The Influence of Baseline Metabolic Rate and Exercise Training on Cardio-Respiratory Dynamics

Speeding the VO2 kinetics results in a reduction of the O2 deficit. Two factors might determine VO2 kinetics: oxygen delivery to muscle (Tschakovsky and Hughson 1999) and a muscle 'metabolic inertia' (Grassi et al. 1996). Therefore, in study 1 we investigated VO2 kinetics and cardiovascular system adaptations during step exercise transitions in different regions of the moderate domain. In study 2 we investigated muscle oxygenation and cardio-pulmonary adaptations during step exercise tests before, after and over a period of training. Study 1 methods: Seven subjects (26 ± 8 yr; 176 ± 5 cm; 69 ± 6 kg) performed 4 types of step transition from rest (0-50W; 0-100W) or elevate baseline (25-75W; 25-125W). GET and VO2max were assessed before testing. O2 uptake and were measured during testing. Study 2 methods: 10 subjects (25 ± 4 yr; 175 ± 9 cm; 71 ± 12 kg) performed a step transition test (0 to 100 W) before, after and during 4 weeks of endurance training (ET). VO2max and GET were assessed before and after of ET (40 minutes, 3 times a week, 60% O2max). VO2 uptake, Q and deoxyheamoglobin were measured during testing. Study 1 results: VO2 τ and the functional gain were slower in the upper regions of the moderate domain. Q increased more abruptly during rest to work condition. Q τ was faster than VO2 τ for each exercise step. Study 2 results: VO2 τ became faster after ET (25%) and particularly after 1 training session (4%). Q kinetics changed after 4 training sessions nevertheless it was always faster than VO2 τ. An attenuation in ∆[HHb] /∆VO2 was detectible. Conclusion: these investigations suggest that muscle fibres recruitment exerts a influence on the VO2 response within the moderate domain either during different forms of step transition or following ET.

Influence of Electromagnetic Fields On Biological Signalling: An Experimental and Theoretical Approach

The primary goals of this study were to develop a cell-free in vitro assay for the assessment of nonthermal electromagnetic (EMF) bioeffects and to develop theoretical models in accord with current experimental observations. Based upon the hypothesis that EMF effects operate by modulating Ca2+/CaM binding, an in vitro nitric oxide (NO) synthesis assay was developed to assess the effects of a pulsed radiofrequency (PRF) signal used for treatment of postoperative pain and edema. No effects of PRF on NO synthesis were observed. Effects of PRF on Ca2+/CaM binding were also assessed using a Ca2+-selective electrode, also yielding no EMF Ca2+/CaM binding. However, a PRF effect was observed on the interaction of hemoglobin (Hb) with tetrahydrobiopterin, leading to the development of an in vitro Hb deoxygenation assay, showing a reduction in the rate of Hb deoxygenation for exposures to both PRF and a static magnetic field (SMF). Structural studies using pyranine fluorescence, Gd3+ vibronic sideband luminescence and attenuated total reflectance Fourier transform infrared (ATR-FTIR) spectroscopy were conducted in order to ascertain the mechanism of this EMF effect on Hb. Also, the effect of SMF on Hb oxygen saturation (SO2) was assessed under gas-controlled conditions. These studies showed no definitive changes in protein/solvation structure or SO2 under equilibrium conditions, suggesting the need for real-time instrumentation or other means of observing out-of-equilibrium Hb dynamics. Theoretical models were developed for EMF transduction, effects on ion binding, neuronal spike timing, and dynamics of Hb deoxygenation. The EMF sensitivity and simplicity of the Hb deoxygenation assay suggest a new tool to further establish basic biophysical EMF transduction mechanisms. If an EMF-induced increase in the rate of deoxygenation can be demonstrated in vivo, then enhancement of oxygen delivery may be a new therapeutic method by which clinically relevant EMF-mediated enhancement of growth and repair processes can occur.

Personalization of Electronic Nicotine Delivery Systems Toxicological impact in in-vivo model

Electronic nicotine delivery systems (ENDS) use has recently grown. E-cig generates carcinogenic chemical compounds and reactive oxygen species (ROS). Carbonyls and ROS are formed when the liquid comes into contact with the heating element. In this study the chemical and biological effects of coil resistance applied on the same device were investigated. A preliminary in-vivo study the new heat-not-burn devices (IQOS®) has been conducted to evaluate the effect of the device on antioxidant biomarkers. The amount of formaldehyde, acetaldehyde, acrolein was measured by GC-MS analysis. The two e-liquids used for carbonyls detection differed only for the presence of nicotine. The nicotine-free liquid was then used for the detection of ROS in the aerosol. The impact of the non-nicotine vapor on cell viability in H1299 human lung carcinoma cells, as well as the biological effects in a rat model of e-cig aerosol exposure, were also evaluated. After the exposure of Sprague Dawley rats to e-cig and IQOS® aerosol, the effect of 28-day treatment was examined on enzymatic and non-enzymatic antioxidant response, lung inflammation, blood homeostasis and tissue damage by using scanning electron microscope (SEM) technique. The results show a significant correlation between the low resistance and the generation of higher concentrations of the selected carbonyls and ROS in aerosols. Cell viability was reduced with an inverse relation to coil resistance. The experimental model highlighted an impairment of the pulmonary antioxidant and detoxifying machinery. Frames from SEM show disorganization of alveolar and bronchial epithelium. IQOS® exposed animals shows a significant production of ROS related to the unbalance of antioxidant defense and alteration of macromolecule integrity. This research demonstrates how several toxicological aspects can potentially occur in e-cig consumers who use low resistance device coupled with nicotine-free liquid. ENDS may expose users to hazardous compounds, which, may promote chronic pathologies and degenerative diseases.