Wk Of Aerobic Exercise Training Research Articles

Effects of aerobic exercise training on cerebral pulsatile hemodynamics in middle-aged adults with elevated blood pressure/stage 1 hypertension.

Mechanisms behind the protective effects of aerobic exercise on brain health remain elusive but may be vascular in origin and relate to cerebral pulsatility. This pilot study investigated the effects of 12-wk aerobic exercise training on cerebral pulsatility and its vascular contributors (large artery stiffness, characteristic impedance) in at-risk middle-aged adults. Twenty-eight inactive middle-aged adults with elevated blood pressure or stage 1 hypertension were assigned to either moderate/vigorous aerobic exercise training (AET) for 3 days/wk or no-exercise control (CON) group. Middle cerebral artery (MCA) pulsatility index (PI), large artery (i.e., aorta, carotid) stiffness, and characteristic impedance were assessed via Doppler and tonometry at baseline, 6, and 12 wk, whereas cardiorespiratory fitness (V̇o2peak) was assessed via incremental exercise test and cognitive function via computerized battery at baseline and 12 wk. V̇o2peak increased 6% in AET and decreased 4% in CON (P < 0.05). Proximal aortic compliance increased (P = 0.04, partial η2 = 0.14) and aortic characteristic impedance decreased (P = 0.02, partial η2 = 0.17) with AET but not CON. Cerebral pulsatility showed a medium-to-large effect size increase with AET, although not statistically significant (P = 0.07, partial η2 = 0.11) compared with CON. Working memory reaction time improved with AET but not CON (P = 0.02, partial η2 = 0.20). Our data suggest 12-wk AET elicited improvements in central vascular hemodynamics (e.g., proximal aortic compliance and characteristic impedance) along with apparent, paradoxical increases in cerebral pulsatile hemodynamics.NEW & NOTEWORTHY We identify differential central versus cerebrovascular responses to 12 wk of aerobic exercise training in middle-aged adults. Although proximal aortic compliance and characteristic impedance improved after 12 wk of exercise, cerebral pulsatility tended to unexpectedly increase. These data suggest short-term aerobic exercise training may lead to more immediate benefits in the central vasculature, whereas longer duration exercise training may be required for beneficial changes in pulsatility within the cerebrovasculature.

Effect of Exercise Training on Blood Pressure in Healthy Postmenopausal Females: A Systematic Review with Meta-analysis.

The prevalence of hypertension is greater in postmenopausal females compared with males of similar age. Previous meta-analyses of normotensive and hypertensive adults have shown that aerobic exercise training reduces systolic blood pressure (SBP) and/or diastolic blood pressure (DBP). However, the effect of aerobic exercise training on blood pressure specifically within healthy postmenopausal females remains unclear. This systematic review with meta-analysis quantified the effect of aerobic exercise training on resting SBP and DBP in healthy postmenopausal females. The systematic review and meta-analysis followed the Preferred Reporting Items for Systematic Review and Meta-analyses guidelines and was registered in PROSPERO (CRD42020198171). The literature search was done in MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials, CINAHL Plus, and SPORTDiscus. Randomized controlled trials involving healthy postmenopausal females with normal or high normal blood pressure and undergoing ≥4 wk of aerobic exercise training were included. The total weighted mean change in SBP and DBP was compared between the exercise and the control interventions. A random-effects model was used to calculate the overall effect sizes of the weighted mean differences and the 95% confidence interval (CI). Twelve studies were included in the meta-analysis (exercise interventions: n = 357, age = 60 ± 4 yr, baseline SBP/DBP = 128 ± 13/79 ± 8 mm Hg; control interventions: n = 330, age = 60 ± 4 yr, baseline SBP/DBP = 126 ± 11/77 ± 6 mm Hg). Compared with the change observed in response to the control interventions, exercise training significantly reduced SBP (-0.43 mm Hg, 95% CI = -0.78 to -0.09, P = 0.02) and DBP (-0.39 mm Hg, 95% CI = -0.73 to -0.05, P = 0.05). Aerobic exercise training significantly reduces resting SBP and DBP in healthy postmenopausal females with normal or high normal blood pressure. However, this reduction is small and of uncertain clinical significance.

Acute Effects of Exercise Intensity on Insulin Sensitivity under Energy Balance.

The primary objective of this study was to assess the effect of 8 to 16 wk of aerobic exercise training on the SI of untrained women under rigorously controlled energy-balanced conditions. The secondary objective was to determine if one acute bout of moderate-intensity continuous (MIC) or high-intensity interval (HII) exercise further affected SI. Insulin sensitivity was assessed in 28 untrained women at baseline, after 8 to 16 wk of training with no-exercise (NE) before assessment, 22 h after MIC (50% V˙O2peak), and 22 h after HII (84% V˙O2peak) using a hyperinsulinemic-euglycemic clamp. Participants were in a whole-room indirect calorimeter during each condition, and food intake was adjusted to ensure energy balance across 23 h before each clamp. There were no significant differences in acute energy balance between each condition. Results indicated a significant main effect of time, such that SI was higher during the HII condition compared with both baseline and NE (P < 0.05). No significant differences in SI were observed after NE or MIC. Widely reported improvements in SI in response to chronic exercise training may be mediated in part by shifts in energy balance. However, an acute bout of HII exercise may increase SI even in the context of energy balance.

Abstract P035: Habitual Aerobic Exercise-Induced Decrease in Circulating C1q Level is Associated With Reduction of Cardiovascular Diseases Risks in the Elderly

Introduction: Habitual aerobic exercise leads to reduction of arterial wall thickness and arterial stiffness with aging. Recently, C1q has been identified as a novel myokine, and the expression of muscle C1q mRNA increases with aging. Additionally, in vivo and in vitro studies, C1q induces proliferation of vascular smooth muscle cells. However, it remains unclear whether the secretion of myokines, C1q, TNF-alpha and IL-6 are related to the changes in cardiovascular disease risk by aging and regular exercise. PURPOSE: This study aimed to clarify whether serum C1q, TNF-alpha and IL-6 levels are associated with the changes in cardiovascular disease risks with aging and regular aerobic exercise. Methods: In a cross-sectional study, 127 healthy male and female subjects (18-81 years) were enrolled in this study. Subjects were divided into two groups; young (&lt;40 year) and middle-aged and older (≥40 year) groups. Serum C1q, TNF-alpha, IL-6 levels were determined by ELISA. Risks of cardiovascular disease were estimated by using carotid-femoral pulse wave velocity (cfPWV) and common carotid intima-media thickness (ccIMT). Additionally, in an intervention study, thirteen older male subjects were randomly divided into two groups: aerobic training group (AT: n=6) and a sedentary control group (Con: n=7). subjects in the AT group completed 8 wk of aerobic exercise training (60-70% peak oxygen uptake for 45 min, 3 days/wk). Results: In the cross-sectional study, serum C1q, TNF-alpha and IL-6 levels, cfPWV and ccIMT were significantly higher in middle-aged and older group as compared with young group (respectively p&lt;0.05). Positive correlations between cfPWV and serum C1q (r=0.41, p&lt;0.05), TNF-alpha (r=0.28, p&lt;0.05) or IL-6 (r=0.26, p&lt;0.05) levels were seen. Additionally, ccIMT was positively correlated with only serum C1q (r=0.67, p&lt;0.05). After adjusting for TNF-alpha and IL-6, the association between the serum C1q and cfPWV (ß=0.44, p&lt;0.05) or ccIMT (ß=0.83, p&lt;0.05) remained statistically significant. Additionally, in the intervention study, cfPWV and serum C1q level significantly decreased after AT intervention (each P&lt;0.05). Furthermore, the AT-induced change in serum C1q level was positively correlated with AT-induced change in cfPWV (r=0.65, P&lt;0.05) and ccIMT (r=0.59, P&lt;0.05). Conclusion: These results suggest that circulating C1q level may reflect the changes of arterial stiffness and thickness with aging and regular exercise, and the reduction of serum C1q level in response to regular aerobic exercise may contribute to the reduction in cardiovascular disease risks in the elderly.

Effects of exercise training and supplementation with selenium nanoparticle on T-helper 1 and 2 and cytokine levels in tumor tissue of mice bearing the 4 T1 mammary carcinoma.

Physical exercise decreases the incidence of breast cancer and also improves survival in breast cancer patients. However, the mechanistic basis of these protective effects of exercise is not well known. Changes in tumor cytokines, such as oncostatin-M (OSM), have been associated with modulation of antitumor immune responses in breast cancer. Exercise and antioxidants such as selenium affect both antitumor immune responses as well as tumor cytokine expression. Thus, the aim of this study was to determine the effects of aerobic exercise training (AET) and selenium nanoparticle (SeNP) administration on T-helper 1 and 2 and tumor tissue cytokines in mice bearing the 4 T1 mammary carcinoma. We examined the effects of 6 wk of AET and SeNP administration (100 μg three times/wk) on tumor size, concentration of tumor necrosis factor (TNF)-α, interleukin (IL)-6, interferon (IFN)-γ, IL-4 and OSM in tumor tissue and INF-γ and IL-4 in splenocytes of 64 mice bearing the 4 T1 mammary carcinoma. AET increased OSM levels in tumor tissue. Moreover, AET increased levels of TNF-α in tumor tissue, whereas SeNP supplementation decreased IL-4 levels tumor tissue. Also, the combination of AET and SeNP administration decreased tumor volume and increased T-helper 1 cytokines in the splenocytes of tumor-bearing mice. These findings suggest that the combination of AET and SeNP supplementation effects antitumor immune responses in splenocytes, whereas AET induced antitumor cytokines, such as OSM and TNF-α in tumor tissue.

Exercise Effects on Adipose Tissue Postprandial Lipolysis and Blood Flow in Children.

To determine if acute bouts of aerobic exercise and/or excise training alter lipolytic and blood flow responses to food intake in lean (LN) and obese (OB) children. Sixty-five children (9-11 yr) were randomized into acute exercise (EX: 16 LN and 28 OB) or control (CON: 9 LN and 12 OB) groups that exercised (EX), or rested (CON) between standardized breakfast and lunch. Microdialysis probes were inserted into the subcutaneous abdominal adipose tissue to monitor interstitial glycerol (lipolysis) and blood flow. Changes in interstitial glycerol and nutritive flow were calculated from dialysate samples before and after each meal. A subgroup (OB = 15 and LN = 9) from the acute exercise group underwent 16 wk of aerobic exercise training. Poor suppression of lipolysis and a blunted increase in adipose tissue nutritive blood flow in response to breakfast was associated with BMI percentile (r = 0.3, P < 0.05). These responses were normalized at lunch in the OB in the EX (P < 0.05), but not in OB in the CON. Sixteen weeks of exercise training did not improve meal-induced blood flow and marginally altered the antilipolytic response to the two meals (P = 0.06). Daily bouts of acute aerobic exercise should be used to improve the antilipolytic and nutritive blood flow response to a subsequent meal in obese children.

Aerobic exercise training-induced changes in serum C1q/TNF-related protein levels are associated with reduced arterial stiffness in middle-aged and older adults

Adiponectin regulates endothelial nitric oxide synthase in endothelial cells, and body fat loss by aerobic exercise training promotes adiponectin secretion. Recently, C1q/tumor necrosis factor-related proteins (CTRPs) have been identified as novel adipokines and are paralogs of adiponectin, but the association between exercise training-induced reduction of arterial stiffness and circulating CTRPs levels remains unclear. This study aimed to clarify whether the reduction of arterial stiffness in middle-aged and older adults is associated with the change in serum levels of CTRPs induced by exercise training. A total of 52 middle-aged and older participants were randomly divided into two groups: a training group ( n = 26) and a sedentary control group ( n = 26). Participants in the training group completed 8 wk of aerobic exercise training (60-70% peak oxygen uptake for 45 min, 3 days/wk). The reduction of percent whole body fat, abdominal visceral fat area, and carotid-femoral pulse-wave velocity (cfPWV) was significantly greater in the training group than in the control group ( P < 0.05). Moreover, the increase in serum adiponectin, CTRP3, and CTRP5 from baseline to 8 wk was significantly higher in the training group compared with the control group ( P < 0.05). Additionally, the training-induced change in cfPWV was negatively correlated with the training-induced change in serum adiponectin, CTRP3, and CTRP5 levels ( r = -0.51, r = -0.48, r = -0.42, respectively, P < 0.05), and increased plasma nitrite/nitrate level by exercise training was correlated only with adiponectin levels ( r = 0.41, P < 0.05). These results suggest that the exercise training-induced increase in serum CTRPs levels may be associated with the reduction of arterial stiffness in middle-aged and older adults.

Exercise training decreases NADPH oxidase activity and restores skeletal muscle mass in heart failure rats.

We have recently demonstrated that NADPH oxidase hyperactivity, NF-κB activation, and increased p38 phosphorylation lead to atrophy of glycolytic muscle in heart failure (HF). Aerobic exercise training (AET) is an efficient strategy to counteract skeletal muscle atrophy in this syndrome. Therefore, we tested whether AET would regulate muscle redox balance and protein degradation by decreasing NADPH oxidase hyperactivity and reestablishing NF-κB signaling, p38 phosphorylation, and proteasome activity in plantaris muscle of myocardial infarcted-induced HF (MI) rats. Thirty-two male Wistar rats underwent MI or fictitious surgery (SHAM) and were randomly assigned into untrained (UNT) and trained (T; 8 wk of AET on treadmill) groups. AET prevented HF signals and skeletal muscle atrophy in MI-T, which showed an improved exercise tolerance, attenuated cardiac dysfunction and increased plantaris fiber cross-sectional area. To verify the role of inflammation and redox imbalance in triggering protein degradation, circulating TNF-α levels, NADPH oxidase profile, NF-κB signaling, p38 protein levels, and proteasome activity were assessed. MI-T showed a reduced TNF-α levels, NADPH oxidase activity, and Nox2 mRNA expression toward SHAM-UNT levels. The rescue of NADPH oxidase activity induced by AET in MI rats was paralleled by reducing nuclear binding activity of the NF-κB, p38 phosphorylation, atrogin-1, mRNA levels, and 26S chymotrypsin-like proteasome activity. Taken together our data provide evidence for AET improving plantaris redox homeostasis in HF associated with a decreased NADPH oxidase, redox-sensitive proteins activation, and proteasome hyperactivity further preventing atrophy. These data reinforce the role of AET as an efficient therapy for muscle wasting in HF.NEW & NOTEWORTHY This study demonstrates, for the first time, the contribution of aerobic exercise training (AET) in decreasing muscle NADPH oxidase activity associated with reduced reactive oxygen species production and systemic inflammation, which diminish NF-κB overactivation, p38 phosphorylation, and ubiquitin proteasome system hyperactivity. These molecular changes counteract plantaris atrophy in trained myocardial infarction-induced heart failure rats. Our data provide new evidence into how AET may regulate protein degradation and thus prevent skeletal muscle atrophy.

Aerobic Exercise Training and Arterial Changes in African Americans versus Caucasians.

African Americans (AA) have increased carotid artery intima-media thickness and decreased vascular function compared with their Caucasian (CA) peers. Aerobic exercise prevents and potentially reverses arterial dysfunction. The purpose of this study was to examine the effect of 8 wk of moderate- to high-intensity aerobic training in young healthy sedentary AA and CA men and women. Sixty-four healthy volunteers (men, 28; women, 36) with mean age 24 yr underwent measures of arterial structure, function, and blood pressure (BP) variables at baseline, after the 4-wk control period, and 8 wk after training. There was a significant increase in VO2peak among both groups after exercise training. Brachial systolic BP decreased significantly after the control period in both groups but not after exercise training. Carotid pulse pressure decreased significantly in both groups after exercise training as compared with that in baseline. There was no change in any of the other BP variables. AA had higher intima-media thickness at baseline and after the control period but it significantly decreased after exercise training compared with that of CA. AA had significantly lower baseline forearm blood flow and reactive hyperemia compared with those of CA, but exercise training had no effect on these variables. There was no significant difference in arterial stiffness (central pulse wave velocity) and wave-reflection (augmentation index) between the two groups at any time point. This is the first study to show that 8 wk of aerobic exercise training causes significant improvement in the arterial structure in young, healthy AA, making it comparable with the CA and with minimal effects on BP variables.

Regulation of cardiac microRNAs induced by aerobic exercise training during heart failure

Exercise training (ET) has beneficial effects on the myocardium in heart failure (HF) patients and in animal models of induced cardiac hypertrophy and failure. We hypothesized that if microRNAs (miRNAs) respond to changes following cardiac stress, then myocardial profiling of these miRNAs may reveal cardio-protective mechanisms of aerobic ET in HF. We used ascending aortic stenosis (AS) inducing HF in Wistar rats. Controls were sham-operated animals. At 18 wk after surgery, rats with cardiac dysfunction were randomized to 10 wk of aerobic ET (HF-ET) or to a heart failure sedentary group (HF-S). ET attenuated cardiac remodeling as well as clinical and pathological signs of HF with maintenance of systolic and diastolic function when compared with that of the HF-S. Global miRNA expression profiling of the cardiac tissue revealed 53 miRNAs exclusively dysregulated in animals in the HF-ET, but only 11 miRNAs were exclusively dysregulated in the HF-S. Out of 23 miRNAs that were differentially regulated in both groups, 17 miRNAs exhibited particularly high increases in expression, including miR-598, miR-429, miR-224, miR-425, and miR-221. From the initial set of deregulated miRNAs, 14 miRNAs with validated targets expressed in cardiac tissue that respond robustly to ET in HF were used to construct miRNA-mRNA regulatory networks that revealed a set of 203 miRNA-target genes involved in programmed cell death, TGF-β signaling, cellular metabolic processes, cytokine signaling, and cell morphogenesis. Our findings reveal that ET attenuates cardiac abnormalities during HF by regulating cardiac miRNAs with a potential role in cardio-protective mechanisms through multiple effects on gene expression.

Improved arterial-ventricular coupling in metabolic syndrome after exercise training: a pilot study.

The metabolic syndrome (MetS) is associated with threefold increased risk of cardiovascular (CV) morbidity and mortality, which is partly due to a blunted CV reserve capacity, reflected by a reduced peak exercise left ventricular (LV) contractility and aerobic capacity and a blunted peak arterial-ventricular coupling. To date, no study has examined whether aerobic exercise training in MetS can reverse peak exercise CV dysfunction. Furthermore, examining how exercise training alters CV function in a group of individuals with MetS before the development of diabetes and/or overt CV disease can provide insights into whether some of the pathophysiological CV changes can be delayed/reversed, lowering their CV risk. The objective of this study was to examine the effects of 8 wk of aerobic exercise training in individuals with MetS on resting and peak exercise CV function. Twenty participants with MetS underwent either 8 wk of aerobic exercise training (MetS-ExT, n = 10) or remained sedentary (MetS-NonT, n = 10) during this period. Resting and peak exercise CV function was characterized using Doppler echocardiography and gas exchange. Exercise training did not alter resting LV diastolic or systolic function and arterial-ventricular coupling in MetS. In contrast, at peak exercise, an increase in LV contractility (40%, P < 0.01), cardiac output (28%, P < 0.05), and aerobic capacity (20%, P < 0.01), but a reduction in vascular resistance (30%, P < 0.05) and arterial-ventricular coupling (27%, P < 0.01), were noted in the MetS-ExT but not in the MetS-NonT group. Furthermore, an improvement in lifetime risk score was also noted in the MetS-ExT group. These findings have clinical importance because they provide insight that some of the pathophysiological changes associated with MetS can be improved and can lower the risk of CV disease.

Aerobic exercise training upregulates skeletal muscle calpain and ubiquitin-proteasome systems in healthy mice

Aerobic exercise training (AET) is an important mechanical stimulus that modulates skeletal muscle protein turnover, leading to structural rearrangement. Since the ubiquitin-proteasome system (UPS) and calpain system are major proteolytic pathways involved in protein turnover, we aimed to investigate the effects of intensity-controlled AET on the skeletal muscle UPS and calpain system and their association to training-induced structural adaptations. Long-lasting effects of AET were studied in C57BL/6J mice after 2 or 8 wk of AET. Plantaris cross-sectional area (CSA) and capillarization were assessed by myosin ATPase staining. mRNA and protein expression levels of main components of the UPS and calpain system were evaluated in plantaris by real-time PCR and Western immunoblotting, respectively. No proteolytic system activation was observed after 2 wk of AET. Eight weeks of AET resulted in improved running capacity, plantaris capillarization, and CSA. Muscle RING finger-1 mRNA expression was increased in 8-wk-trained mice. Accordingly, elevated 26S proteasome activity was observed in the 8-wk-trained group, without accumulation of ubiquitinated or carbonylated proteins. In addition, calpain abundance was increased by 8 wk of AET, whereas no difference was observed in its endogenous inhibitor calpastatin. Taken together, our findings indicate that skeletal muscle enhancements, as evidenced by increased running capacity, plantaris capillarization, and CSA, occurred in spite of the upregulated UPS and calpain system, suggesting that overactivation of skeletal muscle proteolytic systems is not restricted to atrophying states. Our data provide evidence for the contribution of the UPS and calpain system to metabolic turnover of myofibrillar proteins and skeletal muscle adaptations to AET.

Sixteen Weeks of Exercise Reduces C-Reactive Protein Levels in Young Women

Regular exercise has been shown to protect against breast cancer risk, and one possible mechanism is through a reduction in inflammation. The purpose of this study was to examine the effects of 16 wk of aerobic exercise training on adipokines and inflammatory markers in healthy young women. Participants were 319 sedentary women aged 18-30 yr, with body mass index of 18-40 kg · m, randomized to an exercise intervention or no exercise for approximately 16 wk. Adiponectin, leptin, C-reactive protein (CRP), and amyloid A (AA) were measured at baseline and after 16 wk. Adiponectin was measured by enzyme-linked immunosorbent assay, and AA, CRP, and leptin were measured by multiplex bead array assays. Exercise significantly decreased CRP levels in the exercise group compared with the control group (-1.41 mg · L in exercisers vs -0.005 mg · L in controls, P = 0.040), and this effect was largely driven by changes in CRP that occurred in the obese exercisers. There was no effect of exercise on levels of SAA, adiponectin, or leptin. There was also no effect of exercise on stress and depression scores. Neither change in percent body fat nor change in fitness influenced the effects of exercise on these inflammatory markers. This study demonstrated that a 16-wk aerobic exercise program significantly decreased levels of CRP in young women, especially in those who were obese. There was no evidence that this effect was mediated by changes in perceived stress, percent body fat, or fitness. These findings suggest that adopting an exercise routine early in life may decrease future risk of breast cancer and other chronic diseases in obese women.

Aerobic Exercise Training-Induced Decrease in Plasma Visfatin and Insulin Resistance in Obese Female Adolescents

The purpose of this study was to assess differences in the levels of plasma visfatin among female adolescents and changes in plasma visfatin and insulin resistance in obese female adolescents after 12 wk of aerobic exercise training. Twenty normal-weight female students (body-mass index [BMI] < 22.9 kg/m² and body fat ≤ 29.9) and 18 obese female students (BMI ≥ 25 kg/ m² and body fat ≥ 30%) participated in this study. Eleven obese students were assigned to an exercise group and completed a 12-wk aerobic exercise-training program that included four 40- to 50-min sessions per wk with an energy expenditure of 300-400 kcal/d. Seven obese students were assigned to a control group that received no exercise sessions or dietary restriction. The plasma visfatin levels of obese female adolescents were significantly higher (p < .05) than those of the normal-weight female adolescents. The plasma visfatin levels (294.00 ± 124.74 ng/ml to 185.55 ± 67.30 ng/ml, p < .01) and insulin resistance (p < .05) were significantly reduced after 12 wk of aerobic exercise. The results suggest that aerobic exercise resulting in an energy expenditure of 1,200-1,600 kcal/wk for 12 wk decreases plasma visfatin and insulin resistance in obese female adolescents.

Effects of aerobic exercise training on sympathetic and renal responses to mental stress in humans

The effects of aerobic exercise training (ET) on muscle sympathetic nerve activity (MSNA) and renal vascular responses to mental stress (MS) have not been determined in humans. We hypothesized that aerobic ET would reduce MSNA and renal vasoconstriction during MS. MSNA, mean arterial pressure (MAP), heart rate, renal blood flow velocity (RBFV), and peak oxygen uptake (V(O2peak)) were recorded in 23 healthy adults. Fourteen subjects participated in 8 wk of aerobic ET, while nine subjects served as sedentary controls (Con). ET significantly increased V(O2peak) (Delta18 +/- 1%; P < 0.001) and decreased RBFV at rest (60 +/- 4 to 48 +/- 3 cm/s; P < 0.01), whereas Con did not alter V(O2peak) or RBFV. ET did not alter resting MSNA (11 +/- 1 to 9 +/- 1 bursts/min) or MAP (84 +/- 2 to 83 +/- 2 mmHg), and these findings were similar in the Con group. MS elicited similar increases in MSNA (approximately Delta2 bursts/min; P < 0.05), MAP (approximately Delta15 mmHg; P < 0.001), and heart rate (approximately Delta20 beats/min; P < 0.001) before and after ET, and the responses were not different between ET and Con. Likewise, MS elicited similar decreases in RBFV and renal vascular conductance before and after ET, and the responses were not different between ET and Con. Perceived stress levels during MS were similar before and after the 8-wk study in both ET and Con. In conclusion, ET does not alter MSNA and renal vascular responses to MS in healthy humans.

Exercise and diet enhance fat oxidation and reduce insulin resistance in older obese adults

Older, obese, and sedentary individuals are at high risk of developing diabetes and cardiovascular disease. Exercise training improves metabolic anomalies associated with such diseases, but the effects of caloric restriction in addition to exercise in such a high-risk group are not known. Changes in body composition and metabolism during a lifestyle intervention were investigated in 23 older, obese men and women (aged 66 +/- 1 yr, body mass index 33.2 +/- 1.4 kg/m(2)) with impaired glucose tolerance. All volunteers undertook 12 wk of aerobic exercise training [5 days/wk for 60 min at 75% maximal oxygen consumption (Vo(2max))] with either normal caloric intake (eucaloric group, 1,901 +/- 277 kcal/day, n = 12) or a reduced-calorie diet (hypocaloric group, 1,307 +/- 70 kcal/day, n = 11), as dictated by nutritional counseling. Body composition (decreased fat mass; maintained fat-free mass), aerobic fitness (Vo(2max)), leptinemia, insulin sensitivity, and intramyocellular lipid accumulation (IMCL) in skeletal muscle improved in both groups (P < 0.05). Improvements in body composition, leptin, and basal fat oxidation were greater in the hypocaloric group. Following the intervention, there was a correlation between the increase in basal fat oxidation and the decrease in IMCL (r = -0.53, P = 0.04). In addition, basal fat oxidation was associated with circulating leptin after (r = 0.65, P = 0.0007) but not before the intervention (r = 0.05, P = 0.84). In conclusion, these data show that exercise training improves resting substrate oxidation and creates a metabolic milieu that appears to promote lipid utilization in skeletal muscle, thus facilitating a reversal of insulin resistance. We also demonstrate that leptin sensitivity is improved but that such a trend may rely on reducing caloric intake in addition to exercise training.

Aerobic Exercise Training Increases Skeletal Muscle Protein Turnover in Healthy Adults at Rest

The effect of a 4-wk aerobic exercise training program (30-45 min, 3-5 d/wk, >or=65% maximal heart rate) on mixed skeletal muscle protein fractional synthetic rate (FSR), fractional breakdown rate (FBR), and net protein balance (FSR - FBR) (NET) was examined in 8 healthy, previously unfit men and women [21.0+/- 0.4 y, 163.7+/- 4.4 cm, 75.6+/- 5.7 kg, 33.5+/- 4.1% body fat, VO(2 peak) 38.6+/- 2.3 mL/(kg.min)] fed eucaloric diets providing 0.85 g protein/(kg.d) for the 6-wk study. Measurements were made at baseline after 2 wk of diet intervention only, and after 4 wk of aerobic exercise training and diet intervention. Primed continuous infusions of ring-[(2)H(5)]-phenylalanine (2 micromol/kg; 0.05 micromol/(kg.min) and [(15)N]-phenylalanine (2 micromol/kg; 0.05 micromol/(kg.min) were used to assess skeletal muscle protein turnover at rest via the precursor-product method. Endurance training improved cardiovascular fitness, with a significant increase in VO(2 peak) (P<0.01) and a significant decrease in running time on a standard course (P<0.01). There were o significant changes in body mass or composition. There was a significant increase in FSR (0.077+/- 0.007 vs. 0.089+/- 0.006%/h, P<0.05) and decrease in NET (FSR - FBR) (-0.023 +/-0.004 vs. -0.072 +/- 0.012%/h, P < 0.05); FBR tended to increase (0.105+/- 0.014 vs. 0.143+/- 0.018%/h; P=0.06) after training. Findings show that aerobic training for 4 wk increases skeletal muscle protein turnover in previously unfit subjects.

Aerobic Exercise Training Decreases Leucine Oxidation at Rest in Healthy Adults

Both exercise and dietary protein intake affect whole-body protein turnover (WBPTO). Few studies have investigated the effect of aerobic exercise training on WBPTO [leucine rate of appearance (Ra), oxidation (Ox), and nonoxidative leucine disposal (NOLD)] in untrained individuals consuming a specified level of protein. This study examined the effect of aerobic exercise training on WBPTO in untrained men and women during a controlled diet intervention providing 0.88 g protein/(kg . d). After a 2-wk adaptation to the study diet, 7 subjects [3 men, 4 women; 76.1 +/- 5.8 kg, 164.7 +/- 4.4 cm, 30.7 +/- 4.5% body fat, 39.1 +/- 2.8 VO(2max) (maximal oxygen uptake) mL/(kg . min)] participated in 4 wk of aerobic exercise training (running and walking 4-5 times/wk at 65-85% maximal heart rate). WBPTO (determined via constant infusion of 1-[(13)C] leucine), nitrogen balance, and body composition were determined at baseline and after 4 wk of training. Nitrogen balance (-1.0 +/- 0.7 vs. 0.9 +/- 1.1 g N/24 h, P = 0.03) improved with exercise training, whereas body mass and composition did not change. Leucine Ra did not change, Ox decreased [18 +/- 2 to 15 +/- 2 micromol/(kg . h), P </= 0.001], and NOLD tended to increase [128 +/- 18 to 151 +/- 19 micromol/(kg . h), P = 0.09] in response to training. These data indicate improved protein utilization in response to exercise training in weight-stable subjects. This study emphasizes the importance of dietary control, with specific regard to energy and protein intakes, in the characterization of protein utilization in response to an exercise intervention.

Sequence variation in hypoxia-inducible factor 1alpha (HIF1A): association with maximal oxygen consumption.

Hypoxia-inducible factor 1 (HIF1) is a DNA transcription factor composed of two subunits, one of which is regulated by hypoxia (HIF1alpha, encoded by HIF1A). Genes regulated by HIF1 are involved in the processes of angiogenesis, erythropoiesis, and metabolism, making HIF1A a candidate gene in establishing maximal oxygen consumption (VO2 max) before and after aerobic exercise training. The purpose of the present study was to screen HIF1A for sequence variation and determine whether such variation is associated with VO2 max before and after aerobic exercise training. A total of 233 Caucasian and African-American subjects were available for screening of HIF1A and determination of allele frequencies, with 155 of those subjects used to study VO2 max in relation to identified variants. We measured VO2 max before and after 24 wk of aerobic exercise training. Screening revealed several rare and common polymorphisms in HIF1A with race-specific allele frequencies. African Americans with AT or TT genotype at the A-2500T locus exhibited significantly lower baseline VO2 max compared with those of AA genotype (21.9 +/- 0.99 vs. 25.1 +/- 1.0, P = 0.03). An age by P582S (C/T) genotype interaction was observed in Caucasian subjects, such that those of CT or TT genotype exhibited significantly lower change in VO2 max after training than those of CC genotype when compared at ages 65 and 60 yr, but not at age 55 yr. No other significant differences were noted among genotype groups at the A-2500T, P582S, or T+140C sites. Based on these findings, we conclude that HIF1A sequence variation is associated with VO2 max before and after aerobic exercise training in older humans.

Gender-dependent effects of exercise training on serum leptin levels in humans.

Leptin, the product of the ob gene, is elevated in obese humans and appears to be closely related to body fat content. The purpose of the present investigation was to determine the effect of aerobic exercise training on systemic leptin levels in humans. Eighteen sedentary middle-aged men (n = 9) and women (n = 9) who did not differ in aerobic capacity (29.4 +/- 1.2 vs. 27.5 +/- 1.2 ml x kg(-1) x min(-1)) or insulin sensitivity index (3.41 +/- 1.12 vs. 4.88 +/- 0.55) were studied. Fat mass was significantly lower in females vs. males (21.83 +/- 2.25 vs. 26.99 +/- 2.37 kg, P < 0.05). Despite this, fasting serum leptin was significantly higher in the females vs. males (18.27 +/- 2.55 vs. 9.88 +/- 1.26 ng/ml, P < 0.05). Serum leptin concentration decreased 17.5% in females (P < 0.05) after 12 wk of aerobic exercise training (4 day/wk, 30-45 min/day) but was not significantly reduced in males. Fat mass was not altered after training in either group. In contrast, both aerobic capacity (+13% males, +9.1% females) and insulin sensitivity (+35% males, +82% females) were significantly improved subsequent to training. These data suggest that 1) women have higher circulating leptin concentrations despite lower fat mass and 2) exercise training appears to have a greater effect on systemic leptin levels in females than in males.