Table 1.
Summary of exercise training studies of conduit and/or resistance vessel function in healthy humans and subjects with cardiovascular disease and risk factors
| Study | Methods | Exercise training | Effect of NO-mediated vasodilator function | NO improvement? |
|---|---|---|---|---|
| Normal subjects: | ||||
| Localized exercise | ||||
| Green et al. 1994 | Healthy young controls. VOP | Handgrip, 4 weeks, 3 × weekly | No difference in ACh, SNP or l-NMMA responses after training. Peak reactive hyperaemia improved | ↔ |
| Franke et al. 1998 | Young healthy subjects. VOP | Handgrip, 4 weeks, 3 × weekly | Response to exercise increased. No change in ACh + exercise responses | ↔ |
| Bank et al. 1998 | Controls for study of CHF patients. VOP | Handgrip, 30 min, 4–6 times/week | ACh improved after training. No change SNP | ↑ |
| Whole body exercise | ||||
| Kingwell et al. 1997b | Male sedentary 4 week cycle training. VOP | Cycling, 4 weeks, 3 × weekly, 30 min | Training ↑l-NMMA response at 2 μmol only. No difference ACh or SNP | ↔a |
| First suggestion that leg training improves forearm responses | ↑b | |||
| Bergholm et al. 1999 | Fit young males. VOP | Running. High intensity 4 × 1 h running session, weekly | ACh and l-NMMA ↓ after training. No change SNP. Effect may be due to ↓ antioxidant concentrations | ↓ |
| Clarkson et al. 1999 | Healthy army recruits Brachial D/U | Running, 10 weeks Daily 3 mile run + strength sessions High volume exercise | FMD increased from 2.2 to 3.9%. No change GTN | ↑ |
| Higashi et al. 1999a | Middle-aged controls for study of hypertensives. VOP | Walking, 30 mins, 5–7/week, 12 weeks | ACh response increased. No change in isosorbide dinitrate | ↑ |
| DeSouza et al. 2000 | Normal middle aged sedentary. VOP | Walking, 3 months home basedNo control group or period | Training improved ACh responses. No changes in SNP responses | ↑ |
| Maiorana et al. 2001b | Normals. Middle-aged. VOP | Circuit training, 8 weeks, 3 × week | No changes ACh or SNP or l-NMMA | ↔ |
| Goto et al. 2003 | Normal young males. VOP | Cycle exercise, 30 min, 5–7 × weekly, 12 weeks | Moderate intensity improved ACh responses. l-NMMA abolished this improvement | ↔c |
| 25%, 50% and 75% groups | No improvement in low or high intensity groups | |||
| Oxidant stress increased, high intensity group | ↑d | |||
| ↔e | ||||
| CHF | ||||
| Localized exercise | ||||
| Hornig et al. 1996 | Radial artery D/U | Handgrip, 4 weeks training, daily for 30 min | Training improved FMD, especially the l-NMMA sensitive component | ↑ |
| Katz et al. 1997 | VOP | Handgrip, 30 min daily, 8 weeks | Yes ACh ↑. GTN no change | ↑ |
| Bank et al. 1998 | VOP | Handgrip, 30 min, 4-6 times/weeks | No improvement in ACh responses after training. No change SNP | ↔ |
| Hambrecht et al. 2000b | Radial D/U | Handgrip, 6 × daily, 4 weeks | ACh dilatation increased, l-arginine potentiated the effect. No change in GTN | ↑ |
| Whole body exercise | ||||
| Hambrecht et al. 1998 | Doppler flow velocity + angiography of femoral artery | Cycle training, 6 months, 6 × day, 10 min, 80% HRmax | ACh mediated blood flow response increased. l-NMMA response also increased. No change GTN. | ↑ |
| Maiorana et al. 2000 | VOP. | Circuit training, 8 weeks, 3× week | ACh increased. SNP response also significantly improved. | ↑ |
| Linke et al. 2001 | Radial artery D/U. | 4 weeks cycle training, 6 × day, 10 min, 80% HRmax | Leg training improved ACh and FMD responses in the forearm. No change in GTN. | ↑ |
| CAD | ||||
| Whole body exercise | ||||
| Hambrecht et al. 2000c | Coronary bed. Flow wire/Doppler | Cycle training, 6 × day, 10 min, 4 weeks 80% HRmax | ACh responses and peak flow velocity improved. | ↑ |
| Gielen et al. 2003 | Coronary bed Intravascular ultrasound/angiography | Home based follow-up to above study | ACh responses improved, improved flow and velocity to ACh. No changes in response to GTN. | ↑ |
| Bicycle exercise, 20 min daily, 5 months | ||||
| Gokce et al. 2002b | Brachial and tibial D/U | Leg exercise, 40 min, 3x weekly, 10 weeks | FMD increased significantly in the tibial artery, with increase (NS) also in the brachial. No changes in GTN responses. | ↑ |
| Walsh et al. 2003a | Brachial D/U | Circuit training, 8 weeks, 3 × week | FMD improved. No change in GTN | ↑ |
| Hambrecht et al. 2003 | Coronary bed Intravascular ultrasound/angiography | Cycle or rowing, 3 × day, 10 min, 4 weeks | Peak flow velocity response to ACh increased eNOS expression and phosphorylation increased in coronary artery samples. | ↑ |
| Hypertensives | ||||
| Whole body exercise | ||||
| Higashi et al. 1999a | VOP | Walking, 30 mins, 5-7/week, 12 weeks | ACh increase sig in hypertensives. No difference isosorbide dinitrate LNNMA abolished training enhancement in ACh response. | ↑ |
| Higashi et al. 1999b | VOP | Walking, 30 mins, 5-7/week, 12 weeks | Max RHBF response increased only in hypertensives l-NMMA abolished thins enhancement | ↑ |
| Hypercholesterolaemia | ||||
| Whole body exercise | ||||
| Lewis et al. 1999 | Hyperchols not medicated. VOP | Cycle training, 4 weeks, 3 × 30 min/week | l-NMMA responses greater after training at 4 μmol. No effect of training on ACh or SNP responses | ↑f |
| Walsh et al. 2003b | Hyperchols on and off medication.VOP and Brachial D/U | Circuit training, 8 weeks, 3 × week | ACh and FMD responses improved in overall and in medicated subjects. No change SNP or GTN. l-NMMA improved in unmedicated subjects. | ↑h |
| Obesity | ||||
| Whole body exercise | ||||
| Sciacqua et al. 2003 | Adults. VOP | Walking, 30 min daily, 3 × weekly, 10–16 weeks | In those who lost weight: improved response to upper dose of AChNo change in SNP responses | ↑ |
| Watts et al. 2004a | Adolescents. Brachial D/U | Circuit training, 8 weeks, 3 × week | FMD increased. Improvement not related to change in adiposity | ↑ |
| Watts et al. 2004b | Children. Brachial D/U | Structured play/games, 1 h, 3 × week | FMD increased | ↑ |
| Woo et al. 2004 | Overweight children. Brachial D/U | Diet + exercise versus diet alone design | At 6 weeks, both group improved FMD | ↑ |
| Diabetes | ||||
| Whole body exercise | ||||
| Lavrencic et al. 2000 | Polymetabolic syndrome. Brachial D/U | Bicycle exercise, 3 × weekly, 12 weeks | FMD increased. No change in GTN responses | ↑ |
| Maiorana et al. 2001a | Type 2 diabetics. VOP and Brachial D/U | Circuit training, 8 weeks, 3 × week | ACh and FMD increased. No change in SNP or GTN | ↑ |
| Fuchsjager-Mayrl et al. 2002 | Type 1 diabetes. Brachial D/U | Cycle exercise, 1 h, 2–3× weekly, 4 months | FMD increased significantly. No significant change in GTN, despite trend | ↑ |
VOP, venous occlusion plethysmography; D/U, Doppler ultrasound arterial assessment; l-NMMA, NG-monomethyl-l-arginine: ACh, acetylcholine, an endothelium-dependent NO vasodilator; SNP, sodium nitroprusside, an endothelium-independent NO vasodilator; FMD, flow-mediated vasodilatation, an endothelium- and NO-dependent vasodilator stimulus; GTN, glyceryl trinitrate, an endothelium-independent vasodilator; CHF, chronic heart failure; CAD, coronary artery disease; ↑, improvement in NO vasodilator function; ↓, deterioration in NO vasodilator function; ↔, no change in NO vasodilator function. aStimulated function; bbasal function; clow intensity; dmoderate intensity; ehigh intensity; fbasal function; gstimulated function; hbasal function in unmedicated subjects; istimulated function in unmedicated subjects; jmedicated subjects.