Key result
Acute intermittent hypercapnic hypoxia preserved the muscle sympathetic nerve activity response to exercise and metaboreflex activation in healthy males, despite a modest increase in MAP response.
Why the study?
In normotensive OSA patients, the MSNA response to exercise is increased while metaboreflex control is decreased, prompting investigation into whether acute intermittent hypercapnic hypoxia produces similar autonomic alterations in healthy males.
Does acute intermittent hypercapnic hypoxia alter the muscle sympathetic nerve activity response to exercise and metaboreflex activation in healthy males?
Does acute intermittent hypercapnic hypoxia alter the muscle sympathetic nerve activity response to exercise and metaboreflex activation in healthy males?
Absolute Event Rate: 16% vs 14%
p-value: p=<0.01
Acute intermittent hypercapnic hypoxia does not alter sympathetic exercise responses in healthy males; hypothesis-generating for chronic exposure or OSA comorbidities.
PURPOSE: In normotensive patients with obstructive sleep apnea (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 yr) were exposed to 40 min of IHH. Before and after IHH, the pressor response to exercise was studied during 2 min of isometric handgrip exercise (at 30% maximal voluntary contraction), whereas the metaboreflex was studied during 4 min of postexercise 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 was similar before and after IHH (All P > 0.31). During PECO, the change from baseline in MSNA BF and TA was similar after IHH, whereas the change from baseline in MAP (Δ14 mm Hg, 95% CI = 7-19, vs Δ16 mm Hg, 95% CI = 10-21; P < 0.01) was modestly increased. CONCLUSION: After acute IHH, 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.
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Shafer et al. (2021) studied Healthy (n=13). Acute intermittent hypercapnic hypoxia (IHH) vs. Baseline (before IHH) was evaluated on Change from baseline in mean arterial pressure (MAP) during postexercise circulatory occlusion (PECO) (p=<0.01). Acute intermittent hypercapnic hypoxia preserved the muscle sympathetic nerve activity response to exercise and metaboreflex activation in healthy males, despite a modest increase in MAP response.
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