6

19.6

BMI

17.4 ± 1.2

16.8 ± 1.1

15.7 ± 1.9

16.1 ± -2.2

16.7 ±2.4

SUM

17.5 ± 2.5

16.3 ± 2.0

21.2 ±3.8

21.3 ± 5.2

23.5 ± 6.0

LBM

54.3 ± 6.7

52.0 ± 8.4

45.1 ± 10.3

45.2 ± 9.0

44.8 ± 9.8

FBM

0.77 ± 1.0

1.3 ± 2.2

1.9 ±2.8

2.6 ± 4.1

4.2 ± 4.8

BIA

482 ± 110

536 ± 129

643 ± 116

638 ± 92

656 ± 87

TBW

72.7 ± 2

72.4 ± 0.5

73.6 ± 2.3

73.7 ± 1.2

73.4 ± 1.3

Caloric intake

2194 ± 600

2768 ± 1611

1848 ± 480

3605 ±915

3898 ± 634

IGF-1, insulin-like growth factor-1; IGFBP-3, insulin-like-growth-factor binding protein-3; DHEA-S, dehydroepiandros-terone sulfate

Prevention of Lipodystrophy

Strategies for preventing or reducing the risk of lipodystrophy are:

- Avoid combination of PIs and NRTIs

- Early antiretroviral treatment

- Early intervention for metabolic changes

- Dietary advice, dietary supplementation and physical exercise.

Management of Lipodystrophy

In established lipodystrophy, there are four categories of intervention:

- Lifestyle changes regarding diet, physical activity, and smoking

- Changes in the treatment regimen

- Use of specific drug therapies to correct specific abnormalities

- Cosmetic surgery.

Management of Fat Accumulation Diet and Exercise

Specific dietary and exercise intervention, as extrapolated from subjects not infected with HIV [100], seems to be also effective in lipodystrophy for preventing hyperlipidaemia as well as reducing lipid levels and abnormal fat distribution, especially VAT [101-106]. A Mediterranean low-fat diet, rich in vegetables, fresh fruits, fibre, and fish, is recommended for its high content of omega-3 fatty acids. Diets very low in fat [107], i.e. containing < 15% fat calories, are recommended for persons with high cholesterol and TG levels.

A beneficial role of antioxidants, B vitamins, and carnitine in reversing mitochondrial damage induced by NRTI [108], and related to lipodystrophy and lactic acidosis, has been reported by many authors [108-116].Vitamins B1 (thiamine) and B2 (riboflavin) are given at a dose of 100 mg and 50 mg, respectively, in addition to dietary intervention. Improved p-oxidation of long-chain fatty acids is achieved with 100 mg levocarnitine (Sigma-tau, Italy)/kg/day in children and 2-4 g/day in adults. Independent of other specific therapies, we usually administer fish oil or/and vegetable-derived PUFAs [117-119] together with L-carnitine,in order to increase p-oxidation of long-chain fatty acids, and replace saturated fats with polyunsaturated fats (data available on line). Consumption of purified and concentrated preparations of fish-oil derivatives (Enerzona Omega-3Rx, New Vitality, Italy) and adherence to insulin-sparing diets are highly effective in controlling metabolic pathways that can lead to fat disorders (data available on line).

Physical exercise is also prescribed to partly compensate for the reduction of peripheral fat tissue with muscle-mass hypertrophy (body building) [105,106]. Intensive aerobic and anaerobic exercise can decrease VAT in normal and HIV subjects by 17-20% [106, 120]. Exercise increases the production of the adrenergic hormone epinephrine, the lipolytic effect of which is more evident for visceral fat than for peripheral fat. Physical exercise associated with a high-fibre, moderate-fat, low-gly-caemic-index diet ameliorates lipodystrophy patterns [103]. Progressive resistance training decreases truncal fat and improves LBM [106,121,122].

Androgens

Testosterone and other synthetic androgens at low or replacement doses in males with testosterone levels < 250 ng/dl can be used to reduce intra-abdominal fat, but a reduction of peripheral fat is also observed [123].

Insulin-Sensitising Agents (Metformin)

Metformin is a drug that reduces glucose production in the liver. At a dosage of 500-850 mg 2-3 times a day, it decreases VAT, TGs, and LDL, and improves fasting insulin levels and the insulin response in an oral glucose tolerance test [124, 125]; however, serious lactic acidosis can occur during metformin therapy.

Growth Hormone and GH-Releasing Hormone

Prior to the availability of HAART for use in treating AIDS-related wasting, GH had been shown to promote gains in lean mass and loss of fat mass [126, 127]. We demonstrated favourable effects of GH in association with MA [71] in the treatment of wasting syndrome, and the data suggested a role for GH in reducing central fat accumulation and increasing muscle mass. Since the introduction of HAART, studies have pointed out that rhGH improves fat redistribution, reducing waist circumference (VAT) and breast size, while increasing fat-free mass [128, 129]. GH improves fat metabolism and reduces both fat accumulation and lipoatrophy, including loss of facial fat pads. The optimal dose for treating lipodystrophy is not yet established but is less than the 4-6 mg/day administered to patients with wasting [130]. Adverse effects, however, at the doses employed are common and include arthral-gias, myalgias, diabetes, and hypertriglyceridaemia. In addition, there is reversion of truncal adiposity after drug discontinuation, suggesting the need to establish a maintenance dose. In order to maintain physiological levels of GH, which appear to be reduced in lipodystrophic HIV patients, the effect of GHRH in the treatment of lipodystrophy was studied [131]. GHRH, at the dose of 1 mg subcutaneous-ly twice daily, increases LBM and subcutaneous fat, reduces truncal and visceral fat, and increases the concentration of IGF-1.

Leptin

The discovery of leptin, in 1994 [132], and the identification of its role in body weight homeostasis, food intake, energy expenditure, and adipose tissue metabolism represent an enormous progress in understanding and treating lipodystrophy [133-137]. As a result, lipodystrophy may be considered as a localised form of obesity, with associated typical changes in the neuroendocrine system as well as in metabolism and immune functions [137-139]. Low leptin levels or non-functional leptin receptors have been shown in lipodystrophy [140]. Leptin replacement ameliorated hormonal and fat-tissue abnormalities characteristic of the syndrome [141,142] after 4 months of therapy.

Management of Lipoatrophy Switch Therapy

Switch therapy consists of replacing a drug causing fat loss or fat redistribution with another drug that has fewer or none of these effects. The majority of switch studies have focused on replacing a combination of NRTIs and PIs with a PI-sparing regimen [143]; changing from one PI to another does not seem to be useful. The replacement of PIs by NRTIs or NNRTIs leads to significant improvement of metabolic and fat abnormalities [144, 145]. In HAART, NRTIs inhibit DNA polymerase, which ultimately induces lipodystrophic changes [124,144-147], in the following decreasing hierarchic order; zalcitabine > didanosine > stavudine > lamivudine > zidovudine > abacavir. Thus, some studies have demonstrated an improvement in lipoatrophy in response to switching from stavudine or zidovudine to abacavir [148], and from stavudine to abacavir or zidovudine [149,150]. In the TARHEEL study (Trial to Assess the Regression of Hyperlactataemia and to Evaluate the Regression of Established Lipodystrophy) of HIV-1-positive subjects, replacing stavudine with aba-cavir or zidovudine resulted in a median increase in arm fat of 35%, in leg fat of 12%, and in trunk fat of 18%, after 48 weeks of therapy [149].

New antiretroviral drugs with less effects on fat metabolism are espected.

Cosmetic Surgery

Cosmetic surgery for lipodystrophy was introduced to correct both fat accumulation and lipoat-rophy. Anomalous dorsal and abdominal fat accumulations can be reduced with ultrasound-assisted liposuction and endermology, and facial shape can be restored by lipofilling the temple, nasolabial, and cheek areas with fat cells taken from the patient's abdomen [151, 152] or by injecting new fill. These cells remain in place even during lipodystrophy progression.

Traditional plastic surgery approaches have also been used for cosmetic results, mainly for facial changes affecting the nasolabial folds and buccal and temporal fat-pad areas. Implants usually consist of fat transfer and collagen injections, but loss of the implanted fat is a not uncommon risk. Satisfactory results were reported with polylac-tic acid (New-Fill) injections every 15 days for treating facial lipoatrophy [153]. Polylactic acid and similar compounds (e.g. hyaluronic acid), however, are not approved for this type of use in the USA. Success, as judged by evaluating on 3D photos, is around 48% and additional injections are needed within 1-2 years. Side effects include pain in 80%, the development of non-inflammatory small nodules, bleeding, and malaise. New-Fill is not a true filler, like collagen or transferred fat, but stimulates fibroblasts to produce collagen in the injection sites. The product is hypoallergenic and biodegradable over 2 years [154]. Suction-assisted lipotomy has been used to remove 'buffalo hump' but fat deposits can reappear [152,155,156]. Malar atrophy can benefit from surgical correction, with dermafat grafts transferred from the abdominal wall to malar pockets through a transoral approach. The aesthetic results were judged to be satisfactory and persisting during 2 years of follow-up [151].

Correction of Metabolic Abnormalities Associated with Lipodystrophy

Persons infected with HIV could represent an emerging population at higher risk of coronary heart disease (CHD), due to their prolonged life expectancy despite metabolic disturbances induced by therapy [157-160]. Elevated TGs, LDL

cholesterol, and VLDL cholesterol, and reduced levels of high-density lipoprotein (HDL) cholesterol are associated with visceral fat accumulation, peripheral lipodystrophy, lipoatrophy, and CHD. In 5-75% of HIV patients receiving HAART, lipid metabolism and body fat distribution worsen after 10-12 months of therapy.

Patients on HAART at risk of heart disease (CAD, IHD), because of high levels of cholesterol and/or TGs, may benefit from special diet, changes in life style, and drugs. The risk of increases in total cholesterol (> 0.6 mmol/l) is 19.6% for Ritonavir, 8.5% for Nelfinavir, and 3.8% for Indinavir.

Increased lipid concentrations in HIV-infected patients on HAART can be managed following the American National Cholesterol Education Program (NCEP), but new strategies addressed to prevent and manage such emerging disorders [161, 162] are still needed. Our guidelines, based on our own and experience and that of others [163-168] meet the intervention criteria defined by NCEP [169], including evaluation criteria, diet prescription, drugs, exercise, and were preliminarily discussed in The Pavia Consensus Statement, October 2001 [170,171], together with recommendations of the HIV Medicine Association of the Infectious Disease Society of America and the Adult AIDS Clinical Trials Group [172].

Patient Evaluation Criteria

Patients at risk of CHD must be routinely evaluated for risk factors, such as family history, smoking, hypertension, hormonal status, obesity, physical activity, alcohol abuse, hypogonadism, hypothy-roidism, diabetes, and renal or hepatic disease. The guidelines include measurement of total cholesterol, HDL, LDL and VLDL cholesterol, TG, lactate [170-172], body compartments, body circumferences and skinfolds [160], and resting metabolic rate (RMR). The RMR is a measure of the energy expended for maintenance of physiological functions and generally represents the largest portion of daily energy expenditure (60-75%) [163-165]. We use the WHO equations for determining body weights and heights [166], and BIA and indirect calorimetry to predict the RMR and energy expenditure for different age and sex groups [167,168].

Energy production is estimated by measuring O2 consumption and CO2 production using a special calorimeter (e.g. type MBM-200-23-01, Datex-Engstron Division Instrumentarium Corp. Helsinki, Finland). RMR values normally range between 0.7 and 1.6 Kcal/min according to the subject's body composition, gender, and level of training.

Intervention Criteria

Nutritional and Pharmacological Approach There are no universally accepted guidelines for the nutritional treatment of disturbances in lipid metabolism in HIV patients: however, according to NCEP [157,169] and our studies as well as those of other authors [161, 160, 168, 170-173] in patients with preexisting CHD dietary intervention is recommended at LDL cholesterol level between 100 and 130 mg/dl, adding drug therapy if LDL cholesterol exceeds 130 mg/dl. Among patients without CHD, but presenting with two or more risk factors, dietary intervention is strongly indicated when LDL cholesterol is between 130 and 160mg/dl. Drug therapy must be added at LDL levels > 160 mg/dl. With less than two risk factors, dietary modifications should be recommended at LDL levels between 160 and 190 mg/dl; and drug therapy should be considered at LDL > 190 mg/dl. For patients with very high TG levels (> 400 mg/dl) the Adult AIDS Clinical Trials Group (AACTG) [172] suggests dietary intervention at a total cholesterol >240 mg/dl or HDL cholesterol < 35 mg/dl. Patients with isolated hypertriglyceridaemia (fasting serum levels > 200mg/dl) should follow an appropriate diet and a program of physical exercise. If levels exceed 1000 mg/dl, pharmacological therapy is strongly suggested because of the risk of pancreatitis. The same indication is mandatory for patients with a history of pancreatitis and TGs > 500mg/dl.

Diet and exercise in order to reduce hypercho-lesterolaemia are recommended before and during pharmacological intervention. In patients suffering from wasting and from lipid disturbances, it is preferable to treat the wasting first [168,174,175]. In patients without other risk factors, such as smoking, preexisting cardiovascular diseases, and lipid problems, 'wait and see' may be an appropriate strategy [176].

Nutritional intervention must be tailored to the needs of each patient, considering RMR, gut functions, concomitant diseases, hormonal status, appetite, and social conditions [160, 170, 175]. At the first signs of malnutrition, suitable nutritional treatment is advised [168] due to the positive effect on reducing infection and improving the quality of life. A balanced supply of n-6 and n-3 PUFAs, including EPA and DHA (the main components of fish oil) in a ratio of 0.9;1.5, may modulate cytokine production and reduce TGs. EPA, as a direct suppressant of lipid mobilisation factor, counteracts weight loss, lipolysis, and protein catabolism [177]. Amino acids (1.5-2 g/kg per day), of which a portion (< 0.7 g/kg) should be essential, must be administered to block protein loss. Branched-chain amino acids are important when patients present with associated hepatic encephalopathy. Early and aggressive nutritional treatment of wasting and lipid metabolism disturbances improves the general clinical status, thus reducing the length of hospital stay. Unfortunately, national health services do not completely support nutritional therapy programs.

Pharmacological intervention on appetite and on metabolic pathways, by administering drugs, such as cyproheptadine [178], progestin derivatives [174, 179-181], insulin-like growth factor-1 [182], steroids, and GH [160, 183, 184], may contribute to the success of any nutritional program.

Drugs Lowering Lipids

Since diet and physical exercise reduce lipid levels in only 40% of patients, therapy with statins and/or fibrates for hypercholesterolaemia and/or hypertriglyceridaemia is almost always necessary [170,172].

In our opinion, an isolated increase of TGs in a patient with normal HDL values should be treated only when levels of 1000 mg/dl are reached, and the consequent risk of pancreatitis becomes high [105]. In this situation, we also recommend replacement of saturated fats with unsaturated fats and the addition of statin or fibrate drugs, if diet alone fails. In combined disorders (high choles terol, high TGs), statins and fibrates together may control lipid metabolism, but they also cause muscle damage (rhabdomyolysis). In some subjects, Gemfibrozil (600 mg BID), Atorvastatin (10 mg QD), or a combination thereof reduces total cholesterol by, respectively, 32,19, and 30%, with a TG reduction of 59,21, and 60%. Interactions between antiretroviral compounds, lipid-lowering agents, and anti-diabetic drugs are not well-described. What is known is that these drugs carry a risk of toxicity, because the majority of them (Atorvastatin, Lovastatin, Simvastatin, Bezafibrate, Ciprofibrate, Fenofibrate, Gemfibrozil) are metabolised by the same CYP3A liver enzymes as protease inhibitors and other drugs taken by HIV patients. Pravastatin, Cerivastatin, and Fluvastatin in contrast, are mainly excreted by the kidney. PIs, macrolides, and imidazole derivatives inhibit CYP3A and can raise statin levels 10- to 20-fold, leading to increased muscle and liver toxicity with elevation of CPK and ALT. CAD/IHD, due to elevated lipids or diabetes, require 5-10 years to develop, whereas myocardial infarctions are seen after a few weeks or months of PI therapy and have been attributed to thrombosis rather than to atherosclerosis. Metformin can reduce central fat and insulin resistance [186] but it also reduces general fat and muscle mass. Troglitazone (400 mg/day), Rosiglitazone, and Pioglitazone may normalise glucose levels but no effects on lipids and body fat have been observed [187-189]. GH [71, 190] reduces abdominal fat without influencing peripheral fat loss and lipids. Androgenic anabolic steroids (AAS), e.g. oxandrolone, nandrolone, and decanoate, increase muscular body mass without changes in lipids and body fat [191].

Physical Exercise

The effects of exercise have been extensively studied in patients with known coronary artery disease. Exercise induces beneficial adaptation of the cardiovascular system as well as in peripheral muscle mass [168,192-197] (Table 5, Fig. 3).

Aerobic exercise and resistance exercise are the most popular methods to prevent or treat sarcope-nia and increase muscular performance [198]. In our experience, both forms of exercise, together with a personalised training diet, improves muscle endurance and body composition in HIV patients, as reported by Stringer [199] and Smith [193]. For developing complete muscle strength, three exercise methods are commonly used: weight training, isometric training, and isokinetic training. The neck, arms, and shoulders; the chest, abdomen and back; the buttocks and the legs can be conditioned separately by specific exercises. All our exercise programs include progressive resistance training of the major muscle groups.

HDL levels may increase in sedentary people who engage in aerobic training. Concurrently, LDL is lowered so the net result is a considerably improved ratio of HDL to LDL or HDL to total cholesterol. This exercise effect appears to be independent of whether or not the diet is low in fat or whether or not the exerciser is overweight. The effect of regular endurance-type exercise on blood lipid profile is certainly a strong argument for incorporating vigorous physical activity into a total program of health maintenance in HIV

Table 5. Beneficial effects of muscle exercise

Resistance to fatigue

t

Elasticity and flexibility

t

Muscle mass and strength

t

Respiratory capacity

t

Appetite

t

Intestinal functions

t

Stress and insomnia

*

patients receiving HAART. It is well-known that exercise improves myocardial circulation and metabolism and enhances vascularisation, cardiac glycogen stores, and glycolytic capacity,which protect the heart from hypoxic stress [196]. Moreover, the mechanical and contractile properties of the myocardium are improved, enabling the conditioned heart to maintain or increase contractility during specific challenge. Heart rate and blood pressure are reduced, so that the work of the myocardium is significantly reduced at rest and during exercise.

Weekly walking exercise in miles

Walk less than 5 Walk 10-15 Walk 20-25 Walk 30-35

Walk 5-10 Walk 15-20 Walk 25-30

V

On

e mile of wa

Iking burns

about 100 K

cal

\

El

^__

Fig. 3. Regularly walking/jogging more than 3 miles a day proportionally reduces the risk of death. No additional benefits are obtained with energy expenditure beyond 3500 kcal per week (reproduced from [197])

Exercise reduces symptoms and the amount of medication needed; it corrects nutritional imbalance, reduces the side effects of many drugs and of an altered diet. Many clinical signs and symptoms are responsive to exercise: atrophy of muscle and bone, postural hypotension, joint stiffness, reflexes, cardiovascular deconditioning, anorexia, gastrointestinal motility, insomnia, and depression. Exercise stimulates the muscles, which not only improves movement of the body in space but also increases biochemical reactions devoted to produce energy. The predominant energy pathways required for physical activities are the ATP-CP system, the lactic acid system, and the oxygen or aerobic system. These pathways often operate simultaneously (Fig. 4); however, there are marked differences in their relative contributions during exercise to the total energy requirement, which is related directly to the length of time and intensity that a specific activity is performed.

Anaerobic Conditioning. During intense, maximal bursts of energy lasting no more than 6 s, energy is provided anaerobically, almost exclusively by stored high-energy molecules of phosphates, ATP, and CP. Overload of the ATP-CP pool can be achieved by engaging specific muscles in maximum bursts of effort for 5 or 10 s. In physical activities chosen to enhance the ATP-CP energy capacity of specific muscles, a person must perform numerous bouts of intense, short-duration exercise. The energy for a performance lasting between 10 and 90 s is still supplied predominantly by anaerobic reactions, but lactic acid becomes a more important source of energy. To improve the lactic acid energy system, training must be of sufficient intensity and duration to stimulate lactic acid production as well as to overload the ATP-CP energy system. An effective way to increase the latter to near-maximum levels and overload the lactic acid system is repeated bouts of up to 1 min r

Predominant energy pathways Immediate/short-term non aerobic systems Aerobic systems

Strength/power

(power lift, high jump, shot put, golf swing, tennis serve)

ATP-CP

Sustained power

(sprints, fast breaks, football line play)

Anaerobic power/ en durance ATP-CP+LACTIC ACID (200-400 m dash.

Aerobic endurance

(beyond 1/2 mile run, aerobic system becomes progressively more important)

Fig. 4. The three energy systems (ATP-CP system, lactic acid system, aerobic system) involved in physical activities. In exercises requiring an intense, short burst of energy, the energy is provided anaerobically, almost exclusively by stored reserves of ATP and CP. In performances lasting between 10 and 90 s, energy from lactic acid production becomes an important source. After 2-4 min of continuous activity, the energy is released almost exclusively from aerobic reactions (reproduced from [197])

of extreme running, swimming, or cycling stopped 30-40 s before exhaustion. The exercise bout should be repeated several times after 1-2 min of recovery. The recovery time from such forms of exercise can be considerable when large amounts of lactic acid are produced (Fig. 2).

Aerobic Conditioning. After 2-4 min of continuous exercise, any physical activity becomes progressively more dependent on aerobic energy for the resynthesis of phosphates. Under aerobic conditions, pyruvic acid from carbohydrate metabolism and molecules from fat and protein are transformed into various intermediate substances, with the final formation of CO2, H2O, and large amounts of energy. If the O2 supply and O2 utilisation are adequate, lactic acid will not accumulate and fatigue will be absent. It is possible to reach a condition of endurance or aerobic fitness in which the body's ability to generate ATP aerobically exceeds the energy produced from anaerobic reactions. To have a practical measure of a person's cardiovascular capacity, we use the step-up shown in Fig. 5. This system measures the heart rate in response to aerobic exercise: a low heart rate during exercise and a small increment with more intense exercise reflect a high level of cardiovascular fitness. A simple method to recover heart rates for evaluation of relative fitness for aerobic exercise is the Tecumseh step test [193].

The stepping cadence must be 22 steps/min for women and 24 for men, with a stepping height of 20 cm. After 3 min of stepping, the subject, in a standing position and exactly after 30 s after stopping, must measure his or her pulse for 30 s. The number of pulse beats, from 30 s to the 1-min post-exercise phase, is the heart rate score. By means of special equations and taking into account recovery heart rate, maximal O2 consumption can be calculated [194].

Determination of Frequency, Duration, and Intensity of Training. The intensity of training is the most critical factor influencing successful aerobic conditioning. It can be expressed in different ways: as calories consumed, as a percentage of maximal O2 consumption, as heart rate or percentage of maximum heart rate, or as multiples of

Fig. 5. Step-up exercise to evaluate cardiovascular capacity: the heart rate responses of three individuals during 3 min of regular stepping. The subjects have different degrees of condition: A is a professional football player, and at the end of 3 min his heart rate is 115 beats per min; B works out at a gym; her heart rate is 140 beats per min. C is a sedentary young person, his heart rate reaches 170 beats per min. Heart-rate recovery is complete 2 min after the end of exercise (reproduced from [197])

resting metabolic rate required to perform the work. The amount of exercise must be sufficient to produce an increase in heart rate to at least 130-140 beats/min, equivalent to about 50-55% of the maximum aerobic capacity or about 70% of the maximum exercise heart rate (Fig. 6).

Both continuous as well as intermittent overload are effective in improving aerobic capacity. As little as 3-5 min of vigorous exercise performed three times a week improves aerobic capacity and is less exhausting than steady-state exercise performed for 20 min. Our aerobic training program is conducted 3 days a week and includes 20-30 min of continuous exercise of sufficient intensity to expend about 300 kcal. For example, subjects trained on a bicycle ergometer 20-30 min a day (~ 300 kcal), three times a week for 8 weeks, with a training intensity of 85% of maximum heart rate improved maximal O2 uptake by 7.8% [170,195].

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