Cardiovascular benefits and assessment of physical activity and physical fitness in adults.
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Biomedical subjects
Publications and source records attributed to J M Hagberg.
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To evaluate the effects of 26 wk of aerobic and resistance training on the incidence of injury and program adherence in 70- to 79-yr-old men and women, 57 healthy volunteers (25 males, 32 females) were randomly assigned to a walk/jog (W/J, N = 21), strength (STREN, N = 23), or control (CONT, N = 13) group. Walk/jog training was for 30-45 min, 3 d.wk-1 with intensity equal to 40-70% heart rate max reserve (HRmax reserve) during the first 13 wk, and 75-85% HRmax reserve for weeks 14-26. STREN training consisted of one set (10-12 repetitions) each of 10 variable resistance exercises performed to volitional fatigue. Forty-nine of the original participants completed the training program. Walk/jog training increased VO2max from 22.5 to 27.1 ml.kg-1.min-1 (P less than or equal to 0.05) while STREN and CONT showed no change. STREN improved significantly in chest press and leg extension strength (P less than or equal to 0.05) while W/J and CONT showed no change. Adherence to training was 20/23 (87%) and 17/21 (81%) in STREN and W/J, respectively. One repetition maximum (1-RM) strength testing resulted in 11 injuries in the 57 subjects (19.3%) while STREN training resulted in only two injuries in 23 subjects (8.7%). Walk training during weeks 1-13 resulted in one injury in 21 subjects (4.8%). Eight of 14 subjects (57%) who began jogging intervals at week 14 incurred an injury: two of eight (25%) of the men and all of the women (6 of 6). All W/J training injuries were to the lower extremity.(ABSTRACT TRUNCATED AT 250 WORDS)
Exercise training elicits numerous beneficial adaptations in patients with coronary artery disease (CAD), but until 10 yr ago these adaptations were generally believed to be peripheral adaptations rather than improvements in myocardial blood supply. However, animal models of CAD have been shown to elicit improvements in myocardial blood flow and left ventricular performance with prolonged, intense exercise training. More recently we have provided electrocardiographic, echocardiographic hemodynamic, and radionuclide evidence of central cardiovascular adaptations in patients with CAD after a year-long program of 1 h of exercise at 70-90% of VO2max 5 d.wk(-1). These training-induced adaptations are consistent with an improvement in myocardial oxygenation and concomitantly an enhanced left ventricular function in these patients. This program also resulted in improvements in glucose tolerance, insulin sensitivity, and plasma lipoprotein-lipid profile. We have also shown that these beneficial cardiovascular and metabolic adaptations are maintained during six additional years of training in patients with CAD. These results do not imply that all patients with CAD should initiate such an intense training program, but rather that, in selected patients undergoing a training stimulus well in excess of that conventionally prescribed for coronary patients, the training-induced adaptations may be substantially greater than previously believed.
Men and women 70-79 yr of age (N = 49) were studied to assess the effect of 6 months of resistance or endurance exercise training on their blood pressure, hemodynamic parameters, and pressor hormone levels. Resistance training consisted of one set of 8-12 repetitions on ten Nautilus machines three times per week. The endurance training group progressed to training at 75-85% VO2max for 35-45 min three times per week for the last 2 months of training. No changes in body weight or estimated lean body mass occurred; however, the sum of seven skinfolds, as an index of percent body fat, decreased in both exercise groups. Upper and lower body strength increased with resistance training, while VO2max increased by 20% in the endurance training group. Blood pressure did not change with resistance training in individuals with normal or somewhat elevated blood pressures. Diastolic and mean blood pressure decreased significantly, by 5 and 4 mm Hg, with endurance training. Subjects with blood pressure greater than 140/90 reduced their systolic, diastolic, and mean blood pressure by 8, 9, and 8 mm Hg, respectively, with endurance exercise training. Cardiac output, peripheral vascular resistance, and plasma levels of angiotensin I and II and epi- and norepinephrine did not change in any of the groups. Thus, resistance exercise training does not adversely affect, or reduce, blood pressure, while endurance exercise training produces modest reductions in blood pressure in 70-79-yr-old individuals with somewhat elevated blood pressures.
To evaluate the effect of aerobic and variable resistance exercise training on fractionated reaction time (RT) and speed of movement (SM) in elderly individuals, premotor time (PMT), motor time (MT), total RT, and SM were measured in 49 healthy, untrained men and women, 70 to 79 years of age, before and after 6 months of training. Subjects were randomized into either a walk/jog (n = 17), a strength training (n = 20), or a control group (n = 12). Improvements in aerobic capacity were only weakly related to reduced total RT (r = 0.30, p less than .05). Analysis of covariance revealed that there were no differences (p greater than .05) among the three groups after training with respect to PMT, MT, total RT, and SM. These findings indicate that 6 months of aerobic and strength training did not induce significant changes in RT or SM in this group.
This study was designed to measure the O2 uptake (VO2) of cyclists while they rode outdoors at speeds from 32 to 40 km/h. Regression analyses of data from 92 trials using the same wheels, tires, and tire pressure with the cyclists riding in their preferred gear and in an aerodynamic position indicated the best equation (r = 0.84) to estimate VO2 in liters per minute VO2 = -4.50 + 0.17 rider speed + 0.052 wind speed + 0.022 rider weight where rider and wind speed are expressed in kilometers per hour and rider weight in kilograms. Following another rider closely, i.e., drafting, at 32 km/h reduced VO2 by 18 +/- 11%; the benefit of drafting a single rider at 37 and 40 km/h was greater (27 +/- 8%) than that at 32 km/h. Drafting one, two, or four riders in a line at 40 km/h resulted in the same reduction in VO2 (27 +/- 7%). Riding at 40 km/h at the back of a group of eight riders reduced VO2 by significantly more (39 +/- 6%) than drafting one, two, or four riders in a line; drafting a vehicle at 40 km/h resulted in the greatest decrease in VO2 (62 +/- 6%). VO2 was also 7 +/- 4% lower when the cyclists were riding an aerodynamic bicycle. An aerodynamic set of wheels with a reduced number of spokes and one set of disk wheels were the only wheels to reduce VO2 significantly while the cyclists were riding a conventional racing bicycle at 40 km/h.(ABSTRACT TRUNCATED AT 250 WORDS)
This study was designed to determine whether patients with McArdle's disease, who do not increase their blood lactate levels during and after maximal exercise, have a slow "lactacid" component to their recovery O2 consumption (VO2) response after high-intensity exercise. VO2 was measured breath by breath during 6 min of rest before exercise, a progressive maximal cycle ergometer test, and 15 min of recovery in five McArdle's patients, six age-matched control subjects, and six maximal O2 consumption- (VO2 max) matched control subjects. The McArdle's patients' ventilatory threshold occurred at the same relative exercise intensity [71 +/- 7% (SD) VO2max] as in the control groups (60 +/- 13 and 70 +/- 10% VO2max) despite no increase and a 20% decrease in the McArdle's patients' arterialized blood lactate and H+ levels, respectively. The recovery VO2 responses of all three groups were better fit by a two-, than a one-, component exponential model, and the parameters of the slow component of the recovery VO2 response were the same in the three groups. The presence of the same slow component of the recovery VO2 response in the McArdle's patients and the control subjects, despite the lack of an increase in blood lactate or H+ levels during maximal exercise and recovery in the patients, provides evidence that this portion of the recovery VO2 response is not the result of a lactacid mechanism. In addition, it appears that the hyperventilation that accompanies high-intensity exercise may be the result of some mechanism other than acidosis or lung CO2 flux.
Master athletes who exercise regularly appear to avoid the development of insulin resistance and deterioration of glucose tolerance (GT) commonly seen with aging. To evaluate the possibility that exercise prevents rather than masks the aging-related changes responsible for development of insulin resistance, we investigated the effects of 10 days of physical inactivity in 14 master athletes aged 61 +/- 2 (SE) yr. The response of 10 of these men to inactivity was similar to that of young athletes, with an unchanged plasma glucose response and a significantly greater insulin response to an oral glucose tolerance test (OGTT) after 10 days of inactivity. These 10 athletes appeared to have been protected against the aging-related changes in GT because their plasma glucose and insulin levels during the OGTT after 10 days of inactivity were not significantly different from those of young lean sedentary men. In contrast, a deterioration in GT occurred in four of the master athletes during 10 days of inactivity; this was sufficiently marked in two of them to be classified as impaired GT. We conclude that regular exercise may 1) protect against the development of insulin resistance and decline in GT with aging in individuals with normal GT and 2) normalize GT by means of short-term effects of exercise in some individuals with abnormal GT.
Fifteen well-trained master endurance athletes [62.0 +/- 2.3 (SE) yr] and 14 sedentary control subjects (61.4 +/- 1.4 yr) were reevaluated after an average follow-up period of approximately 8 yr to obtain information regarding the effects of physical activity on the age-related decline in maximal O2 uptake capacity (VO2max). The master athletes had been training for 10.2 +/- 2.9 yr before initial testing and continued to train during the follow-up period. The sedentary subjects' VO2max declined by an average of 3.3 ml.kg-1.min-1 (33.9 +/- 1.7 vs. 30.6 +/- 1.6, P less than 0.001) over the course of the study, a decline of 12% per decade. In these subjects maximal heart rate declined 8 beats/min (171 vs. 163) and maximal O2 pulse decreased from 0.20 to 0.18 ml.kg-1.beat (P less than 0.05). The master athletes' VO2 max decreased by an average of 2.2 ml.kg-1.min-1 (54.0 +/- 1.7 vs. 51.8 +/- 1.8, P less than 0.05), a 5.5% decline per decade. The master athletes' maximal heart rate was unchanged (171 +/- 3 beats/min) and their maximal O2 pulse decreased from 0.32 to 0.30 ml.kg-1.beat (P less than 0.05). These findings provide evidence that the age-related decrease in VO2max of master athletes who continue to engage in regular vigorous endurance exercise training is approximately one-half the rate of decline seen in age-matched sedentary subjects. Furthermore our results suggest that endurance exercise training may reduce the rate of decline in maximal heart rate that typically occurs as an individual ages.
This study sought to determine whether 9 months of low- or moderate-intensity exercise training could decrease blood pressure (BP) in hypertensive men and women (mean age 64 +/- 3 years). Patients underwent weekly BP evaluations for 1 month to ensure that they had persistently elevated BP and then completed a maximal treadmill exercise test to exclude those with overt coronary artery disease. The low- and moderate-intensity groups trained at 53 and 73% of maximal oxygen consumption (VO2 max), respectively; however, total caloric expenditure per week was similar in both groups. VO2 max did not increase in the low-intensity group with training, but increased 28% in the moderate-intensity group. Diastolic BP decreased 11 to 12 mm Hg in both training groups. Systolic BP decreased 20 mm Hg in the low-intensity group with training, which was significantly greater than the change in the control and the moderate-intensity groups. Although systolic BP decreased 8 mm Hg in the moderate-intensity training group, this reduction was not significant. Training resulted in a somewhat lower cardiac output at rest in the low-intensity group, whereas total peripheral resistance decreased slightly in the moderate-intensity training group. Plasma and blood volumes, plasma renin levels and urinary sodium excretion did not change in either group with training. Both groups manifested lower plasma norepinephrine levels after training during standing rest, but not while supine. Thus, low-intensity training may lower BP as much or more than moderate-intensity training in older persons with essential hypertension, but the underlying mechanisms are unclear.
This study determined the effects of endurance or resistance exercise training on maximal O2 consumption (VO2max) and the cardiovascular responses to exercise of 70- to 79-yr-old men and women. Healthy untrained subjects were randomly assigned to a control group (n = 12) or to an endurance (n = 16) or resistance training group (n = 19). Training consisted of three sessions per week for 26 wk. Resistance training consisted of one set of 8-12 repetitions on 10 Nautilus machines. Endurance training consisted of 40 min at 50-70% VO2max and at 75-85% VO2max for the first and last 13 wk of training, respectively. The endurance training group increased its VO2max by 16% during the first 13 wk of training and by a total of 22% after 26 wk of training; this group also increased its maximal O2 pulse, systolic blood pressure, and ventilation, and decreased its heart rate and perceived exertion during submaximal exercise. The resistance training group did not elicit significant changes in VO2max or in other maximal or submaximal cardiovascular responses despite eliciting 9 and 18% increases in lower and upper body strength, respectively. Thus healthy men and women in their 70s can respond to prolonged endurance exercise training with adaptations similar to those of younger individuals. Resistance training in older individuals has no effect on cardiovascular responses to submaximal or maximal treadmill exercise.
To determine whether depressed left ventricular (LV) contractile function can occur after prolonged and strenuous exercise, 12 healthy men, 26 +/- 1 years old (mean +/- standard error of the mean) were studied. The subjects exercised on a treadmill at 69 +/- 1% of maximal O2 uptake until exhaustion (170 +/- 10 minutes). Hemodynamic variables were measured before and 10 minutes after exhausting exercise. Baseline systolic blood pressure decreased from 124 +/- 2 to 113 +/- 3 mm Hg (p less than 0.001) after exhausting exercise. LV end-diastolic diameter, measured by echocardiography, decreased from 51 +/- 1.0 to 47 +/- 1.0 mm (p less than 0.005) but LV end-systolic diameter did not change (34 +/- 1.0 vs 34 +/- 1.0 mm). Both LV fractional shortening and the mean velocity of circumferential fiber shortening decreased (33 +/- 1 vs 28 +/- 1%; p less than 0.01 and 1.09 +/- 0.4 vs 0.97 +/- 0.05 circ/s; p less than 0.025) despite a lower end-systolic wall stress (sigma es = 88 +/- 4 vs 82 +/- 5, X 10(3) dynes/cm2; p less than 0.05) after prolonged exhausting exercise. A repeat bout of exercise of the same intensity but brief in duration (10 minutes) resulted in increases in LV fractional shortening (p less than 0.001) and mean velocity of circumferential fiber shortening (p less than 0.001), and a decrease in LV end-diastolic diameter (50 +/- 1.0 to 48 +/- 1.0 mm; p less than 0.05) at heart rates comparable to those attained after prolonged exhausting exercise. The results suggest that prolonged strenuous exercise may result in impaired LV function in healthy young subjects.
Digoxin-like immunoreactive factors (DLIFs) in serum may represent endogenous cardiotropic agents. We determined if blood levels of these endogenous factors changed during prolonged strenuous exercise. Total and loosely protein-bound (LPB) DLIF were measured by radioimmunoassay in the serum of nine healthy subjects during prolonged exercise to exhaustion. Mean total and LPB serum levels of DLIF increased by 72% (580 to 945 pg/mL) and 63% (53 to 91 pg/mL) over baseline values in digoxin equivalents (p less than 0.01), respectively, after three hours of exercise at 70% of VO2max. The prevalent serum nonesterified fatty acids (arachidonic, linoleic, oleic, palmitic, and stearic acids) as well as hydrocortisone did not account for the observed elevations in DLIF. Percent left ventricular fractional shortening (%FS) and mean velocity of left ventricular circumferential fiber shortening (mVCF) measured echocardiographically were lower (-18.0% and -16.4%, respectively, p less than 0.05) after exercise as compared to prior to exercise. Cardiac left ventricular dysfunction as measured by %FS did correlate with blood levels of DLIF (r = -0.680, p less than 0.02). These observations may suggest a relationship between serum levels of DLIF and cardiac fatigue.
This study compared the lung volumes and pulmonary functions of older endurance-trained athletes with those of healthy sedentary age-matched controls, young athletes, and young untrained men to determine whether training affects the age-associated changes in these variables. Despite large differences in maximal 02 consumption (VO2max), the older athletes and their sedentary peers had similar values for all pulmonary variables when expressed as absolute values. However, because the older athletes were shorter than the older sedentary men, their vital capacity, total lung capacity (TLC), and forced expiratory volume in 1 s were significantly larger than those of the older sedentary men when normalized for age and height; the average values for maximal voluntary ventilation and residual volume (RV) were also larger in the older athletes when normalized for age and height, but the differences were not significant. The young trained and untrained men did not differ in any of these measures. TLC was the only pulmonary variable that was the same in the young and older men; RV and the RV-to-TLC ratio were larger, whereas all other pulmonary function and volume measures were lower in the older men compared with the younger men. The older athletes were the only group whose lung volumes and pulmonary function measures were all, except for RV, substantially greater than expected based on their age and height. Thus prolonged strenuous endurance training in these older highly trained endurance athletes appears to have altered the decline in pulmonary function and volumes associated with aging.
This study evaluated the effects of aging and endurance training on the metabolic responses of trained and sedentary young (age 20-32 yr) and older (age 60-70 yr) men to exercise at the same relative exercise stress (70% of maximal O2 consumption). Plasma growth hormone concentrations at rest were similar in all four groups, but both older groups had an attenuated response to exercise. The older trained men appeared to have avoided the age-associated changes that were evident in their sedentary peers with respect to resting plasma insulin, C-peptide, and norepinephrine concentrations. Plasma glucagon concentrations were lower in both older subject groups at rest. Both sedentary groups decreased their plasma glucose concentrations and increased their plasma glucagon concentrations during exercise, whereas the trained groups had increases in their plasma glucose concentrations but had no change in their glucagon concentrations. Thus, although the concentrations of some hormones at rest and during submaximal exercise are unaffected by aging or by training, others are markedly altered by aging, training, or the interaction of the two. However, it appears that older healthy sedentary men undergo less physiological stress than young untrained men during submaximal exercise at the same relative exercise intensity, and they have no responses that would contraindicate their participation in exercise of the duration and intensity usually prescribed in exercise-training programs.
This study was designed to compare the resting and exercise hemodynamics of older adults with moderate hypertension with those of age-matched normotensive controls. Thirty-one hypertensive (20 men, 11 women; mean age, 63.9 +/- 2.8 years) and 28 normotensive subjects (15 men, 13 women; mean age, 62.6 +/- 2.4 years) were studied. There were no differences between the groups in terms of body weight, body composition, and maximal O2 consumption (VO2). At rest, there were no differences in VO2, cardiac output, stroke volume, or heart rate between the two groups, although systolic (158 +/- 13 vs 121 +/- 12 mm Hg) and diastolic blood pressures (94 +/- 7 vs 79 +/- 8 mm Hg) were higher in the hypertensive subjects. The hypertensive subjects' elevated blood pressure at rest was the result of a higher total peripheral resistance. During exercise, the hypertensive subjects had a lower cardiac output and stroke volume, no difference in heart rate and VO2, higher systolic, diastolic, and mean blood pressures, and a higher total peripheral resistance compared with their normotensive peers. The results indicate that older hypertensive persons have an altered cardiovascular response to exercise as compared with age-matched normotensive subjects. The responses also indicate that older essential hypertensive persons do not undergo excessive myocardial demands during exercise of the intensity usually prescribed in rehabilitation programs.
Nine sedentary men (53 +/- 3 yr) were studied before and after 6 d of endurance exercise training to determine the effects on maximal oxygen uptake (VO2max), and on the heart rate, blood pressure, and metabolic responses to a standard bout of steady-state sub-maximal exercise. The subjects exercised approximately 1 h.d-1 at about 68% of VO2max. The 6-d protocol elicited no improvement in VO2max (2.50 +/- 0.14 before vs 2.58 +/- 0.15 l.min-1 after training). Heart rates were significantly lower by 5 to 8 b.min-1, systolic blood pressures were reduced by 16 to 19 mm Hg, and blood lactate concentrations were 25 to 35% less at the same exercise intensities (60, 70, and 80% of VO2max) after 6 d of exercise. Rate pressure product was about 15% lower at the same exercise intensity after 6 d of training (P less than 0.05). The respiratory exchange ratio during submaximal exercise was 0.02 to 0.04 units lower (P less than 0.05; P less than 0.01) after 6 d of exercise, indicating a shift in substrate utilization favoring fat oxidation. These findings suggest that short-term endurance training can induce heart rate, blood pressure, and metabolic adaptations to sub-maximal exercise before there is a significant increase in VO2max in sedentary, middle-aged men who are capable of vigorous exercise.
Eleven healthy, untrained males (age = 44 +/- 1 yr; range = 40 to 55 yr) were studied to determine the effects of 16 wk of high-intensity resistive training on risk factors for coronary artery disease. Lipoprotein-lipid profiles, plasma glucose and insulin responses during an oral glucose tolerance test, and blood pressure at rest were determined before and after training. The training program resulted in a 13% increase in high-density lipoprotein-cholesterol (39 +/- 2 vs 44 +/- 3 mg.dl-1, P less than 0.05), a 43% increase in high-density lipoprotein-cholesterol (7 +/- 2 vs 10 +/- 2 mg.dl-1, P less than 0.05), a 5% reduction in low-density lipoprotein cholesterol (129 +/- 5 vs 122 +/- 5 mg.dl-1, P less than 0.05), and an 8% decrease in the total cholesterol/high-density lipoprotein-cholesterol ratio (5.1 +/- 0.3 vs 4.7 +/- 0.3, P less than 0.01), despite no changes in VO2max, body weight, or percent body fat. Glucose-stimulated plasma insulin concentrations during oral glucose tolerance testing were significantly lower, and supine diastolic blood pressure was reduced (P less than 0.05) as a result of the training program. No changes in any of these variables occurred in a sedentary control group. These findings indicate that resistive training can lower risk factors for coronary artery disease independent of changes in VO2max, body weight, or body composition.