Chapman, Robert F.

Background Exercise tolerance is strongly related the physiological components of the primary (PC) and slow components (SC) of oxygen uptake. Exercise tolerance is reduced in clinical populations and during acute exposure to altitude by factors affecting skeletal muscle oxygenation. The practice of ischemic preconditioning has been shown to improve exercise tolerance or performance in a variety of different testing methods, but the mechanisms behind the improvements in exercise tolerance following IPC are still unclear. Methods Thirteen men (age= 24 ± 4 years, V̇O 2 max= 63.1 ± 5.1 ml·kg −1 ·min −1 ) completed four randomized trials of each combination of hypoxia (F I O 2 = 0.16) or normoxia (F I O 2 = 0.21) with a resting pre‐exercise IPC protocol (4 × 5 min at 220 mmHg) or SHAM procedure. Following the IPC/SHAM protocol subjects completed two constant load cycling bouts at power outputs corresponding to 1) 15% below the normoxic gas exchange threshold (CL #1) and 2) 85% of normoxic V̇O 2 max (CL #2). Breath‐by‐breath V̇O 2 , oxyhemoglobin saturation, and skeletal muscle oxygenation/extraction (measured via near‐infrared spectroscopy) were continuously monitored throughout the trials. V̇O 2 and NIRS kinetics were quantified using a single (for CL#1) or double (for CL#2) exponential term equation with independent time delays for the V̇O 2 /NIRS primary and slow components. Results There was a significant effect of inspirate on deoxyhemoglobin time constant (τ) during CL#1 (Hypoxia: 5.58 ± 2.82 s vs. Normoxia: 8.01 ± 4.71s, P < 0.05) with no effect of IPC treatment (P = 0.84). During CL #2, there was a significant effect of inspirate on V̇O 2 primary amplitude (PC) (Normoxia: 3.13 ± 0.36 L/min vs. Hypoxia: 2.92 ± 0.39 L/min, P < 0.05). IPC did preserve microvascular oxygen extraction during high‐intensity cycling (CL #2) in Hypoxia (IPC: 21.3 ± 11.0 μM vs. SHAM: 19.9 ± 9.9 μM, P < 0.05), but did not affect any of the NIRS or V̇O 2 parameters in Normoxia. Conclusion Oxygen uptake and peripheral oxygen delivery are compromised during high‐intensity exercise in hypoxia. Ischemic preconditioning prior to high‐intensity bouts is effective at mitigating the declines in microvascular oxygen extraction seen during exercise in hypoxia, however the rates (τ) of microvascular extraction and oxygen uptake are not altered following treatment with IPC. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .

Environmental stressors, such as heat or altitude, elicit dissimilar physiological adaptations to endurance training programs. Whether these differences (i.e., increased hemoglobin mass vs plasma volume) differentially influence performance is debated. We review data in support of our novel hypothesis, which proposes altitude as the preferred environmental training stimulus for elite endurance athletes preparing to compete in temperate, sea-level climates (5°C–18°C).

ABSTRACT Introduction An adequate increase in minute ventilation to defend arterial oxyhemoglobin saturation (SpO 2 ) during hypoxic exercise is commonly viewed as an important factor contributing to large inter-individual variations in the degree of exercise performance impairment in hypoxia. Although the hypoxic ventilatory response (HVR) could provide insight into the underpinnings of such impairments, it is typically measured at rest under isocapnic conditions. Thus, we aimed to determine whether 1) HVR at rest and during exercise are similar and 2) exercise HVR is related to the degree of impairment in cycling time trial (TT) performance from normoxia to acute hypoxia (∆TT). Methods Sixteen endurance-trained men (V˙O 2peak , 62.5 ± 5.8 mL·kg −1 ·min −1 ) performed two poikilocapnic HVR tests: one during seated rest (HVR REST ) and another during submaximal cycling (HVR EX ). On two separate visits, subjects ( n = 12) performed a 10-km cycling TT while breathing either room air (F i O 2 = 0.21) or hypoxic gas mixture (F i O 2 = 0.16) in a randomized order. Results HVR EX was significantly ( P < 0.001) greater than HVR REST (1.52 ± 0.47 and 0.22 ± 0.13 L·min −1 ·%SpO 2 −1 , respectively), and these measures were not correlated ( r = −0.16, P = 0.57). ∆TT was not correlated with HVR REST ( P = 0.70) or HVR EX ( P = 0.54), but differences in ventilation and end-tidal CO 2 between hypoxic and normoxic TT and the ventilatory equivalent for CO 2 during normoxic TT explained ~85% of the variance in performance impairment in acute hypoxia ( P < 0.01). Conclusion We conclude that 1) HVR is not an appropriate measure to predict the exercise ventilatory response or performance impairments in acute hypoxia and 2) an adequate and metabolically matched increase in exercise ventilation, but not the gain in the ventilatory response to hypoxia, is essential for mitigating hypoxia-induced impairments in endurance cycling performance.