Alcohol Breath Test: Gas Exchange Issues

The alcohol breath test is reviewed with a focus on gas exchange factors affecting its accuracy. The basis of the alcohol breath test is the assumption that alveolar air reaches the mouth during exhalation with no change in alcohol concentration. Recent investigations have shown that alcohol concentration is altered during its transit to the mouth. The exhaled alcohol concentration is modified by interaction with the mucosa of the pulmonary airways. Exhaled alcohol concentration is not an accurate indicator of alveolar alcohol concentration. Measuring alcohol concentration in the breath is very different process than measuring a blood level from air equilibrated with a blood sample. Airway exchange of alcohol leads to a bias against certain individuals depending on the anatomic and physiologic characteristics. Methodological modifications are proposed to improve the accuracy of the alcohol breath test to become fair to all.

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Separate and combined effects of a 10-d exposure to hypoxia and inactivity on oxidative function in vivo and mitochondrial respiration ex vivo in humans.

An integrative evaluation of oxidative metabolism was carried out in 9 healthy young men (age: 24.1±1.7 years [mean±SD]) prior to (CTRL) and following a 10-day horizontal bed rest, carried out in normoxia (N-BR) or hypoxia (F_IO₂=0.147; H-BR). H-BR was aimed to simulate planetary habitats. Pulmonary O₂ uptake (V'O₂) and vastus lateralis fractional O₂ extraction (changes in deoxygenated hemoglobin+myoglobin concentration, [deoxy(Hb+Mb)]; near-infrared spectroscopy) were evaluated, in normoxia, during an incremental cycle ergometer exercise (CE) and one-leg knee extension exercise (KE) (aimed at reducing cardiovascular constraints to oxidative function). Mitochondrial respiration was evaluated ex vivo by high-resolution respirometry in permeabilized vastus lateralis fibers. During CE V'O₂peak and [deoxy(Hb+Mb)]peak were lower (P<0.05) after both N-BR and H-BR vs. CTRL; during KE the variables were lower after N-BR, but not after H-BR. During CE the "overshoot" of [deoxy(Hb+Mb)] during constant work rate exercise was greater in N-BR and H-BR vs. CTRL, whereas during KE a significant difference vs. CTRL was observed only after N-BR. Maximal mitochondrial respiration determined ex vivo was not affected by both interventions. In N-BR, a significant impairment of oxidative metabolism occurred downstream of central cardiovascular O₂ delivery and upstream of mitochondrial function, possibly at the level of the intramuscular matching between O₂ supply and utilization (see the [deoxy(Hb+Mb)] overshoot) and peripheral O₂ diffusion. Superposition of H on BR did not aggravate, and partially reversed, the impairment of muscle oxidative function in vivo induced by BR. The effects of longer exposures will have to be determined.

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Role of histidyl dipeptides in contractile function of fast and slow motor units in rat skeletal muscle

The physiological role of the muscle histidyl dipeptides carnosine and anserine in contractile function of various types of muscle fibres in vivo is poorly understood. Ten adult male Wistar rats were randomly assigned to two groups: control and supplemented for 10 weeks with beta-alanine, the precursor of carnosine (~640 mg/kg BW/day). Thereafter, contractile properties and fatigability of isolated fast fatigable (FF), fast resistant to fatigue (FR), and slow motor units (MUs) from the medial gastrocnemius were determined in deeply anaesthetized animals. The fatigue resistance was tested with a 40 Hz fatigue protocol followed by a second protocol at 40 Hz in fast and 20 Hz in slow units. In the supplemented rats, histidyl dipeptide concentrations significantly increased (P < 0.05) by 25% in the red portion of the gastrocnemius and carnosine increased by 94% in the white portion. The twitch force of FF units and maximum tetanic force of FR units were significantly increased (P < 0.05) and the half-relaxation time was prolonged in slow units (P < 0.05). FF units showed less fatigue during the first 10 s and FR units between 10 and 60 s during the 40 Hz fatigue test. In slow units, forces declined less during the first 60 s of the 20 Hz test. In conclusion, this in vivo experiment demonstrates that an elevation in muscle histidyl dipeptide content elicits beneficial changes in MU contractile characteristics and fatigue resistance. Carnosine and anserine seem to play an important yet divergent role in various MUs.

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Age-induced oxidative stress: How does it influence skeletal muscle quantity and quality?

With advancing age, skeletal muscle function declines as a result of strength loss. These strength deficits are largely due to reductions in muscle size (i.e., quantity) and its intrinsic force producing capacity (i.e., quality). Age-induced reductions in skeletal muscle quantity and quality can be the consequence of several factors, including accumulation of reactive oxygen and nitrogen species (ROS/RNS), also known as oxidative stress. In old muscle, oxidative stress has the potential to reduce muscle quantity by shifting protein balance in a deficit, and muscle quality by impairing activation at the neuromuscular junction, excitation-contraction (EC) coupling at the ryanodine receptor (RyR) and cross-bridge cycling within the myofibrillar apparatus. Of these, EC coupling failure mediated by RyR dysfunction via oxidation and/or nitrosylation appears to be the strongest candidate based on the publications reviewed. However, it is clear that age-associated oxidative stress has the ability to alter strength through several mechanisms and at various locations of the muscle fiber.

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How does an airway and subsequently the lung become hyperresponsive?

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Static and dynamic stress heterogeneity in a multiscale model of the asthmatic airway wall.

Airway hyper-responsiveness (AHR) is a key characteristic of asthma that remains poorly understood. Tidal breathing and deep inspiration ordinarily cause rapid relaxation of airway smooth muscle(ASM) (as demonstrated via application of length fluctuations to tissue strips) and are therefore implicated in modulation of AHR, but in some cases (such as application of transmural pressure oscillations to isolated intact airways) this mechanism fails. Here we use a multiscale biomechanical model for intact airways, that incorporates strain-stiffening due to collagen recruitment and dynamic force generation by ASM cells, to show that the geometry of the airway, together with interplay between dynamic active and passive forces, give rise to large stress and compliance heterogeneities across the airway wall that are absent in tissue strips. We show further that these stress heterogeneities result in auxotonic loading conditions that are currently not replicated in tissue-strip experiments; stresses in the strip are similar to hoop stress only at the outer airway wall and are under- or over-estimates of stresses at the lumen. Taken together these results suggest that a previously underappreciated factor - stress heterogeneities within the airway wall and consequent ASM cellular response to this micromechanical environment - could contribute to AHR and should be explored further both theoretically and experimentally.

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Exercise-induced endothelial progenitor cell mobilization is attenuated in impaired glucose tolerance and type 2 diabetes

Circulating endothelial progenitor cells (EPCs) contribute to vascular homeostasis and are fewer in those with type 2 diabetes mellitus (T2DM) compared with normal glucose tolerance (NGT), suggesting a link between EPCs and T2DM-associated vasculopathies. The purpose of this study was to assess EPC number and mobilization by acute submaximal exercise in older adults with NGT, impaired glucose tolerance (IGT) or T2DM. We tested the hypothesis that EPC mobilization is lower in IGT compared with NGT and further reduced in older adults with T2DM. Forty-five older (50-75 years of age) men and women with NGT (n=18), IGT (n=10), or T2DM (n=17) were characterized and underwent submaximal aerobic exercise tests with blood sampling for enumeration of vascular endothelial growth factor receptor 2+ (VEGFR2+) cells, CD34+ hematopoetic progenitor cells, and CD34+/VEGFR2+ EPCs by flow cytometry before and after exercise. Basal EPC number was 65% and 61% lower in the IGT and T2DM groups, respectively, compared with the NGT group (P<0.05). EPC number increased 23% after acute exercise in the NGT group (P<0.01), but did not change in the IGT or T2DMgroups. Before and after exercise, VEGFR2+ cell number was lower in a stepwise manner across the NGT, IGT and T2DM groups (P<0.05). Basal CD34+ cell number was lower in the IGT group compared with NGT (P<0.05), but did not change after exercise in any group. These findings suggest a CD34+/VEGFR2+ EPC mobilization defect in IGT and T2DM that could play a role in the cardiovascular diseases and capillary rarefaction associated with insulin resistance.

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