LAUSR

PURPOSE In normotensive patients with OSA, the muscle sympathetic nerve activity (MSNA) response to exercise is increased while metaboreflex control of MSNA is decreased. We tested the hypotheses that acute intermittent hypercapnic hypoxia (IHH) in males free from OSA and associated comorbidities would augment the MSNA response to exercise but attenuate the change in MSNA during metaboreflex activation. METHODS Thirteen healthy males (age = 24 ± 4 years) were exposed to 40 minutes of IHH. Before and after IHH, the pressor response to exercise was studied during 2-minutes of isometric handgrip exercise (at 30% maximal voluntary contraction) while the metaboreflex was studied during 4-minutes of post exercise circulatory occlusion (PECO). Mean arterial pressure (MAP), heart rate (HR), and fibular MSNA were recorded continuously. MSNA was quantified as burst frequency (BF) and total activity (TA). Mixed effects linear models were used to compare the exercise pressor and metaboreflex before and after IHH. RESULTS As expected, IHH led to significant increases in MSNA BF, TA, and MAP at baseline and throughout exercise and PECO. However, during handgrip exercise the change from baseline in MAP, HR, MSNA BF, and TA were similar before and after IHH (All P > 0.31). During PECO, the change from baseline in MSNA BF and TA were similar following IHH while the change from baseline in MAP (Δ14 {95%CI 7,19} vs. Δ16 {10,21}, mmHg; P < 0.01) was modestly increased. CONCLUSION Following acute IHH, the MSNA response to handgrip exercise and metaboreflex activation were preserved in healthy young males despite overall increases in resting MSNA and MAP. Chronic IHH and comorbidities often associated with OSA may be required to modulate the exercise pressor reflex and metaboreflex.