Assessment of running velocity at maximal oxygen uptake

The purpose of the study was to compare the cardiovascular, respiratory and metabolic responses to exercise of highly endurance trained subjects after 3 different nights i.e. a baseline night, a partial sleep deprivation of 3 h in the middle of the night and a 0.25-mg triazolam-induced sleep. Sleep-waking chronobiology and endurance performance capacity were taken into account in the choice of the subjects. Seven subjects exercised on a cycle ergometer for a 10-min warm-up, then for 20 min at a steady exercise intensity (equal to the intensity corresponding to 75% of the predetermined maximal oxygen consumption) followed by an increased intensity until exhaustion. The night with 3 h sleep loss was accompanied by a greater number of periods of wakefulness (P less than 0.01) and fewer periods of stage 2 sleep (P less than 0.05) compared with the results recorded during the baseline night. Triazolam-induced sleep led to an increase in stage 2 sleep (P less than 0.05), a decrease in wakefulness (P less than 0.05) and in stage 3 sleep (P less than 0.05). After partial sleep deprivation, there were statistically significant increases in heart rate (P less than 0.05) and ventilation (P less than 0.05) at submaximal exercise compared with results obtained after the baseline night. Both variables were also significantly enhanced at maximal exercise, while the peak oxygen consumption (VO2) dropped (P less than 0.05) even though the maximal sustained exercise intensity was not different.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cold-induced bradycardia in man during sleep in Arctic winter nights

Two young male Caucasians volunteered for a study on the effects of cold exposure during night sleep in winter in the Arctic. The 14-day experiment was divided in three consecutive periods, baseline (2 nights), cold exposure (10 night) and recovery (2 nights). Both baseline and recovery data were obtained in neutral thermal conditions in a laboratory. The subjects slept in a sleeping bag under an unheated tent during the cold exposure. Apart from polysomnographic and body temperature recordings, electrocardiograms were taken through a telemetric system for safety purposes. Heart rates were noted at 5-min intervals and averaged hourly. In both environmental conditions, heart rate decreased within the first two hours of sleep. Comparison of the data obtained during cold exposure vs. thermal neutrality revealed lower values of heart rate in the cold, while body temperatures remained within normal range. This cold-induced bradycardia supervening during night sleep is discussed in terms of the occurrence of a vagal reflex preventing central blood pressure to rise.     

Sustained maximal ventilation after endurance exercise in athletes

Although impaired respiratory muscle performance that persists up to 5 min after exercise is stopped has been demonstrated during exhaustive exercise in normal young men, it is not known whether impaired respiratory muscle function follows endurance exercise to exhaustion in highly trained athletes. To study the effects of exercise on sustained maximal voluntary ventilation immediately after exercise, eight elite cross-country skiers performed a 4-min maximal sustained ventilation (MSV) test before and immediately after exhaustive exercise. Subjects were encouraged to maintain maximal ventilation (VE) throughout the MSV test. To encourage greater effort, rapid visual feedback of VE was provided on a computer terminal along with a target VE based on their 12-s maximum voluntary ventilation (MVV). The subjects (7 males, 1 female) were 18.5 +/- 0.9 yr old (mean +/- SD) and exercised for 62.5 +/- 16.7 min at 77 +/- 5% of their maximum oxygen consumption during which average VE was 106.7 +/- 24.2 l/min BTPS. The mean MVV was 196.0 +/- 29.9 l/min or 107% of their age- and height-predicted MVV. Before exercise the MSV was 86% of the MVV or 176.7 +/- 30.5 l/min, whereas after exercise the MSV was 90% of the MVV or 180.3 +/- 28.9 l/min (P = NS). The total volume of gas expired during the 4-min MSV was 706.7 +/- 121.9 liters before and 721.2 +/- 115.5 liters after exercise (P = NS). In this group of athletes, exhaustive exercise produced no deleterious effects on the ability to perform a 4-min MSV test immediately after exercise.     

Masking of the circadian rhythms of heart rate and core temperature by the rest-activity cycle in man

Heart rate and core temperature are elevated by physical activity and reduced during rest and/or sleep. These masking effects may confound interpretation of rhythm waveforms, particularly in situations where the rest-activity rhythm has a different period from that of the core temperature rhythm. Such desynchronization often occurs temporarily as an individual adjusts to a new work shift or to a new time zone following rapid transmeridian travel, making it difficult to assess the impact of such schedule changes on the circadian system. The present experiments were designed to estimate the magnitude of these masking effects, by monitoring the heart rate, rectal temperature, and nondominant wrist activity (2-min samples) of 12 male subjects during 6 days of normal routine outside the lab and during 6 days of strict bedrest. Subjects also kept sleep, dietary, and exercise logs throughout the study. Average (20-min) waveforms were computed for each subject and each rhythm, at home and in bedrest. In addition, data were partitioned according to self-reported sleep and wake times and were analyzed separately for each state. Average waveform comparisons indicated that about 45% of the range of the circadian heart rate rhythm during normal routine was attributable to the masking effects of activity during wake, which also produced a 16% elevation in mean heart rate during wake and an 11% increase in mean heart rate overall. (Analysis of variance indicated that mean heart rate during sleep at home was not significantly different from the mean during sleep in bedrest.) On average, about 14% of the range of the circadian temperature rhythm during normal routine was attributable to the effects of activity masking. However, the change in range of the temperature rhythm, from home to bedrest, was very variable between subjects (-41% to +13%). This variability was not accounted for by age or by reported frequency of exercise at home. Normal activity during wake increased the mean temperature during wake by an average of 0.16 degrees C and the overall mean by about 0.12 degrees C. (Analysis of variance indicated that mean temperature during sleep at home was not significantly different from the mean during sleep in bedrest.) A 10-hr "night" (lights-off from 2200 to 0800 hr) was provided during bedrest, within which subjects could select their own sleep times. Times of sleep onset and wake onset were not significantly different between home and bedrest.(ABSTRACT TRUNCATED AT 400 WORDS)     

Prolonged decrease in cardiac volumes after maximal upright bicycle exercise

Sequential exercise-gated cardiac blood pool scintigrams provide a noninvasive technique for evaluating the effect of therapeutic interventions on cardiac volumes and function only if both exercise periods are equivalent in the absence of an intervention. To assess whether they are indeed equivalent, 14 healthy subjects underwent gated blood pool scintigraphy during two maximal upright exercise periods separated by 60 min without changing position. Although resting cardiac output and blood pressure returned to base-line values 60 min after the first exercise period, mean resting heart rate was markedly higher (89.4 +/- 2.7 vs. 66.5 +/- 2.5 beats/min, P less than 0.001) and upright cardiac volumes lower [39.1 +/- 4.9 vs. 56.3 +/- 6.0 ml, P less than 0.001, for end-systolic volume (ESV) and 112.6 +/- 8.0 vs. 144.9 +/- 9.0 ml, P less than 0.001, for end-diastolic volume (EDV)] than before the first exercise period. These differences persisted during low levels of the subsequent exercise but not at high and maximum work loads. Cardiac volumes and heart rate 60 min after an identical exercise protocol in a second group of 22 subjects who received propranolol, 0.15 mg/kg iv, after their initial exercise, however, were the same as those preexercise. Thus higher sympathetic tone may be responsible for the persistently higher heart rate and decreased cardiac volumes after exercise, and the assumption that cardiac volumes and function are similar during two closely spaced sequential exercise studies is not always valid.     

Exercise-induced and nitroglycerin-induced myocardial preconditioning improves hemodynamics in patients with angina

In humans, regional myocardial dysfunction during ischemia may be improved by ischemic and pharmacological preconditioning. We assessed the possibility that exercise- and nitroglycerin-induced myocardial preconditioning may improve global cardiac performance during subsequent efforts in patients with angina. Ten patients suffering from chronic stable angina and ten healthy volunteers were studied. Through impedance cardiography we assessed hemodynamics during a maximal exercise test, which was used as a baseline (Bas test) and considered as a preconditioning exercise. The Bas test was followed by a sequence of maximal efforts performed during the first (FWOP; 30 min after the Bas test) and second (SWOP; 48 h after the Bas test) windows of protection conferred by ischemic preconditioning. Hemodynamics was further evaluated during maximal exercise performed 48 h later with pharmacologically induced SWOP (PI-SWOP) obtained by transdermal administration of 10 mg of nitroglycerin. In the angina patients, FWOP, SWOP, and PI-SWOP delayed the time to ischemia and allowed them to achieve higher workloads compared with the Bas test. Furthermore, heart rate and cardiac output at peak exercise were enhanced during all the preconditioning phases with respect to the Bas test. However, only SWOP and PI-SWOP increased myocardial contractility and stroke volume. No changes in hemodynamics were detectable in the control subjects. This study demonstrates that in patients with stable angina, although hemodynamics during exercise can be positively improved during both FWOP and SWOP, differences exist between these two phases. Furthermore, the mimicking of exercise-induced SWOP by PI-SWOP with transdermal nitroglycerin may represent an important clinical aspect.     

Heart rate and plasma catecholamines during 24 h of everyday life in trained and untrained men.

Physical training decreases resting heart rate as well as heart rate and catecholamine responses to ordinary physical activity and mental stress. These effects have been speculated to diminish cardiac morbidity. However, the sparing of heartbeats and catecholamine production might be outweighed by exaggerated responses during training sessions. To elucidate this issue, heart rate was measured continuously and plasma catecholamine concentrations were measured frequently during 24 h of ordinary living conditions in seven endurance-trained athletes (T) and eight sedentary or untrained (UT) young males. T subjects had lower heart rates than UT subjects during sleep and during nontraining awake periods. However, because of the increase during training, the total 24-h heartbeat number did not differ between groups (107,737 +/- 3,819 for T vs. 113,249 +/- 6,879 for UT, P = 0.731). Neither during sleep nor during awake nontraining periods were catecholamine levels lower in T than in UT subjects. Peak catecholamine levels during exercise in T were much higher than peak levels in UT subjects, and 24-h average epinephrine and norepinephrine concentrations were twice as high. We concluded that in highly trained athletes the total number of heartbeats per day is not decreased and the catecholamine production is, in fact, increased.     

Cardiovascular control during voluntary static exercise in humans with tetraplegia.

The purpose of the present study was 1) to investigate whether an increase in heart rate (HR) at the onset of voluntary static arm exercise in tetraplegic subjects was similar to that of normal subjects and 2) to identify how the cardiovascular adaptation during static exercise was disturbed by sympathetic decentralization. Mean arterial blood pressure (MAP) and HR were noninvasively recorded during static arm exercise at 35% of maximal voluntary contraction in six tetraplegic subjects who had complete cervical spinal cord injury (C(6)-C(7)). Stroke volume (SV), cardiac output (CO), and total peripheral resistance (TPR) were estimated by using a Modelflow method simulating aortic input impedance from arterial blood pressure waveform. In tetraplegic subjects, the increase in HR at the onset of static exercise was blunted compared with age-matched control subjects, whereas the peak increase in HR at the end of exercise was similar between the two groups. CO increased during exercise with no or slight decrease in SV. MAP increased approximately one-third above the control pressor response but TPR did not rise at all throughout static exercise, indicating that the slight pressor response is determined by the increase in CO. We conclude that the cardiovascular adaptation during voluntary static arm exercise in tetraplegic subjects is mainly accomplished by increasing cardiac pump output according to the tachycardia, which is controlled by cardiac vagal outflow, and that sympathetic decentralization causes both absent peripheral vasoconstriction and a decreased capacity to increase HR, especially at the onset of exercise.     

Short-term exercise improves myocardial tolerance to in vivo ischemia-reperfusion in the rat.

These experiments examined the independent effects of short-term exercise and heat stress on myocardial responses during in vivo ischemia-reperfusion (I/R). Female Sprague-Dawley rats (4 mo old) were randomly assigned to one of four experimental groups: 1) control, 2) 3 consecutive days of treadmill exercise [60 min/day at 60-70% maximal O2 uptake (VO2 max)], 3) 5 consecutive days of treadmill exercise (60 min/day at 60-70% VO2 max), and 4) whole body heat stress (15 min at 42 degrees C). Twenty-four hours after heat stress or exercise, animals were anesthetized and mechanically ventilated, and the chest was opened by thoracotomy. Coronary occlusion was maintained for 30-min followed by a 30-min period of reperfusion. Compared with control, both heat-stressed animals and exercised animals (3 and 5 days) maintained higher (P < 0.05) left ventricular developed pressure (LVDP), maximum rate of left ventricular pressure development (+dP/dt), and maximum rate of left ventricular pressure decline (-dP/dt) at all measurement periods during both ischemia and reperfusion. No differences existed between heat-stressed and exercise groups in LVDP, +dP/dt, and -dP/dt at any time during ischemia or reperfusion. Both heat stress and exercise resulted in an increase (P < 0.05) in the relative levels of left ventricular heat shock protein 72 (HSP72). Furthermore, exercise (3 and 5 days) increased (P < 0.05) myocardial glutathione levels and manganese superoxide dismutase activity. These data indicate that 3-5 consecutive days of exercise improves myocardial contractile performance during in vivo I/R and that this exercise-induced myocardial protection is associated with an increase in both myocardial HSP72 and cardiac antioxidant defenses.     

Disturbance of sports performance after partial sleep deprivation

The changes in cardiac and ventilatory responses were measured in 7 endurance athletes during physical exercise on a bicycle ergometer, taking place after a control night and after a night with partial sleep deprivation in the middle of the night. The results show that, despite the maximal work load was not modified with control, heart rate, ventilation and VE/VO2 ratio (ERO2) were greater at the submaximal (75% of the VO2 max) and maximal work load and oxygen consumption decreased at maximal work, after the night of partial sleep deprivation as compared to the control. These findings suggest that acute sleep loss may contribute to alter the endurance performance by impairment of aerobic pathways.     

Diurnal variation in heart rate variability before and after maximal exercise testing

As heart-rate variability (HRV) is under evaluation in clinical applications, the authors sought to better define the interdependent impact of age, maximal exercise, and diurnal variation under physiologic conditions. The authors evaluated the diurnal changes in HRV 24-h pre- and post-maximal aerobic exercise testing to exhaustion in young (19-25 yrs, n?=?12) and middle-aged (40-55 yrs, n?=?12) adults. Subjects wore a portable 5-lead electrocardiogram holter for 48?h (24?h prior to and following a maximal aerobic capacity test). Time-, frequency-, time-frequency-, and scale-invariant-domain measures of HRV were computed from RR-interval data analyzed using a 5-min window size and a 2.5-min step size, resulting in a different set of outputs every 2.5?min. Results were averaged (mean?±?SE) over four prespecified time periods during the morning, afternoon, evening, and night on Day 1 and Day 2. Diurnal changes in HRV in young and middle-aged adults were compared using a two-way, repeated-measures analysis of variance (ANOVA). Young adults demonstrated higher HRV compared to middle-aged adults during periods of wakefulness and sleep prior to maximal exercise stress testing (i.e., high-frequency power during Day 1: young adults: morning 1862?±?496?ms(2), afternoon 1797?±?384?ms(2), evening 1908?±?431?ms(2), and night 3202?±?728?ms(2); middle-aged adults: morning 341?±?53?ms(2), afternoon 405?±?68?ms(2), evening 469?±?80?ms(2), and night 836?±?136?ms(2)) (p < .05). Exercise resulted in reductions in HRV such that multiple measures of HRV were not significantly different between age groups during the afternoon and evening periods. All measures of HRV demonstrated between-group differences overnight on Day 2 (p < .05). Young adults are associated with higher baseline HRV during the daytime. Sleep increases variability equally and proportionally to daytime variability. Given the higher baseline awake HRV and equal rise in HRV during sleep, the change in HRV from sleep to morning with exercise is greater in younger subjects. These physiologic results have clinical significance in understanding the pathophysiology of altered variability in ill patients.     

Acute alterations in stroke volume during exercise at 3,100 m altitude.

Following 3 weeks exposure to an altitude of 3,100 m, the cardiac output response to upright submaximal exercise was examined in 3 healthy subjects breathing ambient air and breathing 60% oxygen. The procedure allowed acute alteration of the 2 conditions within a single testing period of 30 min, 60% oxygen breathing either preceding or following breathing ambient air. Cardiac output was also measured in two of the subjects during maximal exercise under these two conditions. Administration of the high oxygen inspirate during exercise had little effect on the level of cardiac output but resulted in an immediate bradycardia and a dramatic increase of approximately 16% in stroke volume. Stroke volumes during maximal exercise were also increased by approximately 10% by the administration of high oxygen. It is suggested that the condition of decreases exercise stroke volume which develops with chronic exposure to altitude may be largely the result of diminished myocardial contractility stemming from a condition of myocardial hypoxia.     

Temperature sensitivity of the human cardiac pacemaker during exercise

The temperature sensitivity of the human cardiac pacemaker was investigated during exhaustive exercise. From graded runs to exhaustion, we established the relationship between maximum exercise heart rate (HRmax) and rectal temperature (Tr). After warm-up periods of varying intensity and duration, four male subjects completed 4 to 6 runs each, each run performed on a separate day. For every subject there was a strong linear correlation between HRmax and Tr (r = 0.79 to 0.96). Various measures of the temperature sensitivity were: linear sensitivity, 8.8 +/- 4.3 beats min-1.degrees C-1; Q10, 1.6 +/- 0.4 and the Arrhenius constant, mu, 35.9 +/- 16.6 kJ.mol-1. At HRmax the value for linear temperature sensitivity was similar to, but the values for Q10 and mu lower than, those observed previously for intrinsic heart rate. Sympathetic influence on the cardiac pacemaker during exercise may cause this reduction, by shifting the pacemaker location to cells with a lower temperature sensitivity, or by altering a rate-limiting step determining the diastolic pacemaker potential.     

Cardiovascular response to exercise in younger and older men

Measurements of cardiac performance for humans at various ages is influenced by the variable examined, the population and techniques employed, and the factors that co-vary with age, including the presence of disease and physical conditioning. Interstudy differences in the extent to which occult coronary disease is present in older subjects and in the level of physical conditioning among subjects may underlie the variable perspectives contained in the literature of how aging affects cardiovascular function. In carefully screened, highly motivated but not athletically trained community-dwelling subjects, resting cardiovascular parameters are not age related except for systolic blood pressure, which increases with age. During vigorous exercise the mechanisms used to achieve a high level of cardiac output shift from a dependence on a catecholamine-mediated increase in heart rate and inotropy to a dependence on the Frank Starling mechanism. One reason for the age difference in cardiovascular response to exercise may be a diminished responsiveness to beta-adrenergic stimulation in these subjects. In other elderly subjects who cannot exercise to high work loads, a decline in stroke volume as well as heart rate at peak exercise has been observed. Whether the inability of these individuals to augment stroke volume is caused by a decrease in the ability of the heart to increase diastolic filling, by a decrease in systolic pump function caused by an increased afterload, by intrinsic myocardial contractile defects, or by a greater diminution of the cardiovascular response to beta-adrenergic stimuli is presently unknown.     

Determination of cardiac output using ensemble-averaged impedance cardiograms

Although impedance cardiography provides safe and reliable noninvasive estimates of stroke volume in humans, its usefulness is limited by the necessity for subjects to be apneic and motionless. In an effort to circumvent this restriction we studied the validity of ensemble-averaging of impedance data in exercising normal subjects and in intensive-care patients. The correlation coefficient (r value) between 128 ensemble-averaged and standard hand-digitized determinations of stroke volume index from the same records taken during rest and exercise in six normal male subjects was +0.97 (P less than 0.001). The r value for ensemble-averaged stroke volume indices during free breathing and breath hold in the same subjects was +0.92 (P less than 0.001), suggesting that breath hold did not significantly affect the stroke volume estimation. In 14 freely breathing hospital intensive-care patients the r value between simultaneous thermodilution cardiac output readings and ensemble-averaged impedance determinations was +0.87 (P less than 0.01). The results indicate that ensemble-averaging of transthoracic impedance data provides waveforms from which reliable estimates of cardiac output can be made during normal respiration in healthy human subjects at rest and exercise and in critically ill patients.     

Comparison of exercise effects on the hemodynamics of the Bio 14.6 cardiomyopathic hamster.

1. Comparisons of the effects of 4 and 16 weeks of exercise were made on; cardiac output, stroke volume, heart rate, left intraventricular systolic and diastolic pressures, dP/dt, and heart calcium in the Bio 14.6 cardiomyopathic and F1 B hamsters. 2. In the cardiomyopathic hamster the cardiac output, stroke volume, left intraventricular systolic pressure and dP/dt, which were all depressed in the age related sedentary animals, were increased by both periods of exercise. The left intraventricular diastolic pressure which was elevated was likewise decreased by both exercise periods. Only the 16 week exercise period decreased the resting heart rate. 3. In the normal F1 B hamster, both periods of exercise increased the cardiac output and stroke volume while the left intraventricular systolic pressure was decreased. Only the 16 week exercise decreased the resting heart rate and left intraventricular diastolic pressure and increased the left ventricular dP/dt. 4. Both periods of exercise increased the total heart calcium in the Bio 14.6 hamster while the heart calcium in the F1 B was increased only by the 16 week exercise period.     

Elevated variance in heart rate during slow-wave sleep after late-night physical activity

This study investigates the effect of mild physical activity before bedtime on the sleep pattern and heart rate during the night. Nine healthy subjects underwent a habituation night, a reference night, and a physical induction night. The physical induction night did not alter the sleep pattern. Physical activity before bedtime resulted in higher heart rate variance during slow-wave sleep. The low-frequency/high-frequency component (LF/HF) ratio during slow-wave sleep in the physical induction night was significantly higher than during the reference night. Increased mean heart rate and higher LF/HF ratio are related to decreased parasympathetic dominance. Exercise up to 1 h before bedtime thus seems to modify the quality of sleep.     

Changes in the Cardiovascular Function in Healthy Subjects and Patients with Ischemic Heart Disease during Sleep

The purpose of this study was to investigate the autonomic regulation of the cardiovascular system during sleep in health and disease. The examination included 396 subjects: 29 healthy subjects and 367 patients with ischemic heart disease, of whom 149 had left-ventricular failure and 214 hypertension. Sleep quality and the presence of obstructive sleep apnea syndrome were evaluated by polysomnography; the character of autonomic regulation of cardiac rhythm and hemodynamics was determined by computerized testing during night sleep and an active orthostatic test immediately before and after sleep. The results permitted the authors to conclude that autonomic regulation may be restored to various degrees in health and disease, depending on the pathology level. The sleep quality influenced the restoration of hemodynamics more than that of the cardiac rhythm, mainly when obstructive sleep apnea syndrome was present.     

Thermoregulatory adjustments during continuous heat exposure

Body temperature regulation was studied in 6 male subjects during an acclimation procedure involving uninterrupted heat exposure for 5 successive days and nights in a hot dry environment (ambient temperature = 35 degrees C, dew-point temperature = 7 degrees C; air velocity = 0.2 m.s-1). Data were obtained at rest and during exercise (relative mechanical workload = 35% VO2max). At rest, hourly measurements were made of oesophageal and 4 local skin temperatures, to allow the calculation of mean skin temperature, and of body motility and heart rate. During the working periods these measurements were made at 5 min intervals. Hourly whole-body weight loss was measured at rest on a sensitive platform scale while in the working condition just before starting and immediately after completing the bicycle exercise. The results show that, in both exercise and at rest, the successive heat exposures increased the sweat gland output during the first 3 days. Afterwards, sweat rate decreased without any corresponding change in body temperature. For the fixed workload, the sweat rate decline was associated with a decrease in circulatory strain. Adjustments in both sweating and circulatory mechanisms occur in the first 3 days of continuous heat exposure. The overall sweat rate decline could involve a redistribution of the regional sweating rates which enhances the sweat gland activities of skin areas with maximal evaporative efficiencies.     

Daytime cardiac autonomic activity during one week of continuous night shift

Shift workers encounter an increased risk of cardiovascular disease compared to their day working counterparts. To explore this phenomenon, the effects of one week of simulated night shift on cardiac sympathetic (SNS) and parasympathetic (PNS) activity were assessed. Ten (5m; 5f) healthy subjects aged 18-29 years attended an adaptation and baseline night before commencing one week of night shift (2300-0700 h). Sleep was recorded using a standard polysomnogram and circadian phase was tracked using salivary melatonin data. During sleep, heart rate (HR), cardiac PNS activity (RMSSD) and cardiac SNS activity (pre-ejection period) were recorded. Night shift did not influence seep quality, but reduced sleep duration by a mean of 52 +/- 29 min. One week of night shift evoked a small chronic sleep debt of 5 h 14 +/- 56 min and a cumulative circadian phase delay of 5 h +/- 14 min. Night shift had no significant effect on mean HR, but mean cardiac SNS activity during sleep was consistently higher and mean cardiac PNS activity during sleep declined gradually across the week. These results suggest that shiftwork has direct and unfavourable effects on cardiac autonomic activity and that this might be one mechanism via which shiftwork increases the risk of cardiovascular disease. It is postulated that sleep loss could be one mediator of the association between shiftwork and cardiovascular health.