Effects of exercise intensity on clot microstructure and mechanical properties in healthy individuals.

BACKGROUND: Exercise is well established to lead to exercise-induced hypercoagulability, as demonstrated by kinetic coagulation markers. It remains unclear as to whether exercise-induces changes lead in clot development and increased polymerisation. Fractal dimension (df) has been shown to act as a marker of clot microstructure and mechanical properties, and may provide a more meaningful method of determining the relationship between exercise-induced hypercoagulability and potential clot development. METHODS: df was measured in 24 healthy individuals prior to, after 5min of submaximal exercise, following maximal exercise, 45min of passive recovery and following 60min of recovery. Results were compared with conventional markers of coagulation, fibrinolysis and SEM images. RESULTS: Significantly increased df was observed following exercise, returning to resting values following 60min of recovery. The relationship between df and mature clot microstructure was confirmed by SEM: higher df was associated with dense clots formed of smaller fibrin fibres immediately following exercise compared to at rest. Conventional markers of coagulation confirmed findings of previous studies. CONCLUSION: This study demonstrates that df is a sensitive technique which quantifies the structure and properties of blood clots following exercise. In healthy individuals, the haemostatic balance between coagulation and fibrinolysis is maintained in equilibrium following exercise. In individuals with underlying vascular damage who participate in exercise, this equilibrium may be displaced and lead to enhanced clot formation and a prothrombotic state. df may therefore have the potential to not only quantify hypercoagulability, but may also be useful in screening these individuals.

Changes in heart rate variability and QT variability during the first trimester of pregnancy.

The risk of new-onset arrhythmia during pregnancy is high, presumably relating to changes in both haemodynamic and cardiac autonomic function. The ability to non-invasively assess an individual's risk of developing arrhythmia during pregnancy would therefore be clinically significant. We aimed to quantify electrocardiographic temporal characteristics during the first trimester of pregnancy and to compare these with non-pregnant controls. Ninety-nine pregnant women and sixty-three non-pregnant women underwent non-invasive cardiovascular and haemodynamic assessment during a protocol consisting of various physiological states (postural manoeurvres, light exercise and metronomic breathing). Variables measured included stroke volume, cardiac output, heart rate, heart rate variability, QT and QT variability and QTVI (a measure of the variability of QT relative to that of RR). Heart rate (p < 0.0005, p < 0.0005, p < 0.0005) and cardiac output (p = 0.043, p < 0.0005, p < 0.0005) were greater in pregnant women in all physiological states (respectively for the supine position, light exercise and metronomic breathing state), whilst stroke volume was lower in pregnancy only during the supine position (p < 0.0005). QTe (Q wave onset to T wave end) and QTa (T wave apex) were significantly shortened (p < 0.05) and QTeVI and QTaVI were increased in pregnancy in all physiological states (p < 0.0005). QT variability (p < 0.002) was greater in pregnant women during the supine position, whilst heart rate variability was reduced in pregnancy in all states (p < 0.0005). Early pregnancy is associated with substantial changes in heart rate variability, reflecting a reduction in parasympathetic tone and an increase in sympathetic activity. QTVI shifted to a less favourable value, reflecting a greater than normal amount of QT variability. QTVI appears to be a useful method for quantifying changes in QT variability relative to RR (or heart rate) variability, being sensitive not only to physiological state but also to gestational age. We support the use of non-invasive markers of cardiac electrical variability to evaluate the risk of arrhythmic events in pregnancy, and we recommend the use of multiple physiological states during the assessment protocol.

Relationships between oxygen uptake, dynamic body acceleration and heart rate in humans.

AIM: Accurate estimation of energy expenditure (EE) is important in human and animal behavior analysis. Rate of oxygen consumption (VO2) reflects EE during aerobic metabolism but is not always convenient. Alternative methods include heart rate (HR) and overall dynamic body acceleration (ODBA). A favorable ODBA-VO2 relationship was recently reported but the strength of association between VO2, ODBA, HR and its variability (HRV) is less clear. METHOD: Fifteen young (23±4 years) healthy males of similar aerobic fitness (maximal oxygen uptake, VO2max=49.7±8.5 mL·kg(-1)·min(-1)) carried out progressive maximal exercise. ODBA, HRV and V̇O2 were recorded continuously. Relationships between ODBA, HRV and V̇O2 were explored using regression methods. RESULTS: VO2 was strongly related to ODBA and RR during walking (R=0.45,0.30; P<5x10(-5)) and running (R=0.60,0.38; P<5x10(-5)). HRV was related to VO2 during walking only (R=0.11-0.26; 0.005

Influence of long-term oxygen therapy on cardiac acceleration and deceleration capacity in hypoxic patients with chronic obstructive pulmonary disease.

BACKGROUND: There is increasing interest in cardiovascular co-morbidities of chronic obstructive pulmonary disease (COPD). Heart rate turbulence (HRT) and phase-rectified signal averaging (PRSA) techniques quantify the heart's acceleration/deceleration capacities. We postulated that these methods can help assess the integrity of cardiac control in hypoxic COPD. METHODS: Eight hypoxic stable COPD patients, nine healthy age-matched older adults and eight healthy young adults underwent ECG monitoring for 24 h. Patients with COPD were also monitored following 4 weeks of standardized oxygen therapy. HRT measures [turbulence onset (TO), turbulence slope (TS)] and PRSA-derived acceleration/deceleration (AC, DC) indices were quantified within 6-h blocks to assess circadian variation. RESULTS: There were between-group differences for variables TS, DC and AC (P<0·0005, η(2) = 0·54-0·65), attributable solely to differences between healthy young and COPD subjects. Only HR (P<0·0005) and DC index (P = 0·008) showed circadian variation. A significant interaction 'trend' effect for HR (F(9,87) = 2·52, P = 0·015, η(2) = 0·21) reflected the strong influence of COPD on HR circadian variation (afternoon and night values being different to those in healthy subjects). CONCLUSIONS: As expected, heart rate dynamics were substantially diminished in older (healthy and COPD) groups compared with healthy young controls. Patients with COPD showed similar heart rate dynamics compared with age-matched controls, both before and after hypoxia correction. However, there was a suggestion of diminished DC in COPD compared with age-matched controls (P = 0·059) that was absent following oxygen therapy. TS, DC and AC indices were altered by similar degrees in older subjects, apparently indicating equivalent tonic dysfunction of sympathetic/parasympathetic systems with ageing.