Parasympathetic Neural Activity Accounts for the Lowering of Exercise Heart Rate at High Altitude

Boushel, Robert; Calbet, José A. L.; Rådegran, Göran; Söndergaard, Hans Peter; Wagner, Peter D.; Saltin, Bengt

doi:10.1161/hc4001.097040

Cited by 141 publications

(136 citation statements)

References 28 publications

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“…First, with the examination of our own criterion measure of vagal tone in this investigation, i.e., HR at low to moderate levels of activity, human sympathetic responses to dynamic exercise (muscle sympathetic nerve activity, norepinephrine, and epinephrine) begin to increase when HR approaches the level at which vagal withdrawal is nearly complete (5,23,42), indicating that modest levels of sympathetic activity are still present at lower intensities of exertion. Individual differences in physical conditioning may also have impact on the parasympathetic and sympathetic influences on HR at submaximal levels of exertion, although blockade studies suggest similar relations among healthy subjects whether they report regular exercise or not (e.g., 5, 23).…”

Section: Discussionmentioning

confidence: 99%

Respiratory sinus arrhythmia, cardiac vagal control, and daily activity

Grossman¹,

Wilhelm²,

Spoerle³

2004

American Journal of Physiology-Heart and Circulatory Physiology

150

125

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Grossman, P, F. H. Wilhelm, and M. Spoerle. Respiratory sinus arrhythmia, cardiac vagal control, and daily activity. Am J Physiol Heart Circ Physiol 287: H728 -H734, 2004. First published January 29, 2004 10.1152/ajpheart.00825.2003.-Ambulatory respiratory sinus arrhythmia (RSA) or high-frequency heart rate (HR) variability is frequently employed as an index of cardiac parasympathetic control and related to risk or severity of cardiovascular disease. However, laboratory studies indicate variations in physical activity and respiratory parameters of rate and tidal volume may confound estimation of vagal activity. Because little is known about these relations outside the laboratory, we examined ambulatory relations among RSA, respiration, physical activity, and HR during waking hours by employing a multichannel monitoring system. Forty healthy young-to-middle aged adults underwent daytime monitoring that included continuous registration of the ECG, respiration (inductance plethysmography), and accelerometry motion activity. Within-individual regression analyses were performed to examine minute-to-minute relations between RSA and respiration, HR, and indexes of physical activity (minute ventilation and motion). HR changes were assumed to be strongly related to within-individual variations of vagal tone. RSA adjusted for respiratory parameters and unadjusted RSA were compared for strength of prediction of other measures. Unadjusted RSA was related to respiratory parameters (R ϭ 0.80) and moderately predicted minute-tominute HR and activity variances (means ϭ 56%, HR; 48%, minute ventilation; and 37%, motion). Adjusted RSA predicted significantly more HR and activity variance (means ϭ 75%, 76%, and 57%, respectively) with narrower confidence intervals. We conclude that ambulatory RSA magnitude is associated with respiratory variations and physical activity. Adjustment for respiratory parameters substantially improves relations between RSA and significantly vagally mediated HR and physical activity. Concurrent monitoring of respiration and physical activity may enhance HR variability accuracy to predict autonomic control.high-frequency heart rate variability; respiration; autonomic control; ambulatory monitoring; metabolic activity RESPIRATORY SINUS ARRHYTHMIA (RSA), or high-frequency heart rate (HR) variability (HRV), is frequently employed as a measure of cardiac vagal tone under ambulatory conditions. Among both patients and healthy persons, ambulatory RSA measures are increasingly used to elucidate patterns of autonomic modulation of cardiovascular control and to index disease risk or severity (7,10,25,33).A number of human and animal studies confirm that HR changes during mild-to-moderate increase and decrease in physical activity are under parasympathetic control to a significant degree (5, 9, 11, 15, 23, 26, 34, 36, 40 -42, 52). Therefore, fluctuations in daily physical activity, which are typically moderate in magnitude (e.g., walking at slow to moderate pace), should importantly reflect variations in cardiac ...

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Section: Discussionmentioning

confidence: 99%

Respiratory sinus arrhythmia, cardiac vagal control, and daily activity

Grossman¹,

Wilhelm²,

Spoerle³

2004

American Journal of Physiology-Heart and Circulatory Physiology

150

125

View full text Add to dashboard Cite

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“…Acutely raising inspiratory PO 2 to sea level values increased work output and restored cardiac output. 12 These data indicate that enhanced parasympathetic neural activity accounts for the lowering of heart rate during exercise, whereas the reduction in cardiac output in hypoxia may be linked to the decreased maximum work capacity, ie, decreased signals from the skeletal muscle.…”

Section: Heart Ratementioning

confidence: 93%

Effect of Altitude on the Heart and the Lungs

2007

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T his review focuses on the effects of altitude exposure from 1 to several days or weeks as occurs in tourists, trekkers, and mountaineers who visit high altitude and normally reside near sea level. We briefly review the acute physiological adjustments and early acclimatization that occur in the cardiovascular system and the lungs of healthy individuals. These ensure life-sustaining oxygen delivery to the tissues despite a reduction in the partial pressure of inspired oxygen between 20% and 60% at 2500 and 8000 m, respectively. One of the acute adjustments, hypoxic pulmonary vasoconstriction (HPV), may be disadvantageous in those with a vigorous response and lead to 2 potentially lethal illnesses, high-altitude pulmonary edema (HAPE) and subacute mountain sickness (SAMS), which we present in more detail. Finally, on the basis of knowledge about the acute physiological adjustments and acclimatization and, when available, a review of the literature, we discuss the highaltitude tolerance of patients with coronary artery disease, congestive heart failure, arrhythmias, systemic hypertension, and pulmonary hypertension. Effects of Exposure to High Altitude on the Normal Cardiovascular System CirculationThe major effects of acute hypoxia on the heart and lung are shown in Figure 1. Hypoxia directly affects the vascular tone of the pulmonary and systemic resistance vessels and increases ventilation and sympathetic activity via stimulation of the peripheral chemoreceptors. 1 Interactions occur between the direct effects of hypoxia on blood vessels and the chemoreceptor-mediated responses in the systemic and pulmonary circulation. Unraveling the underlying mechanisms of the hypoxic vasodilatation of systemic arterioles is an active area of research. Several mechanisms appear to regulate local oxygen delivery according to the needs of the tissues 2,3 ; for instance, the release of ATP from red blood cells and the generation of NO by various ways appear to regulate local oxygen delivery according to the needs of the tissue. These mechanisms may decrease with prolonged stay at high altitude when oxygen content of the blood increases because of ventilatory acclimatization, an increase in hematocrit associated with plasma volume reduction, and an increase in red blood cell mass due to erythropoiesis.Peripheral chemoreceptor afferent activity rises hyperbolically as hypoxia increases. 4 Ventilation and sympathetic activity are augmented, as demonstrated by increased urinary and plasma concentration of catecholamines 5 and skeletal muscle sympathetic activity. 6 With exposure over days to weeks, the sensitivity of the peripheral chemoreceptors to hypoxia increases, leading to further enhancement of ventilation (ventilatory acclimatization). This presumably also accounts for the further increase of sympathetic activity documented by microneurography after 3 weeks at 5200 m 6 and elevated catecholamines in urine and plasma. 5 As shown in Figure 1, there is antagonism between the direct effects of hypoxia on the resistance vessels ...

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“…Cardiac output was measured by indocyanine (ICG, Akon Inc) dye dilution. 10 LBF was determined by the constant-infusion thermodilution technique. 11,12 Heart rate was obtained from the continuously recorded ECG signal.…”

Section: Methodsmentioning

confidence: 99%

Reductions in Systemic and Skeletal Muscle Blood Flow and Oxygen Delivery Limit Maximal Aerobic Capacity in Humans

2003

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Background-A classic, unresolved physiological question is whether central cardiorespiratory and/or local skeletal muscle circulatory factors limit maximal aerobic capacity (V O 2 max) in humans. Severe heat stress drastically reduces V O 2 max, but the mechanisms have never been studied. Methods and Results-To determine the main contributing factor that limits V O 2 max with and without heat stress, we measured hemodynamics in 8 healthy males performing intense upright cycling exercise until exhaustion starting with either high or normal skin and core temperatures (ϩ10°C and ϩ1°C). Heat stress reduced V O 2 max, 2-legged V O 2 , and time to fatigue by 0.4Ϯ0.1 L/min (8%), 0.5Ϯ0.2 L/min (11%), and 2.2Ϯ0.4 minutes (28%), respectively (all PϽ0.05), despite heart rate and core temperature reaching similar peak values. However, before exhaustion in both heat stress and normal conditions, cardiac output, leg blood flow, mean arterial pressure, and systemic and leg O 2 delivery declined significantly (all 5% to 11%, PϽ0.05), yet arterial O 2 content and leg vascular conductance remained unchanged. Despite increasing leg O 2 extraction, leg V O 2 declined 5% to 6% before exhaustion in both heat stress and normal conditions, accompanied by enhanced muscle lactate accumulation and ATP and creatine phosphate hydrolysis. Conclusions-These results demonstrate that in trained humans, severe heat stress reduces V O 2 max by accelerating the declines in cardiac output and mean arterial pressure that lead to decrements in exercising muscle blood flow, O 2 delivery, and O 2 uptake. Furthermore, the impaired systemic and skeletal muscle aerobic capacity that precedes fatigue with or without heat stress is largely related to the failure of the heart to maintain cardiac output and O 2 delivery to locomotive muscle. Key Words: hemodynamics Ⅲ blood flow, regional Ⅲ cardiac output Ⅲ hemodynamics Ⅲ heat stress D uring heavy exercise, large volumes of oxygen are transported through the links of the cardiorespiratory transport system to mitochondrial cytochromes for synthesis of ATP in the electron transport chain. The fastest rate at which the body can utilize O 2 during heavy exercise is defined as the maximum rate of oxygen uptake (V O 2 max), which is an index of maximal cardiovascular function, provided pulmonary function and ambient O 2 concentration are normal. 1 The working skeletal muscle cells, which account for more than 90% of the energy spent during severe exercise, largely determine V O 2 max. 1-4 Long-standing yet unresolved debates center on whether central cardiorespiratory and/or local skeletal muscle circulatory and metabolic factors limit V O 2 max. [1][2][3][4][5][6][7] Severe heat stress has been shown to markedly suppress V O 2 max and work capacity without altering the initial rate of rise in whole-body V O 2 . 8 The mechanisms underlying the compensatory adjustments to heat stress early in exercise and the subsequent precipitated fatigue have never been investigated. During heavy exercise in normal environments, f...

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Parasympathetic Neural Activity Accounts for the Lowering of Exercise Heart Rate at High Altitude

Cited by 141 publications

References 28 publications

Respiratory sinus arrhythmia, cardiac vagal control, and daily activity

Respiratory sinus arrhythmia, cardiac vagal control, and daily activity

Effect of Altitude on the Heart and the Lungs

Reductions in Systemic and Skeletal Muscle Blood Flow and Oxygen Delivery Limit Maximal Aerobic Capacity in Humans

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