Exercise and the Aging Endothelium

Table 1

Selected recent clinical trials (last 5 years) about the effects of exercise in elderly.

References	Patient groups and characteristics	Intervention and follow-up	Measured parameters	Outcome
[20]	(i) 57 subjects with a mean age of 65.6 ± 3.8 y divided to: (ii) Control placebo; (iii) Resistance training (RT); (iv) Vit C/E supplementation (VS); (v) RT + VS	(i) RT performed 3 times a week for 6 months.; (ii) Vit supplement was 1000 mg Vit C + Vit E 400 IU daily for 6 month	(i) Oxidative stress status and metabolic and lipid profile were determined at baseline and after 6 months.; (ii) Fat mass and fat-free mass measured by DXA; (iii) Muscle strength	After 6 months: (i) No difference in muscle strength; (ii) RT + VS had a positive effect on the plasma antioxidant profile but not on the prooxidant status
[21]	(i) 34 healthy, obese, older women (55–79 y old) with mild to moderate physical impairments divided to into the following groups for 24 weeks: (ii) Weight loss plus exercise (WL + E); (iii) Educational control	(i) WL + E was weight management sessions + 3 supervised exercise sessions/w; (ii) Educational group had monthly health lectures	(i) Body weight; (ii) Walk speed; (iii) Short physical performance battery (SPPB); (iv) Knee extension isokinetic strength	(i) WL + E lost more weight and walking speed increased significantly.; (ii) SPPB improved in both groups with significant differences between groups.
[22]	(i) Peripheral blood mononuclear cells (PBMC) from 25 young adult (18–33 y old) and 40 older subjects (50–76 y old)	(i) 2 months of aerobic exercise (brisk walking 6 days/w, 50 min/day, 70% of maximal HR)	(i) mRNA expression of NF-κB, receptor for AGEs; (ii) Proinflammatory cytokines including TNF-α, MCP-1, NADPH-oxidase, iNOS	(i) In older subjects VO2 max and exercise time were increased; (ii) Expression of proinflammatory genes was decreased
[23]	(i) 173 overweight or obese, postmenopausal, sedentary women randomized to: (ii) Aerobic exercise intervention; (iii) Stretching control group for 12 months.	(i) Exercise intervention was 60–75% of maximal HR for ≥ 45 min per day, 5 days/w	(i) F2-isoprostane, VO2 max, body weight, body fat percentage, waist circumference, intra-abdominal fat surface area	(i) VO2 max increased and body weight decreased in exercise group.; (ii) F2-isoprostane decreased in exercise group and increased in control group.
[24]	(i) Six older (71 ± 2 y) healthy men with mild hypertension	All subjects received the antioxidant cocktail and placebo in a double blind, balanced, crossover design and participated in the exercise protocol.	(i) Plasma free radical concentrations were verified via EPR spectroscopy; (ii) Endothelial function was evaluated via FMD	(i) Prior to training, acute antioxidant exposure did not change resting BP or FMD. Six weeks exercise reduced BP.; (ii) Antioxidant administration after exercise negated improvements.
[25]	Patients with IGT and CAD were randomly assigned to: (i) Exercise training (𝑛=13); (ii) Rosiglitazone (8 mg, 𝑛=11); (iii) Control group (𝑛=10)	Exercise training consisted of 6 × 15 min/d in the 1st week followed by 30 min/d submaximal ergometer for 3 weeks	(i) FBS, lipid profile, HbA1c; (ii) CRP, fibrinogen; (iii) BMI; (iv) FMD	(i) Triglycerides and uric acid decreased in exercise group; (ii) FBS, HbA1c, LDL, HDL, CRP, fibrinogen, and BMI did not differ between groups; (iii) In the exercise group, exercise capacity and FMD increased significantly
[26]	(i) 14 young subjects (25.7 ± 5.4 y); (ii) 13 older people (65.6 ± 10.7 y)	(i) 30 min of dynamic handgrip exercise at a moderate intensity	(i) Brachial artery diameter and blood flow were measured by Doppler ultrasound; (ii) vWF was measured before, immediately and 30 min after exercise	(i) The change in plasma vWF was linearly correlated with the increase in shear stress during exercise in older individuals, but not in the young subjects.
[27]	(i) EPCs from elderly (𝑛=25, 67.8 ± 3.38 years) and young men (𝑛=22, 26.3 ± 3.15 y)	(i) 12 weeks of physical exercise	(i) In vitro endothelial function and in vivo reendothelialization capacity of EPCs; (ii) Expression of CXCR4 and JAK-2 were measured	(i) In vitro function and in vivo reendothelialization capacity were reduced in elderly; (ii) Exercise increased CXCR4 protein expression and JAK-2 phosphorylation
[28]	(i) 11 middle-aged/older men; (ii) 15 postmenopausal women	(i) 8 weeks of brisk walking (6 days/w, 50 min/d)	(i) FMD	(i) FMD increased >50% in men but did not change in postmenopausal women
[29]	(i) 13 young men (27 ± 1 y); (ii) 15 older men (62 ± 2 y)	(i) 3-month aerobic exercise intervention in older subjects	(i) FBF was measured in response to ET-1 and selective (BQ-123) and nonselective (BQ-788) ET-1 inhibitors	(i) Vasoconstrictor response to ET-1 was blunted in older subjects; (ii) BQ-123 increase FBF in the older subjects; (iii) After 3-month exercise, vasoconstrictor responses to ET-1 increased in older people, while BQ-123 added modestly to this response
[30]	31 patients with type 2 diabetes and metabolic syndrome (mean age = 58 ± 6 years) were divided to: (i) High-intensity exercise (𝑛=10); (ii) Low-intensity exercise (𝑛=10); (iii) Controls (𝑛=11)	(i) 6 weeks of training	(i) Endothelial function examined by a high resolution ultrasound of the brachial artery, before and after 6 weeks training	(i) High intensity aerobic training improved endothelium dependent vasodilator response.
[31]	38 patients with type 2 diabetes divided to: (i) Exercise group (𝑛=21); (ii) Control (𝑛=17)	(i) Aerobic and resistance exercise for 3 months	(i) Endothelial function (FMD); (ii) Insulin resistance; (iii) Adipocytokines; (iv) Inflammatory markers; (v) Incidence of CVE after 24 months	(i) HbA1c decreased in both groups; (ii) FMD increased only in exercise group; (iii) Incidence of CVE was higher in control group
[32]	209 patients with recent AMI divided to; (i) Aerobic group (ET, 𝑛=52, 56 ± 6 y); (ii) Resistance training (RT, 𝑛=54, 57 ± 8 y); (iii) RT + ET (𝑁=53, 55 ± 9 y); (iv) No training (𝑛=50, 58 ± 7 y)	(i) 4 weeks of exercise training; (ii) 1 month of detraining	(i) Endothelial function (FMD); (ii) vWF	(i) FMD increased in all 3 exercise groups independently of the type of exercise; (ii) vWF decreased in all exercised groups; (iii) Detraining returned FMD to baseline.

CRP: C reactive protein, CVE: cardiovascular events, EPR: electron paramagnetic resonance, FBF: forearm blood flow, FMD: flow-mediated dilation, HDL: high-density lipoprotein, HR: heart rate, IU: international unit, LDL: low-density lipoproteins, MCP-1: monocyte chemoattractant protein-1, NADPH-oxidase: nicotinamide adenine dinucleotide phosphate-oxidase, vit: vitamin, VO₂ max= maximal oxygen consumption, vWF: von Willebrand factor, w: week, Y: years.