Key pointsr Intermittent hypoxia leads to long-lasting increases in muscle sympathetic nerve activity and blood pressure, contributing to increased risk for hypertension in obstructive sleep apnoea patients.r We determined whether augmented vascular responses to increasing sympathetic vasomotor outflow, termed sympathetic neurovascular transduction (sNVT), accompanied changes in blood pressure following acute intermittent hypercapnic hypoxia in men.r Lower body negative pressure was utilized to induce a range of sympathetic vasoconstrictor firing while measuring beat-by-beat blood pressure and forearm vascular conductance. r IH reduced vascular shear stress and steepened the relationship between diastolic blood pressure and sympathetic discharge frequency, suggesting greater systemic sNVT.r Our results indicate that recurring cycles of acute intermittent hypercapnic hypoxia characteristic of obstructive sleep apnoea could promote hypertension by increasing sNVT.Abstract Acute intermittent hypercapnic hypoxia (IH) induces long-lasting elevations in sympathetic vasomotor outflow and blood pressure in healthy humans. It is unknown whether IH alters sympathetic neurovascular transduction (sNVT), measured as the relationship between sympathetic vasomotor outflow and either forearm vascular conductance (FVC; regional sNVT) or diastolic blood pressure (systemic sNVT). We tested the hypothesis that IH augments sNVT by exposing healthy males to 40 consecutive 1 min breathing cycles, each comprising 40 s of hypercapnic hypoxia (P ETCO 2 : +4 ± 3 mmHg above baseline; P ETO 2 : 48 ± 3 mmHg) and 20 s of Troy J. R. Stuckless is a native of Bayside, Ontario in Canada. He attained his Bachelor of Science in Kinesiology from Queen's University and practiced as a kinesiologist in Calgary before pursuing an Master of Science from the University of British Columbia's Okanagan Campus under the supervision of Dr Glen Foster. His research interests include vascular endothelial cell function and interactions between the autonomic nervous system and cardiovascular health. Troy is currently completing the Doctor of Dental Surgery Program at the University of Toronto.normoxia (n = 9), or a 40 min air-breathing control (n = 7). Before and after the intervention, lower body negative pressure (LBNP; 3 min at -15, -30 and -45 mmHg) was applied to elicit reflex increases in muscle sympathetic nerve activity (MSNA, fibular microneurography) when clamping end-tidal gases at baseline levels. Ventilation, arterial pressure [systolic blood pressure, diastolic blood pressure, mean arterial pressure (MAP)], brachial artery blood flow (Q BA ), FVC (Q BA /MAP) and MSNA burst frequency were measured continuously. Following IH, but not control, ventilation [5 L min -1 ; 95% confidence interval (CI) = 1-9] and MAP (5 mmHg; 95% CI = 1-9) were increased, whereas FVC (-0.2 mL min -1 mmHg -1 ; 95% CI = -0.0 to -0.4) and mean shear rate (-21.9 s -1 ; 95% CI = -5.8 to -38.0; all P < 0.05) were reduced. Systemic sNVT was increased following IH (0.25 mmHg burst -1...

Ventilatory long-term facilitation (vLTF) refers to respiratory neuroplasticity that develops following intermittent hypoxia in both healthy and clinical populations. r A sustained hypercapnic background is argued to be required for full vLTF expression in humans. r We determined whether acute intermittent hypercapnic hypoxia elicits vLTF during isocapnic-normoxic recovery in healthy males and females. We further assessed whether tonic peripheral chemoreflex drive is necessary and contributes to the expression of vLTF. r Following 40 min of intermittent hypercapnic hypoxia, minute ventilation was increased throughout 50 min of isocapnic-normoxic recovery. Inhibition of peripheral chemoreflex drive with hyperoxia attenuated the magnitude of vLTF. r Males and females achieve vLTF through different respiratory recruitment patterns.

The purpose of this study was to examine the independent and combined effects of carbohydrate and caffeine ingestion on performance and various physiological parameters during aerobic cycling (∼1 h). Ten male cyclists (28 ± 9 years, 73 ± 6 kg, 66 ± 9 mL·kg(-1)·min(-1) maximal oxygen consumption) performed 20 min of steady-state (SS) cycling (60% peak power (W(max))) followed by a simulated 20-km time trial (TT) under placebo (PLA), carbohydrate (CHO), caffeine (CAF), and combined CAF-CHO conditions, all of which were performed in the fed state. CAF-CHO improved TT performance by 3.4% ± 2% (84 ± 57 s) compared with PLA (p < 0.05), whereas no differences were detected among CHO, CAF, and PLA. The SS respiratory exchange ratio was elevated in CHO (0.92 ± 0.03), CAF (0.96 ± 0.07), and CAF-CHO (0.95 ± 0.02) compared with PLA (0.89 ± 0.03) (p < 0.05). Post-SS and post-TT blood glucose levels were also elevated in CAF-CHO (88.3 ± 16.7 mg·dL(-1) and 111.2 ± 33.5 mg·dL(-1), respectively) compared with PLA (74.5 ± 9.8 mg·dL(-1) and 85.4 ± 17.6 mg·dL(-1), respectively) (p < 0.05). Treatment conditions did not differentially impact SS pulmonary ventilation, oxygen consumption, heart rate, peak quadriceps muscle strength, rating of perceived exertion, or blood lactate. CAF and CHO improved TT performance when taken together but not independently. Although the present work did not yield any definitive physiological mechanisms for the performance findings, these data suggest that cyclists in the fed state should ingest carbohydrate and caffeine together to improve time trial performance.

Findings suggest that OSA results in decreased cardiac function in patients entering CR, likely because of pressure and volume changes associated with apneic events. This may place those individuals at a disadvantage in recovering from their cardiac event, and place them at increased risk for secondary complications.