Journal of applied physiology
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Restriction of total lung capacity (TLC) is found in some obese subjects, but the mechanism is unclear. Two hypotheses are as follows: 1) increased abdominal volume prevents full descent of the diaphragm; and 2) increased intrathoracic fat reduces space for full lung expansion. We have measured total intrathoracic volume at full inflation using magnetic resonance imaging (MRI) in 14 asymptomatic obese men [mean age 52 yr, body mass index (BMI) 35-45 kg/m2] and 7 control men (mean age 50 yr, BMI 22-27 kg/m2). ⋯ The difference in gas volume at TLC between the six obese men with restriction, TLC<80% predicted (OR), and the eight obese men with TLC>80% predicted (ON) was 26% predicted TLC. Mediastinal volume was similar in OR (1.84 liter) and ON (1.73 liter), but total intrathoracic volume was 19% predicted TLC smaller in OR than in ON. We conclude that the major factor restricting TLC in some obese men was reduced thoracic expansion at full inflation.
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Phenylephrine decreases frontal lobe oxygenation at rest but not during moderately intense exercise.
Whether sympathetic activity influences cerebral blood flow (CBF) and oxygenation remains controversial. The influence of sympathetic activity on CBF and oxygenation was evaluated by the effect of phenylephrine on middle cerebral artery (MCA) mean flow velocity (Vmean) and the near-infrared spectroscopy-derived frontal lobe oxygenation (ScO2) at rest and during exercise. At rest, nine healthy male subjects received bolus injections of phenylephrine (0.1, 0.25, and 0.4 mg), and changes in mean arterial pressure (MAP), MCA Vmean, internal jugular venous O2 saturation (SjvO2), ScO2), and arterial PCO2 (PaCO2) were measured and the cerebral metabolic rate for O2 (CMRO2) was calculated. ⋯ MAP increased after the administration of phenylephrine during low-intensity exercise (approximately 15%), but this was attenuated (approximately 10%) during high-intensity exercise (P<0.001). The reduction in ScO2 after administration of phenylephrine was attenuated during low-intensity exercise (-5%, P<0.001) and abolished during high-intensity exercise (-3%, P=not significant), where PaCO2 decreased 7% (P<0.05) and CMRO2 increased 17% (P<0.05). These results suggest that the administration of phenylephrine reduced ScO2 but that the increased cerebral metabolism needed for moderately intense exercise eliminated that effect.
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We previously proposed 5'-AMP-activated protein kinase (AMPK) dephosphorylation within immune cells as an intracellular mechanism linking exercise and immunosuppression. In this study, AMPK phosphorylation underwent transient (<1 h) decreases (53.8+/-7.2% basal) immediately after exercise (45 min of cycling at 70% VO2max) in a cohort of 16 adult male participants. Similar effects were seen with running. ⋯ By analogy, the fact that exercise decreased mononuclear cell ROS content (32.8+/-16.6% basal), possibly due to downregulation (43.4+/-8.0% basal) of mRNA for NOX2, the catalytic subunit of the cytoplasmic ROS-generating enzyme NADPH oxidase, may provide an explanation for the AMPK-dephosphorylating effect of exercise. In contrast, exercise-induced Ca2+ signaling events did not seem to be coupled to changes in AMPK activity. Thus we propose that the exercise-induced decreases in both intracellular ROS and AMPK phosphorylation seen in this study constitute evidence supporting a role for ROS in controlling AMPK, and hence immune function, in the context of exercise-induced immunosuppression.
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Randomized Controlled Trial
Supine cycling plus volume loading prevent cardiovascular deconditioning during bed rest.
There are two possible mechanisms contributing to the excessive fall of stroke volume (and its contribution to orthostatic intolerance) in the upright position after bed rest or spaceflight: reduced cardiac filling due to hypovolemia and/or a less distensible heart due to cardiac atrophy. We hypothesized that preservation of cardiac mechanical function by exercise training, plus normalization of cardiac filling with volume infusion, would prevent orthostatic intolerance after bed rest. Eighteen men and three women were assigned to 1) exercise countermeasure (n=14) and 2) no exercise countermeasure (n=7) groups during bed rest. ⋯ We conclude that daily supine cycle exercise sufficient to prevent cardiac atrophy can prevent orthostatic intolerance after bed rest only when combined with plasma volume restoration. This maintenance of orthostatic tolerance was achieved by neither exercise nor dextran infusion alone. Cardiac atrophy and hypovolemia are likely to contribute independently to orthostatic intolerance after bed rest.
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Effects of hypoxia on cerebral circulation are important for occupational, high-altitude, and aviation medicine. Increased risk of fainting might be attributable to altered cerebral circulation by hypoxia. Dynamic cerebral autoregulation is reportedly impaired immediately by mild hypoxia. ⋯ Furthermore, transfer function gain and coherence in the very-low-frequency range increased significantly at the beginning of hypoxia, indicating impaired dynamic cerebral autoregulation. However, contrary to the proposed hypothesis, indexes of dynamic cerebral autoregulation showed no significant restoration despite ETCO2 reductions, resulting in persistent higher values of very-low-frequency power of CBF velocity variability during hypoxia (214+/-40% at 5 h of hypoxia vs. control) without significant increases in blood pressure variability. These results suggest that sustained mild hypoxia reduces steady-state CBF and continuously impairs dynamic cerebral autoregulation, implying an increased risk of shortage of oxygen supply to the brain.