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The effect of exercise training on human hypertension: a review.

Numerous sources of information in both the medical and exercise physiology areas state that exercise training lowers blood pressure at rest and during submaximal exercise in normotensive and hypertensive individuals. Based on these statements, the medical community is currently recommending regular exercise as a non-pharmacological therapy for reducing blood pressure in hypertensive patients. The purpose of this review was to assess the existing literature in this area to determine whether a basis exists for this recommendation. Our findings indicate that most of the studies reviewed reported modest reductions in blood pressure (means less than or equal to 10 mmHg) at rest and during submaximal exercise after training. However, even the modest reductions in blood pressure reported in these studies must be interpreted with caution because of numerous methodological shortcomings and inadequate study design, most notably the omission of non-exercising hypertensive control groups. Therefore, the evidence available at the present time is inadequate to recommend exercise training as a non-pharmacological therapy in hypertension.

Adolescent↗

8-Oxoguanosine and uracil repair of nuclear and mitochondrial DNA in red and white skeletal muscle of exercise-trained old rats.

Oxoguanine DNA glycosylase (OGG1) and uracil DNA glycosylase (UDG) are two of the most important repair enzymes that are involved in the base excision repair processes to eliminate oxidative damage from mammalian DNA, which accumulates with aging. Red and white skeletal muscle fibers have very different antioxidant enzyme activities and resistance to oxidative stress. In this paper, we demonstrate that the activity of OGG1 is significantly higher in the red type of skeletal muscle compared with white fibers from old rats. Exercise training resulted in increased OGG1 activity in the nuclei of red fibers and decreased activity in nuclei of white fibers and in the mitochondria of both red and white fibers. The activities of UDG were similar in both red and white muscle fibers. Exercise training appears to increase the activity of UDG in the nuclei and mitochondria. However, exercise training affects the activity of OGG1 in nuclei and mitochondria differently, suggesting different regulation of the enzymes. In contrast, UDG showed similar activities in nuclei and mitochondrial extracts of exercise-trained animals. These data provide evidence for differential regulation of UDG and OGG1 in maintaining fidelity of DNA in oxidatively stressed cells.

Age Factors↗

Assessment by a microprocessor of adherence to home-based moderate-intensity exercise training in healthy, sedentary middle-aged men and women.

Research in exercise training of healthy persons, which has been conducted almost exclusively in supervised group programs, is relatively expensive for the investigator and inconvenient for the participant. To overcome these obstacles, self-monitored moderate-intensity home-based exercise training was prescribed for 28 middle-aged men and 26 middle-aged women. The median energy expenditure prescribed for each of 5 weekly exercise sessions was 4 cal/kg body weight, or 317 kcal for men and 265 kcal for women, corresponding to a median duration of 45 and 60 minutes, respectively. In the next 24 weeks, peak oxygen uptake increased 13.7% in men who exercised, from 31 +/- 4 to 37 +/- 4 ml/kg/min, and 10% in women who exercised, from 26 +/- 4 to 29 +/- 5 ml/kg/min (p less than 0.001 for both comparisons). The proportion of prescribed caloric expenditure per session, which was documented by a solid-state heart rate recorder, was 108% in men and 90% in women. The duration of training at heart rates above the prescribed range approximated 10 minutes per session for both men and women; the proportion of total caloric expenditure represented by exercise at heart rates exceeding the prescribed limit was 9% for men and 4% for women. The proportion of time spent within the prescribed heart rate range during training sessions was 76% for men and 84% for women. Training-induced musculoskeletal problems were reported by 6 men and no women. No subject sought medical attention and all resumed training within 1 week.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Effect of exercise training and sucrose feeding on insulin-stimulated glucose uptake in rats with streptozotocin-induced insulin-deficient diabetes.

The effect of exercise training and a sucrose-rich diet on insulin-stimulated glucose disposal was studied in rats with streptozotocin-induced insulin deficiency. Rats were injected with streptozotocin (40 mg/kg), and 3 days later divided into three groups with equal degrees of hyperglycemia. One group of rats was allowed to run spontaneously on exercise wheels, another group remained sedentary but ate a sucrose-rich diet (66% sucrose), and the third also remained sedentary but consumed conventional rat chow. Three weeks later, we determined the effect of these various programs on postabsorptive plasma glucose and insulin levels, as well as on the ability of exogenous insulin to stimulate disposal of a glucose load during a period in which endogenous insulin was suppressed by epinephrine and propanolol. Basal plasma insulin levels were the same in all three groups, but plasma glucose levels were significantly lower (P less than 0.001) in exercise-trained rats, and significantly higher (P less than 0.05) in sucrose-fed rats, than in chow-fed diabetic rats. The inference that exercise training markedly enhanced insulin action in rats with insulin deficiency was borne out by direct estimation of insulin-stimulated glucose disposal. In contrast, sucrose-fed diabetic rats seemed to be more insulin-resistant than chow-fed diabetic rats. These results provide direct evidence that spontaneous exercise can dramatically attenuate the severity of diabetes in insulin-deficient rats by enhancing insulin action. DIABETES 32:165-168, February 1983.

Animals↗

Effects of exercise training on left ventricular function evaluated by the Tei index in patients with myocardial infarction.

BACKGROUND: This study investigated the influence of exercise training on left ventricular (LV) function in patients with acute myocardial infarction (AMI) using a new index of cardiac function, the Tei index. METHODS AND RESULTS: The study enrolled 53 consecutive patients (36 males, 17 females; mean age: 65+/-10 years) with AMI. Exercise training was performed for 6 months; peak VO2 and the Tei index were measured at the start of the cardiac rehabilitation program and 1, 3, and 6 months later. The peak VO2 improved from 14.3+/-3.3 to 18.5+/-5.2 ml.min -1.kg-1 after 6 months (p<0.01). Although there were no significant changes in LV ejection fraction over the 6 months, the Tei index improved from 0.50+/-0.18 to 0.41+/-0.19 (p<0.05). When the DeltaTei index was compared among the 3 groups classified by the Tei index at baseline, the values improved in the groups with high/slightly high values compared with the normal group. CONCLUSION: Both cardiac function, as evaluated by the Tei index, and exercise capacity improved after exercise training in patients with AMI. The greater improvement was seen in the population with the higher value (lower cardiac function) according to this index.

Acute Disease↗

Antioxidative effects of exercise training in patients with chronic heart failure: increase in radical scavenger enzyme activity in skeletal muscle.

BACKGROUND: In chronic heart failure (CHF), cross-talk between inflammatory activation and oxidative stress has been anticipated in skeletal muscle (SM). The role of the radical scavenger enzymes superoxide dismutase (SOD), catalase (Cat), and glutathione peroxidase (GPX), which remove oxygen radicals, has never been assessed in the SM in this context. Moreover, it remains unknown whether exercise training augments the activity of these enzymes in CHF. METHODS AND RESULTS: Twenty-three patients with CHF were randomized to either 6 months of exercise training (T) or a sedentary lifestyle (C); 12 age-matched healthy subjects (HS) were studied in parallel. Activity of Cat, SOD, and GPX was assessed in SM biopsies before and after 6 months (6 months). Oxidative stress was determined by measuring nitrotyrosine formation. SOD, Cat, and GPX activity was reduced by 31%, 57%, and 51%, respectively, whereas nitrotyrosine formation was increased by 107% in SM in CHF (P<0.05 versus HS). In CHF, exercise training augmented GPX and Cat activity in SM by 41% (P<0.05 versus before and group C) and 42% (P<0.05 versus before and group C), respectively, and decreased nitrotyrosine production by 35% (from 3.8+/-0.4% tissue area before to 2.5+/-0.3% after 6 months; P<0.05 versus before). CONCLUSIONS: The reduced activity of major antioxidative enzymes in the SM of CHF patients is associated with increased local oxidative stress. Exercise training exerts antioxidative effects in the SM in CHF, in particular, due to an augmentation in activity of radical scavenger enzymes.

Case-Control Studies↗

Regional vascular resistance during exercise: role of cardiac afferents and exercise training.

This study was designed to determine whether cardiac vagal afferents exert an inhibitory influence on increases in regional vascular resistance during exercise and to determine whether endurance exercise training enhances the inhibitory influence of cardiac vagal afferents. We measured changes in regional vascular resistance in 12 rabbits at rest and during running at 12.6 m/min, 20% grade, before and after reversible denervation of cardiac afferents (intrapericardial procainamide HCl, 2%). In addition, these procedures were repeated in five of these rabbits following an 8-wk endurance exercise training program. Because intrapericardial injections of procainamide anesthetize both the efferent as well as the afferent innervation to the heart, it was necessary to determine the effects of blocking the efferent innervation on the regulation of regional vascular resistance during exercise. Rabbits were instrumented with Doppler ultrasonic flow probes around the renal (R), mesenteric (M), ascending, and terminal aortic (TA) arteries. Catheters were positioned in the central ear artery and vein and pericardial sac. Mean arterial pressure, heart rate, cardiac output, R, M, TA, and systemic (S) resistances were determined. Exercise changed R (+37 +/- 4%), M (+88 +/- 9%), TA (-62 +/- 6%), and S (-34 +/- 3) resistances. Subsequent cardiac efferent blockade alone had no significant effect on regional vascular resistance during exercise. Combined efferent and afferent blockade resulted in significant increases in R (+62 +/- 6%) and M resistance (+134 +/- 13%) but did not alter TA (-51 +/- 4%) or S (-27 +/- 2%) resistance during exercise. Exercise training significantly enhanced the inhibitory influence of cardiac afferents on R and M regional vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗

Swimming exercise training prior to acute myocardial infarction attenuates left ventricular remodeling and improves left ventricular function in rats.

The effect of exercise training prior to acute myocardial infarction (AMI) on left ventricular (LV) remodeling is poorly understood. This study investigated the protective effect of 3 weeks of swimming exercise training prior to AMI on cardiac morphology and function. Male Sprague-Dawley rats (n = 35) were randomly assigned to 3 groups: swimming training (n = 14, 90 min, 5 days/wk, 3 wk), sedentary (n =14), and controls (n = 7, no exercise, no MI). At the end of the training/sedentary period, rats were subjected to AMI (ExMI and SedMI) induced by surgical ligation of the left coronary artery. Thereafter, the rats remained sedentary for a 4-wk recovery period. Trans-thoracic echocardiography was performed in each group at the end of the exercise/sedentary period (pre-AMI), 24 hr after AMI, and following recovery (4 wk after AMI). No differences were observed in LV dimensions and function pre-AMI among the 3 groups; however, LV-end systolic diameter (LVESD) and LV-end systolic area (LVES-area) were significantly lower in the prior trained rats, 24 hr post-AMI with no additional change 4 wk post-AMI, during remodeling. Both LV-shortening fraction (SF%) and fractional area change (FAC%) were higher in the trained animals 4 wk post-AMI (39+/-12% vs 23+/-8%; p 0.002, and 48+/-14% vs. 38+/-9%; p 0.07, respectively). In conclusion, 3 wk of swimming exercise training prior to AMI significantly attenuated LV remodeling and improved LV function, despite no changes in LV dimensions or systolic function at the end of the exercise session. The data suggest that even a short-term training period is sufficient to induce cardiac protection.

Acute Disease↗

Effects of whole-body exercise training on body composition and functional capacity in normal-weight patients with COPD.

BACKGROUND: Skeletal muscle wasting is related to muscle dysfunction, exercise intolerance, and increased mortality risk in patients with COPD. STUDY OBJECTIVES: The aims of this study were to investigate the effects of whole-body exercise training on body composition in normal-weight patients with COPD, and to study the relationship between changes in body composition and functional capacity. SETTING AND PARTICIPANTS: Fifty patients with COPD (FEV(1), 39% of predicted [SD, 16]) admitted to the pulmonary rehabilitation center at Hornerheide, and 36 healthy age-matched control subjects (for baseline comparison) were included. INTERVENTIONS: Patients participated in a standardized inpatient exercise training program consisting of daily submaximal cycle ergometry, treadmill walking, weight training, and gymnastics during 8 weeks. MEASUREMENTS: Fat-free mass (FFM) was measured by bioelectrical impedance analysis. None of the patients met the criteria for nutritional supplementation (body mass index </= 21, or FFM index </= 15 kg/m(2) in women and </= 16 kg/m(2) in men). Exercise capacity was measured using incremental cycle ergometry. Isokinetic quadriceps strength was measured with a Biodex dynamometer (Biodex Medical Corporation; Shirley, NY). RESULTS: At baseline, patients were characterized by a significantly lower FFM than the control subjects. Age and FFM were independent predictors of skeletal muscle function and exercise capacity in patients. After rehabilitation, weight (72.4 +/- 9.8 to 73.0 +/- 9.4 kg, p < 0.05) significantly increased, as a result of increased FFM (52.4 +/- 7.3 to 53.4 +/- 7.7 kg, p < 0.05), while fat mass (20.0 +/- 6.1 to 19.6 +/- 5.7 kg) tended to decrease. Peak work rate (63 +/- 29 to 84 +/- 42 W, p < 0.001), maximal oxygen consumption (O(2)max) [1,028 +/- 307 to 1,229 +/- 421 mL/min, p < 0.001], and isokinetic quadriceps strength (82.5 +/- 36.4 to 90.3 +/- 34.9 Newton-meters, p < 0.05) all improved. Changes in FFM were proportionally smaller than functional improvements, and were related to changes in O(2)max (r = 0.361, p < 0.05), but not to other changes in functional capacity. CONCLUSIONS: Intensive exercise training per se is able to induce an anabolic response in normal-weight patients with COPD classified into Global Initiative for Chronic Obstructive Lung Disease stages III-IV. Improvements in exercise performance and muscle function are proportionally larger than increases in FFM.

Aged↗

Streptozotocin-induced diabetes and the effects of endurance exercise training.

The purpose of this investigation was to determine if endurance exercise training would alter the degenerative effects of streptozotocin diabetes on cardiac function and alter the responses of streptozotocin diabetic rats to induced myocardial ischemia. Diabetic rats experienced a significant (p < 0.05) reduction in cardiac function as evidenced by left ventricular peak systolic pressure (LVPSP), maximal time rate of change of pressure (+dP/dTmax), rate pressure product (RPP), and heart rate (HR). Exercise training apparently reduced the effect of diabetes since the function of non-ischemic hearts from trained diabetic rats was not different from that of non-diabetic rats. It also was not different from the sedentary diabetic rat hearts. Training did not alter the response of the hearts of either group of diabetic rats to induced myocardial ischemia.

Analysis of Variance↗

Impact of high- and low-intensity targeted exercise training on the type of substrate utilization in obese boys submitted to a hypocaloric diet.

BACKGROUND: We assessed the effect of two programs combining a hypocaloric diet with low-intensity (LI) or high-intensity (HI) exercise training, during two months, on substrate utilization at exercise in obese children. METHODS: Fifteen obese boys participated in a combined program of exercise and caloric restriction-induced weight loss (diet starting two weeks before the training program). The maximal fat oxidation point (Lipox max) was determined to individualize exercise training. Training consisted of cycling at either LI (Lipox max) for seven children or HI (Lipoxmax+40% Lipox max) for eight children. RESULTS: All children exhibited a decrease in weight (LI: -5.2 kg +/- 0.7 (P<0.01), HI: -7 kg +/- 0.7 (P<0.01)). While in the LI group, both fat and CHO oxidation were unchanged after training, HI group oxidize less fat and more CHO after training when exercising at 20% and 30% Wmax th (P = 0.02). DISCUSSION: While a LI exercise training program maintains (but does not improve) the ability to oxidize fat at exercise, HI training actually shifts towards CHO the balance of substrate oxidation during exercise. Thus, a low intensity training protocol seems to counteract to some extent the decline in lipid oxidation at exercise that occurs after a hypocaloric diet, and is thus likely to be synergistic to diet in the weight lowering strategy.

Adipose Tissue↗

Interaction of exercise training and chronic ethanol ingestion on hepatic and plasma antioxidant system in rat.

This study was undertaken in order to investigate the interactive effects of exercise training and chronic ethanol consumption on the antioxidant system in rat liver and plasma. Fisher-344 rats were treated in separate groups as follows: sedentary control (SC); exercise training (ET) for 6.5 weeks; ethanol 20% (2.0 g kg-1, p.o.) for 6.5 weeks; and ET and ethanol administration. In liver, ET significantly decreased the malondialdehyde (MDA) level (73% of SC). Chronic ethanol significantly increased catalase (CAT) activity and MDA levels (126% and 135% of SC), respectively, and also depleted the reduced glutathione (GSH) level and the reduced to oxidized glutathione (GSH/GSSG) ratio (81% and 38% of SC), respectively. Exercise training plus ethanol significantly increased CAT and glutathione reductase (GR) activity (126% and 118% of SC), respectively, and decreased the MDA level (67% of SC). In plasma, ethanol significantly enhanced CAT activity and MDA levels (173% and 221% of SC), respectively. Ethanol ingestion also increased the CAT/superoxide dismutase (SOD) ratio (216% of SC) in plasma. Training plus ethanol ingestion significantly increased CAT activity and MDA levels (208% and 148% of SC), respectively, and increased CAT/SOD and glutathione peroxidase (GSH-Px)/SOD ratios (279% and 142% of SC), respectively. The data indicate that the combination of exercise and ethanol ingestion resulted in an enhanced hepatic CAT and GR activity to eliminate H2O2 and to maintain endogenous GSH levels. Thus, training ameliorated the ethanol-induced oxidative injury in the liver. The ratio of CAT/SOD in plasma increased twofold due to chronic ethanol intake and threefold due to the combination, which may be used as an index of oxidative stress.

Animals↗

Cardiac effects of prolonged and intense exercise training in patients with coronary artery disease.

The effects of intense and prolonged exercise training on the heart were studied with echocardiography in eight men with coronary artery disease with a mean age (+/- standard error of the mean) of 52 +/- 3 years. Training consisted of endurance exercise 3 times/week at 50 to 60 percent of the measured maximal oxygen uptake for 3 months followed by exercise 4 to 5 days/week at 70 to 80 percent of maximal oxygen uptake for 9 months. Maximal oxygen uptake capacity increased by 42 percent (26 +/- 1 versus 37 +/- 2 ml/kg per min; p less than 0.001). Heart rate at rest and submaximal heart rate and systolic blood pressure at a given work rate were significantly lower after training. Systolic blood pressure at the time of maximal exercise increased (145 +/- 9 before versus 166 +/- 8 mm Hg after training; probability [p] less than 0.01). Left ventricular end-diastolic diameter was increased after 12 months of training (from 47 +/- 1 to 51 +/- 1 mm; p less than 0.01). Left ventricular fractional shortening and mean velocity of circumferential shortening decreased progressively in response to graded isometric handgrip exercise before training but not after training. At comparable levels of blood pressure during static exercise, mean velocity of circumferential shortening was significantly higher after training (0.76 +/- 0.04 versus 0.98 +/- 0.07 diameter/sec, p less than 0.01). No improvement in echocardiographic or exercise variables was observed over a 12 month period in another group of five patients who did not exercise. Thus the data suggest that prolonged and vigorous exercise training in selected patients with coronary artery disease can elicit cardiac adaptations.

Adaptation, Physiological↗

Immune response to exercise training and/or energy restriction in obese women.

PURPOSE: The effect of exercise training (five 45-min walking sessions/wk at 60-75% maximum heart rate) and/or moderate energy restriction (4.19-5.44 MJ or 1,200-1,300 kcal x d(-1)) on innate and adaptive immunity (including mitogen-stimulated lymphocyte proliferation (MSLP), natural killer cell activity (NKCA), and monocyte and granulocyte phagocytosis and oxidative burst (MGPOB) was studied in obese women (N = 91, age 45.6 +/- 1.1 yr, body mass index 33.1 +/- 0.6 kg x m(-2)) randomized to one of four groups: control (C), exercise (E), diet (D), exercise, and diet (ED). METHODS: Aerobic power, body composition, and immune function were measured in all subjects before and after a 12-wk diet intervention period, with data analyzed using a 4 x 2 repeated measures design. All subjects self-reported symptoms of sickness in health logs using a precoded checklist. Statistical significance was set at P < or = 0.05. RESULTS: Data from this study indicate that although exercise training was unrelated to any significant changes in resting immune function, the number of days with symptoms of upper respiratory tract infection (URTI) was reduced relative to subjects in the nonexercise groups (5.6 +/- 0.9 and 9.4 +/- 1.1 sickness days, respectively, P < 0.05). Energy restriction and weight loss (7.9 +/- 0.7 kg) was associated with a significant decrease in MSLP, but no change in NKCA, MGPOB, or URTI. CONCLUSION: The data are consistent the viewpoint that weight loss, even at a moderate rate, is associated with a decrease in mitogen-stimulated lymphocyte proliferation without a change in various measures of innate immunity of the blood compartment.

Adult↗

Exercise training increases GLUT-4 protein concentration in previously sedentary middle-aged men.

The purpose of this study was to determine if 14 wk of exercise training would increase insulin-sensitive glucose transporter protein (GLUT-4) concentration in skeletal muscle of previously sedentary middle-aged men (47.2 +/- 1.3 yr; n = 13). Muscle samples (lateral gastrocnemius) and insulin action [insulin sensitivity index (ISI), minimal model] were obtained in the sedentary condition and 48 h after the final training bout. GLUT-4 protein concentration increased (P < 0.001, 2,629 +/- 331 to 4,140 +/- 391 absorbance units/100 micrograms protein) with exercise training by 1.8-fold. ISI increased by twofold (P < 0.05, 2.1 +/- 0.5 to 3.4 +/- 0.7 SI x 10(5) min/pM) with training. The percentage of GLUT-4 rich type IIa muscle fibers increased by approximately 10% (P < 0.01), which may have contributed to the elevation in transporter protein. GLUT-4 concentration and citrate synthase activity (1.7-fold, P < 0.001) also increased by similar increments. These findings indicate that GLUT-4 protein concentration is elevated in middle-aged individuals with exercise training.

Body Composition↗

Cardiovascular drugs: effects on exercise testing and exercise training of the coronary patient.

The exercise test response and exercise capacity of patients with atherosclerotic coronary heart disease may be significantly altered by a number of commonly used cardiovascular drugs, alone or in combination, via complex interactions of hemodynamic and electrophysiologic changes. The clinician must assess the effects of pharmacotherapy when evaluating the results of exercise testing as well as when prescribing a rehabilitative exercise training regimen.

Adrenergic beta-Antagonists↗

Exercise training alters myogenic responses in porcine coronary resistance arteries.

The purpose of this study was to test the hypothesis that myogenic responsiveness in porcine coronary resistance arteries is attenuated by exercise training. Twenty-four female Yucatan miniature swine were randomly separated into two groups of 12 pigs: exercise trained (ET) and sedentary control (SED). The ET pigs were trained on a motor-driven treadmill for 16-22 wk while the SED pigs remained confined to their pens. After training, heart weight-to-body weight ratio, skeletal muscle oxidative capacity, and exercise tolerance were significantly increased in ET pigs compared with SED pigs. Coronary resistance arteries 75-150 microns diam were isolated for in vitro evaluation of myogenic responses to changes in intraluminal pressure in the absence of intraluminal flow. Coronary resistance arteries from ET and SED pigs developed spontaneous tone at 40 mmHg intraluminal pressure. Active changes in diameter measured in response to intraluminal pressures < 40 mmHg were similar in coronary resistance arteries from ET and SED pigs. When pressure was raised above 40 mmHg, myogenic constriction was greater in coronary resistance arteries from ET pigs, as indicated by significantly greater reductions in diameter. At 60 and 70 mmHg intraluminal pressure, constriction was 8 and 16% greater, respectively, in resistance arteries from ET pigs. After maximal relaxation with sodium nitroprusside (100 microM), passive diameter changes measured in response to changes in intraluminal pressure from 10 to 80 mmHg were not significantly different in coronary resistance arteries from ET and SED pigs. We conclude that, contrary to our hypothesis, exercise training in pigs enhances myogenic constrictor responses in coronary resistance arteries.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effect of exercise training on oxidized LDL-mediated platelet function in rats.

This study investigates how exercise training affects Oxidized LDL (Ox-LDL) mediated-platelet activation. Five-week-old male Wistar rats were assigned to either control or trained groups. Trained rats were treadmill-trained for 10 weeks after familiarization. The following measurements were taken in both control and trained groups: Ox-LDL-mediated platelet aggregability and [Ca2+]i, plasma and platelet-derived nitric oxide (NO) metabolite (nitrite plus nitrate) levels, and antiaggregating activity of NO derived from endothelial cells. Based on those measurements, major findings in this study can be summarized as follows: 1) the trained group had a higher plasma -NO metabolite level than the control group; 2) the trained group had a lower platelet aggregability and [Ca2+]i elevation and a higher platelet derived-NO metabolite level than the control group; 3) the trained group had lower Ox-LDL-potentiated platelet aggregability and [Ca2+]i elevation and Ox-LDL-attenuated NO metabolite in platelet than the control group; 4) treating the platelet with L-arginine inhibited Ox-LDL-potentiated platelet activation in both control and trained groups; 5) Ox-LDL enhances platelet aggregation directly although impairing NO bioactivity but not guanylate cyclase activity in both control and trained groups. Results in this study demonstrate that exercise training decreases Ox-LDL-potentiated platelet activation most likely by enhancing platelet-derived NO release.

Adenosine Diphosphate↗