Acute exposure to hypoxia provokes a decrease in peak oxygen consumption ( V(O)(2peak)). At and a... more Acute exposure to hypoxia provokes a decrease in peak oxygen consumption ( V(O)(2peak)). At and above 4000 m, the decrease in V(O)(2peak) is greater than expected from the decrease in arterial oxygen content (C(a)O(2)) suggesting the participation of other factors. We hypothesized that O(2) transfer within the active muscle may play a role. Therefore we used Near Infra Red Spectroscopy (NIRS) to assess oxy (O2Hb) and deoxyhemoglobin (HHb) concentration in the vastus lateralis of trained athletes (TA) and untrained subjects (US) exercising at various inspired oxygen pressure (PI(O)(2), 131.4, 107.3 and 87.0 mmHg). A mathematical model has been developed to compute: (i) the pulmonary (K(p)) and muscular (K(tm)) O(2) diffusion coefficients and (ii) the proportion of arteriolar:capillary:venous blood participating in the NIRS signal at every exercise intensity from rest to peak exercise in the normoxic and various hypoxic conditions. In TA, O2Hb decreased near maximal exercise at 2500 and 4000 m, while in US, altitude had no effect. In normoxia O2Hb was higher in TA than in US, the difference disappearing in hypoxia. K(tm) increased linearly with workload and altitude and was higher in TA than US while K(p) plateaued near maximal exercise, which was consistent with athletes' greater decrease in C(a)O(2). The greater participation of arterial blood in the NIRS signal in TA at altitudes account for their higher O2Hb values as well as the greater decrease they underwent in hypoxia. At 4000m, athletes loose their advantages of adaptation to training due to a reduced arterial content, and both from NIRS variables and model output, characteristics of O(2) transfer of TA converge toward those of US.
Cerebral hypoxaemia associated with rapid ascent to high altitude can be life threatening; yet, w... more Cerebral hypoxaemia associated with rapid ascent to high altitude can be life threatening; yet, with proper acclimatization, cerebral function can be maintained well enough for humans to thrive. We investigated adjustments in global and regional cerebral oxygen delivery (DO2) as 21 healthy volunteers rapidly ascended and acclimatized to 5260 m. Ultrasound indices of cerebral blood flow in internal carotid and vertebral arteries were measured at sea level, upon arrival at 5260 m (ALT1; atmospheric pressure 409 mmHg) and after 16 days of acclimatization (ALT16). Cerebral DO2 was calculated as the product of arterial oxygen content and flow in each respective artery and summed to estimate global cerebral blood flow. Vascular resistances were calculated as the quotient of mean arterial pressure and respective flows. Global cerebral blood flow increased by ∼70% upon arrival at ALT1 (P < 0.001) and returned to sea-level values at ALT16 as a result of changes in cerebral vascular resistance. A reciprocal pattern in arterial oxygen content maintained global cerebral DO2 throughout acclimatization, although DO2 to the posterior cerebral circulation was increased by ∼25% at ALT1 (P = 0.032). We conclude that cerebral DO2 is well maintained upon acute exposure and acclimatization to hypoxia, particularly in the posterior and inferior regions of the brain associated with vital homeostatic functions. This tight regulation of cerebral DO2 was achieved through integrated adjustments in local vascular resistances to alter cerebral perfusion during both acute and chronic exposure to hypoxia.
The Richalet hypoxia sensitivity test (RT), which quantifies the cardiorespiratory response to ac... more The Richalet hypoxia sensitivity test (RT), which quantifies the cardiorespiratory response to acute hypoxia during exercise at an intensity corresponding to a heart rate of ~130 bpm in normoxia, can predict susceptibility of altitude sickness. Its ability to predict exercise performance in hypoxia is unknown. Investigate: (1) whether cerebral blood flow (CBF) and cerebral tissue oxygenation (O2Hb; oxygenated hemoglobin, HHb; deoxygenated hemoglobin) responses during RT predict time-trial cycling (TT) performance in severe hypoxia; (2) if subjects with blunted cardiorespiratory responses during RT show greater impairment of TT performance in severe hypoxia. Thirteen men [27 ± 7 years (mean ± SD), Wmax: 385 ± 30 W] were evaluated with RT and the results related to two 15 km TT, in normoxia and severe hypoxia (FIO2 = 0.11). During RT, mean middle cerebral artery blood velocity (MCAv: index of CBF) was unaltered with hypoxia at rest (p > 0.05), while it was increased during normoxic (+22 ± 12 %, p < 0.05) and hypoxic exercise (+33 ± 17 %, p < 0.05). Resting hypoxia lowered cerebral O2Hb by 2.2 ± 1.2 μmol (p < 0.05 vs. resting normoxia); hypoxic exercise further lowered it to -7.6 ± 3.1 μmol below baseline (p < 0.05). Cerebral HHb, increased by 3.5 ± 1.8 μmol in resting hypoxia (p < 0.05), and further to 8.5 ± 2.9 μmol in hypoxic exercise (p < 0.05). Changes in CBF and cerebral tissue oxygenation during RT did not correlate with TT performance loss (R = 0.4, p > 0.05 and R = 0.5, p > 0.05, respectively), while tissue oxygenation and SaO2 changes during TT did (R = -0.76, p < 0.05). Significant correlations were observed between SaO2, MCAv and HHb during RT (R = -0.77, -0.76 and 0.84 respectively, p < 0.05 in all cases). CBF and cerebral tissue oxygenation changes during RT do not predict performance impairment in hypoxia. Since the changes in SaO2 and brain HHb during the TT correlated with performance impairment, the hypothesis that brain oxygenation plays a limiting role for global exercise in conditions of severe hypoxia remains to be tested further.
This study aimed to determine the cardiovascular responses during a prolonged exercise with volun... more This study aimed to determine the cardiovascular responses during a prolonged exercise with voluntary hypoventilation (VH). 7 men performed 3 series of 5-min exercise at 65% of normoxic maximal O (2) uptake under 3 conditions: (1) normal breathing (NB) in normoxia (NB (0.21)), (2) VH in normoxia (VH (0.21)), (3) NB in hypoxia (NB (0.157), inspired oxygen fraction=0.157). In both VH (0.21) and NB (0.157), there was a similar drop in arterial oxygen saturation and arterial O (2) content (CaO (2)) which were lower than in NB (0.21). Heart rate (HR), stroke volume, and cardiac output (-) were higher in VH (0.21) than in NB (0.21) during most parts of exercise whereas there was no difference between NB (0.157) and VH (0.21) or NB (0.21). HR variability analysis suggested an increased sympathetic modulation in VH (0.21) only. O (2) transport and oxygen uptake were generally not different between interventions. Mixed venous O (2) content (C-O (2)) was lower in NB (0.157) than in both VH (0...
Acute exposure to hypoxia provokes a decrease in peak oxygen consumption ( V(O)(2peak)). At and a... more Acute exposure to hypoxia provokes a decrease in peak oxygen consumption ( V(O)(2peak)). At and above 4000 m, the decrease in V(O)(2peak) is greater than expected from the decrease in arterial oxygen content (C(a)O(2)) suggesting the participation of other factors. We hypothesized that O(2) transfer within the active muscle may play a role. Therefore we used Near Infra Red Spectroscopy (NIRS) to assess oxy (O2Hb) and deoxyhemoglobin (HHb) concentration in the vastus lateralis of trained athletes (TA) and untrained subjects (US) exercising at various inspired oxygen pressure (PI(O)(2), 131.4, 107.3 and 87.0 mmHg). A mathematical model has been developed to compute: (i) the pulmonary (K(p)) and muscular (K(tm)) O(2) diffusion coefficients and (ii) the proportion of arteriolar:capillary:venous blood participating in the NIRS signal at every exercise intensity from rest to peak exercise in the normoxic and various hypoxic conditions. In TA, O2Hb decreased near maximal exercise at 2500 and 4000 m, while in US, altitude had no effect. In normoxia O2Hb was higher in TA than in US, the difference disappearing in hypoxia. K(tm) increased linearly with workload and altitude and was higher in TA than US while K(p) plateaued near maximal exercise, which was consistent with athletes' greater decrease in C(a)O(2). The greater participation of arterial blood in the NIRS signal in TA at altitudes account for their higher O2Hb values as well as the greater decrease they underwent in hypoxia. At 4000m, athletes loose their advantages of adaptation to training due to a reduced arterial content, and both from NIRS variables and model output, characteristics of O(2) transfer of TA converge toward those of US.
Cerebral hypoxaemia associated with rapid ascent to high altitude can be life threatening; yet, w... more Cerebral hypoxaemia associated with rapid ascent to high altitude can be life threatening; yet, with proper acclimatization, cerebral function can be maintained well enough for humans to thrive. We investigated adjustments in global and regional cerebral oxygen delivery (DO2) as 21 healthy volunteers rapidly ascended and acclimatized to 5260 m. Ultrasound indices of cerebral blood flow in internal carotid and vertebral arteries were measured at sea level, upon arrival at 5260 m (ALT1; atmospheric pressure 409 mmHg) and after 16 days of acclimatization (ALT16). Cerebral DO2 was calculated as the product of arterial oxygen content and flow in each respective artery and summed to estimate global cerebral blood flow. Vascular resistances were calculated as the quotient of mean arterial pressure and respective flows. Global cerebral blood flow increased by ∼70% upon arrival at ALT1 (P < 0.001) and returned to sea-level values at ALT16 as a result of changes in cerebral vascular resistance. A reciprocal pattern in arterial oxygen content maintained global cerebral DO2 throughout acclimatization, although DO2 to the posterior cerebral circulation was increased by ∼25% at ALT1 (P = 0.032). We conclude that cerebral DO2 is well maintained upon acute exposure and acclimatization to hypoxia, particularly in the posterior and inferior regions of the brain associated with vital homeostatic functions. This tight regulation of cerebral DO2 was achieved through integrated adjustments in local vascular resistances to alter cerebral perfusion during both acute and chronic exposure to hypoxia.
The Richalet hypoxia sensitivity test (RT), which quantifies the cardiorespiratory response to ac... more The Richalet hypoxia sensitivity test (RT), which quantifies the cardiorespiratory response to acute hypoxia during exercise at an intensity corresponding to a heart rate of ~130 bpm in normoxia, can predict susceptibility of altitude sickness. Its ability to predict exercise performance in hypoxia is unknown. Investigate: (1) whether cerebral blood flow (CBF) and cerebral tissue oxygenation (O2Hb; oxygenated hemoglobin, HHb; deoxygenated hemoglobin) responses during RT predict time-trial cycling (TT) performance in severe hypoxia; (2) if subjects with blunted cardiorespiratory responses during RT show greater impairment of TT performance in severe hypoxia. Thirteen men [27 ± 7 years (mean ± SD), Wmax: 385 ± 30 W] were evaluated with RT and the results related to two 15 km TT, in normoxia and severe hypoxia (FIO2 = 0.11). During RT, mean middle cerebral artery blood velocity (MCAv: index of CBF) was unaltered with hypoxia at rest (p > 0.05), while it was increased during normoxic (+22 ± 12 %, p < 0.05) and hypoxic exercise (+33 ± 17 %, p < 0.05). Resting hypoxia lowered cerebral O2Hb by 2.2 ± 1.2 μmol (p < 0.05 vs. resting normoxia); hypoxic exercise further lowered it to -7.6 ± 3.1 μmol below baseline (p < 0.05). Cerebral HHb, increased by 3.5 ± 1.8 μmol in resting hypoxia (p < 0.05), and further to 8.5 ± 2.9 μmol in hypoxic exercise (p < 0.05). Changes in CBF and cerebral tissue oxygenation during RT did not correlate with TT performance loss (R = 0.4, p > 0.05 and R = 0.5, p > 0.05, respectively), while tissue oxygenation and SaO2 changes during TT did (R = -0.76, p < 0.05). Significant correlations were observed between SaO2, MCAv and HHb during RT (R = -0.77, -0.76 and 0.84 respectively, p < 0.05 in all cases). CBF and cerebral tissue oxygenation changes during RT do not predict performance impairment in hypoxia. Since the changes in SaO2 and brain HHb during the TT correlated with performance impairment, the hypothesis that brain oxygenation plays a limiting role for global exercise in conditions of severe hypoxia remains to be tested further.
This study aimed to determine the cardiovascular responses during a prolonged exercise with volun... more This study aimed to determine the cardiovascular responses during a prolonged exercise with voluntary hypoventilation (VH). 7 men performed 3 series of 5-min exercise at 65% of normoxic maximal O (2) uptake under 3 conditions: (1) normal breathing (NB) in normoxia (NB (0.21)), (2) VH in normoxia (VH (0.21)), (3) NB in hypoxia (NB (0.157), inspired oxygen fraction=0.157). In both VH (0.21) and NB (0.157), there was a similar drop in arterial oxygen saturation and arterial O (2) content (CaO (2)) which were lower than in NB (0.21). Heart rate (HR), stroke volume, and cardiac output (-) were higher in VH (0.21) than in NB (0.21) during most parts of exercise whereas there was no difference between NB (0.157) and VH (0.21) or NB (0.21). HR variability analysis suggested an increased sympathetic modulation in VH (0.21) only. O (2) transport and oxygen uptake were generally not different between interventions. Mixed venous O (2) content (C-O (2)) was lower in NB (0.157) than in both VH (0...
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