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At least 667 records · Page 37Linked to original sources

PubMed2005

Dietary whey protein downregulates fatty acid synthesis in the liver, but upregulates it in skeletal muscle of exercise-trained rats.

OBJECTIVE: This study compared the effects of casein and whey protein as the source of dietary protein on the activity of lipogenic enzymes and mRNA levels in the liver and skeletal muscle of exercise-trained rats. METHODS: Twenty-eight male Sprague-Dawley rats were randomly assigned to one of four groups (n = 7/group). Rats were assigned to sedentary or exercise-trained groups and were fed the casein or whey protein diet. Rats in the exercise groups were trained for 2 wk using a swimming exercise for 120 min/d and 6 d/wk. RESULTS: A significant decrease in the activity of the hepatic lipogenic enzymes, glucose-6-phosphate dehydrogenase, malic enzyme, adenosine triphosphate citrate lyase, acetyl-coenzyme A carboxylase, and fatty acid synthase (FASN) was observed in rats fed whey protein compared with animals fed casein. Compared with the casein diet, the whey protein diet also lowered mRNA expression of these enzymes, except for FASN. In contrast to the findings in liver, whey protein, as compared with casein, increased skeletal muscle FASN activity and mRNA. Further, exercise training resulted in increased skeletal muscle glucose-6-phosphate dehydrogenase and FASN activity and adenosine triphosphate citrate lyase, acetyl-coenzyme A carboxylase-1, and FASN mRNA expression. CONCLUSIONS: Exercise training or whey protein may play an important role in suppressing hepatic fatty acid synthesis, thereby decreasing accumulation of body fat and stimulating the skeletal muscle to increase energy substrate as fat during prolonged exercise.

Analysis of Variance↗

PubMed2004

Effect of exercise training on endothelium-derived nitric oxide function in humans.

Vascular endothelial function is essential for maintenance of health of the vessel wall and for vasomotor control in both conduit and resistance vessels. These functions are due to the production of numerous autacoids, of which nitric oxide (NO) has been the most widely studied. Exercise training has been shown, in many animal and human studies, to augment endothelial, NO-dependent vasodilatation in both large and small vessels. The extent of the improvement in humans depends upon the muscle mass subjected to training; with forearm exercise, changes are restricted to the forearm vessels while lower body training can induce generalized benefit. Increased NO bioactivity with exercise training has been readily and consistently demonstrated in subjects with cardiovascular disease and risk factors, in whom antecedent endothelial dysfunction exists. These conditions may all be associated with increased oxygen free radicals which impact on NO synthase activity and with which NO reacts; repeated exercise and shear stress stimulation of NO bioactivity redresses this radical imbalance, hence leading to greater potential for autacoid bioavailability. Recent human studies also indicate that exercise training may improve endothelial function by up-regulating eNOS protein expression and phosphorylation. While improvement in NO vasodilator function has been less frequently found in healthy subjects, a higher level of training may lead to improvement. Regarding time course, studies indicate that short-term training increases NO bioactivity, which acts to homeostatically regulate the shear stress associated with exercise. Whilst the increase in NO bioactivity dissipates within weeks of training cessation, studies also indicate that if exercise is maintained, the short-term functional adaptation is succeeded by NO-dependent structural changes, leading to arterial remodelling and structural normalization of shear. Given the strong prognostic links between vascular structure, function and cardiovascular events, the implications of these findings are obvious, yet many unanswered questions remain, not only concerning the mechanisms responsible for NO bioactivity, the nature of the cellular effect and relevance of other autacoids, but also such practical questions as the optimal intensity, modality and volume of exercise training required in different populations.

Endothelium, Vascular↗

PubMedDate not supplied

Exercise training improves diastolic perfusion time in patients with coronary artery disease.

Exercise training elicits an improvement in work capacity and in left-ventricular function in patients with coronary artery disease. An improvement in myocardial oxygen supply accounts for these effects. The aim of this study was to test the hypothesis that exercise training could favorably influence diastolic perfusion time, a major determinant of subendocardial perfusion. Twenty-two male patients with coronary artery disease were randomized to a training or control group. At the study entry and after one year, all patients underwent an exercise stress test. After one year, rest heart rate was lower and diastolic perfusion time was higher in the training group but not in the control group. At peak of exercise, diastolic perfusion time increased and ST-segment depression decreased significantly in the training group but not in the control group. A significant relation was found between the R-R interval and the diastolic perfusion time either before or after training, with a difference in the intercepts of two regressions. Training shifted updown-line regression, effecting a higher value of diastolic perfusion time for a given value of heart rate. Thus, training increases diastolic perfusion time, independently from the effect on heart rate. This mechanism may contribute to the improvement of myocardial perfusion.

Blood Flow Velocity↗

PubMed2004

Cardiovascular adaptations to exercise training in postmenopausal women with type 2 diabetes mellitus.

BACKGROUND: Type 2 diabetes mellitus (DM-2) is one of the most prevalent chronic diseases of the aged and contributes to a significant amount of cardiovascular disease morbidity and mortality. Exercise training may be beneficial in attenuating the cardiovascular maladaptations associated with DM-2. The purpose of this study was to examine the effects of exercise training on left ventricular (LV) and vascular function in a sample of postmenopausal women with DM-2. METHODS: Twenty-eight postmenopausal women with DM-2 (age: 59 +/- 7 yrs) were assigned to either an exercise training (ET) (n = 17) or control group (CT) (n = 7). Cardiorespiratory fitness (VO2peak), LV filling dynamics and arterial compliance were assessed at baseline in all participants. The ET group performed a supervised aerobic and resistance training intervention three days per week for a period of 10 weeks, while the CT group continued normal activities of daily living. RESULTS: Body mass index, VO2peak, age and duration of diabetes were similar between the ET and CT groups at baseline. VO2peak (21.3 +/- 3.3 to 24.5 +/- 4.2 ml.kg-1.min-1, p < 0.05) and large artery compliance (1.0 +/- 0.4 to 1.2 +/- 0.4 mL.mmHg-1, p < 0.05), increased significantly in the ET group following training despite no change in LV filling dynamics, blood pressure, lipid profile or insulin sensitivity. All variables remained unchanged in the CT group. CONCLUSIONS: Exercise training improves large artery compliance and cardiorespiratory fitness in postmenopausal women with DM-2, without any appreciable changes in LV filling dynamics or conventional risk factors for cardiovascular disease.

Journal Article↗

PubMed1983

Sensitivity to insulin of glycolysis and glycogen synthesis of isolated soleus-muscle strips from sedentary, exercised and exercise-trained rats.

The half-maximal stimulation of the rates of glycolysis and glycogen synthesis in soleus-muscle strips from sedentary animals occurred at a concentration of insulin of about 100 microunits/ml. In soleus-muscle strips from exercise-trained rats (5 weeks of treadmill training), half-maximal stimulation of the rate of glycolysis occurred at about 10 microunits of insulin/ml, whereas that for glycogen synthesis occurred between 10 and 100 microunits of insulin/ml. The sensitivity of glycolysis to insulin after exercise training is similar to that of adipose tissue from sedentary animals. This finding suggests that, in sedentary animals, the effects of normal changes in insulin concentration may affect muscle primarily indirectly via the anti-lipolytic effect on adipose tissue, whereas after training insulin may effect the rate of glycolysis in muscle directly. A single period of exercise did not change the sensitivity of glycolysis in soleus muscle to insulin, nor probably that of glycogen synthesis. It is suggested that the improvement in insulin sensitivity of glycolysis in muscle caused by exercise-training could account, in part, for the well-established improvement in glucose tolerance and insulin sensitivity observed in man and rats after exercise-training.

Animals↗

PubMed1998

Effect of exercise training on quality of life in patients with chronic heart failure.

The effect of exercise training on quality of life and exercise capacity was studied in 67 patients with mild to moderate chronic heart failure (CHF; age: 65.6+/-8.3 years; left ventricular ejection fraction: 26.5+/-9.6%). Patients were randomly allocated to either a training group or to a control group. After intervention a significantly larger decrease in Feelings of Being Disabled (a subscale of the Heart Patients Psychological Questionnaire) and a significantly larger increase in the Self-Assessment of General Well-Being (SAGWB) were observed in the training group. Exercise time and anaerobic threshold were increased in the training group only. The increase in exercise time was related to both Feelings of Being Disabled and SAGWB. We conclude that supervised exercise training improves both quality of life and exercise capacity and can be safely performed by chronic heart failure patients.

Aged↗

PubMed1987

Effectiveness of self-monitored, home-based, moderate-intensity exercise training in middle-aged men and women.

The effects of 6 months of self-monitored, home-based exercise training on maximal oxygen uptake (VO2 max), body composition and plasma lipid levels of healthy, sedentary, middle-aged persons were evaluated in 60 men, aged 49 +/- 6 years, and 60 women, aged 47 +/- 5 years. Moderate-intensity training was performed 5 times per week in sessions of 47 +/- 7 minutes and 54 +/- 8 minutes for men and women, respectively. The individually prescribed range of heart rate corresponded to 65 to 77% of the peak value during symptom-limited treadmill testing (mean of 72% for men and 69% for women). Caloric expenditure per training session was approximately 345 kcal for men and 235 kcal for women. VO2 max increased 15% in men and 9% in women (both p less than 0.01). The greater increase in VO2 max in men than in women primarily reflected greater adherence to training in men (greater than or equal to 90% vs greater than or equal to 75%). The increase in VO2 max in women who showed very high adherence was comparable to that of men. Body weight decreased, by 1.5 +/- 10 kg, in men (p less than 0.05) but not in women undergoing training. No significant training-induced changes in plasma lipid levels were noted in either men or women. Baseline orientation and follow-up telephone calls required less than 1 hour of staff time per participant. Self-monitored, moderate-intensity, home-based exercise training significantly increases functional capacity in healthy, middle-aged men and women. Such training provides an alternative to group-based exercise training.

Adult↗

PubMed1998

Endurance exercise training increases peripheral vascular response in human fingers.

The purpose of this study was to clarify whether peripheral vascular response to alteration of transmural pressure is changed by endurance exercise training. The healthy male subjects (training group; n = 6) performed endurance exercise training that consisted of cycle ergometer exercise 5 d.week-1 and 30 min.d-1 for a period of 8 weeks. Changes in the peripheral vascular response to alteration of transmural pressure in the human finger were measured by a differential digital photoplethysmogram (DeltaDPG) and blood pressure during passive movement of the arm to different vertical hand positions relative to heart level. Following 8 weeks of endurance training, percent changes in DeltaDPG from heart level in the training group increased significantly (mean +/- SD, -48.1 +/- 7. 3 to -58.7 +/- 9.3% at the lowered position, 46.1 +/- 13.4 to 84.6 +/- 8.8% at the elevated position, p<0.05). Similarly, the arterial compliance index, which was calculated from DeltaDPG-P wave amplitude and arterial pulse pressure, also significantly changed in the training group over the 8 weeks (5.6 +/- 1.3 to 2.7 +/- 1.6 mV. V-1.s-1.mmHg-1 at the lowered position, 30.0 +/- 12.4 to 54.4 +/- 18. 9 mV.V-1.s-1.mmHg-1 at the elevated position ). Maximal oxygen uptake (V.O2 max) was significantly increased in the training group. On the other hand, the control group (n = 6) showed no significant changes in all parameters for 8 weeks. Therefore these results suggest that endurance exercise training induces an increase in peripheral vascular response to alteration of transmural pressure in the human finger.

Adult↗

PubMed2006

Influence of endurance exercise training and sex on intramyocellular lipid and mitochondrial ultrastructure, substrate use, and mitochondrial enzyme activity.

Impaired mitochondrial function and structure and intramyocellular lipid (IMCL) accumulation have been associated with obesity and Type 2 diabetes. We examined whether endurance exercise training and sex influenced IMCL and mitochondrial morphology using electron microscopy, whole-body substrate use, and mitochondrial enzyme activity. Untrained men (n = 5) and women (n = 7) were tested before and after 7 wk of endurance exercise training. Testing included 90 min of cycle ergometry at 60% Vo(2 peak) with preexercise muscle biopsies analyzed for IMCL and mitochondrial size/area using electron microscopy and short-chain beta-hydroxyacyl-CoA dehydrogenase (SCHAD) and citrate synthase (CS) enzyme activity. Training increased the mean lipid area density (P = 0.090), the number of IMCL droplets (P = 0.055), the number of IMCL droplets in contact with mitochondria (P = 0.010), the total mitochondrial area (P < 0.001), and the size of individual mitochondrial fragments (P = 0.006). Women had higher mean lipid area density (P = 0.030) and number of IMCL droplets (P = 0.002) before and after training, but higher individual IMCL area only before training (P = 0.013), compared with men. Women oxidized more fat (P = 0.027) and less carbohydrate (P = 0.032) throughout the study. Training increased Vo(2 peak) (P < 0.001), %fat oxidation (P = 0.018), SCHAD activity (P = 0.003), and CS activity (P = 0.042). In summary, endurance exercise training increased IMCL area density due to an increase in the number of lipid droplets, whereas the increase in total mitochondrial area was due to an increase in the size of individual mitochondrial fragments. In addition, women have higher IMCL content compared with men due mainly to a greater number of individual droplets. Finally, endurance exercise training increased the proportion of IMCL in physical contact with mitochondria.

3-Hydroxyacyl CoA Dehydrogenases↗

PubMed2005

Exercise training in patients receiving maintenance hemodialysis: a systematic review of clinical trials.

BACKGROUND: Exercise is not routinely advocated in patients with end-stage renal disease (ESRD) receiving maintenance hemodialysis (HD), compared to best practice in other chronically diseased cohorts. Lack of widespread awareness of the exercise in HD literature may be contributing to these shortcomings of clinical practice. Therefore, our objectives are: (1) to systematically review trials of exercise training involving adult HD patients; (2) to provide empirical evidence that exercise can elicit health-related adaptations in this cohort, and (3) to provide recommendations for future investigations. METHOD: A systematic review of the literature using computerized databases was performed. RESULTS: According to the 29 trials reviewed, HD patients can safely derive a myriad of health-related adaptations from engaging in appropriately structured exercise regimens involving aerobic and/or resistance training. However, methodological limitations within this body of literature may be partially responsible for minimal advocacy for exercise in this cohort. CONCLUSIONS: Robustly designed RCTs with thorough, standardized reporting are required if clinical practice and quality of life of this cohort is to be enhanced through the integration of exercise training and mainstream medical practice. Future trials should demonstrate the clinical importance, and long-term feasibility and applicability of exercise training for this vulnerable patient population.

Adaptation, Physiological↗

PubMed1985

Effects of exercise training on coronary transport capacity.

Coronary transport capacity was estimated in eight sedentary control and eight exercise-trained anesthetized dogs by determining the differences between base line and the highest coronary blood flow and permeability-surface area product (PS) obtained during maximal adenosine vasodilation with coronary perfusion pressure constant. The anterior descending branch of the left coronary artery was cannulated and pump-perfused under constant-pressure conditions (approximately equal to 100 Torr) while aortic, central venous, and coronary perfusion pressures, heart rate, electrocardiogram, and coronary flow were monitored. Myocardial extraction and PS of 51Cr-labeled ethylenediaminetetraacetic acid were determined with the single-injection indicator-diffusion method. The efficacy of the 16 +/- 1 wk exercise training program was shown by significant increases in the succinate dehydrogenase activities of the gastrocnemius, gluteus medialis, and long head of triceps brachii muscles. There were no differences between control and trained dogs for either resting coronary blood flow or PS. During maximal vasodilation with adenosine, the trained dogs had significantly lower perfusion pressures with constant flow and, with constant-pressure vasodilation, greater coronary blood flow and PS. It is concluded that exercise training in dogs induces an increased coronary transport capacity that includes increases in coronary blood flow capacity (26% of control) and capillary diffusion capacity (82% of control).

Adenosine↗

PubMed2004

Effect of moderate exercise training on peripheral glucose effectiveness, insulin sensitivity, and endogenous glucose production in healthy humans estimated by a two-compartment-labeled minimal model.

For examining the effects of moderate exercise training on peripheral glucose effectiveness (S(g)(2)*), insulin sensitivity (S(i)(2)*), and endogenous glucose production (EGP), seven men and one woman (24.8 +/- 1.8 years) participated in cycle ergometer training at lactate threshold intensity for 60 min/day, 5 days/week for 12 weeks. Stable-labeled frequently sampled intravenous glucose tolerance tests were performed before and 16 h and 1 week after the last training session. S(g)(2)* (pre 0.71 +/- 0.03 x 10(-2), 16 h 0.85 +/- 0.02 x 10(-2) dl. kg(-1). min(-1)) and S(i)(2)* (pre 12.6 +/- 2.6 x 10(-4), 16 h 19.7 +/- 3.3 x 10(-4) dl. kg(-1). min(-1). [ micro U/ml](-1)), analyzed using the two-compartment minimal model, were significantly elevated 16 h after the last training session. The elevated S(g)(2)* remained higher despite the cessation of exercise training for 1 week (1.00 +/- 0.03 x 10(-2) dl. kg(-1). min(-1)). EGP was suppressed within 20 min after glucose bolus, and the suppression of EGP was followed by their overshoot. The time course of EGP during the intravenous glucose tolerance test remained similar after the training period. In conclusion, moderate exercise training at lactate threshold improves not only peripheral insulin sensitivity but also peripheral glucose effectiveness with no change in the effect of glucose and/or insulin to suppress EGP in healthy humans.

Adult↗

PubMed1991

Reductions in exercise lactic acidosis and ventilation as a result of exercise training in patients with obstructive lung disease.

Though exercise training is part of most pulmonary rehabilitation programs, whether there is a physiologic basis for increased exercise tolerance is unclear. We sought to determine whether patients with chronic obstructive pulmonary disease (COPD) are capable of obtaining a physiologic training effect, as manifested by a reduction in blood lactate and ventilation (VE) at a given level of exercise. We also sought to determine whether training work rate determines the size of the training effect. Nineteen participants with COPD of predominantly moderate severity in an inpatient rehabilitation program performed two cycle ergometer exercise tests at a low and a high work rate for 15 min or to tolerance and also an incremental exercise test to tolerance. Arterial blood was sampled for blood gas and lactate analyses. Identical tests were performed before and after 5-day-per-week cycle ergometer training for 8 wk either for 45 min/day at a high work rate (average, 71 W) or for a proportionally longer time at a low work rate (average, 30 W). Average FEV1 was 56 +/- 12% predicted and did not change with training. Peak exercise lactate (average, 6.5 mEq/L) was not correlated with FEV1. For the high work rate training group, identical work rates engendered less lactate (4.5 versus 7.2 mEq/L) and less VE (48 versus 55 L/min) after training; the low work rate training group had significantly less lactate and VE decrease (p less than 0.01). Further, endurance time for the high constant work rate increased 73% in the high work rate training group but only 9% in the low work rate training group. At identical work rates, VE decrease average 2.5 L/min per mEq/L decrease in lactate (r = 0.75). We conclude that most COPD subjects studied increased blood lactate at low work rates. Many of these patients were able to achieve a physiologic training effect. Though total work was the same, training at a high work rate was more effective than was training at a low work rate. The lower VE requirement to perform exercise was in proportion to the lower lactate level, but the VE decrease for a given decrease in lactate was smaller than that seen in normal subjects (7.2 L/min/mEq/L), apparently because patients with COPD fall to hyperventilate in response to lactic acidosis (PaCO2 does not drop). These findings provide a physiologic rationale for exercise training of patients with COPD.

Acidosis, Lactic↗

PubMed2004

Effects of acute exhaustive exercise and chronic exercise training on type 1 and type 2 T lymphocytes.

The present study examined the effects of acute exhaustive exercise and chronic exercise training on type 1 and type 2 T lymphocyte distribution and intracellular cytokine production. Seven endurance-trained male cyclists completed exercise trials to exhaustion before, immediately after, and following 2 weeks of resting recovery from a 6-day intensified training period (ITP). During each trial, resting and post-exercise blood samples were incubated with phorbol 12-myristate 13-acetate (PMA) and ionomycin and stained for T lymphocyte surface antigens (CD3). Cells were then permeabilised, stained for intracellular cytokines and analysed using flow cytometry. Acute exhaustive exercise before and following 2 weeks of recovery from the ITP, but not immediately after the ITP, significantly reduced the circulating percentage and number of lFN-gamma+ (type 1) T cells (P<0.05). In addition, the amount of IFN-gamma produced by stimulated T lymphocytes was decreased (P<0.05) post-exercise during each trial. The percentage and number of interferon (IFN)-gamma+ T lymphocytes was decreased (P<0.05) at rest immediately after the ITP compared with before and following 2 weeks of resting recovery from the ITP. However, the amount of IFN-gamma produced by stimulated T lymphocytes at rest was unaltered following the ITP. Neither acute exercise nor chronic exercise training caused an alteration in the circulating percentage or number of interleukin (IL)-4+ (type 2) T lymphocytes. These results suggest a possible mechanism for the increased incidence of infection reported during chronic exercise training via modulation of type 1/type 2 T lymphocyte distribution.

Adult↗

PubMed1993

Cardiorespiratory responses to exercise training in septuagenarian women.

Cardiorespiratory responses to a 12wk moderate exercise training program were examined in 30 sedentary elderly women (mean age = 73.6 +/- 0.7 yr). In addition, 12 highly conditioned (HC) older women (mean age = 72.5 +/- 1.8 yr; 11.2 +/- 1.2 yr training; 1.6 +/- 0.2 hr.d-1 aerobic activity) were tested at baseline for cross-sectional comparisons. The VO2max and VEmax of the HC subjects were 67% and 36% higher, respectively, (p < 0.001) than the combined sedentary subjects at baseline. Sedentary subjects were randomly assigned to a walking (WALK) or calisthenics control (CAL) group. The WALK group exercised 5 d.wk-1 for 30-40 min per session at 60.0 +/- 1.9% heart rate reserve while the CAL group engaged in mild musculoskeletal exercise. The WALK group demonstrated significant improvement in VO2max compared to CAL subjects at 12 wk (12.6% vs 2.2%, F = 5.74, p = 0.005). These data show that septuagenarian women demonstrate significant improvement in maximal cardiorespiratory fitness through moderate exercise training.

Aged↗

PubMed2003

A quantitative trait locus on 7q31 for the changes in plasma insulin in response to exercise training: the HERITAGE Family Study.

Several genome-wide linkage scans have been carried out to identify quantitative trait loci for type 2 diabetes and related metabolic phenotypes. However, no previous linkage scans have focused on the response to exercise training of relevant metabolic traits. We performed a genome-wide linkage scan for baseline fasting glucose, insulin, and C-peptide and their responses to a 20-week exercise training program in nondiabetic white and black men and women from the HERITAGE Family Study. In SIBPAL linkage analyses, the maximum number of sibpairs available was 344 and 93 for baseline phenotypes and 300 and 72 for exercise training response phenotypes in whites and blacks, respectively. A total of 509 markers with an average spacing of 6.0 Mb were used. The strongest linkage was found for the changes in fasting insulin in response to exercise training with a marker in the leptin gene on 7q31 (empirical multipoint P = 0.0004) in whites. In blacks, the strongest linkage was observed for baseline fasting glucose on 12q13-q14 (empirical multipoint P = 0.0006). These regions harbor several potential candidate genes. The present findings may be important in identifying individuals at increased risk of developing type 2 diabetes and who are most likely to benefit from a physically active lifestyle.

Black People↗

PubMed1985

Effects of exercise training on in vivo insulin action in individual tissues of the rat.

It has previously been suggested that exercise training leads to increased whole body insulin sensitivity. However, the specific tissues and metabolic pathways involved have not been examined in vivo. By combining the euglycemic clamp with administration of glucose tracers, [3H]2-deoxyglucose (2DG), [14C]glucose, and [3H]glucose, in vivo insulin action at the whole body level and within individual tissues has been assessed in exercise-trained (ET, running 1 h/d for 7 wk) and sedentary control rats at four insulin doses. Whole body insulin sensitivity was significantly increased in ET. In addition, the skeletal muscles, soleus, red and white gastrocnemius, extensor digitorum longus (EDL), and diaphragm all showed increased sensitivity of insulin-stimulated 2DG uptake with training. With the exception of EDL, no significant difference in insulin-mediated glycogen synthesis between control and ET could be found. Therefore, the increased insulin-induced 2DG uptake observed in muscle following training is apparently directed towards glucose oxidation. In ET animals, adipose tissue exhibited a significant increase in insulin-mediated 2DG uptake and [14C]glucose incorporation into free fatty acids but there was no difference from control in any parameters measured in lung or liver. EDL and white gastrocnemius, which are not primarily involved during exercise of this type, also demonstrated increased insulin sensitivity following training. In conclusion, exercise training results in a marked increase in whole body insulin sensitivity related mainly to increased glucose oxidation in skeletal muscle. This effect may be mediated by systemic as well as local factors and is likely to be of therapeutic value in pathological conditions exhibiting insulin resistance.

Adipose Tissue↗

PubMed1986

Exercise training and hypertension.

Hypertension is a major health dilemma in the world today because of its high rate of incidence. Exercise training is usually mentioned as a useful nonpharmacological therapy for essential hypertension. Seventeen studies have assessed the effect of exercise training in individuals with essential hypertension. The majority of the results indicate that both systolic and diastolic blood pressure may be lowered by approximately 10 mmHg with training, however, this conclusion must be interpreted in light of numerous design deficiencies, methodological shortcomings, and the limited populations studied in these investigations. Some studies appear to indicate that mild to moderate intensity training may be as useful in lowering blood pressure as higher intensity training. Very little data is available to indicate if cardiac output and/or total peripheral resistance are reduced to bring about the reduction in blood pressure. Clearly more studies are required to evaluate the belief that exercise training is beneficial in essential hypertension and to determine the responsible mechanisms.

Child↗