During intense exercise in COPD, restriction of intercostal muscle perfusion but preservation of quadriceps muscle blood flow along with attainment of a plateau in cardiac output represents the inability of the circulatory system to satisfy the energy demands of locomotor and respiratory muscles.

Cerebral blood flow (CBF) is regulated to secure brain O delivery while simultaneously avoiding hyperperfusion; however, both requisites may conflict during sprint exercise. To determine whether brain O delivery or CBF is prioritized, young men performed sprint exercise in normoxia and hypoxia (PO = 73 mmHg). During the sprints, cardiac output increased to ∼22 L min, mean arterial pressure to ∼131 mmHg and peak systolic blood pressure ranged between 200 and 304 mmHg. Middle-cerebral artery velocity (MCAv) increased to peak values (∼16%) after 7.5 s and decreased to pre-exercise values towards the end of the sprint. When the sprints in normoxia were preceded by a reduced PCO, CBF and frontal lobe oxygenation decreased in parallel ( r = 0.93, P < 0.01). In hypoxia, MCAv was increased by 25%, due to a 26% greater vascular conductance, despite 4-6 mmHg lower PaCO in hypoxia than normoxia. This vasodilation fully accounted for the 22 % lower CaO in hypoxia, leading to a similar brain O delivery during the sprints regardless of PO. In conclusion, when a conflict exists between preserving brain O delivery or restraining CBF to avoid potential damage by an elevated perfusion pressure, the priority is given to brain O delivery.

Non-technical summary Exercise capacity is limited at high altitude where hypoxia (i.e. decreased amount of inspired oxygen resulting in decreased oxygen in the blood) is present, but it is unknown whether a reduction in the oxygen delivered to the brain constitutes the signal to the brain to prematurely terminate exercise. We show that during hypoxic exercise equivalent to exercise at ∼4000 m above sea-level, the oxygen delivered to the brain during intense exercise is ∼60% less than that delivered to the brain at comparable exercise intensity at sea-level. These results show that reduction in the oxygen delivered to the brain could constitute the signal to limit maximal exercise capacity in hypoxia, and help us understand better why exercise capacity is limited at high altitude. Moreover, a plausible mechanism of exercise limitation in patients who present decreased oxygen in the blood during exercise due to pulmonary and/or cardiac disease is revealed.Abstract During maximal hypoxic exercise, a reduction in cerebral oxygen delivery may constitute a signal to the central nervous system to terminate exercise. We investigated whether the rate of increase in frontal cerebral cortex oxygen delivery is limited in hypoxic compared to normoxic exercise. We assessed frontal cerebral cortex blood flow using near-infrared spectroscopy and the light-absorbing tracer indocyanine green dye, as well as frontal cortex oxygen saturation (S tO 2 %) in 11 trained cyclists during graded incremental exercise to the limit of tolerance (maximal work rate, WR max ) in normoxia and acute hypoxia (inspired O 2 fraction (F IO 2 ), 0.12). In normoxia, frontal cortex blood flow and oxygen delivery increased (P < 0.05) from baseline to sub-maximal exercise, reaching peak values at near-maximal exercise (80% WR max : 287 ± 9 W; 81 ± 23% and 75 ± 22% increase relative to baseline, respectively), both leveling off thereafter up to WR max (382 ± 10 W). Frontal cortex S tO 2 % did not change from baseline (66 ± 3%) throughout graded exercise. During hypoxic exercise, frontal cortex blood flow increased (P = 0.016) from baseline to sub-maximal exercise, peaking at 80% WR max (213 ± 6 W; 60 ± 15% relative increase) before declining towards baseline at WR max (289 ± 5 W). Despite this, frontal cortex oxygen delivery remained unchanged from baseline throughout graded exercise, being at WR max lower than at comparable loads (287 ± 9 W) in normoxia (by 58 ± 12%; P = 0.01). Frontal cortex S tO 2 % fell from baseline (58 ± 2%) on light and moderate exercise in parallel with arterial oxygen saturation, but then remained unchanged to exhaustion (47 ± 1%). Thus, during maximal, but not light to

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Background No consensus exists on how to average data to optimize trueV˙O2max assessment. Although the trueV˙O2max value is reduced with larger averaging blocks, no mathematical procedure is available to account for the effect of the length of the averaging block on trueV˙O2max. Aims To determine the effect that the number of breaths or seconds included in the averaging block has on the trueV˙O2max value and its reproducibility and to develop correction equations to standardize trueV˙O2max values obtained with different averaging strategies. Methods Eighty‐four subjects performed duplicate incremental tests to exhaustion (IE) in the cycle ergometer and/or treadmill using two metabolic carts (Vyntus and Vmax N29). Rolling breath averages and fixed time averages were calculated from breath‐by‐breath data from 6 to 60 breaths or seconds. Results trueV˙O2max decayed from 6 to 60 breath averages by 10% in low fit (trueV˙O2max < 40 mL kg−1 min−1) and 6.7% in trained subjects. The trueV˙O2max averaged from a similar number of breaths or seconds was highly concordant (CCC > 0.97). There was a linear‐log relationship between the number of breaths or seconds in the averaging block and trueV˙O2max (R2 > 0.99, P < 0.001), and specific equations were developed to standardize trueV˙O2max values to a fixed number of breaths or seconds. Reproducibility was higher in trained than low‐fit subjects and not influenced by the averaging strategy, exercise mode, maximal respiratory rate, or IE protocol. Conclusions The trueV˙O2max decreases following a linear‐log function with the number of breaths or seconds included in the averaging block and can be corrected with specific equations as those developed here.