This study assessed the intra-individual reliability of oxygen saturation in intercostal muscles (SmO₂-m.intercostales) during an incremental maximal treadmill exercise by using portable NIRS devices in a test-retest study. Fifteen marathon runners (age, 24.9 ± 2.0 years; body mass index, 21.6 ± 2.3 kg·m⁻²; V̇O₂-peak, 63.7 ± 5.9 mL·kg⁻¹·min⁻¹) were tested on two separate days, with a 7-day interval between the two measurements. Oxygen consumption (V̇O₂) was assessed using the breath-by-breath method during the V̇O₂-test, while SmO₂ was determined using a portable commercial device, based in the near-infrared spectroscopy (NIRS) principle. The minute ventilation (VE), respiratory rate (RR), and tidal volume (Vt) were also monitored during the cardiopulmonary exercise test. For the SmO₂-m.intercostales, the intraclass correlation coefficient (ICC) at rest, first (VT1) and second ventilatory (VT2) thresholds, and maximal stages were 0.90, 0.84, 0.92, and 0.93, respectively; the confidence intervals ranged from −10.8% – +9.5% to −15.3% – +12.5%. The reliability was good at low intensity (rest and VT1) and excellent at high intensity (VT2 and max). The Spearman correlation test revealed (p ≤ 0.001) an inverse association of SmO₂-m.intercostales with V̇O₂ (ρ = −0.64), VE (ρ = −0.73), RR (ρ = −0.70), and Vt (ρ = −0.63). The relationship with the ventilatory variables showed that increased breathing effort during exercise could be registered adequately using a NIRS portable device.

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This study aimed to evaluate if the changes in oxygen saturation levels at intercostal muscles (SmO₂-m.intercostales) assessed by near-infrared spectroscopy (NIRS) using a wearable device could determine the respiratory compensation point (RCP) during exercise. Fifteen healthy competitive triathletes (eight males; 29 ± 6 years; height 167.6 ± 25.6 cm; weight 69.2 ± 9.4 kg; $\dot{\mathrm{V}}$O₂-máx 58.4 ± 8.1 mL·kg⁻¹·min⁻¹) were evaluated in a cycle ergometer during the maximal oxygen-uptake test ($\dot{\mathrm{V}}$O₂-máx), while lung ventilation ($\dot{\mathrm{V}}$E), power output (watts, W) and SmO₂-m.intercostales were measured. RCP was determined by visual method (RCP_visual: changes at ventilatory equivalents ($\dot{\mathrm{V}}$E·$\dot{\mathrm{V}}$CO₂⁻¹, $\dot{\mathrm{V}}$E·$\dot{\mathrm{V}}$O₂⁻¹) and end-tidal respiratory pressure (PetO₂, PetCO₂) and NIRS method (RCP_NIRS: breakpoint of fall in SmO₂-m.intercostales). During exercise, SmO₂-m.intercostales decreased continuously showing a higher decrease when $\dot{\mathrm{V}}$E increased abruptly. A good agreement between methods used to determine RCP was found (visual vs NIRS) at %$\dot{\mathrm{V}}$O₂-máx, $\dot{\mathrm{V}}$O₂, $\dot{\mathrm{V}}$E, and W (Bland-Altman test). Correlations were found to each parameters analyzed (r = 0.854; r = 0.865; r = 0.981; and r = 0,968; respectively. p < 0.001 in all variables, Pearson test), with no differences (p < 0.001 in all variables, Student’s t-test) between methods used (RCP_visual and RCP_NIRS). We concluded that changes at SmO₂-m.intercostales measured by NIRS could adequately determine RCP in triathletes.

The study aimed to evaluate the association between the changes in ventilatory variables (tidal volume (Vt), respiratory rate (RR) and lung ventilation ($\stackrel{.}{\mathrm{V}}$E)) and deoxygenation of m.intescostales (∆SmO₂-m.intercostales) during a maximal incremental exercise in 19 male high-level competitive marathon runners. The ventilatory variables and oxygen consumption ($\stackrel{.}{\mathrm{V}}$O₂) were recorded breath-by-breath by exhaled gas analysis. A near-infrared spectroscopy device (MOXY^®) located in the right-hemithorax allowed the recording of SmO₂-m.intercostales. To explore changes in oxygen levels in muscles with high demand during exercise, a second MOXY^® records SmO₂-m.vastus laterallis. The triphasic model of exercise intensity was used for evaluating changes in SmO₂ in both muscle groups. We found that ∆SmO₂-m.intercostales correlated with $\stackrel{.}{\mathrm{V}}$O_2-peak (r = 0.65; p = 0.002) and the increase of $\stackrel{.}{\mathrm{V}}$E (r = 0.78; p = 0.001), RR (r = 0.54; p = 0.001), but not Vt (p = 0.210). The interaction of factors (muscles × exercise-phases) in SmO₂ expressed as an arbitrary unit (a.u) was significant (p = 0.005). At VT1 there was no difference (p = 0.177), but SmO₂-m.intercostales was higher at VT2 (p < 0.001) and $\stackrel{.}{\mathrm{V}}$O_2-peak (p < 0.001). In high-level competitive marathon runners, the m.intercostales deoxygenation during incremental exercise is directly associated with the aerobic capacity and increased lung ventilation and respiratory rate, but not tidal volume. Moreover, it shows less deoxygenation than m.vastus laterallis at intensities above the aerobic ventilatory threshold.

Respiratory muscle training (RMT) improves physical performance, although it is still debated whether this effect depends on the type of training. The purpose of this study was to compare the effects of two different types of RMT, i.e., voluntary isocapnic hyperpnea (VIH) and inspiratory threshold loading (ITL), on the deoxygenation of intercostal (ΔSmO₂-m. intercostales) and vastus lateralis (ΔSmO₂-m. vastus lateralis) muscles during exercise. Twenty-four participants performed eight weeks of RMT by: (i) VIH (3 days·week⁻¹ for 12 min at 60% maximal voluntary ventilation) or (ii) ITL (5 sets·week⁻¹ of 30 breaths·minute⁻¹ at 60% maximal inspiratory pressure). Cardiopulmonary exercise testing (CPET) included ΔSmO₂ (the change from baseline to end of test) of intercostal and vastus lateralis muscles. After RMT, both groups showed decreased ΔSmO₂-m. intercostales (VIH = 12.8 ± 14.6%, p = 0.04 (effect size, ES = 0.59), and ITL = 8.4 ± 9.8%, p = 0.04 (ES = 0.48)), without a coincident change of ∆SmO_2-m. vastus lateralis. ITL training induced higher $\dot{V}$O_2-peak absolute values than VIH (mean Δ post–pre, ITL = 229 ± 254 mL·min⁻¹ [95% CI 67–391] vs. VIH, 39 ± 153 mL·min⁻¹ [95% CI −58–136.0], p = 0.01). In conclusion, both RMT improved the balance between supply and oxygen consumption levels of m. intercostales during CPET, with ITL also inducing an increase of aerobic capacity.