RESUMEN
The short-term scaling exponent of detrended fluctuation analysis (DFAα1) applied to interbeat intervals may provide a method to identify ventilatory thresholds and indicate systemic perturbation during prolonged exercise. The purposes of this study were to (i) identify the gas exchange threshold (GET) and respiratory compensation point (RCP) using DFAα1 values of 0.75 and 0.5 from incremental exercise, (ii) compare DFAα1 thresholds with DFAα1 measures during constant-speed running near the maximal lactate steady state (MLSS), and (iii) assess the repeatability of DFAα1 between MLSS trials. Twelve runners performed an incremental running test and constant-speed running 5% below, at, and 5% above the MLSS, plus a repeat trial at MLSS. During 30-min running trials near MLSS, DFAα1 responses were variable (i.e., 0.27-1.24) and affected by intensity (p = 0.031) and duration (p = 0.003). No difference in DFAα1 was detected between MLSS trials (p = 0.597). In the early phase (~ 8 min), DFAα1 measures at MLSS (0.71 [0.13]) remained higher than the DFAα1 identified at RCP from the incremental test (0.57 [0.13]; p = 0.024). In addition, following ~ 18 min of constant speed running at MLSS, DFAα1 measures (0.64 [0.14]) remained higher than 0.5 (p = 0.011)-the value thought to demarcate the boundaries between heavy and severe exercise intensities. Accordingly, using fixed DFAα1 values associated with the RCP from incremental exercise to guide constant-speed exercise training may produce a greater than expected exercise intensity, however; the dependency of DFAα1 on intensity and duration suggest its potential utility to quantify systemic perturbations imposed by continuous exercise.
RESUMEN
Nitric oxide is a gaseous signaling molecule that participates in a large variety of physiological functions and may have a role in the pathology of altitude illnesses, such as acute mountain sickness (AMS). The effect of normobaric hypoxia on the fraction of exhaled NO ( [Formula: see text] ) is a controversial area of high altitude physiology, with the effect varying widely across studies. We exposed 19 male subjects to normobaric hypoxia for 6h and measured [Formula: see text] and AMS (via Lake Louise Score) each hour. For data analysis, subjects were divided into AMS-positive and AMS-negative groups based on their Lake Louise Scores during exposure. Eighteen subjects completed the study, and the incidence of AMS was 50%. Mean [Formula: see text] was unchanged at hour 1 but was significantly elevated above baseline for the remainder of the normobaric hypoxia exposure (p<0.001). Subjects who developed AMS had a significantly lower mean [Formula: see text] at baseline compared to resistant subjects (p=0.013). Further investigations are warranted to confirm our results and to understand the physiological basis of this association.