Cerebral blood flow (CBF) is regulated to secure brain O₂ delivery while simultaneously avoiding hyperperfusion; however, both requisites may conflict during sprint exercise. To determine whether brain O₂ delivery or CBF is prioritized, young men performed sprint exercise in normoxia and hypoxia (P_IO₂ = 73 mmHg). During the sprints, cardiac output increased to ∼22 L min⁻¹, 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 P_ETCO₂, 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 PaCO₂ in hypoxia than normoxia. This vasodilation fully accounted for the 22 % lower CaO₂ in hypoxia, leading to a similar brain O₂ delivery during the sprints regardless of P_IO₂. In conclusion, when a conflict exists between preserving brain O₂ delivery or restraining CBF to avoid potential damage by an elevated perfusion pressure, the priority is given to brain O₂ delivery.

To determine whether task failure during incremental exercise to exhaustion (IE) is principally due to reduced neural drive and increased metaboreflex activation eleven men (22±2 years) performed a 10s control isokinetic sprint (IS; 80 rpm) after a short warm-up. This was immediately followed by an IE in normoxia (Nx, PIO2:143 mmHg) and hypoxia (Hyp, PIO2:73 mmHg) in random order, separated by a 120 min resting period. At exhaustion, the circulation of both legs was occluded instantaneously (300 mmHg) during 10 or 60s to impede recovery and increase metaboreflex activation. This was immediately followed by an IS with open circulation. Electromyographic recordings were obtained from the vastus medialis and lateralis. Muscle biopsies and blood gases were obtained in separate experiments. During the last 10s of the IE, pulmonary ventilation, VO2, power output and muscle activation were lower in hypoxia than in normoxia, while pedaling rate was similar. Compared to the control sprint, performance (IS-Wpeak) was reduced to a greater extent after the IE-Nx (11% lower P<0.05) than IE-Hyp. The root mean square (EMGRMS) was reduced by 38 and 27% during IS performed after IE-Nx and IE-Hyp, respectively (Nx vs. Hyp: P<0.05). Post-ischemia IS-EMGRMS values were higher than during the last 10s of IE. Sprint exercise mean (IS-MPF) and median (IS-MdPF) power frequencies, and burst duration, were more reduced after IE-Nx than IE-Hyp (P<0.05). Despite increased muscle lactate accumulation, acidification, and metaboreflex activation from 10 to 60s of ischemia, IS-Wmean (+23%) and burst duration (+10%) increased, while IS-EMGRMS decreased (-24%, P<0.05), with IS-MPF and IS-MdPF remaining unchanged. In conclusion, close to task failure, muscle activation is lower in hypoxia than in normoxia. Task failure is predominantly caused by central mechanisms, which recover to great extent within one minute even when the legs remain ischemic. There is dissociation between the recovery of EMGRMS and performance. The reduction of surface electromyogram MPF, MdPF and burst duration due to fatigue is associated but not caused by muscle acidification and lactate accumulation. Despite metaboreflex stimulation, muscle activation and power output recovers partly in ischemia indicating metaboreflex activation has a minor impact on sprint performance.

Torres-Peralta, Rafael, José Losa-Reyna, Miriam González-Izal, Ismael Perez-Suarez, Jaime Calle-Herrero, Mikel Izquierdo, and José A.L. Calbet. Muscle activation during exercise in severe acute hypoxia: Role of absolute and relative intensity. High Alt Med Biol 15:472–482, 2014.—The aim of this study was to determine the influence of severe acute hypoxia on muscle activation during whole body dynamic exercise. Eleven young men performed four incremental cycle ergometer tests to exhaustion breathing normoxic (F _I o ₂ =0.21, two tests) or hypoxic gas (F _I o ₂ =0.108, two tests). Surface electromyography (EMG) activities of rectus femoris (RF), vastus medialis (VL), vastus lateralis (VL), and biceps femoris (BF) were recorded. The two normoxic and the two hypoxic tests were averaged to reduce EMG variability. Peak V o ₂ was 34% lower in hypoxia than in normoxia ( p <0.05). The EMG root mean square (RMS) increased with exercise intensity in all muscles ( p <0.05), with greater effect in hypoxia than in normoxia in the RF and VM ( p <0.05), and a similar trend in VL ( p =0.10). At the same relative intensity, the RMS was greater in normoxia than in hypoxia in RF, VL, and BF ( p <0.05), with a similar trend in VM ( p =0.08). Median frequency increased with exercise intensity ( p <0.05), and was higher in hypoxia than in normoxia in VL ( p <0.05). Muscle contraction burst duration increased with exercise intensity in VM and VL ( p <0.05), without clear effects of F _I o ₂ . No significant F _I o ₂ effects on frequency domain indices were observed when compared at the same relative intensity. In conclusion, muscle activation during whole body exercise increases almost linearly with exercise intensity, following a muscle-specific pattern, which is adjusted depending on the F _I o ₂ and the relative intensity of exercise. Both VL and VM are increasingly involved in power output generation with the increase of intensity and the reduction in F _I o ₂ .

Negative arterial to end‐tidal pco₂ differences ((a‐ET)pco₂) have been reported in normoxia. To determine the influence of blood temperature on (a‐ET)pco₂, 11 volunteers (21 ± 2 years) performed incremental exercise to exhaustion in normoxia (Nx, P_io₂: 143 mmHg) and hypoxia (Hyp, P_io₂: 73 mmHg), while arterial blood gases and temperature (ABT) were simultaneously measured together with end‐tidal pco₂ (P_Etco₂). After accounting for blood temperature, the (a‐ET) pco₂ was reduced (in absolute values) from −4.2 ± 1.6 to −1.1 ± 1.5 mmHg in normoxia and from −1.7 ± 1.6 to 0.9 ± 0.9 mmHg in hypoxia (both P < 0.05). The temperature corrected (a‐ET)pco₂ was linearly related with absolute and relative exercise intensity, VO₂, VCO₂, and respiratory rate (RR) in normoxia and hypoxia (R²: 0.52–0.59). Exercise CO₂ production and P_Etco₂ values were lower in hypoxia than normoxia, likely explaining the greater (less negative) (a‐ET)pco₂ difference in hypoxia than normoxia (P < 0.05). At near‐maximal exercise intensity the (a‐ET)pco₂ lies close to 0 mmHg, that is, the mean P_aco₂ and the mean P_Etco₂ are similar. The mean exercise (a‐ET)pco₂ difference is closely related to the mean A‐aDO₂ difference (r = 0.90, P < 0.001), as would be expected if similar mechanisms perturb the gas exchange of O₂ and CO₂ during exercise. In summary, most of the negative (a‐ET)pco₂ values observed in previous studies are due to lack of correction of P_aco₂ for blood temperature. The absolute magnitude of the (a‐ET)pco₂ difference is lower during exercise in hypoxia than normoxia.