86,608 research outputs found
Cardiovascular determinants of maximal oxygen consumption in upright and supine posture at the end of prolonged bed rest in humans.
No full textWe tested the hypothesis that, after bed rest, maximal oxygen consumption ( VO2max ) decreases more upright than supine, because of adequate cardiovascular response supine, but not upright. On 9 subjects, we determined VO2max and maximal cardiac output (Q ) upright and supine, before and after (reambulation day upright, the following day supine) 35-day bed rest, by classical steady state protocol. Oxygen consumption, heart rate (f(H)) and stroke volume (Q(st)) were measured by a metabolic cart, electrocardiography and Modelflow from pulse pressure profiles, respectively. We computed Q as f(H) times Q(st), and systemic oxygen flow ( QaO2) as Q. times arterial oxygen concentration, obtained after haemoglobin and arterial oxygen saturation measurements. Before bed rest, all parameters at maximal exercise were similar upright and supine. After bed rest, VO2max was lower (p<0.05) than before, both upright (-38.6%) and supine (-17.0%), being 30.8% higher supine than upright. Maximal Q(st) decreased upright (-44.3%), but not supine (+3.7%), being 98.9% higher supine than upright. Maximal Q decreased upright (-45.1%), but not supine (+9.0%), being higher supine than upright (+98.4%). Maximal QaO2 decreased upright (-37.8%), but not supine (+14.8%), being higher (+74.8%) upright than supine. After bed rest, the cardiovascular response (i) did not affect VO2max supine, (ii) partially explained the VO2max decrease upright, and (iii) caused the VO2max differences between postures. We speculate that impaired peripheral oxygen transfer and/or utilisation may explain the VO2max decrease supine and the fraction of VO2max decrease upright unexplained by cardiovascular responses
Simultaneous determination of kinetics of cardiac output, systemic O2 delivery, and lung O2 uptake at exercise onset in men.
No full textWe tested whether the kinetics of systemic O(2) delivery (QaO(2)) at exercise start was faster than that of lung O(2) uptake (Vo(2)), being dictated by that of cardiac output (Q), and whether changes in Q would explain the postulated rapid phase of the Vo(2) increase. Simultaneous determinations of beat-by-beat (BBB) Q and QaO(2), and breath-by-breath Vo(2) at the onset of constant load exercises at 50 and 100 W were obtained on six men (age 24.2 +/- 3.2 years, maximal aerobic power 333 +/- 61 W). Vo(2) was determined using Grønlund's algorithm. Q was computed from BBB stroke volume (Q(st), from arterial pulse pressure profiles) and heart rate (f(h), electrocardiograpy) and calibrated against a steady-state method. This, along with the time course of hemoglobin concentration and arterial O(2) saturation (infrared oximetry) allowed computation of BBB QaO(2). The Q, QaO(2) and Vo(2) kinetics were analyzed with single and double exponential models. f(h), Q(st), Q, and Vo(2) increased upon exercise onset to reach a new steady state. The kinetics of QaO(2) had the same time constants as that of Q. The latter was twofold faster than that of Vo(2). The Vo(2) kinetics were faster than previously reported for muscle phosphocreatine decrease. Within a two-phase model, because of the Fick equation, the amplitude of phase I Q changes fully explained the phase I of Vo(2) increase. We suggest that in unsteady states, lung Vo(2) is dissociated from muscle O(2) consumption. The two components of Q and QaO(2) kinetics may reflect vagal withdrawal and sympathetic activation
Simultaneous determination of the kinetics of cardiac output, systemic O2 delivery and lung O2 uptake at exercise onset in men.
No full textWe tested whether the kinetics of systemic O2 delivery (Q'aO2) at exercise start was faster than that of lung O2 uptake (V' O2), being dictated by that of cardiac output (Q'), and whether changes in Q' would explain the postulated rapid phase of the V'O2 increase. Simultaneous determinations of beat-by-beat (BBB) Q' and Q' aO2, and breath-by-breath V'O2 at the onset of constant load exercises at 50 and 100 W were obtained on six men (age 24.2 +/-3.2 years, maximal aerobic power 333 +/- 61 W). V'O2 was determined using Grønlund’s algorithm. Q' was computed from BBB stroke volume (Qst, from arterial pulse pressure profiles) and heart rate (fH, electrocardiograpy) and calibrated against a steadystate method. This, along with the time course of hemoglobin concentration and arterial O2 saturation (infrared oximetry) allowed computation of BBB Q'aO2. The Q', Q'aO2 and V'O2 kinetics were analyzed with single and double exponential models. fH, Qst, Q', and V'O2 increased upon exercise onset to reach a new steady state. The
kinetics of Q'aO2 had the same time constants as that of Q'. The latter was twofold faster than that of V'O2. The V'O2 kinetics were faster than previously reported for muscle phosphocreatine decrease. Within a two-phase model, because of the Fick equation, the amplitude of phase I Q' changes fully explained the phase I of V'O2 increase. We suggest that in unsteady states, lung V' O2 is dissociated from muscle
O2 consumption. The two components of Q' and Q'aO2 kinetics may reflect vagal withdrawal and sympathetic activation
Factors determining the time course of VO2 max decay during badrest: implications for VO2 max limitation.
No full text[no abstract available
Variations on the Author
No full text“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
Factors determining the kinetics of VO2max decay during bed-rest: implications for VO2max limitation
No full textThe aim of this study was to characterize the time course of maximal oxygen consumption (V'O2 max) changes during bedrests longer than 30 days, on the hypothesis that the decrease in V'O2 max tends to asymptote. On a total of 26 subjects who participated in one of three bedrest campaigns without countermeasures, lasting 14, 42 and 90 days, respectively, V'O2 max, maximal cardiac output (Qmax) and maximal systemic O2 delivery (QaO2max) were measured. After
all periods of HDT, V'O2 max; Qmax and QaO2max were significantly lower than before. The V'O2 max decreased less than Qmax after the two shortest bedrests, but its percent decay was about 10% larger than that of Qmax after 90-day bedrest. The V'O2 max decrease after 90-day bedrest was larger than after 42- and 14-day bedrests, where it was similar. The Qmax and QaO2max decline after 90-day bedrest was equal to those after 14- and 42-day bedrest. The average daily rates of the V'O2 max; Qmax and QaO2max decay during bedrest were less if the bedrest duration was longer, with the exception of that of V'O2 max in the longest bedrest. The asymptotic V'O2 max decay demonstrates the possibility that humans could keep working effectively even after an extremely long time in microgravity. Two components in the V'O2 max decrease were identified, which we postulate were related to cardiovascular deconditioning and to impairment of peripheral gas exchanges due to a possible muscle function deterioration
[Newspaper Clipping: Author Claims Evidence of Second JFK Assassin #1]
No full textNewspaper article titled "Author Claims Evidence of Second JFK Assassin." The article states that author Richard J. Whalen concluded "that there is circumstantial evidence to support the theory of a second assassin in the shooting of President John F. Kennedy.
Factors determining the time course of V'O2 max decay during bedrest: implications for V'O2 max limitation.
No full textThe aim of this study was to characterizethe time course of maximal oxygen consumption (V'O2 max) changes during bedrests longer than 30 days,on the hypothesis that the decrease in V'O2 max tends toasymptote. On a total of 26 subjects who participatedin one of three bedrest campaigns without countermeasures,lasting 14, 42 and 90 days, respectively,_VO2 max maximal cardiac output (Qmax) and maximalsystemic O2 delivery (QaO2max) were measured. Afte rall periods of HDT, V'O2 max; Q'max and Q'aO2max weresignificantly lower than before. The 'V O2 max decreasedless than 'Qmax after the two shortest bedrests, but itsper cent decay was about 10% larger than that of _Qmaxafter 90-day bedrest. The 'V O2 max decrease after90-day bedrest was larger than after 42- and 14-daybedrests, where it was similar. The 'Qmax and 'QaO2maxdeclines after 90-day bedrest was equal to those after14- and 42-day bedrest. The average daily rates of the_VO2 max; Q'max and Q'aO2max decay during bedrest wereless if the bedrest duration were longer, with theexception of that of V'O2 max in the longest bedrest. Theasymptotic V'O2 max decay demonstrates the possibilitythat humans could keep working effectively even afteran extremely long time in microgravity. Two componentsin the 'VO2 max decrease were identified, which wepostulate were related to cardiovascular deconditioningand to impairment of peripheral gas exchanges dueto a possible muscle function deterioration
Prolonged head down bed rest-induced inactivity impairs tonic autonomic regulation while sparing oscillatory cardiovascular rhythms in healthy humans
No full textBackground: Physical inactivity represents a major risk for cardiovascular disorders, such as hypertension, myocardial infarction or sudden death; however, underlying mechanisms are not clearly elucidated. Clinical and epidemiological investigations suggest, beyond molecular changes, the possibility of an induced impairment in autonomic cardiovascular regulation. However, this hypothesis has not been tested directly. Methods: Accordingly, we planned a study with noninvasive, minimally intrusive, techniques on healthy volunteers. Participants were maintained for 90 days strictly in bed, 24 h a day, in head-down (-6 degrees ) position (HDBR). Physical activity was thus virtually abolished for the entire period of HDBR. We examined efferent muscle sympathetic nerve activity, as a measure of vascular sympathetic control, baroreceptor reflex sensitivity, heart rate variability (assessing cardiovagal regulation), RR and systolic arterial pressure and low-frequency and high-frequency normalized components (as a window on central oscillatory regulation). Measures were obtained at rest and during simple maneuvers (moderate handgrip, lower body negative pressure and active standing) to assess potential changes in autonomic cardiovascular responsiveness to standard stimuli and the related oscillatory profiles. Results: HDBR transiently reduced muscle sympathetic nerve activity, RR, heart rate variability and baroreceptor reflex sensitivity late during HDBR or early during the recovery phase. Conversely, oscillatory profiles of RR and systolic arterial pressure variability were maintained throughout. Responsiveness to test stimuli was also largely maintained. Conclusion: Prolonged inactivity as induced by HDBR in healthy volunteers reduces both cardiovagal and vascular sympathetic regulation, while largely maintaining peripheral responsiveness to standardized stimuli and sparing the functional structure of central oscillatory cardiovascular regulation
- …
