China
Africa
Explore chapters and articles related to this topic
Physical properties of the body fluids and the cell membrane
Published in Ronald L. Fournier, Basic Transport Phenomena in Biomedical Engineering, 2017
The first stage of an action potential is a rapid depolarization of the cell membrane. The cell membrane becomes very permeable to sodium ions because of the opening of the voltage-gated sodium channels. This rapid influx of sodium ions, carrying a positive charge, increases the membrane potential in the positive direction and, in some cases, can result in a positive membrane potential (overshoot) for a brief period of time. This depolarization phase may last only a few tenths of a millisecond. Following the depolarization of the membrane, the sodium channels close and the potassium channels, which are now fully opened, allow for the rapid loss of positively charged potassium ions from the cell, thus reestablishing within milliseconds the normal negative resting potential of the cell membrane (repolarization). However, for a brief period of time following an action potential, the sodium channels remain inactive and they cannot open again, regardless of external stimulation, for several milliseconds. This is known as the refractory period.
Electrocardiogram
Published in Kayvan Najarian, Robert Splinter, Biomedical Signal and Image Processing, 2016
Kayvan Najarian, Robert Splinter
A cardiac muscle contraction is a direct result of the cellular electric excitation described by the ECG. The depolarization initiates the shortening of each individual muscle cell. The electric activation of each cell is an indication of the functioning of that cell. Therefore, the ECG is the result of depolarization of the heart muscle in a controlled repetitive fashion. By tracking the process of electric depolarization of the cardiac muscle cells, an impression of the heart’s functionality can be formed and used to recognize regions in the heart structure that are not functioning to specifications and may require medical attention. Any deviation from the typical ECG observed in the recorded electric depolarization signal is analyzed and classified as a certain cardiac disorder.
X-Nuclei MRI and Energy Metabolism
Published in Guillaume Madelin, X-Nuclei Magnetic Resonance Imaging, 2022
AP generation. An action potential (AP) is a rapid rise and fall of the membrane potential Vm, which occurs in excitable cells such as neurons, muscle cells or endocrine cells [1–5, 10–12, 30–32]. In neurons, the AP can rapidly propagate along the axons and act as an electric signal which enables them to communicate with other neurons, muscles or glands. The AP can be divided into 3 distinct phases which can happen within a few milliseconds: Depolarization. At rest, the membrane is negatively polarized due to the different overall charge on each side. During depolarization, the membrane potential Vm increases rapidly to a positive value when the membrane changes its Na+ permeability to allow Na+ ions them to flow inside the cell and make the intracellular space more positive.Repolarization. The Na+ permeability then decreases quickly and the K+ permeability rapidly increases to allow K+ ions to flow out of the cell in order to return to the negative resting value of Vm.Hyperpolarization. When returning to its resting value, the membrane potential becomes slightly more negative that its resting value, before reaching back its resting state.
A Functional BCI Model by the P2731 working group: Physiology
Published in Brain-Computer Interfaces, 2021
Ali Hossaini, Davide Valeriani, Chang S. Nam, Raffaele Ferrante, Mufti Mahmud
Like all cells, a membrane separates the interior of neurons from their surroundings which are typically other cells and extracellular fluids. Neuronal membranes are selectively permeable to ions, and they use ion pumps to actively maintain a voltage difference of −40 mV to −90 mV with their surroundings. This difference is known as the neuron’s resting potential. Resting potential resists perturbations up to a certain threshold, but, when a stimulus is strong enough to cross the threshold, a neuron rapidly changes polarity by reversing its ionic balance as shown in Figure 10. In a matter of milliseconds, the neuron’s interior becomes as much as 50 mV positive relative to its external medium, and, during the course of its response, it may change polarity several times before returning to its resting state. This radical depolarization causes the neuron to ‘fire’, that is, to transmit signals to connected neurons. After depolarization, a neuron typically passes through a refractory period where no level of stimulus will change its polarity. A depolarization event is known as the action potential or firing of a neuron, and its propagation to connected neurons via axons form the fundamental signals of mental activity [75].
Exertional rhabdomyolysis and acute kidney injury in endurance sports: A systematic review
Published in European Journal of Sport Science, 2021
Daniel Rojas-Valverde, Braulio Sánchez-Ureña, Jennifer Crowe, Rafael Timón, Guillermo J. Olcina
More commonly reported physiological symptoms and biomarkers indicators for ER and AKI were S-Cr and S-CK (74.42%). ER is the result of muscle damage induced by exercise. This damage is represented in myocyte damage and energy depletion at the cellular level (Hernández-Contreras et al., 2015; Stella & Shariff, 2012). During rest, ion channels (Na+ / K+ pump and Na+ / Ca+ exchange) located in the plasma membrane (sarcolemma) of muscle cells, maintain low intracellular concentrations of Na+ and Ca+ and high concentrations of K+. Muscular depolarization causes Ca+ release from the reserves located in the sarcoplasmic reticulum to the cytoplasm or sarcoplasm, causing actin–myosin binding. These changes are the result of insufficient energy in the form of ATP. Any adverse event that causes injury to the ion channels or availability of ATP, would cause an imbalance in the electrolyte concentration. In the case of myocyte injury and ATP depletion, an intracellular increase in Na+, causes a flow of water into the intracellular space, and an intracellular increase of Ca+, which causes sustained myofibrillary contractions. This leads to a decrease in ATP (Al-Ismaili, Piccioni, & Zappitelli, 2011) and mitochondrial dysfunction resulting in the production of oxygen radicals and increasing cell damage (Patel, Gyamfi, & Torres, 2009).
The acute angiogenic signalling response to low-load resistance exercise with blood flow restriction
Published in European Journal of Sport Science, 2018
Richard A. Ferguson, Julie E. A. Hunt, Mark P. Lewis, Neil R. W. Martin, Darren J. Player, Carolin Stangier, Conor W. Taylor, Mark C. Turner
The greater phosphorylation of p38MAPK is perhaps not surprising given it is considered to be a stress-activated kinase and has been repeatedly shown to be activated in response to various exercise modalities including resistance training (Camera, Hawley, & Coffey, 2015). p38MAPK lies downstream of the calcium/calmodulin-dependent protein kinase (CAMK) which is activated by cytosolic increases in Ca2+, that ultimately leads to increased PGC-1α expression (Wright et al., 2007). The key physiological stimulus causing the release of Ca2+ from the sarcoplasmic reticulum is depolarisation of the muscle surface membrane in the form of an action potential (Endo, 1977). Thus, an increase in motor unit activity (i.e. EMG activity) which has been reported during BFR resistance exercise (Fatela, Reis, Mendonca, Avela, & Mil-Homens, 2016) likely explains the greater phosphorylation of p38MAPK. Moreover, ROS generated in response to ischaemia-reperfusion and muscle contraction can also activate MAPK and PGC-1α signalling pathways (Kang et al., 2009) and may contribute to the phosphorylation of p38MAPK following BFR resistance exercise. However, ROS production during BFR resistance exercise may be minor given that levels of oxidative stress markers are unaltered post-exercise (Nielsen et al., 2017). It is, however, surprising that AMPK was not similarly activated given the additional metabolic stimulus BFR has been purported to provide (Krustrup et al., 2009; Suga et al., 2009). This may be reflected by the specific protocol used in the present study (1 × 30 reps, 2 × 15 reps, 1× reps to fatigue, with 30 s recovery between sets) which may not have been as metabolically challenging as expected.