Claus, Paul

Hypoxia during exercise augments vasodilation and blood flow to ensure adequate delivery of O 2 to active muscles. However, the impact of hyperoxia on skeletal muscle blood flow during exercise is poorly understood. Therefore, we tested the hypothesis that the hyperemic response to exercise with hyperbaric hyperoxia would be blunted compared to exercise during normoxia. Seven subjects (6M/1F; 26 ± 2 years) performed forearm exercise (20% of maximum) under normoxic and hyperoxic conditions. Forearm blood flow (FBF; ml/min) was measured using Doppler ultrasound. Forearm vascular conductance (FVC; ml/min/100mmHg) was calculated from FBF and blood pressure (mmHg; brachial arterial catheter). Studies were performed in a hyperbaric chamber with the subjects supine at 1 ATA (sea level) and 2.8 ATA while breathing normoxic (21% O 2 , 1 ATA; F I O 2 ≈ 150 mmHg), hyperbaric normoxic (7% O 2 , 2.8 ATA, F I O 2 ≈ 150 mmHg) and hyperoxic (7% O 2 , 2.8 ATA, F I O 2 ≈ 2100 mmHg) gas. The change in FBF and FVC (Δ from rest) during exercise under normoxia and hyperbaric normoxia did not differ (P > 0.05). However, the ΔFBF and ΔFVC during exercise under hyperoxia were attenuated by ~18–29% compared to both normoxic conditions (P ≤ 0.01). Our data suggest that exercise hyperemia in skeletal muscle is highly dependent on oxygen availability during hyperoxia as well as hypoxia. NIH HL46493 (MJJ), AR55819 (DPC) and RR‐024150.

AbstractLate‐onset HC is a well‐recognized complication associated with cyclophosphamide/acrolein‐induced toxicity. It poses a management challenge when hyperhydration and bladder irrigation do not result in clinical improvement as desired. The data regarding use of hyperbaric oxygen therapy (HBO2) as an early treatment modality in this clinical setting are limited. We present 2 cases, that were refractory to hyperhydration and bladder irrigation but responded to HBO2. They were treated with 20‐30 daily sessions over weekdays with 100% oxygen for 90 minutes at 2 atmospheric pressure units (2 atm). Both patients reported improved symptoms within the first 15 sessions, and hematuria diminished by 20 sessions. Hyperbaric oxygen is a less invasive, outpatient therapy that is effective for treatment of HC and is tolerated well by young patients.

Large increases in systemic oxygen content cause substantial reductions in exercising forearm blood flow (FBF) due to increased vascular resistance. We hypothesized that 1) functional sympatholysis (blunting of sympathetic α-adrenergic vasoconstriction) would be attenuated during hyperoxic exercise and 2) α-adrenergic blockade would limit vasoconstriction during hyperoxia and increase FBF to levels observed under normoxic conditions. Nine male subjects (age 28 ± 1 yr) performed forearm exercise (20% of maximum) under normoxic and hyperoxic conditions. Studies were performed in a hyperbaric chamber at 1 atmosphere absolute (ATA; sea level) while breathing 21% O2 and at 2.82 ATA while breathing 100% O2 (estimated change in arterial O2 content ∼6 ml O2/100 ml). FBF (ml/min) was measured using Doppler ultrasound. Forearm vascular conductance (FVC) was calculated from FBF and blood pressure (arterial catheter). Vasoconstrictor responsiveness was determined using intra-arterial tyramine. FBF and FVC were substantially lower during hyperoxic exercise than normoxic exercise (∼20–25%; P < 0.01). At rest, vasoconstriction to tyramine (% decrease from pretyramine values) did not differ between normoxia and hyperoxia ( P > 0.05). During exercise, vasoconstrictor responsiveness was slightly greater during hyperoxia than normoxia (−22 ± 3 vs. −17 ± 2%; P < 0.05). However, during α-adrenergic blockade, hyperoxic exercise FBF and FVC remained lower than during normoxia ( P < 0.01). Therefore, our data suggest that although the vasoconstrictor responsiveness during hyperoxic exercise was slightly greater, it likely does not explain the majority of the large reductions in FBF and FVC (∼20–25%) during hyperbaric hyperoxic exercise.

Hypoxia during exercise augments blood flow in active muscles to maintain the delivery of O2 at normoxic levels. However, the impact of hyperoxia on skeletal muscle blood flow during exercise is not completely understood. Therefore, we tested the hypothesis that the hyperemic response to forearm exercise during hyperbaric hyperoxia would be blunted compared with exercise during normoxia. Seven subjects (6 men/1 woman; 25 ± 1 yr) performed forearm exercise (20% of maximum) under normoxic and hyperoxic conditions. Forearm blood flow (FBF; in ml/min) was measured using Doppler ultrasound. Forearm vascular conductance (FVC; in ml·min−1·100 mmHg−1) was calculated from FBF and blood pressure (in mmHg; brachial arterial catheter). Studies were performed in a hyperbaric chamber with the subjects supine at 1 atmospheres absolute (ATA) (sea level) while breathing normoxic gas [21% O2, 1 ATA; inspired Po2 (PiO2) ≈ 150 mmHg] and at 2.82 ATA while breathing hyperbaric normoxic (7.4% O2, 2.82 ATA, PiO2 ≈ 150 mmHg) and hyperoxic (100% O2, 2.82 ATA, PiO2 ≈ 2,100 mmHg) gas. Resting FBF and FVC were less during hyperbaric hyperoxia compared with hyperbaric normoxia ( P < 0.05). The change in FBF and FVC (Δ from rest) during exercise under normoxia (204 ± 29 ml/min and 229 ± 37 ml·min−1·100 mmHg−1, respectively) and hyperbaric normoxia (203 ± 28 ml/min and 217 ± 35 ml·min−1·100 mmHg−1, respectively) did not differ ( P = 0.66–0.99). However, the ΔFBF (166 ± 21 ml/min) and ΔFVC (163 ± 23 ml·min−1·100 mmHg−1) during hyperbaric hyperoxia were substantially attenuated compared with other conditions ( P < 0.01). Our data suggest that exercise hyperemia in skeletal muscle is highly dependent on oxygen availability during hyperoxia.