Acute respiratory muscle unloading improves time-to-exhaustion during moderate- and heavy-intensity cycling in obese adolescent males.

Obesity significantly impairs breathing during exercise. The aim was to determine, in male obese adolescents (OB), the effects of acute respiratory muscle unloading, obtained by switching the inspired gas from ambient air (AIR) to a normoxic helium + oxygen gas mixture (HeO2) (AIR → HeO2) during moderate [below gas exchange threshold (GET)] and heavy [above GET] constant work rate cycling. Ten OB [age 16.0 ± 2.0 years (mean ± SD); body mass index (BMI) 38.9 ± 6.1 kg/m2] and ten normal-weight age-matched controls (CTRL) inspired AIR for the entire exercise task, or underwent AIR → HeO2 when they were approaching volitional exhaustion. In OB time to exhaustion (TTE) significantly increased in AIR → HeO2 vs. AIR during moderate [1524 ± 480 s vs. 1308 ± 408 (P = 0.024)] and during heavy [570 ± 306 s vs. 408 ± 150 (P = 0.0154)] exercise. During moderate exercise all CTRL completed the 40-min task. During heavy exercise no significant differences were observed in CTRL for TTE (582 ± 348 s [AIR → HeO2] vs. 588 ± 252 [AIR]). In OB, but not in CTRL, acute unloading of respiratory muscles increased TTE during both moderate- and heavy-exercise. In OB, but not in CTRL, respiratory factors limit exercise tolerance during both moderate and heavy exercise.

Changes in Skeletal Muscle Oxidative Capacity After a Trail Running Race.

PURPOSE: to evaluate the effects of a trail-running race on muscle oxidative function by measuring pulmonary gas exchange variables and muscle fractional O2 extraction. METHODS: Eighteen athletes were evaluated before (PRE) and after (POST) a trail running competition of 32-km or 50-km with 2000 m or 3500 m of elevation gain, respectively. During the week before the race, runners performed an incremental uphill running test and an incremental exercise by utilizing a one-leg knee-extension (KE) ergometer. The KE exercise was repeated after the end of the race. During the KE test we measured oxygen uptake (V'O2) and micromolar changes in deoxygenated hemoglobin (Hb)+myoglobin (Mb) concentrations (Δ[deoxy(Hb+Mb)]) on vastus lateralis with a portable near-infrared spectroscopy. RESULTS: V'O2peak was lower at POST vs. PRE (-23.9±9.0%, p<0.001). V'O2peak at POST was lower than V'O2 at the same workload at PRE (-8.4±15.6%, p<0.050). Peak power output and time to exhaustion decreased at POST by -23.7±14.3% and -18.3±11.3%, respectively (p<0.005). At POST the increase of Δ[deoxy(Hb + Mb)] as a function of work rate, from unloaded to peak, was less pronounced (from 20.2±10.1 to 64.5±21.1% of limb ischemia at PRE to 16.9±12.7 to 44.0±18.9% at POST). Peak Δ[deoxy(Hb+Mb)] values were lower at POST (by -31.2±20.5%; p<0.001). CONCLUSIONS: trail running leads to impairment in skeletal muscle oxidative metabolism, possibly related to muscle damage from repeated eccentric contractions. In association with other mechanisms, the impairment of skeletal muscle oxidative metabolism is likely responsible of the reduced exercise capacity and tolerance during and following these races.

Air blood barrier phenotype correlates with alveolo-capillary O2 equilibration in hypobaric hypoxia.

The O2 diffusion limitation across the air blood barrier (DO2 and subcomponents Dm and Vc) was evaluated in 17 healthy participants exposed to hypobaric hypoxia (HA, 3840m, PIO2 ∼90mmHg). A 10% decrease in alveolar volume (VA) in all participants suggested the development of sub-clinical interstitial lung edema. In >80% of participants DO2/VA increased, reflecting an individual strategy to cope with the hypoxia stimulus by remodulating Vc or Dm. Opposite changes in Dm/Vc ratio were observed and participants decreasing Vc showed reduced alveolar blood capillary transit time. The interplay between diffusion and perfusion (cardiac output) was estimated in order to investigate the individual adaptive response to hypoxia. It appears remarkable that despite individual differences in the adaptive response to HA, diffusion limitation did not exceed ∼11% of the alveolar-venous PO2 gradient, revealing an admirable functional design of the air-blood barrier to defend the O2 diffusion/perfusion function when facing hypobaric hypoxia corresponding to 50mmHg decreased PAO2.

Reappraisal of DLCO adjustment to interpret the adaptive response of the air-blood barrier to hypoxia.

DLCO measured in hypoxia must be corrected due to the higher affinity (increase in coefficient θ) of CO with Hb. We propose an adjustment accounting for individual changes in the equation relating DLCO to subcomponents Dm (membrane diffusive capacity) and Vc (lung capillary volume): 1/DLCO=1/Dm+1/θVc. We adjusted the individual DLCO measured in hypoxia (HA, 3269m) by interpolating the 1/DLCO to the sea level (SL) 1/θ value. Nineteen healthy subjects were studied at SL and HA. Based on the proposed adjustment, DLCO increased in HA in 53% of subjects, reflecting the increase in Dm that largely overruled the decrease in Vc. We hypothesize that a decrease in Vc (buffering microvascular filtration) and the increase in Dm (possibly resulting from a decrease in thickness of the air-blood barrier) represent the anti-edemagenic adaptation of the lung to hypoxia exposure. The efficiency of this adaptation varied among subjects as DLCO did not change in 31% of subjects and decreased in 16%.