Repeated change-of-direction test for collegiate male soccer players.

AIM: The aim of the study was to investigate the applicability of a repeated change-of-direction (RCoD) test for NCAA Division-I male soccer players. METHODS: The RCoD test consisted of 5 diagonal direction changes per repetition with a soccer ball to be struck at the end. Each player performed 15 repetitions with approximately 10 seconds to jog back between repetitions. Data were collected in two sessions. In the first session, 13 players were examined for heart rate responses and blood lactate concentrations. In the second session, 22 players were examined for the test's ability to discriminate the primary from secondary players (78.0±16.1 and 10.4±13.3 minutes per match, respectively). RESULTS: Heart rate data were available only from 9 players due to artifacts. The peak heart rate (200.2±6.6 beats∙min-1: 99.9±3.0% maximum) and blood lactate concentration (14.8±2.4 mmol∙L-1 immediately after) resulted in approximately 3.5 and 6.4-fold increases from the resting values, respectively. These values appear comparable to those during intense periods of soccer matches. In addition, the average repetition time of the test was found to discriminate the primary (4.85±0.23 s) from the secondary players (5.10±0.24 s) (P=0.02). CONCLUSION: The RCoD test appears to induce physiological responses similar to intense periods of soccer matches with respect to heart rate and blood lactate concentration. Players with better average repetition times tend to be those who play major minutes.

Bone mineral density and content of collegiate throwers: influence of maximum strength.

AIM: Bone changes in size and density in response to different levels of stress. Alterations to bone mineral density (BMD) appear to occur in a site specific manner. Even though BMD has been examined in many populations there is a paucity of data looking at strength-power athletes, such as throwers. Therefore, the purpose of this study was to examine the BMD of a group of USA Division I collegiate throwers (e.g. shot put, discus, etc.). METHODS: Seven throwers (4 males; 3 females) who were 19.0 + or - 0.9 years had their BMD compared to an age matched control group (n = 14; 8 women and 6 men) and normative data. BMD was measured with dual X-ray absorptometry. Potential right/left side and sex difference in BMD were also examined. Maximal isometric strength was assessed using a mid-thigh pull while standing on a forceplate which generated force-time curves. Peak force (PF) and normalized peak force (PFa) were then correlated with BMDs. RESULTS: Generally, throwers had denser bones with male throwers tending to have a greater total BMD (P < or = 0.05). The dominant arm BMD was slightly greater when compared to non-dominant arm (P < or = 0.05). Furthermore, total body BMD was related to PF (r = 0.68, r(2) = 0.46) and PFa (r = 0.56, r(2) = 0.31). CONCLUSIONS: Throwers have greater BMDs than non-athletes and most other athletes. However, throwers only showed a small indication of sidedness. It is likely that the BMDs observed in this study stem from the training intervention (e.g. whole body heavy lifting) undertaken by this population.

Dietary supplementation with marine omega-3 fatty acids improve systemic large artery endothelial function in subjects with hypercholesterolemia.

OBJECTIVE: This work was undertaken to determine whether dietary supplementation with marine omega-3 fatty acids improve systemic large artery endothelial function in subjects with hypercholesterolemia. BACKGROUND: Marine omega-3 fatty acids improve vascular function, but the underlying mechanism(s) are unclear. We studied the effects of marine omega-3 fatty acids on large artery endothelial function in subjects with hypercholesterolemia. METHODS: Hypercholesterolemic subjects with no other known cause for endothelial dysfunction were recruited to a prospective, placebo-controlled, randomized, double-blind, parallel-group study. Treatment with omega-3 fatty acids at a dose of 4 g/day (n = 15/group) was compared with placebo, at the beginning (day 0) and end (day 120) of a four-month treatment period. Endothelial function was assessed pre- and posttreatment by noninvasive ultrasonic vessel wall tracking of brachial artery flow-mediated dilation (FMD). RESULTS: Treatment with marine omega-3 fatty acids resulted in a significant improvement in FMD (0.05 +/- 0.12 to 0.12 +/- 0.07 mm, p < 0.05) and a significant reduction in triglycerides (2.07 +/- 1.13 to 1.73 +/- 0.95 mmol/liter, p < 0.05), whereas treatment with placebo resulted in no change in FMD (0.03 +/- 0.10 to 0.04 +/- 0.10 mm) or triglycerides (2.29 +/- 2.09 to 2.05 +/- 1.36 mmol/liter) (both p < 0.05 treated compared with control). Responses to sublingual glyceryl trinitrate were unchanged. CONCLUSIONS: Marine omega-3 fatty acids improve large artery endothelium-dependent dilation in subjects with hypercholesterolemia without affecting endothelium-independent dilation.

Endothelial function is impaired in fit young adults of low birth weight.

OBJECTIVE: Non-insulin-dependent diabetes, hypertension and ischaemic heart disease, with insulin resistance, are associated with low birth weight (the 'Small Baby Syndrome'). Common to these adult clinical conditions is endothelial dysfunction. We tested the hypothesis that endothelial dysfunction could precede their development in those of low birth weight. METHODS: Endothelial function was measured by ultrasonic 'wall-tracking' of flow-related brachial artery dilatation in fit 19-20 year old subjects randomly selected (blind to the investigators throughout the study) from low (< 2.5 kg) and normal (3.0-3.8 kg) birth weight subjects in the 1975-7 cohort of the Cardiff Births Survey and with no known cause for endothelial dysfunction. RESULTS: Flow-related dilatation was impaired in low birth weight relative to normal birth weight subjects (median 0.04 mm [1.5%] [n = 22] cf. 0.11 mm [4.1%] [n = 17], p < 0.05; 0.04 mm [1.5%] [n = 15] cf. 0.12 mm [4.4%] [n = 12], p < 0.05 after exclusion of inadvertently included ever-smokers). CONCLUSION: The findings suggest that endothelial dysfunction is a consequence of foetal malnutrition, consistent with contributing to the clinical features of the 'Small Baby Syndrome' in later adult life.

Differences in pollinator effectiveness of birds and insects visiting Banksia menziesii (Proteaceae).

The effectiveness of nectarivorous birds, introduced honey bees and staphylined beetles as pollinators of Banksia menziesii was assessed. Staphylinids removed substantial amounts of pollen but did not deposit any onto stigmata. Abundance of beetles on inflorescences was related to the mean number of florets opening per day. Honey bees collecting pollen were more likely to effect pollination than those collecting nectar which only contacted stigmata when arriving or leaving an inflorescence. Nectar-foraging birds probed between florets 10.2±0.8 (±SE) times, contacting 8-16 stigmata during each probe. Bees visited inflorescences ten times more frequently than birds although they deposited only 25% of the pollen that birds did on stigmata. Fruit set was ten times greater on inflorescences visited by birds than on inflorescences visited by bees. Bees were capable of removing as much pollen as birds but, because of direct pollen transfer to birds when florets opened during foraging, actual removal was probably much less. Selection for floret opening during nectar foraging by birds may have resulted from pollen removal by non-pollinating animals, such as staphylinids.

Non-invasive measurement of pulse wave velocity using transputer-based analysis of Doppler flow audio signals.

A system for the measurement of arterial pulse wave velocity is described. A personal computer (PC) plug-in transputer board is used to process the audio signals from two pocket Doppler ultrasound units. The transputer is used to provide a set of bandpass digital filters on two channels. The times of excursion of power through thresholds in each filter are recorded and used to estimate the onset of systolic flow. The system does not require an additional spectrum analyser and can work in real time. The transputer architecture provides for easy integration into any wider physiological measurement system.

Real-time measurement of pulse wave velocity from arterial pressure waveforms.

Instrumentation for the real-time clinical measurement of pulse wave velocity (PWV) from intra-arterial pressure waveforms is presented. This time delay between pressure waveforms (obtained from two intra- arterial catheter-mounted transducers 5 cm apart) is calculated by a transputer using multiple comparisons between discrete sections of the waveforms. The method is validated by analysis of digital and analogue signals with known time delays and is used to measure changes in PWV in the right common iliac artery (RCIA) during infusions of acetylcholine (2.4, 24 and 240 micrograms ml-1) in six healthy subjects. The system measures the delay between digitally shifted triangular waveforms and pressure waveforms to a precision of about 50 microseconds, and it is superior to measurements performed by hand using a high-performance digital storage oscilloscope. When used to measure the effects of acetylcholine on the RCIA, dose-dependent reductions in PWV are recorded (-85%, -11.6%, -14.5%). It is concluded that the instrumentation enables PWV to be measured with high accuracy and precision in real time, if the pressure signals are of high fidelity and the relative amplification of the signals is carefully balanced.

The role of endothelial dysfunction in the pathophysiology of erectile dysfunction in diabetes and in determining response to treatment.

BACKGROUND: Erectile dysfunction (ED) in diabetes is related to autonomic neuropathy and endothelial dysfunction. We studied the relative importance of these factors in diabetic and non-diabetic men with ED and determined if they predict responses to treatment with sildenafil. METHODS: Thirty-three men, aged 35-65 years, with ED (20 diabetic, 13 non-diabetic), 15 of whom were sildenafil responders and 18 non-responders, were compared with 30 age and risk-matched control subjects (15 diabetic, 15 non-diabetic). Subjects with ED completed the International Index of Erectile Function (IIEF) questionnaire. Endothelial function was assessed by changes in brachio-radial and femoro-tibial arterial pulse-wave velocity (pulse-wave velocity) during reactive hyperaemia, expressed as percentage endothelium-dependent dilatation. Autonomic function was assessed by heart rate variation during expiration and inspiration (E/I ratio) and during the valsalva manoeuvre. RESULTS: The respective changes in pulse-wave velocity, in the arm and leg [mean (sd)] were 0.71 (6.5)% and 3.5 (6.4)% in the impotent diabetic men, 0.7 (7.6)% and 2.4 (5.9)% in the non-diabetic impotent men, -0.68 (5.7)% and -1.31 (7.2)% in the non-impotent diabetic men and 7.7 (3.7)% and 7.6 (3.4)% in the control subjects. There was a significant interaction between ED and diabetic status such that there was significantly impaired vascular response in the diabetic group (both with and without ED) and in the non-diabetic group with ED compared with the non-diabetic control group (P = 0.01 and P = 0.001 for brachio-radial and femoro-tibial measures, respectively). The E/I ratios of the diabetic men were significantly lower than those of the control subjects [1.17 (0.14) vs. 1.33 (0.16), P < 0.02), but there were no differences in the measures of autonomic neuropathy between the groups with ED and those with normal erectile function. Amongst diabetic men, the initial IIEF scores (maximum score 30, low score indicates more severe ED) were significantly higher in sildenafil-responders than non-responders [16.3 (8.4), vs. 6.8 (7 1), P < 0.02]. The rate of sildenafil response was not significantly affected by the measures of endothelial or autonomic function. CONCLUSIONS: ED in both diabetic and non-diabetic men is characterized by marked endothelial dysfunction in comparison with non-diabetic control subjects. Response to sildenafil is not predicted by either endothelial function or autonomic function, but in diabetic men appears to be related to the initial degree of erectile dysfunction.

Spontaneous closure of an acquired ventricular septal defect.

Ventricular septal defect (VSD) is a rare but serious complication of acute myocardial infarction requiring early surgical intervention. A patient with acquired VSD that spontaneously closed over three months is presented. The literature on spontaneous closure of acquired VSDs is also reviewed.

Arterial wave intensity and ventriculoarterial interaction.

Wave intensity analysis has been applied to the study of arterial hemodynamics. It is a measure of the power transported by waves as they propagate within the arteries and may provide quantitative information about both upstream and downstream conditions. This paper discusses the physical meaning of wave intensity, its measurement using invasive and noninvasive methods, and the effects of physical and pharmacological interventions.

Oral folate enhances endothelial function in hyperhomocysteinaemic subjects.

BACKGROUND: Elevated plasma homocysteine (Hcy) is a risk factor for vascular disease. A postulated mechanism is vascular endothelial damage by homocysteine. Hcy levels are inversely related to blood concentrations of folate and can be lowered by folate supplements. The effect of oral folic acid on endothelial function was investigated in healthy adults with mild hyperhomocysteinaemia. PATIENTS AND METHODS: Eighteen healthy subjects (Hcy > 13 micromol L-1 at entry), from a screening population of 890 volunteers, were entered into a randomised double-blind placebo-controlled crossover study of oral folic acid (5 mg daily for six weeks) with a six week interval between treatments. Flow-mediated (endothelium-dependent) and (endothelial-independent) glyceryl trinitrate (GTN)-mediated brachial artery dilatation were measured by high resolution wall tracking. RESULTS: Folate supplementation enhanced endothelium-dependent responses (+0.08 +/- 0.05 vs. +0.04 +/- 0.04 mm, P = 0.015) but endothelium-independent responses (GTN) were unchanged. Folate reduced Hcy (8.7 +/- 2.5 vs. 12.1 +/- 3.6 micromol L-1). CONCLUSION: High dose folic acid supplementation enhances endothelium-dependent vascular function and lowers plasma Hcy. This provides preliminary evidence that folate may have beneficial cardiovascular effects in adults with mild hyperhomocysteinaemia.

Endothelial control of arterial distensibility is impaired in chronic heart failure.

BACKGROUND: Vascular tone is a determinant of conduit artery distensibility. The aim of this study was to establish whether endothelium-derived relaxing factor (EDRF) influences the distensibility of conduit arteries and whether endothelium-mediated increases in distensibility are impaired in chronic heart failure (CHF). METHODS AND RESULTS: Conduit artery distensibility was measured by two methods in healthy subjects and in nine patients with CHF caused by dilated cardiomyopathy. In the first method, pulse-wave velocity (PWV) was measured in the right common iliac artery at rest and during local infusions of acetylcholine (10(-7) to 10(-5) mol/L) or adenosine (2 x 10(-7) to 2 x 10(-5) mol/L), with correction for systemic effects. Acetylcholine induced concentration-dependent local reductions of PWV in healthy subjects (-5%, -15%, and -26%) but not in CHF patients (3%, 1%, -4%, P < .01), whereas adenosine induced similar reductions of PWV in healthy subjects and CHF patients. In the second method, brachial artery diameter, blood flow, and blood pressure were measured noninvasively by high-resolution ultrasound, continuous-wave Doppler, and photoplethysmography during reactive hyperemia in the hand and after sublingual glyceryl trinitrate (GTN, 400 micrograms). Hyperemic flow, similar in healthy subjects and CHF patients, was associated with increases in diameter and distensibility in healthy subjects (8.8% and 18.4%, respectively) but not in CHF patients (0.3% and -4.5%), whereas GTN induced similar effects in healthy subjects and CHF patients. CONCLUSIONS: These data indicate that conduit artery distensibility is increased by acetylcholine and increased blood flow in healthy subjects but not in CHF patients, whereas the effects of adenosine and GTN on distensibility are preserved in CHF patients. This implies that EDRF-mediated increases in distensibility are impaired in CHF patients, thus adding to cardiac work.

Flosequinan in chronic heart failure: how is exercise capacity improved?

OBJECTIVE: Diuretics, angiotensin converting enzyme inhibitors and digoxin have become "standard" triple therapy for many patients with chronic cardiac failure. Flosequinan increases exercise duration and improves symptoms when added to standard triple therapy. Despite intensive study, the clinical pharmacology of flosequinan remains uncertain. SETTING: The University Hospital of Wales, a Regional Cardiac Centre. PATIENTS: Twenty four patients with chronic heart failure who remained symptomatic despite standard therapy including ACE inhibitors. METHODS: A double-blind placebo-controlled parallel group study of 100 mg daily of flosequinan. We measured changes in exercise duration using cardiorespiratory exercise testing and changes in large artery distensibility using Doppler ultrasound. RESULTS: Exercise duration after 8 weeks flosequinan treatment was significantly greater than following placebo treatment. The flosequinan-related increase in exercise duration (+14%) was associated with a significant reduction in VE/VCO2 slope (-16%). Brachial-radial pulse wave velocities were unaltered by flosequinan treatment. CONCLUSIONS: Our results confirm that flosequinan improves exercise duration in patients with chronic heart failure. They suggest that this observed beneficial effect is independent of any change in large artery distensibility and that in the presence of ACE inhibitors, this improvement may be independent of any vasodilating action of flosequinan. Although this study confirms the beneficial symptomatic effects of flosequinan in chronic cardiac failure, clinical trials have subsequently demonstrated an overall increase in mortality in patients treated with 100 mg flosequinan daily. This has resulted in the withdrawal of flosequinan from routine clinical use.

Endothelial function in Marfan syndrome: selective impairment of flow-mediated vasodilation.

BACKGROUND: The cardiovascular complications of Marfan syndrome arise due to alterations in the structural and functional properties of fibrillin, a constituent of vascular connective tissues. Fibrillin-containing microfibrils are closely associated with arterial endothelial cells, indicating a possible functional role for fibrillin in the endothelium. Plasma concentrations of endothelial cell products are elevated in Marfan subjects, which indirectly indicates endothelial dysfunction. This study directly assessed flow- and agonist-mediated endothelium-dependent brachial artery reactivity in Marfan subjects. METHODS AND RESULTS: In 20 Marfan and 20 control subjects, brachial artery diameter, blood flow, and blood pressure were measured by ultrasonic wall tracking, Doppler ultrasound, and photoplethysmography, respectively. Measurements were taken during hand hyperemia (a stimulus for endothelium-derived nitric oxide [NO] release in the upstream brachial artery) and after sublingual administration of the endothelium-independent vasodilator nitroglycerin. In 9 Marfan and 6 control subjects, the above parameters were also assessed during intra-arterial infusions of acetylcholine and bradykinin (agonists that stimulate NO production) and NG-monomethyl-L-arginine (L-NMMA, an inhibitor of NO production). Flow-mediated responses differed markedly between Marfan and control subjects (-1.6+/-3.5% versus 6. 50+/-4.1%, respectively; P<0.0001), whereas nitroglycerin produced similar vasodilation (14.2+/-5.7% versus 15.2+/-7.8%; P=NS). Agonist-induced vasodilation to incremental intra-arterial infusions of acetylcholine and bradykinin were not significantly different between Marfan and control subjects, and intra-arterial L-NMMA produced similar reductions in brachial artery diameter in both groups. CONCLUSIONS: These data demonstrate impaired flow-mediated but preserved agonist-mediated endothelium-dependent vasodilation in Marfan subjects and suggest preservation of basal NO release. Selective loss of flow-mediated dilation suggests a role for fibrillin in endothelial cell mechanotransduction.

Hyperhomocysteinemia after an oral methionine load acutely impairs endothelial function in healthy adults.

BACKGROUND: Elevated plasma homocysteine is a risk factor for arteriosclerosis, but a cause-and-effect relationship remains to be fully established. Endothelial dysfunction, an early event in the atherogenic process, has been shown to be associated with hyperhomocysteinemia in experimental and human studies. To further establish a direct relationship between changes in plasma homocysteine and endothelial dysfunction, we investigated whether moderate hyperhomocysteinemia induced by an oral methionine load would acutely impair flow-mediated endothelium-dependent vasodilatation in healthy adults. METHODS AND RESULTS: Twenty-four healthy volunteers completed a randomized crossover study in which an oral methionine load (0.1 g/kg) was administered on 1 of 2 study days, 7 days apart. At each visit, plasma homocysteine and brachial artery endothelium-dependent and -independent dilatation were measured at baseline and at 4 hours. To further elucidate the temporal relationship between methionine, homocysteine, and endothelial function, an oral methionine load was administered in 10 subjects on a separate visit, and the time courses of plasma methionine, homocysteine, and flow-mediated brachial artery dilatation were measured at baseline and after 1, 2, 3, 4, and 8 hours. After oral methionine, plasma homocysteine increased from 7. 9+/-2.0 micromol/L at baseline to 23.1+/-5.4 micromol/L at 4 hours (P<0.0001, n=24) and was associated with a decrease in flow-mediated brachial artery dilatation from 0.12+/-0.09 to 0.06+/-0.09 mm (P<0. 05). The time course of the impairment of flow-mediated vasodilatation mirrored the time course of the increase in homocysteine concentration. CONCLUSIONS: Oral methionine loading raises plasma homocysteine and impairs flow-mediated endothelium-dependent vasodilatation. This supports the view that homocysteine may promote vascular disease by inducing endothelial dysfunction.