The Effect of Caffeine Intake on Body Fluids Replacement after Exercise-Induced Dehydration

We studied the effect of a plain espresso coffee (171 ± 8.9 mg caffeine) which is roughly the amount in a cup of regular coffee or caffeine soda drink on fluid replacement in mildly dehydrated healthy subjects following moderate exercise, which induced dehydration to approximately 1.2% of their body weight. Subjects then rehydrated by drinking either water alone as control or caffeinated beverage plus up to 150% of the body weight they had lost. All subjects underwent both conditions. There were differences between the control and caffeine in urine specific gravity (control: 1.018 ± 0.00 vs caffeine: 1.024 ± 0.00, P =.001), urine volume (control: 200 ±71 mL vs caffeine: 302 ± 151 mL, P =.05), and urine color (control: 2 ± 0.9 and caffeine: 4 ± 1.66, P =.00). We conclude that intake of an espresso coffee possibly impedes replacement of body fluids. © 2020 Wolters Kluwer Health, Inc. All rights reserved

The effect of exercise-induced hypoxemia on blood redox status in well-trained rowers

Exercise-induced arterial hypoxemia (EIAH), characterized by decline in arterial oxyhemoglobin saturation (SaO2), is a common phenomenon in endurance athletes. Acute intensive exercise is associated with the generation of reactive species that may result in redox status disturbances and oxidation of cell macromolecules. The purpose of the present study was to investigate whether EIAH augments oxidative stress as determined in blood plasma and erythrocytes in well-trained male rowers after a 2,000-m rowing ergometer race. Initially, athletes were assigned into either the normoxemic (n = 9, SaO 2 [92%, V O2max: 62.0 ± 1.9 ml kg-1 min-1) or hypoxemic (n = 12, SaO2\92%, V O2max: 60.5 ± 2.2 ml kg-1 min-1, mean ± SEM) group, following an incremental V O2max test on a wind resistance braked rowing ergometer. On aseparate day the rowers performed a 2,000-m all-out effort on the same rowing ergometer. Following an overnight fast, blood samples were drawn from an antecubital vein before and immediately after the termination of the 2,000-mall-out effort and analyzed for selective oxidative stress markers. In both the normoxemic (SaO2: 94.1 ± 0.9%) and hypoxemic (SaO2: 88.6 ± 2.4%) rowers similar and significant exercise increase in serum thiobarbituric acidreactive substances, protein carbonyls, catalase and total antioxidant capacity concentration were observed post-2,000 m all-out effort. Exercise significantly increased the oxidized glutathione concentration and decreased the ratio of reduced (GSH)-to-oxidized (GSSG) glutathione in the normoxemic group only, whereas the reduced form of glutathione remained unaffected in either groups. The increased oxidation of GSH to GSSG in erythrocytes of normoxemic individuals suggest that erythrocyte redox status may be affected by the oxygen saturation degree of hemoglobin. Our findings indicate that exercise-induced hypoxemia did not further affect the increased blood oxidative damage of lipids and proteins observed after a2,000-m rowing ergometer race in highly-trained male rowers. The present data do not support any potential link between exercise-induced hypoxemia, oxidative stress increase and exercise performance. © 2011 Springer-Verlag

The effect of exercise-induced hypoxemia on blood redox status in well-trained rowers

Exercise-induced arterial hypoxemia (EIAH), characterized by decline in arterial oxyhemoglobin saturation (SaO(2)), is a common phenomenon in endurance athletes. Acute intensive exercise is associated with the generation of reactive species that may result in redox status disturbances and oxidation of cell macromolecules. The purpose of the present study was to investigate whether EIAH augments oxidative stress as determined in blood plasma and erythrocytes in well-trained male rowers after a 2,000-m rowing ergometer race. Initially, athletes were assigned into either the normoxemic ( = 9, SaO(2) > 92%, : 62.0 +/- A 1.9 ml kg(-1) min(-1)) or hypoxemic ( = 12, SaO(2) < 92%, : 60.5 +/- A 2.2 ml kg(-1) min(-1), mean +/- A SEM) group, following an incremental test on a wind resistance braked rowing ergometer. On a separate day the rowers performed a 2,000-m all-out effort on the same rowing ergometer. Following an overnight fast, blood samples were drawn from an antecubital vein before and immediately after the termination of the 2,000-m all-out effort and analyzed for selective oxidative stress markers. In both the normoxemic (SaO(2): 94.1 +/- A 0.9%) and hypoxemic (SaO(2): 88.6 +/- A 2.4%) rowers similar and significant exercise increase in serum thiobarbituric acid-reactive substances, protein carbonyls, catalase and total antioxidant capacity concentration were observed post-2,000 m all-out effort. Exercise significantly increased the oxidized glutathione concentration and decreased the ratio of reduced (GSH)-to-oxidized (GSSG) glutathione in the normoxemic group only, whereas the reduced form of glutathione remained unaffected in either groups. The increased oxidation of GSH to GSSG in erythrocytes of normoxemic individuals suggest that erythrocyte redox status may be affected by the oxygen saturation degree of hemoglobin. Our findings indicate that exercise-induced hypoxemia did not further affect the increased blood oxidative damage of lipids and proteins observed after a 2,000-m rowing ergometer race in highly-trained male rowers. The present data do not support any potential link between exercise-induced hypoxemia, oxidative stress increase and exercise performance

Contribution of respiratory muscle blood flow to exercise-induced diaphragmatic fatigue in trained cyclists

We investigated whether the greater degree of exercise-induced diaphragmatic fatigue previously reported in highly trained athletes in hypoxia (compared with normoxia) could have a contribution from limited respiratory muscle blood flow. Seven trained cyclists completed three constant load 5 min exercise tests at inspired O2 fractions (FIO2 of 0.13, 0.21 and 1.00 in balanced order. Work rates were selected to produce the same tidal volume, breathing frequency and respiratory muscle load at each (63 ± 1, 78 ± 1 and 87 ± 1% of normoxic maximal work rate, respectively). Intercostals and quadriceps muscle blood flow (IMBF and QMBF, respectively) were measured by near-infrared spectroscopy over the left 7th intercostal space and the left vastus lateralis muscle, respectively, using indocyanine green dye. The mean pressure time product of the diaphragm and the work of breathing did not differ across the three exercise tests. After hypoxic exercise, twitch transdiaphragmatic pressure fell by 33.3 ± 4.8%, significantly (P &amp;lt; 0.05) more than after both normoxic (25.6 ± 3.5% reduction) and hyperoxic (26.6 ± 3.3% reduction) exercise, confirming greater fatigue in hypoxia. Despite lower leg power output in hypoxia, neither cardiac output nor QMBF (27.6 ± 1.2 l min-1 and 100.4 ± 8.7 ml (100 ml)-1 min-1, respectively) were significantly different compared with normoxia (28.4 ± 1.9 l min-1 and 94.4 ± 5.2 ml (100 ml)-1 min-1, respectively) and hyperoxia (27.8 ± 1.6 l min-1 and 95.1 ± 7.8 ml (100 ml)-1 min-1, respectively). Neither IMBF was different across hypoxia, normoxia and hyperoxia (53.6 ± 8.5, 49.9 ± 5.9 and 52.9 ± 5.9 ml (100 ml)-1 min-1, respectively). We conclude that when respiratory muscle energy requirement is not different between normoxia and hypoxia, diaphragmatic fatigue is greater in hypoxia as intercostal muscle blood flow is not increased (compared with normoxia) to compensate for the reduction in, thus further compromising O2 supply to the respiratory muscles. © 2008 The Authors. Journal compilation © 2008 The Physiological Society

Human respiratory muscle blood flow measured by near-infrared spectroscopy and indocyanine green

Measurement of respiratory muscle blood flow (RMBF) in humans has important implications for understanding patterns of blood flow distribution during exercise in healthy individuals and those with chronic disease. Previous studies examining RMBF in humans have required invasive methods on anesthetized subjects. To assess RMBF in awake subjects, we applied an indicator-dilution method using near-infrared spectroscopy (NIRS) and the light-absorbing tracer indocyanine green dye (ICG). NIRS optodes were placed on the left seventh intercostal space at the apposition of the costal diaphragm and on an inactive control muscle (vastus lateralis). The primary respiratory muscles within view of the NIRS optodes include the internal and external intercostals. Intravenous bolus injection of ICG allowed for cardiac output (by the conventional dye-dilution method with arterial sampling), RMBF, and vastus lateralis blood flow to be quantified simultaneously. Esophageal and gastric pressures were also measured to calculate the work of breathing and transdiaphragmatic pressure. Measurements were obtained in five conscious humans during both resting breathing and three separate 5-min bouts of constant isocapnic hyperpnea at 27.1 ± 3.2, 56.0 ± 6.1, and 75.9 ± 5.7% of maximum minute ventilation as determined on a previous maximal exercise test. RMBF progressively increased (9.9 ± 0.6, 14.8 ± 2.7, 29.9 ± 5.8, and 50.1 ± 12.5 ml·100 ml·-1·min -1, respectively) with increasing levels of ventilation while blood flow to the inactive control muscle remained constant (10.4 ± 1.4, 8.7 ± 0.7, 12.9 ± 1.7, and 12.2 ± 1.8 ml·100 ml -1·min-1, respectively). As ventilation rose, RMBF was closely and significantly correlated with 1) cardiac output (r = 0.994, P = 0.006), 2) the work of breathing (r = 0.995, P = 0.005), and 3) transdiaphragmatic pressure (r = 0.998, P = 0.002). These data suggest that the NIRS-ICG technique provides a feasible and sensitive index of RMBF at different levels of ventilation in humans. Copyright © 2008 the American Physiological Society

Effects of hypoxia on diaphragmatic fatigue in highly trained athletes

Previous work suggests that exercise-induced arterial hypoxaemia (EIAH), causing only moderate arterial oxygen desaturation (SaO2 92 ± 1%), does not exaggerate diaphragmatic fatigue exhibited by highly trained endurance athletes. Since changes in arterial O2 tension have a significant effect on the rate of development of locomotor muscle fatigue during strenuous exercise, the present study investigated whether hypoxia superimposed on EIAH exacerbates the exercise-induced diaphragmatic fatigue in these athletes. Eight trained cyclists (V̇O2max 67.0 ± 2.6 ml kg-1 min-1; mean ± s.e.m.) completed in balanced order four 5 min exercise tests leading to different levels of end-exercise SaO2 (64 ± 2, 83 ± 1, 91 ± 1 and 96 ± 1%) via variations in inspired O2 fraction (FIO2 0.13, 0.17, 0.21 and 0.26, respectively). Measurements were made at corresponding intensities (65 ± 3, 80 ± 3, 85 ± 3 and 90 ± 3% of normoxic maximal work rate, respectively) in order to produce the same tidal volume, breathing frequency and respiratory muscle load at each FIO2. The mean pressure time product of the diaphragm did not differ across the four exercise tests and ranged between 312 ± 28 and 382 ± 22 cmH2O s min-1. Ten minutes into recovery, twitch transdiaphragmatic pressure (Pdi,tw) determined by bilateral phrenic nerve stimulation, was significantly (P=0.0001) reduced after all tests. After both hypoxic tests (FIO2: 0.13, 0.17) the degree of fall in Pdi,tw (by 26.9 ± 2.7 and 27.4 ± 2.6%, respectively) was significantly greater (P&amp;lt;0.05) than after the normoxic test (by 20.1 ± 3.4%). The greater amount of diaphragmatic fatigue in hypoxia at lower leg work rates (presumably requiring smaller leg blood flow compared with normoxia at higher leg work rates), suggests that when ventilatory muscle load is similar between normoxia and hypoxia, hypoxia exaggerates diaphragmatic fatigue in spite of potentially greater respiratory muscle blood flow availability. © 2007 The Authors. Journal compilation © 2007 The Physiological Society