Progenitor cells and age: can we fight aging with exercise?
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Adult Stem Cells↗
Biomedical subjects
James M Hagberg
Publications and source records attributed to James M Hagberg.
Reduction in midthigh low-density muscle with aerobic exercise training and weight loss impacts glucose tolerance in older men.
CONTEXT: Intramuscular lipid content increases with aging and obesity and is directly related to impaired glucose tolerance and insulin resistance. OBJECTIVE: Our purpose was to determine the effects of aerobic exercise training (AEX) with and without weight loss (WL) on midthigh low-density muscle (LDM; a measure of im lipid) and whether changes in LDM impact glucose tolerance in sedentary older men. DESIGN: Forty-six men (60.4 +/- 1.1 yr) completed 6 months of AEX (n = 34) or AEX + WL (n = 12) and had oral glucose tolerance tests (OGTTs) and computed tomography measures of LDM and regional abdominal and thigh fat depot areas. RESULTS: At baseline, LDM area directly correlated with fasting plasma glucose (FPG), 120-min glucose (G(120)), and glucose area under the curve (G(AUC)) during an OGTT (r = 0.44, r = 0.51, and r = 0.54, respectively, P < 0.01). After the interventions, the AEX + WL group had greater decreases in LDM (-13.5 vs. +1.3%, respectively), FPG (-8.3 vs. +2.1%, respectively), G(120) (-22.5 vs. -3.6%, respectively), and G(AUC) (-17.3 vs. - 3.1%, respectively) than the AEX group. In the entire sample, the decreases in LDM correlated with reductions in FPG, G(120), and G(AUC) during an OGTT (r = 0.31, r = 0.34, and r = 0.41, P < 0.05). Changes in other regional fat depots did not independently correlate with glucose tolerance or insulin responses. CONCLUSION: AEX + WL is more efficacious than AEX for reducing LDM and glucose tolerance. The improvement in glucose tolerance may be partially mediated by decreases in LDM in older men.
Blood Glucose↗
FABP2 Ala54Thr genotype is associated with glucoregulatory function and lipid oxidation after a high-fat meal in sedentary nondiabetic men and women.
BACKGROUND: A common functional missense mutation [Ala54Thr of the fatty acid-binding protein 2 gene (FABP2)] has previously been studied for associations with glucoregulation, postprandial lipemia, and lipid oxidation rates. However, most of those studies have not accounted for the interactive and potentially confounding effects of habitual physical activity and diet. OBJECTIVE: We tested the hypothesis that, in sedentary nondiabetic subjects following a low-fat diet, Thr54 FABP2 carriers have lower glucoregulatory function, greater postprandial lipemia, and greater lipid oxidation rates than do their Ala54 FABP2-homozygous counterparts. DESIGN: Men and women (n = 122) aged 50-75 y who were following a low-fat diet were genotyped and underwent oral-glucose-tolerance tests. A subgroup (n = 36) also underwent postprandial lipemia tests with lipid oxidation rate measurements. RESULTS: Thr54 carriers were less likely to have normal glucose tolerance (P = 0.05) and had higher fasting glucose concentrations (P = 0.003) than did Ala54 homozygotes. In Thr54 carriers, the insulin sensitivity index was lower (P = 0.02), and the fasting insulin and the oral-glucose-tolerance test insulin area under the curve were higher (P = 0.05 and 0.03, respectively) than in Ala54 homozygotes. FABP2 genotype was not associated with fasting or postprandial lipemia test triacylglycerol or free fatty acids (P > or = 0.22 for all), but postprandial lipid oxidation rates were higher (P = 0.01), which suggests that fat absorption is higher in Thr54 carriers than in Ala54 homozygotes. CONCLUSIONS: In sedentary nondiabetic persons following a low-fat diet, FABP2 Thr54 carriers have lower glucose tolerance and lower insulin action than do Ala54-homozygous persons. Furthermore, FABP Thr54 carriers have higher lipid oxidation rates, which may be the mechanism of glucoregulatory dysfunction.
Aged↗
Hemostatic response to postprandial lipemia before and after exercise training.
Chronic hypertriglyceridemia is thought to be atherogenic and is associated with an elevated thrombotic potential, both of which may be improved with aerobic exercise training. Eight subjects were tested for aerobic capacity, body composition, and postprandial lipemia (PPL), followed by 6 mo of exercise training and final testing. Blood samples were obtained for measurement of free fatty acid (FFA), triglycerides (TG), insulin (Ins), and glucose (Glu). Hemostatic variables including factor VII activity (FVIIa), tissue factor pathway inhibitor-factor Xa complex (TFPI/Xa), and plasminogen activator inhibitor-1 (PAI-1) antigen/activity as well as leukocyte tumor necrosis factor-alpha (TNF-alpha) gene expression were determined among four subjects. We found that the exercise training was of sufficient intensity to increase aerobic capacity (P < 0.0001) and improve body composition (P = 0.04). There were no differences between tests among PPL responses of FFA, TG, Ins, or Glu; however, the mean TG response and fat oxidation rate improved. PAI-1 antigen/activity, FVIIa, TFPI/Xa, and TNF-alpha gene expression were all improved after exercise training after adjusting for confounders. We conclude that aerobic exercise training reduces the potential for coagulation, improves fibrinolytic potential, and reduces leukocyte TNF-alpha gene expression after the ingestion of a high-fat meal.
Aged↗
C-reactive protein genotype affects exercise training-induced changes in insulin sensitivity.
An etiologic role for chronic inflammation in the development of insulin resistance has been hypothesized. We determined whether the -732A/G and +219G/A C-reactive protein (CRP) gene variants affect insulin and glucose measures and whether these variants affect training-related changes in insulin sensitivity and glucose measures. Men and women 50 to 75 years old (n = 61) underwent baseline testing that included glucose tolerance, maximal oxygen consumption, body composition, CRP levels, and genotyping assessments. Tests were repeated after 24 weeks of aerobic exercise training. In bivariate analyses, CRP -732A/G G allele carriers had significantly lower baseline postprandial plasma glucose and after-training CRP levels. After exercise training, the -732A/G G allele carriers had approximately 28% increase in insulin sensitivity index (ISI) and approximately 26% reduction in insulin area under the curve (AUC), compared with the approximately 7% increase in ISI and approximately 15% reduction in insulin AUC in the A allele homozygotes (P = .03). The significant enhancement of ISI in -732A/G G allele carriers remained evident in analyses limited to those with normal glucose tolerance. Multivariate analyses adjusted for demographic and biologic variables confirmed the significant enhancement of training-induced improvement in ISI by the CRP gene variant. In addition, the CRP -732A/G and +219G/A haplotype significantly associated with training-induced improvements in ISI and insulin AUC in separate multivariate models. In conclusion, the CRP -732A/G variant modulates exercise training-related improvements in ISI and glucose AUC, and the haplotype of the CRP -732A/G and +219G/A variants significantly affected training-induced changes in ISI and insulin AUC.
Aged↗
The human gene map for performance and health-related fitness phenotypes: the 2005 update.
The current review presents the 2005 update of the human gene map for physical performance and health-related fitness phenotypes. It is based on peer-reviewed papers published by the end of 2005. The genes and markers with evidence of association or linkage with a performance or fitness phenotype in sedentary or active people, in adaptation to acute exercise, or for training-induced changes are positioned on the genetic map of all autosomes and the X chromosome. Negative studies are reviewed, but a gene or locus must be supported by at least one positive study before being inserted on the map. By the end of 2000, in the early version of the gene map, 29 loci were depicted. In contrast, the 2005 human gene map for physical performance and health-related phenotypes includes 165 autosomal gene entries and QTL, plus five others on the X chromosome. Moreover, there are 17 mitochondrial genes in which sequence variants have been shown to influence relevant fitness and performance phenotypes. Thus, the map is growing in complexity. Unfortunately, progress is slow in the field of genetics of fitness and performance, primarily because the number of laboratories and scientists focused on the role of genes and sequence variations in exercise-related traits continues to be quite limited.
Anthropometry↗
Identification of a novel mutation combination in factor XIII deficiency: genetic update to the first reported case in the United States.
A 1967 report described the first known case of congenital factor XIII (FXIII) deficiency in the United States in a male patient with a severe hemorrhagic disorder. The patient's family presented no symptoms of the disorder, but the members were found to have half the normal FXIII activity. Although the molecular basis of the disorder could not be evaluated at the time, the results suggested an autosomal recessive inherited disorder. We sequenced all of the exons and the flanking regions in the genes for the FXIII A and B subunits of the patient, his family, and 18 unrelated individuals. We report the novel combination of an Arg-to-Cys mutation at codon 78 and a G-to-C mutation at the intron 5/exon 6 splice junction in the patient's FXIIIA gene. The missense-splice junction mutation combination appears to have caused the patient's FXIIIA deficiency, because the remaining family members, who present no symptoms and have no clinical diagnoses of FXIII deficiency, have one or the other of the 2 mutations but not both. Additionally, the 18 unrelated individuals are homozygous wild type at these loci. The molecular consequences of these mutations appear to be an abnormality in protein conformation or folding and/or a reduced production of messenger RNA transcripts of varying length that likely result in a nonfunctional, unstable FXIII protein.
Adult↗
Abdominal adiposity is a stronger predictor of insulin resistance than fitness among 50-95 year olds.
OBJECTIVE: Physical inactivity and increased adiposity contribute to insulin resistance; less is known, however, about the relative contributions of these factors in older adults. The aim of this study was to determine whether cardiovascular fitness, whole-body adiposity, or abdominal adiposity is the strongest predictor of insulin resistance into old age. RESEARCH DESIGN AND METHODS: Subjects included 407 men and women aged 50-95 years (means +/- SD 69 +/- 11 years). Insulin resistance was estimated using the insulin sensitivity index (ISI) of Matsuda and DeFronzo [ISI = 10,000/square root of (fasting glucose x fasting insulin) x (mean glucose x mean insulin during an oral glucose tolerance test); lower ISI = greater insulin resistance]. Fitness was determined with a treadmill maximal oxygen consumption (Vo(2max)) test. Whole-body adiposity measures included BMI and percent fat by dual-energy X-ray absorptiometry or hydrodensitometry; abdominal adiposity was estimated by waist circumference. RESULTS: Waist circumference was the strongest independent correlate of ISI (r = -0.52, P < 0.0001), explaining 28% of the variance when controlling for sex, BMI, percent fat, and Vo(2max). BMI (r = -0.45), percent fat (r = -0.40), and Vo(2max) (r = 0.22) independently predicted ISI (all P < 0.0001); however, after controlling for waist circumference, only Vo(2max) remained significant (r = 0.13, P = 0.009). CONCLUSIONS: Adiposity and fitness continue to be significant predictors of insulin sensitivity into old age, with abdominal obesity being the most important single factor. These findings support the measurement of waist circumference to assess health risk among older adults.
Abdominal Fat↗
DNA sequence variation in the promoter region of the VEGF gene impacts VEGF gene expression and maximal oxygen consumption.
In its role as an endothelial cell proliferation and migration factor, vascular endothelial growth factor (VEGF) can affect peripheral circulation and therefore impact maximal oxygen consumption (Vo2 max). Because of the role of VEGF, and because variation in the VEGF gene has the ability to alter VEGF gene expression and VEGF protein level, we hypothesized that VEGF gene polymorphisms are related to VEGF gene expression in human myoblasts and Vo2 max before and after aerobic exercise training. We analyzed the effects of the VEGF -2578/-1154/-634 promoter region haplotype on VEGF gene expression by using a luciferase reporter assay in cultured human myoblasts and found that the AAG and CGC haplotypes resulted in significantly higher hypoxia-stimulated VEGF gene expression than the AGG and CGG haplotypes. Consistent with these results, we found that individuals with at least one copy of the AAG or CGC haplotype had higher Vo2 max before and after aerobic exercise training than did subjects with only the AGG and/or CGG haplotype. In conclusion, we found that VEGF -2578/-1154/-634 haplotype impacts VEGF gene expression in human myoblasts and is associated with Vo2 max. These results have potential implications for aerobic exercise training and may prove relevant in the study of pathological conditions that can be affected by angiogenesis, such as coronary artery disease and peripheral artery disease.
Aged↗
Human gender differences in fibrinolytic responses to exercise training and their determinants.
Endurance exercise training improves fibrinolysis, but this training-induced adaptation may differ somewhat between men and women. We sought to determine whether the potential gender differences in training-induced changes in selected fibrinolysis measures were related to changes in adiposity and/or plasma lipoprotein lipid levels. Seventeen men and 28 women, 50-75 years old, who were generally overweight to obese, were assessed for plasminogen activator inhibitor-1 (PAI-1) and tissue plasminogen activator (t-PA) activity, t-PA antigen and plasma lipoprotein-lipid levels, and body composition before and after 6 months of endurance exercise training while on a low-fat diet. At baseline, there were no differences in fibrinolytic measures between the men and women. Baseline levels of these fibrinolytic markers in both men and women were primarily related to other fibrinolytic measures and body composition, with a smaller contribution from plasma high-density lipoprotein cholesterol (HDL-C) levels. Exercise training reduced t-PA antigen levels in both men and women, but the reduction was significantly greater in men (-1.6 +/- 0.3 versus -0.5 +/- 0.2 ng ml(-1), P = 0.007). Exercise training decreased PAI-1 activity more in men than in women (-2.6 +/- 1.4 versus +0.9 +/- 0.9 IU ml(-1), P = 0.03). Men and women both showed increased t-PA activity with exercise training to the same extent (+0.38 +/- 0.12 versus +0.36 +/- 0.24 U ml(-1)). The changes in fibrinolytic measures with exercise training in men and women were correlated with changes in other fibrinolytic measures, although in men abdominal fat changes were a strong predictor of fibrinolytic changes with training. These findings suggest that training-induced improvements in endogenous fibrinolysis markers are somewhat greater in men compared to women and may be more strongly associated with abdominal obesity in men.
Aged↗
NADPH oxidase p22phox gene variants are associated with systemic oxidative stress biomarker responses to exercise training.
Systemic oxidative stress plays a role in many degenerative diseases. Although regular physical activity has been known as the most effective nonpharmacological intervention to alleviate the oxidative stress, the beneficial effect varies between individuals. We investigated whether NADPH oxidase p22phox gene C242T and A640G polymorphisms are associated with systemic oxidative stress level response to exercise training (ExTr). Fifty-nine sedentary middle-aged to older Caucasians with relatively high cardiovascular disease risk factors underwent a 6-mo standardized ExTr program. Body mass index, plasma lipoprotein-lipid profiles, cardiovascular fitness, and plasma thiobarbituric acid reactive substances (TBARS) were measured before and after ExTr. Demographic and initial levels of cardiovascular disease risk factors were similar among genotype groups for both polymorphisms. Overall, TBARS was decreased by 16% with ExTr in the entire group (P < 0.001). There was no significant difference in TBARS changes with ExTr among the C242T genotype groups. However, A allele carriers showed greater reduction in TBARS than noncarriers at the A640G locus (P = 0.05). There was a significant interaction (P = 0.05) between ExTr and A640G polymorphism in TBARS changes with ExTr. This interaction remained after accounting for age and baseline TBARS level. Furthermore, diplotype analysis showed that TBARS was decreased to a greater extent in the C242/A640 haplotype carriers compared with the noncarriers (P < 0.05). We found that p22phox polymorphisms, especially A640G, were associated with differential changes in systemic oxidative stress with aerobic exercise training.
Aged↗
Vitamin D receptor FokI genotype influences bone mineral density response to strength training, but not aerobic training.
To determine the influence of the vitamin D receptor (VDR) gene FokI and BsmI genotype on bone mineral density response to two exercise training modalities, 206 healthy men and women (50-81 years old) were studied before and after approximately 5-6 months of either aerobic exercise training (AT) or strength training (ST). A totla of 123 subjects completed AT (51 men, 72 women) and 83 subjects completed ST (40 men, 43 women). DNA was extracted from blood samples of all subjects and genotyping was performed at the VDR FokI and BsmI locus to determine its association to training response. Total body, greater trochanter and femoral neck bone mineral density (BMD) were measured before and after both training programmes using dual-energy X-ray absorptiometry. VDR BsmI genotype was not significantly related to BMD at baseline or after ST or AT. However, VDR FokI genotype was significantly related to ST- but not AT-induced changes in femoral neck BMD (P < 0.05). The heterozygotes (Ff) in the ST group approached a significantly greater increase in femoral neck BMD (P = 0.058) compared to f homozygotes. There were no significant genotype relationships in the AT group. These data indicate that VDR FokI genotype may influence femoral neck BMD response to ST, but not AT.
Absorptiometry, Photon↗
Interleukin-6 genotype is associated with high-density lipoprotein cholesterol responses to exercise training.
BACKGROUND: High-density lipoprotein cholesterol (HDL-C) and its subfractions are modifiable with exercise training and these responses are heritable. The interleukin-6 (IL6)-174G/C polymorphism may be associated with HDL-C levels. We hypothesized that the IL6-174G/C polymorphism would be associated with plasma HDL-C response to exercise training. METHODS AND RESULTS: Sixty-five 50- to 75-year-olds on a standardized diet were studied before and after 24 weeks of aerobic exercise training. Significant differences existed among genotype groups for change with exercise training in HDL-C, HDL3-C, integrated HDL4,5NMR-C, and HDLsize. The CC genotype group increased HDL-C more than the GG (7.0 +/- 1.3 v. 1.0 +/- 1.1 mg/dL, p = 0.001) and GC groups (3.3 +/- 0.9 mg/dL, p = 0.02); for HDL3-C, the CC group increased more than the GG (6.1 +/- 1.0 v. 0.9 +/- 0.9, mg/dL p < 0.001) and GC groups (2.5 +/- 0.7 mg/dL, p = 0.006). Integrated HDL4,5NMR-C increased more in the CC than GG group (6.5 +/- 1.6 mg/dL v. 1.0 +/- 1.3 mg/dL, p = 0.01), as did HDLsize compared to the GG (CC: 0.3 +/- 0.1 v. GG: 0.1 +/- 0.1 nm, p = 0.02) and GC (0.0 +/- 0.0 nm, p = 0.007) groups. CONCLUSIONS: IL6 genotype is associated with HDL-C response to exercise training.
Aged↗
Endurance training-induced changes in the insulin response to oral glucose are associated with the peroxisome proliferator-activated receptor-gamma2 Pro12Ala genotype in men but not in women.
The present study sought to investigate, in sedentary men and women, (a) whether a common functional gene variant (peroxisome proliferator-activated receptor-gamma2 [PPARgamma2] Pro12Ala) predicts insulin action and (b) whether improvements in insulin action in response to endurance exercise training are associated with PPARgamma2 Pro12Ala. Sedentary, 50- to 75-year-old men and women (N = 73) were genotyped and underwent oral glucose tolerance tests (OGTTs) before and after 6 months of endurance training. At baseline, men heterozygous for the Pro12Ala variant had a greater OGTT insulin area under the curve (AUC) as compared with Pro12 homozygous men (P = .009). Endurance training resulted in a significantly greater improvement in insulin AUC in Pro12Ala heterozygous men as compared with Pro12 homozygous men (P = .003) despite no genotype-specific differences with respect to training-induced changes in body weight, body mass index, and percent body fat. No differences between genotype groups were present at baseline or in response to training in women. Training did not alter the OGTT glucose AUC for the group as a whole, and the baseline, final, and change in glucose AUC were not dependent on PPARgamma2 genotype and/or sex. In conclusion, these findings suggest that sedentary men with the PPARgamma2 Pro12Ala variant have lower insulin action on glucose disposal as compared with their counterparts. However, these men are particularly responsive with respect to the magnitude of endurance training-induced improvement in insulin action.
Aged↗
The human gene map for performance and health-related fitness phenotypes: the 2004 update.
We began this series in 2000 with the aim of making available in an easily accessible format all the advances on the genetic basis of a large family of exercise-related traits. The current review presents the 2004 update of the human gene map for physical performance and health-related fitness phenotypes. It is based on peer-reviewed papers published by the end of 2004. The genes and markers with evidence of association or linkage with a performance or fitness phenotype in sedentary or active people, in adaptation to acute exercise, or for training-induced changes are positioned on the genetic map of all autosomes and the X chromosome. Negative studies are reviewed but a gene or locus must be supported by at least one positive study before being inserted on the map. One new feature is that we have incorporated the genes whose sequence variants have been associated with either the level of physical activity or indicators of sedentarism. By the end of 2000, in the early version of the gene map, 29 loci were depicted. In contrast, the 2004 human gene map for physical performance and health-related phenotypes includes 140 autosomal gene entries and quantitative trait loci, plus four on the X chromosome. Moreover, there are 16 mitochondrial genes in which sequence variants have been shown to influence relevant fitness and performance phenotypes. Thus, the map is growing in complexity and progress is being made. The number of laboratories and scientists concerned by the role of genes and sequence variations in exercise-related traits is rising. But exercise science and sports medicine is generally lagging behind in terms of utilizing the advances in genetic and genomic technologies.
Anthropometry↗
C-reactive protein genotypes affect baseline, but not exercise training-induced changes, in C-reactive protein levels.
OBJECTIVE: The goal of this study is to determine whether C-reactive protein (CRP) gene variants affect baseline and training-induced changes in plasma CRP levels. METHODS AND RESULTS: Sixty-three sedentary men and women aged 50 to 75 years old underwent baseline testing (Vomax, body composition, CRP levels). They repeated these tests after 24 weeks of exercise training while on a low-fat diet. The CRP +219G/A variant significantly associated with CRP levels before and after training after accounting for the effects of demographic and biological variables. CRP -732A/G genotype was significantly related on a univariate basis to CRP levels after training. The CRP +29T/A variant did not affect CRP levels before or after training. In regression analyses, the +219 and -732 variants each had significant effects on CRP levels before and after training. Subjects homozygous for the common A/G -732/+219 haplotype exhibited the highest CRP levels, and having the rare allele at either site was associated with significantly lower CRP levels. CRP levels decreased significantly with training (-0.38+/-0.18 mg/L; P=0.03). However, none of the CRP variants was associated with the training-induced CRP changes. CONCLUSIONS: CRP +219G/A and -732A/G genotypes and haplotypes and exercise training appear to modulate CRP levels. However, training-induced CRP reductions appear to be independent of genotype at these loci.
Adenine↗
Influence of the interleukin-6 -174 G/C gene polymorphism on exercise training-induced changes in glucose tolerance indexes.
A polymorphism in the IL-6 gene, a G-to-C substitution 176 bp upstream of the ATG translation initiation site, has been associated with diabetes prevalence and insulin resistance. Interventions including exercise training are frequently used to modify cardiovascular disease risk factors. Consequently, this project examined associations between the IL-6 -174 genotype and oral glucose tolerance test outcomes in 50- to 75-yr-old sedentary men and postmenopausal women before and after aerobic exercise training. Among the 87 individuals who started the study, 56 were retested after 6 mo of aerobic exercise training. Subject characteristics at baseline did not differ between the IL-6 genotype groups with the exception of fasting glucose, which was higher (P = 0.02, covariates age, gender, and ethnicity) in the CC genotype group. The training-induced change in glucose area under the curve during the oral glucose tolerance test varied between the IL-6 -174 genotype groups (P = 0.05, covariates age, gender, ethnicity, baseline glucose area under the curve, and percent body fat change) with a significant decrease occurring only in the GG genotype group. Insulin outcomes did not differ among the groups at baseline or after training. Training-induced changes in weight, percent body fat, maximal oxygen consumption, fasting glucose, and an insulin sensitivity index also changed similarly among the genotype groups. In conclusion, fasting glucose and the extent to which glucose tolerance changes with exercise training may be influenced by the IL-6 -174 gene polymorphism.
Age Factors↗
Plasma nitrate/nitrite response to an oral glucose load and the effect of endurance training.
To assess the role of circulating nitric oxide (NO) production in glucose homeostasis, plasma nitrate/nitrite (NO(x)) was assessed during oral glucose tolerance tests (OGTTs) on 64 sedentary subjects and in a subset 40 subjects before and after 6 months of endurance exercise training. NO(x) decreased with the oral glucose load (P </=.001 for linear and quadratic effects). OGTT NO(x) response indices (NO(x) response area (NO(x) AREA), change in NO(x) from baseline to the minimum (DeltaNO(x)), and NO(x) time-to-minimum) were not associated with OGTT insulin or glucose areas under the curve (AUCs) or with insulin sensitivity index (ISI). Training did not alter NO(x) AREA, or DeltaNO(x), however, NO(x) time-to-minimum occurred later after training (P =.038). Training-induced insulin AUC and ISI changes were not associated with OGTT NO(x) index changes; however, glucose total AUC changes were associated with changes in NO(x) AREA (r =.42, P =.007) and DeltaNO(x) (r =.37, P =.019). In conclusion, these data suggest that circulating NO production is not involved in glycemic control after an oral glucose load in sedentary adults. In response to endurance training, however, it appears that the time required to reach minimum NO(x) levels after a glucose load is greater after training. Furthermore, although the magnitude of NO(x) response (as indicated by NO(x) AREA and DeltaNO(x)) to an oral glucose load does not appear to change with training for all individuals, individual training-induced changes in the NO(x) response magnitude are partly explained by training-induced changes in OGTT glucose responses.
Administration, Oral↗