Cardiovascular Response in Partly Mechanized Willow Planting Operations Indicates a Low to Moderate Intensity of Work

This study tested the hypothesis that pregnancy affects the cardiovascular responses to hypoxia by altering the outputs of the peripheral components of the stress system and independent of changes in P(a)CO(2). Comparison of cardiovascular and endocrine responses to acute isocapnic hypoxia between pregnant and non-pregnant ewes. Experimental laboratory. Fifteen pregnant (118 days of gestation; term is ca. 145 days) and 8 non-pregnant sheep. Chronically instrumented pregnant and non-pregnant ewes were subjected to 1 hour normoxia, 1 hour of acute systemic isocapnic hypoxia and 1 hour recovery. Arterial blood pressure, heart rate, femoral blood flow and femoral vascular conductance were recorded continuously throughout and arterial blood samples were taken during normoxia, hypoxia and recovery for the measurement of blood gas, metabolic and endocrine status. Basal blood pressure and blood glucose and lactate concentrations were lower in pregnant animals (P < 0.05). In contrast, basal cardiovascular variables and plasma concentrations of noradrenaline, adrenaline, neuropeptide Y, adrenocorticotropic hormone (ACTH) and cortisol were similar in pregnant and non-pregnant ewes. During hypoxia similar reductions in P(a)O(2) occurred in pregnant and non-pregnant animals, without alterations in P(a)CO(2) or pH(a). In non-pregnant ewes, acute hypoxia induced a transient increase in arterial pressure and sustained tachycardia without significant changes in femoral haemodynamics. Pregnancy attenuated the cardiovascular response, significantly diminishing the magnitude of the increment in heart rate throughout the hypoxic challenge (P < 0.001). However, hypoxia did not induce significant changes in blood metabolites or in plasma concentrations of any stress hormone measured in either pregnant or non-pregnant animals. Pregnancy not only affects basal but also stimulated cardiovascular function in the mother. The diminished chronotropic response to hypoxia in pregnancy is mediated via mechanisms independent of changes in P(a)CO(2) or in plasma concentrations of hormones or metabolites associated with activation of the stress system.

1. The cardiovascular responses to sustained hand-grip contractions at 20, 30 and 50% maximal voluntary contraction (MVC) were measured in subjects who were engaged in treadmill walking at three different rates with oxygen intakes of 1.1, 1.7 and 2.8l./min. The increments in heart rate and blood pressure at tensions of 20 and 30% MVC were similar at all rates of walking, but the response to a contraction at 50% MVC was lower at the hardest work rate than at the two easier rates.2. When two or more muscle groups contracted at the same relative tension, the increments in heart rate and blood pressure were the same, whether they contracted separately or together.3. When two or more muscle groups contracted simultaneously at different relative tensions, the increments in heart rate and blood pressure were the same as when the muscle group, at the higher relative tension, contracted separately at that tension.4. The blood flow to a muscle engaged in sustained contraction was increased when a second muscle group contracted at a higher relative tension.

OBJECTIVES Heart rate (HR) is a crucial health indicator and is also one of the health factors we need to pay explicit attention to. Body Mass Index (BMI) is considered a cofactor in heart-related issues like heart rate increment and recovery. Thus a study was conducted to determine the relationship between BMI and the rate of heart rate increment and recovery. METHODOLOGY 24 participants aged 17-20 were examined during elliptical machine training once a week continuously for three months. Their regular resting heart rate and change in heart rate during and after the elliptical workout were recorded and compared with BMI. RESULTS The HR increments were noted alongside BMI for male participants below BMI 21.13, and female participants below BMI 20.16. The heart rate increment tempo decreases alongside the increased BMI for both sexes afterwards. The heart rate recovery (HRrecovery) for male participants falls with the BMI increase to ~25 and increases thereafter. The female participants show a differing trend: HRrecovery rates increase following BMI growth till BMI ~ 20 and then decrease parabolically till the maximum BMI among female participants. The findings suggest no linear and non-significant correlation between BMI and heart rate increment or HRrecovery. The coefficient of determination is too tiny (R2 = 0.1395 for males and R2 = 0.003 for females) to indicate the causation between BMIs and HRrecovry. CONCLUSION This is the first study scrutinizing the role of body mass index on heart rate increment and heart rate recovery. Thus BMI should not be used as the cofactor or risk for heart activity or impaired functions.

Coronary artery disease is the leading cause of morbidity and mortality around the world. Autonomic nervous system abnormalities are associated with coronary artery disease and its complications. Exercise stress tests are routinely used for the detection of the presence of coronary artery disease. In this study, we observed the association between heart rate profile during exercise and the severity of coronary artery disease. One hundred and sixty patients with abnormal exercise treadmill test (> or =1 mm horizontal or downsloping ST-segment depression; 119 men, 41 women; mean age = 57 +/- 9 years) were included in the study. Use of any drug affecting heart rate was not permitted. Resting heart rate before exercise, maximum heart rate during exercise, and resting heart rate after exercise (5 min later) were measured and two parameters were calculated: heart rate increment (maximum heart rate - resting heart rate before exercise) and heart rate decrement (maximum heart rate - resting heart rate after exercise). All patients underwent selective coronary angiography and subclassified into two groups according to stenotic lesion severity. Group 1 had at least 50% of stenotic lesion and group 2 had less than 50%. Patients in the first group had increased resting heart rate, decreased maximum heart rate, decreased heart rate increment, and decreased heart rate decrement compared with second group. All patients were classified into tertiles of resting heart rate, heart rate increment, and heart rate decrement level to evaluate whether these parameters were associated with severity of coronary artery stenosis in the study. The multiple-adjusted odds ratio of the risk of severe coronary atherosclerosis was 21.888 (95% confidence interval 6.983-68.606) for the highest tertile of resting heart rate level compared with the lowest tertile. In addition, the multiple-adjusted odds ratio of the risk of severe coronary atherosclerosis was 20.987 (95% confidence interval 6.635-66.387) for the lowest tertile of heart rate increment level compared with the highest tertile and 2.360 (95% confidence interval 1.004-5.544) for the lowest tertile of heart rate decrement level compared with the highest tertile. Altered autonomic nervous system regulation affects heart rate profile, increased resting heart rate, decreased heart rate increment, and decreased heart rate decrement, during exercise and this effect is strongly and independently associated with the severity of coronary artery disease.

The psychophysiological responses to laboratory stressors are often examined because it is believed that such responses relate to responsiveness in real life situations. This belief has seldom been tested. The changes in heart rate, pulse transit time, and respiration rate produced by a variety of laboratory tasks (active and passive coping and physical exercise) were related to ambulatory measures of heart rate in 32 young men. The field measures were the difference in heart rate between the waking day and when asleep, and estimates of the variability of heart rate during the day, derived from time series analyses. Average changes in heart rate and pulse transit time during specific tasks did not relate consistently to heart rate in the field. However, an active coping index, derived from the ratio of the peak heart rate during an active coping task to the peak during physical exercise related to all the field measures of heart rate responsiveness. This index, which may relate to measures of additional heart rate and heightened sympathetic response to stress, also correlated positively with Trait Anxiety and elevated basal sympathetic arousal, as measured by skin conductance level. Measures of the cardiovascular response to a passive coping task, the cold pressor, and exercise did not relate to heart rate responses in the field. The findings suggest that heightened cardiac responsiveness in real life is exhibited by subjects who show elevated peak responses to active coping stressors specifically.

Background: Postural tachycardia syndrome (POTS) is defined as heart rate (HR) increments ≥30 bpm on head-up tilt (HUT) associate with orthostatic symptoms (lightheadedness, dizziness, palpitations, etc.). A large proportion of asymptomatic young adults naturally express excessive HR increments on HUT, which has raised questions regarding whether revision to the diagnostic criteria for POTS in younger patient populations is needed. In addition, poor adaptation to environmental stressors may contribute to the disability experienced by POTS patients. Objectives: 1) determine whether asymptomatic patients were predisposed to developing constitutional symptoms that could result in the full syndrome of POTS, and 2) determine whether these symptoms correlated to postural HR or orthostatic symptoms. Methods: HR response to HUT and orthostatic and constitutional symptoms in 30 asymptomatic POTS patients were evaluated after 1 year. Results: HR increment at follow-up demonstrated no correlation with general fatigue (r = 0.006), body vigilance (r = 0.195), physical (r = -0.087) and mental (r = -0.137) health, or orthostatic scores (r = 0.04). Orthostatic scores significantly correlated with general fatigue (r = 0.374) and body vigilance (r = 0.392) (p&lt;0.05). Conclusion: These data support that the majority of young individuals express benign orthostatic tachycardia and further argue for re-evaluation of the HR criteria for diagnosing POTS in younger populations.

Influence of heart rate on mortality among persons with hypertension: The Framingham Study

Stimuli that evoke pain stimulate the sympathetic nervous system leading to downstream vascular and hemodynamic adjustments. In clinical populations and older individuals, the perception of pain is associated with cardiovascular responses (e.g., heart rate, blood pressure, and arterial stiffness). However, there are extensive inter‐individual differences in the perception of pain, pain perception may be influenced by age, and it’s unclear if pain is associated with cardiovascular responses in younger adults.PURPOSETherefore, we sought to determine whether heart rate, blood pressure, and arterial stiffness responses to sympathoexcitatory stimuli were associated with perceived pain, in apparently healthy young adultsMETHODS17 young adults (21.6±3.9 yrs; BMI: 24.4±2.8 kg/m2;Mean±SD) participated in this investigation. Following 10‐min of supine rest, we measured heart rate (HR) and mean arterial pressure (MAP), via pulse wave analysis (PWA), and arterial stiffness via carotid‐femoral pulse wave velocity (cf‐PWV). Measures were obtained in duplicate then averaged for analysis. Participants then performed a 3‐min isometric handgrip exercise (HG) at 30% of maximum voluntary contraction, which was immediately followed by 3‐min of brachial cuff‐occlusion at 240mmHg. Perceived pain was assessed via visual analog scale (0‐10; 0=no pain, 10=most pain) at the first minute of each stimulus. HR and MAP were assessed at minute two and arterial stiffness was acquired in the final minute of each stimulus. Associations between perceived pain scores during HG and cuff‐occlusion with percent change in cardiovascular responses were assessed using Spearman’s correlations (α=0.05)RESULTSDuring HG, significant (P&lt;0.01) increases in HR (pre: 63±6 vs. post: 78±11 bpm; 23±15 %), MAP (pre: 86±9 vs. post: 105±14 mmHg; 22±10 %), and cf‐PWV (pre: 6.5±1.7 vs. post: 7.2±1.0 m/s; 13±26 %) were observed. During cuff‐occlusion, relative to pre, significant (P&lt;0.05) increases in MAP (post: 100±13 mmHg; 18±15%) and cf‐PWV (post: 7.2±1.4 m/s; 14±13%), but not (P&gt;0.05) HR (post: 64±7 bpm; 7±6%) were observed. Perceived pain during cuff‐occlusion (3.73±1.79 A.U.) was significantly greater (P=0.01) than during HG (1.88±1.20 A.U.). While no relationships were observed between perceived pain and cardiovascular responsiveness during HG (P&gt;0.05) with HR (r=0.28; P=0.28), BP (r=0.45; P=0.07), or cf‐PVW (r=0.28; P=0.28), perceived pain was associated with increases in BP (r=0.57; P=0.02) and cf‐PWV (r=0.55; P=0.02;), but not HR (r=0.19; P=0.47), during cuff‐occlusion.CONCLUSIONSWhile pain during HG was not associated with cardiovascular responses, significantly greater cuff‐occlusion evoked pain was associated with cardiovascular responsiveness. Our data suggests that the relation between perceived pain and cardiovascular responsiveness to sympathoexcitatory stimuli exists in younger adults, although additional data in larger cohorts and using varied stimuli are warranted.

The mechanism responsible for the attenuated heart rate (HR) response to exercise in patients with congestive heart failure (CHF) was investigated in 46 normal subjects and 59 patients with CHF stratified by peak exercise oxygen consumption (VO2). The peak exercise HR and the increment in HR from rest to peak exercise were decreased in CHF patients, and both correlated strongly with peak VO2 (r = 0.810, p less than 0.0001; r = 0.863, p less than 0.0001, respectively). Peak exercise norepinephrine level (NE) and the increment in NE from rest to peak exercise were not attenuated in CHF patients. Resting NE was elevated in CHF patients and correlated inversely with peak VO2 (r = -0.595, p less than 0.001). However, no significant correlation occurred between peak VO2 and either peak exercise NE or the exercise increment in NE. The ratio of the exercise increments in HR and NE, and indirect index of sinoatrial node sympathetic responsiveness, was markedly reduced in CHF patients and was inversely related to the severity of exercise impairment. Likewise, the HR response to a graded isoproterenol infusion was markedly reduced in CHF patients. Age-matching of normal subjects and CHF patients did not affect the foregoing observations. Infusion of CHF patients with the phosphodiesterase inhibitor milrinone caused a significant increase in the ratio of the exercise increments in HR and NE. These data strongly suggest that the attenuated HR response to exercise in CHF patients is due, at least in part, to postsynaptic desensitization of the beta-adrenergic receptor pathway.

The purposes of this study were to determine the role of the sympathetic and parasympathetic nervous systems in producing the heart rate (HR) response to dynamic exercise in rats and to determine the effect of attenuation of the HR response to exercise on blood flow redistribution. Sprague-Dawley rats (n = 10) were instrumented with arterial and venous catheters and Doppler flow probes. Mean arterial pressure (MAP), HR, mesenteric blood flow (MBF), and iliac blood flow (IBF) were determined during four exercise tests. On 4 consecutive days, rats were treated with saline (SAL, 1 mg/kg iv), atropine methyl nitrate (ATR, 2 mg/kg), timolol maleate (TIM, 0.5 mg/kg), and combined timolol and atropine. One minute of mild exercise (10 m/min) produced an increase in HR of 90 +/- 6 beats/min after SAL treatment, which was significantly less than the increment after ATR (56 +/- 5 beats/min) or TIM (4 +/- 3 beats/min). For the remainder of graded exercise, ATR treatment produced a modest attenuation in the increment in HR and no effect on MAP, IBF, and MBF. At 30 m/min, TIM markedly blunted the exercise-induced increment in HR (SAL, 138 +/- 8 beats/min; TIM, 53 +/- 4 beats/min) and IBF (SAL, 324 +/- 33%; TIM, 197 +/- 33%) with no effect on MAP or MBF. The results suggest that 1) the sympathetic nervous system is an important mediator of exercise-induced tachycardia in rats and 2) exercised-induced hyperemia, but not MAP, is attenuated by nonselective beta-blockade during exercise in rats.

Psychological disturbances, including anxiety and depression, are common during human pregnancy. Our objective was to determine whether these maternal disturbances influence cardiovascular responses of the offspring. The psychological status of 231 pregnant women was determined. Offspring (216) of these women were subsequently exposed to a video challenge stress when aged 7-9 years. Heart rate (HR) and blood pressure (BP) of the children were determined at rest, in response to video stress and during subsequent recovery. Children's resting and stress-induced increases in HR (bpm), systolic (SBP, mm Hg) and diastolic (DBP, mm Hg) BP were all greater in children whose mothers reported anxiety during pregnancy. Values (mean±s.d.) for resting HR, SBP and DBP were 75.15±5.87, 95.37±2.72 and 66.39±4.74 for children whose mothers reported no anxiety and an average of 81.62±6.71, 97.26±2.90 and 68.86±2.82 for children whose mothers reported anxiety at any level. Respective values for stress-induced increments in HR, SBP and DBP were 14.83.±2.14, 16.41±1.97 and 12.72±2.69 for children whose mothers reported no anxiety and 17.95±3.46, 18.74±2.46 and 14.86±2.02 for children whose mothers reported any level of anxiety. Effects of maternal depression were less consistent. The effects of maternal anxiety remained in multivariate analyses, which also included children's birth weight. The results indicate a long-term influence of maternal psychological status during pregnancy on the cardiovascular responses to stress among offspring. These effects may contribute to prenatal influences on subsequent health of the offspring.

Inappropriate response and magnitude of cardiovascular reactivity (CVR) to stress is a proposed mechanism through which environmental stressors are linked with poor cardiovascular health outcomes (Chida & Steptoe, 2010; Krantz & Manuck, 1984). Studies of reactivity to various laboratory tasks commonly control for factors known to influence CVR such as smoking, medication use, caffeine intake, and BMI; however, few have considered the influence of sleep on CVR. In order to determine whether sleep characteristics need to be assessed and considered in studies of CVR, this study aimed to examine the association between indices of sleep quality and the magnitude and patterning of CVR to an acute virtual stress task protocol. Fifty undergraduate participants were recruited to complete three nights of sleep measurement via actigraphy, followed by a virtual stress task during the daytime after the third night. The stress protocol involved both a mental arithmetic and Raven’s matrices task that were completed under time and accuracy pressure. Tasks were completed in counterbalanced order across participants to control for order effects, and CVR measures included heart rate (HR) and heart rate variability (HRV). It was hypothesized that decreases in total sleep time (TST) as well as decreases in sleep efficiency (SE; e.g., increased sleep disruption) would be significantly associated with increases in CVR to both stress tasks. Results did not reveal a significant association between CVR and three-day average as well as prior night measures of TST and SE. However, a significant association was observed between three-day wake after sleep onset (WASO) and measures of HR and HRV reactivity. Increased frequency of WASO was associated with both increased heart rate reactivity and decreased heart rate variability reactivity (less vagal reaction) to mental stress. Although no associations were observed between affective responses to the two tasks and any sleep parameter, decreased SE was associated with increased ratings of stressfulness to the Raven's task and decreased TST was associated with lower ratings of perseverance to the Raven's task. At least one parameter of sleep quality (i.e., WASO) was associated with cardiovascular reactions to mental stress in the current study and may influence risk for cardiovascular health as measured by CVR. Congruent with other studies examining the relation between sleep parameters and CVR, findings from the current study suggest that quality of sleep may be important to evaluate in future studies of CVR.

Previous research has produced mixed results regarding the relationship between sleep and cardiovascular reactivity to acute mental stress. This study aimed to re-analyze this relationship as well as test the relationship between sleep and stress-related changes in baroreflex function in order to further clarify the relationship between sleep and stress reactivity. Participants (N = 127, 84 female, mean age = 20.64, 78 White) completed a mental arithmetic stress task, while measures of heart rate (HR), blood pressure (BP), and baroreflex function were undertaken. Participants self-reported sleep duration, timing, efficiency, quality, latency, and wake after sleep onset the night prior to testing. Mental stress caused significant increases in HR and BP and significant decreases in baroreflex sensitivity and effectiveness (all p < 0.001). However, no statistically significant relationships were found between any measures of sleep and HR or BP reactivity (all p ≥ 0.05). Similarly, stress-induced changes in baroreflex function were not associated with any measures of sleep (all p ≥ 0.05). Results suggest that self-reported sleep is not related to cardiovascular or baroreflex reactivity to acute mental stress.

Office and out of office heart rate measurements: which clinical value?

A43 The effect of hydrocortisone on the growth of preterm infants on prolonged mechanical ventilation