Effect of pulsed electromagnetic fields (pemfs) on muscle activity, tissue oxygenation and vo2 during exercise.

PEMF are a medical and non-invasive therapy successfully used for clinical treatments of bone disease, due to the piezoelectric effect that improve bone mass and density, by the stimulation of osteoblastogenesis, with modulation of calcium storages and mineral metabolism. PEMF enhance tissue oxygenation, microcirculation and angiogenesis, in rats and cells erythrocytes, in cells-free assay. Such responses could be caused by a modulation of nitric oxide signal and interaction between PEMF and Ca2+/NO/cGMP/PKG signal. PEMF improve blood flow velocity of smallest vein without changing their diameter. PEMF therapy helpful in patients with diabetes, due to increased microcirculation trough enhance capillary blood velocity and diameter. We investigated the influence of stimulation on muscular activity, tissue oxygenation and pulmonary VO2, during exercise, on different intensity, as heavy or moderate, different subjects, as a athlete or sedentary, and different sport activity, as a cycling or weightlifting. In athletes, we observed a tendency for a greater change and a faster kinetic of HHb concentration. PEMF increased the velocity and the quantity of muscle O2 available, leading to accelerate the HHb kinetics. Stimulation induced a bulk muscle O2 availability and a greater muscle O2 extraction, leading to a reduced time delay of the HHb slow component. Stimulation increased the amplitude of muscle activity under different conditions, likely caused by the effect of PEMF on contraction mechanism of muscular fibers, by the change of membrane permeability and Ca2+ channel conduction. In athletes, we observed an increase of overall activity during warm-up. In sedentary people, stimulation increased the magnitude of muscle activity during moderate constant-load exercise and warm-up. In athletes and weightlifters, stimulation caused an increase of blood lactate concentration during exercise, confirming a possible influence of stimulation on muscle activity and on glycolytic metabolism of type-II muscular fibers

The effect of cycling positions on cardiorespiratory and aerodynamic parameters for road cyclists

Second study used a coasting-down technique for obtaining Cd value. Four subjects were investigated with velocity of 25 and 15 km/h of 20 trials of the same three positions on a flat floor 50-m long in sports hall. The velocity-time function was measured by a tachogenerator mounted with a telemetry bicycle. Least squares method was used to estimate the Cd value. The results showed that the mean of Cd for DP and AP less than UP

The role of glycogen and lactate in supporting action potential conduction in mouse central white matter and peripheral nerve

Central white matter and peripheral nerves function by conducting action potentials, which rely on the presence of transmembrane potentials generated by ion gradients. The maintenance of these transmembrane potentials is the main energy-dependent process in the nervous system. In this thesis I investigated the ability of endogenous glycogen to support the energy requirements of nervous tissue and the role of lactate in this process. Glycogen in the CNS is located in astrocytes but is capable of supporting axonal conduction, implying axon-glial metabolic interactions. These interactions were investigated in both the mouse optic nerve (MON), a central white matter tract, and the mouse sciatic nerve (MSN), a mixed peripheral nerve. Electrophysiological techniques were used to record action potential conduction in the nerves as an index of nerve function. Parallel experiments to quantify glycogen content using biochemical assay, or simultaneous real-time measurement of lactate release from the nerves using enzyme-based lactate biosensors, correlated action potential conduction with glycogen content, or lactate release, respectively. Depletion of glycogen leaves the MON vulnerable to irreversible injury to a greater extent than exposure to moderate hyperthermia during aglycemia. Glycogen also greatly enhanced the neuroprotective effects of mild hypothermia during aglycemia. Under resting conditions lactate in the immediate vicinity of the MON was stable at ~0.5 mM, a concentration that increased with axonal activity, dependent upon stimulus intensity. Raising extracellular K+ evoked lactate release, suggesting that increased neuronal activity promotes lactate release. Inhibition of glycogen metabolism, partly reduced lactate release from the MON, implying that glycogen metabolism is important under normal physiological conditions. The relative contribution of glycogen to lactate release increased with axonal activity, consistent with activity-induced glycogenolysis. These studies were then extended to the peripheral nervous system as the role of glycogen in this tissue has not previously been considered. Glycogen, which was present in Schwann cells, supported myelinated, but not un-myelinated axons during aglycemia, suggesting a more complex and selective neuroprotective role than that in central white matter. These results advance our understanding of white matter energy metabolism in relation to both the contributions of glycogen and lactate. The novel functional role of glycogen in supporting peripheral nerve function has also been described

The role of glycogen and lactate in supporting action potential conduction in mouse central white matter and peripheral nerve

Central white matter and peripheral nerves function by conducting action potentials, which rely on the presence of transmembrane potentials generated by ion gradients. The maintenance of these transmembrane potentials is the main energy-dependent process in the nervous system. In this thesis I investigated the ability of endogenous glycogen to support the energy requirements of nervous tissue and the role of lactate in this process. Glycogen in the CNS is located in astrocytes but is capable of supporting axonal conduction, implying axon-glial metabolic interactions. These interactions were investigated in both the mouse optic nerve (MON), a central white matter tract, and the mouse sciatic nerve (MSN), a mixed peripheral nerve. Electrophysiological techniques were used to record action potential conduction in the nerves as an index of nerve function. Parallel experiments to quantify glycogen content using biochemical assay, or simultaneous real-time measurement of lactate release from the nerves using enzyme-based lactate biosensors, correlated action potential conduction with glycogen content, or lactate release, respectively. Depletion of glycogen leaves the MON vulnerable to irreversible injury to a greater extent than exposure to moderate hyperthermia during aglycemia. Glycogen also greatly enhanced the neuroprotective effects of mild hypothermia during aglycemia. Under resting conditions lactate in the immediate vicinity of the MON was stable at ~0.5 mM, a concentration that increased with axonal activity, dependent upon stimulus intensity. Raising extracellular K+ evoked lactate release, suggesting that increased neuronal activity promotes lactate release. Inhibition of glycogen metabolism, partly reduced lactate release from the MON, implying that glycogen metabolism is important under normal physiological conditions. The relative contribution of glycogen to lactate release increased with axonal activity, consistent with activity-induced glycogenolysis. These studies were then extended to the peripheral nervous system as the role of glycogen in this tissue has not previously been considered. Glycogen, which was present in Schwann cells, supported myelinated, but not un-myelinated axons during aglycemia, suggesting a more complex and selective neuroprotective role than that in central white matter. These results advance our understanding of white matter energy metabolism in relation to both the contributions of glycogen and lactate. The novel functional role of glycogen in supporting peripheral nerve function has also been described