245 resultados para cinética do VO2


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We investigated the effects of aerobic training on the efferent autonomic control of heart rate (HR) during dynamic exercise in middle-aged men, eight of whom underwent exercise training (T) while the other seven continued their sedentary (S) life style. The training was conducted over 10 months (three 1-h sessions/week on a field track at 70-85% of the peak HR). The contribution of sympathetic and parasympathetic exercise tachycardia was determined in terms of differences in the time constant effects on the HR response obtained using a discontinuous protocol (4-min tests at 25, 50, 100 and 125 watts on a cycle ergometer), and a continuous protocol (25 watts/min until exhaustion) allowed the quantification of the parameters (anaerobic threshold, VO2 AT; peak O2 uptake, VO2 peak; power peak) that reflect oxygen transport. The results obtained for the S and the T groups were: 1) a smaller resting HR in T (66 beats/min) when compared to S (84 beats/min); 2) during exercise, a small increase in the fast tachycardia (D0-10 s) related to vagal withdrawal (P<0.05, only at 25 watts) was observed in T at all powers; at middle and higher powers a significant decrease (P<0.05 at 50, 100 and 125 watts) in the slow tachycardia (D1-4 min) related to a sympathetic-dependent mechanism was observed in T; 3) the VO2 AT (S = 1.06 and T = 1.33 l/min) and VO2 peak (S = 1.97 and T = 2.47 l/min) were higher in T (P<0.05). These results demonstrate that aerobic training can induce significant physiological adaptations in middle-aged men, mainly expressed as a decrease in the sympathetic effects on heart rate associated with an increase in oxygen transport during dynamic exercise.

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The purpose of the present study was to evaluate the effects of aerobic physical training (APT) on heart rate variability (HRV) and cardiorespiratory responses at peak condition and ventilatory anaerobic threshold. Ten young (Y: median = 21 years) and seven middle-aged (MA = 53 years) healthy sedentary men were studied. Dynamic exercise tests were performed on a cycloergometer using a continuous ramp protocol (12 to 20 W/min) until exhaustion. A dynamic 24-h electrocardiogram was analyzed by time (TD) (standard deviation of mean R-R intervals) and frequency domain (FD) methods. The power spectral components were expressed as absolute (a) and normalized units (nu) at low (LF) and high (HF) frequencies and as the LF/HF ratio. Control (C) condition: HRV in TD (Y: 108, MA: 96 ms; P<0.05) and FD - LFa, HFa - was significantly higher in young (1030; 2589 ms²/Hz) than in middle-aged men (357; 342 ms²/Hz) only during sleep (P<0.05); post-training effects: resting bradycardia (P<0.05) in the awake condition in both groups; VO2 increased for both groups at anaerobic threshold (P<0.05), and at peak condition only in young men; HRV in TD and FD (a and nu) was not significantly changed by training in either groups. The vagal predominance during sleep is reduced with aging. The resting bradycardia induced by short-term APT in both age groups suggests that this adaptation is much more related to intrinsic alterations in sinus node than in efferent vagal-sympathetic modulation. Furthermore, the greater alterations in VO2 than in HRV may be related to short-term APT.

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We investigate whether combined treatment with losartan, an angiotensin II receptor blocker, and exercise training (ET) in spontaneously hypertensive rats (SHR) would have an additive effect in reducing hypertension and improving baroreflex sensitivity when compared with losartan alone. Male SHR (8 weeks old) were assigned to 3 groups: sedentary placebo (SP, N = 16), sedentary under losartan treatment (SL, N = 11; 10 mg kg-1 day-1, by gavage), and ET under losartan treatment (TL, N = 10). ET was performed on a treadmill 5 days/week for 60 min at 50% of peak VO2, for 18 weeks. Blood pressure (BP) was measured with a catheter inserted into the carotid artery, and cardiac output with a microprobe placed around the ascending aorta. The baroreflex control of heart rate was assessed by administering increasing doses of phenylephrine and sodium nitroprusside (iv). Losartan significantly reduced mean BP (178 ± 16 vs 132 ± 12 mmHg) and left ventricular hypertrophy (2.9 ± 0.4 vs 2.5 ± 0.2 mg/g), and significantly increased baroreflex bradycardia and tachycardia sensitivity (1.0 ± 0.3 vs 1.7 ± 0.5 and 2.0 ± 0.7 vs 3.2 ± 1.7 bpm/mmHg, respectively) in SL compared with SP. However, losartan combined with ET had no additional effect on BP, baroreflex sensitivity or left ventricular hypertrophy when compared with losartan alone. In conclusion, losartan attenuates hypertension and improves baroreflex sensitivity in SHR. However, ET has no synergistic effect on BP in established hypertension when combined with losartan, at least at the dosage used in this investigation.

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The mechanisms underlying the loss of resting bradycardia with detraining were studied in rats. The relative contribution of autonomic and non-autonomic mechanisms was studied in 26 male Wistar rats (180-220 g) randomly assigned to four groups: sedentary (S, N = 6), trained (T, N = 8), detrained for 1 week (D1, N = 6), and detrained for 2 weeks (D2, N = 6). T, D1 and D2 were treadmill trained 5 days/week for 60 min with a gradual increase towards 50% peak VO2. After the last training session, D1 and D2 were detrained for 1 and 2 weeks, respectively. The effect of the autonomic nervous system in causing training-induced resting bradycardia and in restoring heart rate (HR) to pre-exercise training level (PET) with detraining was examined indirectly after cardiac muscarinic and adrenergic receptor blockade. T rats significantly increased peak VO2 by 15 or 23.5% when compared to PET and S rats, respectively. Detraining reduced peak VO2 in both D1 and D2 rats by 22% compared to T rats, indicating loss of aerobic capacity. Resting HR was significantly lower in T and D1 rats than in S rats (313 ± 6.67 and 321 ± 6.01 vs 342 ± 12.2 bpm) and was associated with a significantly decreased intrinsic HR (368 ± 6.1 and 362 ± 7.3 vs 390 ± 8 bpm). Two weeks of detraining reversed the resting HR near PET (335 ± 6.01 bpm) due to an increased intrinsic HR in D2 rats compared with T and D1 rats (376 ± 8.8 bpm). The present study provides the first evidence of intrinsic HR-mediated loss of resting bradycardia with detraining in rats.

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Several studies have indicated that depressive states may lead to hypokinesia with diminished metabolic rate and energy use. Hypokinesia associated with certain eating behaviors may lead to an unfavorable energy balance that can contribute to the emergence and prevalence of obesity among children and adults. The purpose of the present study was to examine the possibility of reducing depression inventory scores in female adolescents with third-degree obesity while testing the effectiveness of different exercise programs in reducing anxiety and depression scores. The sample consisted of 40 female subjects (mean age 16 ± 1.56 years) divided into 4 groups (aerobic training, anaerobic training, leisure activities, and control). Subjects had a body mass index of 95% or more in relation to the 50th percentile. The aerobic program consisted of three ergometric bicycle sessions per week over a 3-month period (12 weeks) and the activities were prescribed after determining the anaerobic ventilatory threshold (VO2 threshold). Anaerobic training was based on the Wingate anaerobic power test. The leisure program consisted of a varied range of activities (games, exercises, etc.). A nutritionist interviewed the members of these two groups and the control group every week in order to adapt them to the nutritional guidelines proposed for the study. The study showed that all three programs (aerobic exercise, anaerobic exercise and leisure activities) were effective in reducing body mass. However, we found a significant reduction when analyzing the depression scores only for aerobic exercise (18.9 ± 9.33 to 10.6 ± 9.56 or 43.9%) but no significant alterations for anaerobic exercise (11.36 ± 5.23 to 9.63 ± 4.78 or 15.22%) and leisure (17.28 ± 7.55 to 15.07 ± 7.54 or 12.78%), thus indicating that in principle this type of activity could be included to improve emotional well-being of obese adolescent girls.

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We tested the hypothesis that the inability to increase cardiac output during exercise would explain the decreased rate of oxygen uptake (VO2) in recent onset, ischemia-induced heart failure rats. Nine normal control rats and 6 rats with ischemic heart failure were studied. Myocardial infarction was induced by coronary ligation. VO2 was measured during a ramp protocol test on a treadmill using a metabolic mask. Cardiac output was measured with a flow probe placed around the ascending aorta. Left ventricular end-diastolic pressure was higher in ischemic heart failure rats compared with normal control rats (17 ± 0.4 vs 8 ± 0.8 mmHg, P = 0.0001). Resting cardiac index (CI) tended to be lower in ischemic heart failure rats (P = 0.07). Resting heart rate (HR) and stroke volume index (SVI) did not differ significantly between ischemic heart failure rats and normal control rats. Peak VO2 was lower in ischemic heart failure rats (73.72 ± 7.37 vs 109.02 ± 27.87 mL min-1 kg-1, P = 0.005). The VO2 and CI responses during exercise were significantly lower in ischemic heart failure rats than in normal control rats. The temporal response of SVI, but not of HR, was significantly lower in ischemic heart failure rats than in normal control rats. Peak CI, HR, and SVI were lower in ischemic heart failure rats. The reduction in VO2 response during incremental exercise in an ischemic model of heart failure is due to the decreased cardiac output response, largely caused by depressed stroke volume kinetics.

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Several methods are used to estimate anaerobic threshold (AT) during exercise. The aim of the present study was to compare AT obtained by a graphic visual method for the estimate of ventilatory and metabolic variables (gold standard), to a bi-segmental linear regression mathematical model of Hinkley's algorithm applied to heart rate (HR) and carbon dioxide output (VCO2) data. Thirteen young (24 ± 2.63 years old) and 16 postmenopausal (57 ± 4.79 years old) healthy and sedentary women were submitted to a continuous ergospirometric incremental test on an electromagnetic braking cycloergometer with 10 to 20 W/min increases until physical exhaustion. The ventilatory variables were recorded breath-to-breath and HR was obtained beat-to-beat over real time. Data were analyzed by the nonparametric Friedman test and Spearman correlation test with the level of significance set at 5%. Power output (W), HR (bpm), oxygen uptake (VO2; mL kg-1 min-1), VO2 (mL/min), VCO2 (mL/min), and minute ventilation (VE; L/min) data observed at the AT level were similar for both methods and groups studied (P > 0.05). The VO2 (mL kg-1 min-1) data showed significant correlation (P < 0.05) between the gold standard method and the mathematical model when applied to HR (r s = 0.75) and VCO2 (r s = 0.78) data for the subjects as a whole (N = 29). The proposed mathematical method for the detection of changes in response patterns of VCO2 and HR was adequate and promising for AT detection in young and middle-aged women, representing a semi-automatic, non-invasive and objective AT measurement.

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Therapy with bone marrow-derived cells has been used in ischemic patients with reported success. The aim of this study was to determine the therapeutic efficacy of fresh and frozen human umbilical cord blood cells (hUCB) in Wistar rats submitted to permanent occlusion of the left coronary artery. Three hours after myocardial infarction, 2 x 10(7) hUCB cells or vehicle were administered by intramyocardial injection. The animals were divided into five groups: control (N = 10), sham operated (N = 10), infarcted that received vehicle (N = 9), infarcted treated with cryopreserved hUCB (N = 7), and infarcted treated with fresh hUCB (N = 5). Cardiac function was evaluated by electrocardiogram (ECG) and echocardiogram (ECHO) before cell therapy, and by ECG, ECHO, cardiopulmonary test, and left ventricular pressure measurements 3 weeks later. After 3 weeks, both groups treated with hUCB still had Q wave present in L1, âQRS >90° and reduced shortening fraction (less than 50%). In addition, cardiac indexes of left ventricular contractility and relaxation were 5484 ± 875 and -4032 ± 643 mmHg (cryopreserved hUCB) and 4585 ± 955 and -2862 ± 590 mmHg (fresh hUCB), respectively. These values were not statistically different from those of saline-treated animals. Cardiopulmonary exercise test profile was typical of infarcted hearts; exercise time was about 14 min and maximal VO2 was 24.77 ± 5.00 mL·kg-1·min-1. These data show that hUCB therapy did not improve the cardiac function of infarcted animals or prevent cardiac remodeling.

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During cardiopulmonary exercise testing (CPET), stroke volume can be indirectly assessed by O2 pulse profile. However, for a valid interpretation, the stability of this variable over time should be known. The objective was to analyze the stability of the O2 pulse curve relative to body mass in elite athletes. VO2, heart rate (HR), and relative O2 pulse were compared at every 10% of the running time in two maximal CPETs, from 2005 to 2010, of 49 soccer players. Maximal values of VO2 (63.4 ± 0.9 vs 63.5 ± 0.9 mL O2•kg-1•min-1), HR (190 ± 1 vs188 ± 1 bpm) and relative O2 pulse (32.9 ± 0.6 vs 32.6 ± 0.6 mL O2•beat-1•kg-1) were similar for the two CPETs (P > 0.05), while the final treadmill velocity increased from 18.5 ± 0.9 to 18.9 ± 1.0 km/h (P < 0.01). Relative O2 pulse increased linearly and similarly in both evaluations (r² = 0.64 and 0.63) up to 90% of the running time. Between 90 and 100% of the running time, the values were less stable, with up to 50% of the players showing a tendency to a plateau in the relative O2 pulse. In young healthy men in good to excellent aerobic condition, the morphology of the relative O2 pulse curve is consistent up to close to the peak effort for a CPET repeated within a 1-year period. No increase in relative O2pulse at peak effort could represent a physiologic stroke volume limitation in these athletes.

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Resistance training increases muscle strength in older adults, decreasing the effort necessary for executing physical tasks, and reducing cardiovascular load during exercise. This hypothesis has been confirmed during strength-based activities, but not during aerobic-based activities. This study determined whether different resistance training regimens, strength training (ST, constant movement velocity) or power training (PT, concentric phase performed as fast as possible) can blunt the increase in cardiovascular load during an aerobic stimulus. Older adults (63.9 ± 0.7 years) were randomly allocated to: control (N = 11), ST (N = 13, twice a week, 70-90% 1-RM) and PT (N = 15, twice a week, 30-50% 1-RM) groups. Before and after 16 weeks, oxygen uptake (VO2), systolic blood pressure (SBP), heart rate (HR), and rate pressure product (RPP) were measured during a maximal treadmill test. Resting SBP and RPP were similarly reduced in all groups (combined data = -5.7 ± 1.2 and -5.0 ± 1.7%, respectively, P < 0.05). Maximal SBP, HR and RPP did not change. The increase in measured VO2, HR and RPP for the increment in estimated VO2 (absolute load) decreased similarly in all groups (combined data = -9.1 ± 2.6, -14.1 ± 3.9, -14.2 ± 3.0%, respectively, P < 0.05), while the increments in the cardiovascular variables for the increase in measured VO2 did not change. In elderly subjects, ST and PT did not blunt submaximal or maximal HR, SBP and RPP increases during the maximal exercise test, showing that they did not reduce cardiovascular stress during aerobic tasks.

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The oxygen uptake efficiency slope (OUES) is a submaximal index incorporating cardiovascular, peripheral, and pulmonary factors that determine the ventilatory response to exercise. The purpose of this study was to evaluate the effects of continuous exercise training and interval exercise training on the OUES in patients with coronary artery disease. Thirty-five patients (59.3±1.8 years old; 28 men, 7 women) with coronary artery disease were randomly divided into two groups: continuous exercise training (n=18) and interval exercise training (n=17). All patients performed graded exercise tests with respiratory gas analysis before and 3 months after the exercise-training program to determine ventilatory anaerobic threshold (VAT), respiratory compensation point, and peak oxygen consumption (peak VO2). The OUES was assessed based on data from the second minute of exercise until exhaustion by calculating the slope of the linear relation between oxygen uptake and the logarithm of total ventilation. After the interventions, both groups showed increased aerobic fitness (P<0.05). In addition, both the continuous exercise and interval exercise training groups demonstrated an increase in OUES (P<0.05). Significant associations were observed in both groups: 1) continuous exercise training (OUES and peak VO2 r=0.57; OUES and VO2 VAT r=0.57); 2) interval exercise training (OUES and peak VO2 r=0.80; OUES and VO2 VAT r=0.67). Continuous and interval exercise training resulted in a similar increase in OUES among patients with coronary artery disease. These findings suggest that improvements in OUES among CAD patients after aerobic exercise training may be dependent on peripheral and central mechanisms.

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The aim of this study was to measure the energy expenditure for locomotor activities usually performed by soccer referees during a match (walking, jogging, and running) under laboratory conditions, and to compare forward with backward movements. The sample was composed by 10 male soccer referees, age 29±7.8 years, body mass 77.5±6.2 kg, stature 1.78±0.07 m and professional experience of 7.33±4.92 years. Referees were evaluated on two separate occasions. On the first day, maximal oxygen uptake (VO2max) was determined by a maximal treadmill test, and on the second day, the oxygen consumption was determined in different speeds of forward and backward movements. The mean VO2max was 41.20±3.60 mL·kg-1·min-1 and the mean heart rate achieved in the last stage of the test was 190.5±7.9 bpm. When results of forward and backward movements were compared at 1.62 m/s (walking speed), we found significant differences in VO2, in metabolic equivalents, and in kcal. However, the same parameters in forward and backward movements at jogging velocities (2.46 m/s) were not significantly different, showing that these motor activities have similar intensity. Backward movements at velocities equivalent to walking and jogging are moderate-intensity activities, with energy expenditure less than 9 kcal. Energy expenditure was overestimated by at least 35% when calculated by mathematical equations. In summary, we observed that backward movements are not high-intensity activities as has been commonly reported, and when calculated using equations available in the literature, energy expenditure was overestimated compared to the values obtained by indirect calorimetry.

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As atividades de polifenoloxidases do feijão (Phaseolus vulgaris L.), cultivares: (Aruã, Aporé, A774, Carioca, Diamante Negro, Ouro Branco, Pérola, RAO 33 e Rudá) foram investigadas sob condições de cinética enzimática. O pH ótimo para o extrato bruto das nove cultivares foi em pH 7,2 utilizando catecol como substrato. Nenhuma atividade PPO foi observada na presença do ácido gálico ou D,L- DOPA.

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En este trabajo se determinó la vida útil de una fórmula dietética para niños con síndrome diarréico, empleando la disminución de lisina disponible como indicador de deterioro. Muestras del producto fueron empacadas en envases de material multilaminado (papel-plástico-aluminio) y almacenadas a 25, 30 y 35°C, por dos meses. La lisina disponible fue medida con una frecuencia semanal y los datos fueron analizados para determinar la cinética de la reacción de deterioro y su relación con la temperatura. Al finalizar el estudio, la cantidad de lisina disponible remanente fue de 38,5% (a 25°C); 15,3 % (a 30°C) y 14,1% (a 35°C). La cinética de la reacción de deterioro fue de orden uno, dependiente de la temperatura de almacenamiento, según la ecuación de interrelación de Arrhenius, con un valor de energía de activación de 15,17 kcal/mol, por lo que cae dentro del rango de las reacciones de oxidación de lípidos. De acuerdo a las características del producto [contenido de lípidos (17,5%), proteínas (17,3%) y una actividad de agua de 0,46], la disminución de lisina pudiera ser explicada por la interacción de productos de oxidación de lípidos con proteínas. Considerando un valor de 0,422g lis/100g producto como punto crítico, se predijo la vida útil del producto a temperaturas diferentes a las evaluadas. Condiciones de almacenamiento por debajo de 30°C, garantizan un mayor período de vida útil: hasta 9 meses a 15°C, 6 meses a 20°C y 3 meses a 28°C, en función del indicador de deterioro evaluado.

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A acerola é um fruto altamente perecível e que contém altos teores de vitamina C, sendo este o seu principal atrativo em termos nutricionais. A atual legislação brasileira prevê uma variação de, no máximo, 20% do teor dos nutrientes especificados no rótulo. Devido a essa exigência seria importante que os fabricantes considerassem tanto o teor inicial de vitamina C quanto a perda ao longo da armazenagem dos produtos de acerola. Neste trabalho, foi feito o acompanhamento da estabilidade da vitamina C em polpa pasteurizada e acerola in natura congeladas, ambas armazenadas a -12ºC e -18ºC, e em suco de acerola pasteurizado engarrafado, mantido a temperatura ambiente, ao longo de 4 meses de armazenagem. As polpas congeladas não apresentaram degradação significativa durante este período, já as in natura apresentaram cinética de degradação de 1ª ordem e o suco de ordem zero. Após 4 meses de armazenagem as acerolas armazenadas a -12ºC e -18ºC apresentaram teores de 869±12 e 1.223±148 mg vit.C/100g, representando uma perda de 43% e 19%, respectivamente, em relação ao teor inicial. Polpas a -12ºC e -18ºC apresentaram teores de 1.314±6 e 1.322±2 mg vit.C/100g, respectivamente, representando uma perda de, aproximadamente, 3% e o suco apresentou uma perda de 32%, correspondendo a um teor final de 673±17mg vit.C/100g.