| 1. |
- Linnarsson, D, et al.
(författare)
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Baroreflex impairment during rapid posture changes at rest and exercise after 120 days of bed rest.
- 2006
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Ingår i: European Journal of Applied Physiology. - : Springer Science and Business Media LLC. - 1439-6319 .- 1439-6327. ; 96:1, s. 37-45
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Tidskriftsartikel (refereegranskat)abstract
- Orthostatic intolerance is common after space flight and head-down tilt (HDT) bed rest. We hypothesized that HDT-induced impairments of arterial blood pressure (AP) control would be more marked during exercise and that recovery of baroreflex function after very long-term HDT would be delayed. Six subjects were studied before (BDC) during (day 60, D60; D113) and after (recovery day 0, R0; R3; R15) 120 days of HDT. Supine resting subjects were exposed to repeated 1 min passive tilts to upright at 3-min interval. During 50 W steady-state exercise corresponding tilt had a 2-min duration at 4-min interval. The amplitudes of the tilt-induced transient beat-by-beat deviations in AP and rate (HR) were determined during the gravity transients. At rest these deviations did not change over time, but during exercise the total peak-to-nadir range of deviations in systolic AP (SAP) at up-tilt and down-tilt increased to 168+/-16% (mean+/-SEM) of BDC at D113 with no clear recovery upto and including R15. Counter-regulatory HR responses were not increased proportionally and especially not tachycardic responses to up-tilt, resulting in a reduction of baroreflex sensitivity (deltaRR-interval/deltaSAP) by 55+/-9% of BDC at D113 with no recovery upto and including R15. We conclude that prolonged bed rest cause long-lasting impairments in AP control and baroreflex function in exercising humans.
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| 2. |
- Montmerle, S, et al.
(författare)
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Lung function during and after prolonged head-down bed rest
- 2002
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Ingår i: Journal of applied physiology (Bethesda, Md. : 1985). - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 92:1, s. 75-83
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Tidskriftsartikel (refereegranskat)abstract
- We determined the effects of prolonged head-down tilt bed rest (HDT) on lung mechanics and gas exchange. Six subjects were studied in supine and upright postures before (control), during [ day 113(D113)], and after (R + number of days of recovery) 120 days of HDT. Peak expiratory flow (PF) never differed between positions at any time and never differed from controls. Maximal midexpiratory flow (FEF25–75%) was lower in the supine than in the upright posture before HDT and was reduced in the supine posture by about 20% between baseline and D113, R + 0, and R + 3. The diffusing capacity for carbon monoxide corrected to a standardized alveolar volume (volume-corrected Dl CO) was lower in the upright than in the supine posture and decreased in both postures by 20% between baseline and R + 0 and by 15% between baseline and R + 15. Pulmonary blood flow (Q˙C) increased from R + 0 to R + 3 by 20 (supine) and 35% (upright). As PF is mostly effort dependent, our data speak against major respiratory muscle deconditioning after 120 days of HDT. The decrease in FEF25–75% suggests a reduction in elastic recoil. Time courses of volume-corrected Dl CO andQ˙C could be explained by a decrease in central blood volume during and immediately after HDT.
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| 3. |
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| 4. |
- Spaak, J, et al.
(författare)
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Human carotid baroreflex during isometric lower arm contraction and ischemia.
- 1998
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Ingår i: American Journal of Physiology. - 0002-9513 .- 2163-5773. ; 275:3 Pt 2, s. H940-945
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Tidskriftsartikel (refereegranskat)abstract
- Our aim was to determine the roles of somatomotor activation and muscle ischemia for the tachycardia and hypertension of isometric arm contraction. Carotid-cardiac and carotid-mean arterial pressure (MAP) baroreflex response curves were determined in 10 men during rest, during isometric arm contraction at 30% of maximum, and during postcontraction ischemia. Carotid distending pressure (CDP) was changed by applying pressure and suction in a neck chamber. Pressures ranged from +40 to -80 mmHg and were applied repeatedly for 15 s during the three conditions. Maximum slopes and ranges of the response curves did not differ among conditions. The heart rate (HR) curve was shifted to a 14 +/- 1.8 (mean +/- SE) beats/min higher HR and a 9 +/- 5.7 mmHg higher CDP during contraction and to a 14 +/- 5.9 mmHg higher CDP during postcontraction ischemia with no change of HR compared with rest. The MAP curve was shifted to a 20 +/- 2.8 mmHg higher MAP and to a 18 +/- 5.4 mmHg higher CDP during contraction, and the same shifts were recorded during postcontraction ischemia. We conclude that neither somatomotor activation nor muscle ischemia changes the sensitivity of arterial baroreflexes. The upward shift of the MAP response curve, with no shift of the HR response curve during postexercise ischemia, supports the notion of parallel pathways for MAP and HR regulation in which HR responses are entirely caused by somatomotor activation and the pressor response is mainly caused by muscle ischemia.
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| 5. |
- Spaak, J, et al.
(författare)
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Impaired pressor response after spaceflight and bed rest: evidence for cardiovascular dysfunction.
- 2001
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Ingår i: European Journal of Applied Physiology. - : Springer Science and Business Media LLC. - 1439-6319 .- 1439-6327. ; 85:1-2, s. 49-55
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Tidskriftsartikel (refereegranskat)abstract
- We hypothesized that impaired cardiovascular responses to isometric muscle action contribute to the cardiovascular deconditioning that occurs after space flight (SF) and head-down-tilt bed rest (HDT). Six subjects were studied before, during and after 120 days of -6 degrees HDT, and four subjects were studied before, during (two subjects) and after 179-389 days of SF. Subjects performed a sustained handgrip (SHG) at a force equivalent to 30% of maximum contraction force for 2 min, and heart-rate (HR) and pressor (mean arterial pressure, deltaMAP) responses were recorded. At the same relative force, both deltaHR and deltaMAP were significantly reduced during the first days after HDT (-54%, P<0.05 and -43%, P<0.05). In two subjects studied within 24 h after their return from SF, deltaMAP was practically absent (-79%, P<0.05) whereas in four subjects studied 1-4 days after return from SF, deltaMAP was reduced by 35% (P<0.05). deltaHR was not significantly changed. Our finding of attenuated pressor responses to SHG after HDT and SF supports the notion of impairments at both the neurocirculatory control and effector organ levels.
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| 6. |
- Spaak, J, et al.
(författare)
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Long-term bed rest-induced reductions in stroke volume during rest and exercise : cardiac dysfunction vs. volume depletion
- 2005
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Ingår i: Journal of applied physiology. - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 98:2, s. 648-654
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Tidskriftsartikel (refereegranskat)abstract
- Long-term head-down-tilt bed rest (HDT) causes cardiovascular deconditioning, attributed to reflex dysfunctions, plasma volume reduction, or cardiac impairments. Our objective with the present study was to evaluate the functional importance and relative contribution of these during rest and exercise in supine and upright postures. We studied six subjects before (baseline), during [days 60 (D60) and 113 (D113)], and after [recovery days 0 (R0), 3 (R3), and 15 (R15)] 120 days of -6 degrees HDT. We determined cardiac output, stroke volume (SV), mean arterial pressure, and heart rate during rest and exercise in supine and upright postures. Cardiac output and SV decreased significantly in all four conditions, but the time courses differed for rest and exercise. Upright resting SV was decreased by 24 +/- 9% at D60 compared with baseline but had recovered already at R3. Supine exercise SV decreased more slowly (by 5 +/- 8% at D60 and by 18 +/- 4% at D113) and recovered more slowly after HDT termination. Steady-state mean arterial pressure showed no changes. Heart rate had increased by 18 +/- 4% at D60 and had recovered partially at R3. Our data indicate that long-term HDT causes both a rapid, preload-dependent reduction in SV, most evident during rest in the upright position, and a more slowly developing cardiac dysfunction, most evident during supine exercise. However, the ability to maintain blood pressure and to perform sustained low levels of dynamic exercise is not influenced by HDT.
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| 7. |
- Sundblad, Patrik, et al.
(författare)
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Cardiovascular responses to upright and supine exercise in humans after 6 weeks of head-down tilt (-6 degrees).
- 2000
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Ingår i: European Journal of Applied Physiology. - : Springer Science and Business Media LLC. - 1439-6319 .- 1439-6327. ; 83:4-5, s. 303-309
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Tidskriftsartikel (refereegranskat)abstract
- Seven healthy men performed steady-state dynamic leg exercise at 50 W in supine and upright postures, before (control) and repeatedly after 42 days of strict head-down tilt (HDT) (-6 degrees) bedrest. Steady-state heart rate (fc), mean arterial blood pressure, cardiac output (Qc), and stroke volume (SV) were recorded. The following data changed significantly from control values. The fc was elevated in both postures at least until 12 days, but not at 32 days after bedrest. Immediately after HDT, SV and Qc were decreased by 25 (SEM 3)% and 19 (SEM 3)% in supine, and by 33 (SEM 5)% and 20 (SEM 3)% in upright postures, respectively. Within 2 days there was a partial recovery of SV in the upright but not in the supine posture. The SV and Qc during supine exercise remained significantly decreased for at least a month. Submaximal oxygen uptake did not change after HDT. We concluded that the cardiovascular response to exercise after prolonged bedrest was impaired for so long that it suggested that structural cardiac changes had developed during the HDT period.
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| 8. |
- Sundblad, Patrik, et al.
(författare)
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Haemodynamic and baroreflex responses to whole-body tilting in exercising men before and after 6 weeks of bedrest.
- 2000
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Ingår i: European Journal of Applied Physiology. - : Springer Science and Business Media LLC. - 1439-6319 .- 1439-6327. ; 82:5-6, s. 397-406
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Tidskriftsartikel (refereegranskat)abstract
- We sought to determine whether the cardiovascular deconditioning that occurs in exercising men after prolonged (42 days) bedrest in the head-down tilt (HDT) position is primarily related to mechanical changes in the heart or to an impaired arterial-cardiacchronotropic baroreflex. Seven subjects were studied before (C, control) and repeatedly after HDT with rapid tilting between the upright and supine positions during steady-state 50-W dynamic leg exercise. Ventricular interdependence was assumed to be an index of cardiac size; it was assessed on the basis of the initial dip of arterial pulse pressure (PP) induced by a sudden tilt from the upright to the supine position (down-tilt). Arterialcardiac-chronotropic baroreflex sensitivity (ABS) was assessed as the ratio between tilt-induced heart rate transients and the preceding (and reciprocal) transient in arterial pressure. On the first day of recovery, the initial PP dip was -4 (2) mmHg (where 1 mmHg is 0.13 kPa), less than half of the control value; on subsequent recovery days, the initial PP dip was not significantly different from the control value. When tilting from the upright to the supine position, mean ABS ranged from 1.02 to 1.06 bpm/mmHg during three separate control sessions. Tilts in the opposite direction gave lower ABS values because of the more sluggish HR response and ranged from 0.43 to 0.45 bpm/mmHg in the control situations. ABS did not change after HDT. Our results indicate that impairments of the cardiovascular system after long-term bedrest are of haemodynamic rather than baroreflex origin.
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