筋収縮後の再酸素化実験に関する研究

博甲第38号生命システム科学博士県立広島大

Endurance training facilitates myoglobin desaturation during muscle contraction in rat skeletal muscle.

At onset of muscle contraction, myoglobin (Mb) immediately releases its bound O2 to the mitochondria. Accordingly, intracellular O2 tension (PmbO2) markedly declines in order to increase muscle O2 uptake (mVO2). However, whether the change in PmbO2 during muscle contraction modulates mVO2 and whether the O2 release rate from Mb increases in endurance-trained muscles remain unclear. The purpose of this study was, therefore, to determine the effect of endurance training on O2 saturation of Mb (SmbO2) and PmbO2 kinetics during muscle contraction. Male Wistar rats were subjected to a 4-week swimming training (Tr group; 6 days per week, 30 min × 4 sets per day) with a weight load of 2% body mass. After the training period, deoxygenated Mb kinetics during muscle contraction were measured using near-infrared spectroscopy under hemoglobin-free medium perfusion. In the Tr group, the VmO2peak significantly increased by 32%. Although the PmbO2 during muscle contraction did not affect the increased mVO2 in endurance-trained muscle, the O2 release rate from Mb increased because of the increased Mb concentration and faster decremental rate in SmbO2 at the maximal twitch tension. These results suggest that the Mb dynamics during muscle contraction are contributing factors to faster VO2 kinetics in endurance-trained muscle

Intracellular oxygen tension limits muscle contraction-induced change in muscle oxygen consumption under hypoxic conditions during Hb-free perfusion.

Under acute hypoxic conditions, the muscle oxygen uptake (mV˙O2) during exercise is reduced by the restriction in oxygen-supplied volume to the mitochondria within the peripheral tissue. This suggests the existence of a factor restricting the mV˙O2 under hypoxic conditions at the peripheral tissue level. Therefore, this study set out to test the hypothesis that the restriction in mV˙O2 is regulated by the net decrease in intracellular oxygen tension equilibrated with myoglobin oxygen saturation (∆PmbO2) during muscle contraction under hypoxic conditions. The hindlimb of male Wistar rats (8 weeks old, n = 5) was perfused with hemoglobin-free Krebs-Henseleit buffer equilibrated with three different fractions of O2 gas: 95.0%O2, 71.3%O2, and 47.5%O2 The deoxygenated myoglobin (Mb) kinetics during muscle contraction were measured under each oxygen condition with a near-infrared spectroscopy. The ∆[deoxy-Mb] kinetics were converted to oxygen saturation of myoglobin (SmbO2), and the PmbO2 was then calculated based on the SmbO2 and the O2 dissociation curve of the Mb. The SmbO2 and PmbO2 at rest decreased with the decrease in O2 supply, and the muscle contraction caused a further decrease in SmbO2 and PmbO2 under all O2 conditions. The net increase in mV˙O2 from the muscle contraction (∆mV˙O2) gradually decreased as the ∆PmbO2 decreased during muscle contraction. The results of this study suggest that ΔPmbO2 is a key determinant of the ΔmV˙O2

An electrooptical muscle contraction sensor

An electrooptical sensor for the detection of muscle contraction is described. Infrared light is injected into the muscle, the backscattering is observed, and the contraction is detected by measuring the change, that occurs during muscle contraction, between the light scattered in the direction parallel and perpendicular to the muscle cells. With respect to electromyography and to optical absorption-based sensors, our device has the advantage of lower invasiveness, of lower sensitivity to electromagnetic noise and to movement artifacts, and of being able to distinguish between isometric and isotonic contractions

Monitoring muscle fatigue following continuous load changes

Department of Human Factors EngineeringPrevious studies related to monitoring muscle fatigue during dynamic motion have focused on detecting the accumulation of muscle fatigue. However, it is necessary to detect both accumulation and recovery of muscle fatigue in dynamic muscle contraction while muscle load changes continuously. This study aims to investigate the development and recovery of muscle fatigue in dynamic muscle contraction conditions following continuous load changes. Twenty healthy males conducted repetitive elbow flexion and extension using 2kg and 1kg dumbbell, by turns. They performed the two tasks of different intensity (2kg intensity task, 1kg intensity task) alternately until they felt they could no longer achieve the required movement range or until they experienced unacceptable biceps muscle discomfort. Meanwhile, using EMG signal of biceps brachii muscle, fatigue detections were performed from both dynamic measurements during each dynamic muscle contraction task and isometric measurements during isometric muscle contraction right before and after each task. In each of 2kg and 1kg intensity tasks, pre, post and change value of EMG amplitude (AEMG) and center frequency were computed respectively. They were compared to check the validity of the muscle fatigue monitoring method using Wavelet transform with EMG signal from dynamic measurements. As a result, a decrease of center frequency in 2kg intensity tasks and an increase of center frequency in 1kg intensity tasks were detected. It shows that development and recovery of muscle fatigue were detected in 2kg and 1kg intensity tasks, respectively. Also, the tendency of change value of center frequency from dynamic measurements were corresponded with that from isometric measurements. It suggests that monitoring muscle fatigue in dynamic muscle contraction conditions using wavelet transform was valid to detect the development and recovery of muscle fatigue continuously. The result also shows the possibility of monitoring muscle fatigue in real-time in industry and it could propose a guideline in designing a human-robot interaction system based on monitoring user's muscle fatigue.clos

Vascular smooth muscle contraction in hypertension

Hypertension is a major risk factor for many common chronic diseases, such as heart failure, myocardial infarction, stroke, vascular dementia and chronic kidney disease. Pathophysiological mechanisms contributing to the development of hypertension include increased vascular resistance, determined in large part by reduced vascular diameter due to increased vascular contraction and arterial remodelling. These processes are regulated by complex interacting systems such as the renin angiotensin aldosterone system (RAAS), sympathetic nervous system, immune activation and oxidative stress, which influence vascular smooth muscle function. Vascular smooth muscle cells are highly plastic and in pathological conditions undergo phenotypic changes from a contractile to a proliferative state. Vascular smooth muscle contraction is triggered by an increase in intracellular free calcium concentration ([Ca2+]i), promoting actin-myosin cross-bridge formation. Growing evidence indicates that contraction is also regulated by calcium-independent mechanisms involving RhoA-Rho kinase (ROCK), protein kinase C (PKC) and mitogen-activated protein kinase (MAPK) signaling, reactive oxygen species and reorganization of the actin cytoskeleton. Activation of immune/inflammatory pathways and noncoding RNAs are also emerging as important regulators of vascular function. Vascular smooth muscle cell [Ca2+]i, not only determines the contractile state but also influences activity of many calcium-dependent transcription factors and proteins thereby impacting the cellular phenotype and function. Perturbations in vascular smooth muscle cell signaling and altered function influence vascular reactivity and tone, important determinants of vascular resistance and blood pressure. Here we discuss mechanisms regulating vascular reactivity and contraction in physiological and pathophysiological conditions and highlight some new advances in the field, focusing specifically on hypertension

Muscle contractibility and protein turnover

Skeletal, cardiac, and smooth muscle contraction, protein turnover and other research are reported

DEVELOPMENT OF PORTABLE SYSTEM FOR MUSCLE TWITCH EXPERIMENT MEASUREMENT OF MUSCLE CONTRACTION TIME

The muscle contraction time of fish can be the good index for swimming capability to estimate the maximum swimming speed, by defining the maximum tail beating performance. The muscle contraction time of jack mackerel, Thachurus japonicus (18.0 – 19.4 cm of fork length (FL), n = 15) was measured with newly developed portable systemand compared with the conventional setup with the electric stimulation pulse from generator and battery system.The muscle contraction profile was not different among each measurementeven with the different pulse pattern of electric stimulation between portable and conventional setup. The shortest recording of muscle contraction time with the portable system was 22.6 ± 2.1 ms, not different to the conventional system as 24.3 ± 1.9 ms with the generator and 24.2 ± 2.0 mswith the battery system. Time duration and the pulse pattern of the electric stimulus do not affect the muscle contraction time. The portable system can be used to measure the muscle contraction time of fish for the field experiment and onboard the fishing boat without alternating current (AC) electricity supply. Keywords: Muscle contraction time, jack mackerel, portable system, electric stimulus, muscle twitch experiment.

Multiscale Modeling of Skeletal Muscle Active Contraction in Relation to Mechanochemical Coupling of Molecular Motors

In this work, a mathematical model was developed to relate the mechanochemical characterizations of molecular motors with the macroscopic manifestation of muscle contraction. Non-equilibrium statistical mechanics were used to study the collective behavior of myosin molecular motors in terms of the complex conformation change and multiple chemical states in one working cycle. The stochastic evolution of molecular motor probability density distribution during the contraction of sarcomere was characterized by the Fokker-Planck Equation. Quick muscle contraction was demonstrated by the collective dynamic behavior of myosin motors, the muscle contraction force, and the muscle contraction velocity-force relation. Our results are validated against published experiments, as well as the predictions from the Hill’s model. The quantitative relation between myosin molecular motors and muscle contraction provides a novel way to unravel the mechanism of force generation