Journal of applied physiology
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In patients with chronic obstructive pulmonary disease (COPD), one of the proposed mechanisms for improving exercise tolerance, when work of breathing is experimentally reduced, is redistribution of blood flow from the respiratory to locomotor muscles. Accordingly, we investigated whether exercise capacity is improved on the basis of blood flow redistribution during exercise while subjects are breathing heliox (designed to primarily reduce the mechanical work of breathing) and during exercise with oxygen supplementation (designed to primarily enhance systemic oxygen delivery but also to reduce mechanical work of breathing). Intercostal, abdominal, and vastus lateralis muscle perfusion were simultaneously measured in 10 patients with COPD (forced expiratory volume in 1 s: 46 ± 12% predicted) by near-infrared spectroscopy using indocyanine green dye. ⋯ At exhaustion, intercostal and abdominal muscle blood flow during heliox (9.5 ± 0.6 and 8.0 ± 0.7 ml · min(-1)·100 g(-1), respectively) was greater compared with room air (6.8 ± 0.5 and 6.0 ± 0.5 ml·min(-1)·100 g·, respectively; P < 0.05), whereas neither intercostal nor abdominal muscle blood flow differed between oxygen and air breathing. Quadriceps muscle blood flow was also greater with heliox compared with room air (30.2 ± 4.1 vs. 25.4 ± 2.9 ml·min(-1)·100 g(-1); P < 0.01) but did not differ between air and oxygen breathing. Although our findings confirm that reducing the burden on respiration by heliox or oxygen breathing prolongs time to exhaustion (at 75% of maximal capacity) in patients with COPD, they do not support the hypothesis that redistribution of blood flow from the respiratory to locomotor muscles is the explanation.
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The role of autonomic nervous system (ANS) in adapting cerebral blood flow (CBF) to arterial blood pressure (ABP) fluctuations [cerebral autoregulation (CA)] is still controversial. We aimed to study the repercussion of autonomic failure (AF) on dynamic CA during the Valsalva maneuver (VM). Eight AF subjects with familial amyloidotic polineuropahty (FAP) were compared with eight healthy controls. ⋯ ARI(t) showed a biphasic variation in controls with initial increase followed by a decrease during phase II but in FAP this response was blunted (5.4 ± 3.0 and 2.0 ± 2.9; P = 0.033). Our data suggest that dynamic cerebral autoregulatory response is a time-varying phenomena during VM and that it is disturbed by autonomic dysfunction. This study also emphasizes the fact that RAP + CrCP model allowed additional insights into understanding of cerebral hemodynamics, showing a higher vasodilatory response expressed by RAP in AF and an equal CrCP response in both groups during the increased intracranial and intrathoracic pressure, while classical CVRi paradoxically suggests a cerebral vasoconstriction.
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Short-term, high-altitude (HA) exposure raises pulmonary artery systolic pressure (PASP) and decreases left-ventricular (LV) volumes. However, relatively little is known of the long-term cardiac consequences of prolonged exposure in Sherpa, a highly adapted HA population. To investigate short-term adaptation and potential long-term cardiac remodeling, we studied ventricular structure and function in Sherpa at 5,050 m (n = 11; 31 ± 13 yr; mass 68 ± 10 kg; height 169 ± 6 cm) and lowlanders at sea level (SL) and following 10 ± 3 days at 5,050 m (n = 9; 34 ± 7 yr; mass 82 ± 10 kg; height 177 ± 6 cm) using conventional and speckle-tracking echocardiography. ⋯ We propose that this was consequent to a persistently higher PASP. In contrast to the RV, remodeling of LV volumes and normalization of systolic mechanics indicate structural and functional adaptation to HA. However, altered LV diastolic relaxation after chronic hypoxic exposure may reflect differential remodeling of systolic and diastolic LV function.
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Although rats are a frequent model for studies of plasticity in respiratory motor control, the relative capacity of rat accessory respiratory muscles to express plasticity is not well known, particularly in unanesthetized animals. Here, we characterized external intercostal (T2, T4, T5, T6, T7, T8, T9 EIC) and abdominal muscle (external oblique and rectus abdominis) electromyogram (EMG) activity in unanesthetized rats via radiotelemetry during normoxia (Nx: 21% O2) and following acute intermittent hypoxia (AIH: 10 × 5-min, 10.5% O2; 5-min intervals). Diaphragm and T2-T5 EIC EMG activity, and ventilation were also assessed during maximal chemoreceptor stimulation ( ⋯ 7% CO2, 10.5% O2) and sustained hypoxia (SH: 10.5% O2). In Nx, T2 EIC exhibits prominent inspiratory activity, whereas T4, T5, T6, and T7 EIC inspiratory activity decreases in a caudal direction. T8 and T9 EIC and abdominal muscles show only tonic or sporadic activity, without consistent respiratory activity. MCS increases diaphragm and T2 EIC EMG amplitude and tidal volume more than SH (0.94 ± 0.10 vs. 0.68 ± 0.05 ml/100 g; P < 0.001). Following AIH, T2 EIC EMG amplitude remained above baseline for more than 60 min post-AIH (i.e., EIC long-term facilitation, LTF), and was greater than diaphragm LTF (41.5 ± 1.3% vs. 19.1 ± 2.0% baseline; P < 0.001). We conclude that 1) diaphragm and rostral T2-T5 EIC muscles exhibit inspiratory activity during Nx; 2) MCS elicits greater ventilatory, diaphragm, and rostral T2-T5 EIC muscle activity vs. SH; and 3) AIH induces greater rostral EIC LTF than diaphragm LTF.
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The purpose of this study was to compare hemodynamic and blood analyte responses to reduced central venous pressure (CVP) and pulse pressure (PP) elicited during graded lower body negative pressure (LBNP) to those observed during graded blood loss (BL) in conscious humans. We hypothesized that the stimulus-response relationships of CVP and PP to hemodynamic responses during LBNP would mimic those observed during BL. We assessed CVP, PP, heart rate, mean arterial pressure (MAP), and other hemodynamic markers in 12 men during LBNP and BL. ⋯ The PP-heart rate trajectory was the only PP-response slope that was statistically different during LBNP compared with BL (-1.85 ± 0.45 vs. -0.46 ± 0.27; P = 0.024). Norepinephrine, hematocrit, and hemoglobin were all lower at termination in the BL protocol compared with LBNP (P < 0.05). Consistent with our hypothesis, LBNP mimics the hemodynamic stimulus-response trajectories observed during BL across a significant range of CVP in humans.