We employ 130 low‐frequency earthquake (LFE) templates representing tremor sources on the plate boundary below southern Vancouver Island to examine LFE magnitudes. Each template is assembled from hundreds to thousands of individual LFEs, representing over 269,000 independent detections from major episodic‐tremor‐and‐slip (ETS) events between 2003 and 2013. Template displacement waveforms for direct P and S waves at near epicentral distances are remarkably simple at many stations, approaching the zero‐phase, single pulse expected for a point dislocation source in a homogeneous medium. High spatiotemporal precision of template match‐filtered detections facilitates precise alignment of individual LFE detections and analysis of waveforms. Upon correction for 1‐D geometrical spreading, attenuation, free surface magnification and radiation pattern, we solve a large, sparse linear system for 3‐D path corrections and LFE magnitudes for all detections corresponding to a single‐ETS template. The spatiotemporal distribution of magnitudes indicates that typically half the total moment release occurs within the first 12–24 h of LFE activity during an ETS episode when tidal sensitivity is low. The remainder is released in bursts over several days, particularly as spatially extensive rapid tremor reversals (RTRs), during which tidal sensitivity is high. RTRs are characterized by large‐magnitude LFEs and are most strongly expressed in the updip portions of the ETS transition zone and less organized at downdip levels. LFE magnitude‐frequency relations are better described by power law than exponential distributions although they exhibit very high b values ≥∼5. We examine LFE moment‐duration scaling by generating templates using detections for limiting magnitude ranges (MW<1.5, MW≥2.0). LFE duration displays a weaker dependence upon moment than expected for self‐similarity, suggesting that LFE asperities are limited in fault dimension and that moment variation is dominated by slip. This behavior implies that LFEs exhibit a scaling distinct from both large‐scale slow earthquakes and regular seismicity.

The effect of isometric exercise on blood flow, blood pressure, intramuscular pressure as well as lactate and potassium efflux from exercising muscle was examined. The contractions performed were continuous or intermittent (5 s on, 5 s off) and varied between 5% and 50% maximal voluntary contraction (MVC). A knee-extensor and a hand-grip protocol were used. Evidence is presented that blood flow through the muscle is sufficient during low-level sustained contractions (less than 10% MVC). Despite this muscle fatigue occurs during prolonged contractions. One mechanism for this fatigue may be the disturbance of the potassium homeostasis. Such changes may also play a role in the development of fatigue during intermittent isometric contractions and even more so in the recovery from such exercise. In addition the role of impaired transport of substances within the muscle, due to long-lasting daily oedema formation, is discussed in relation to fatigue in highly repetitive, monotonous jobs.

The effect of heat stress on blood flow and metabolism in an exercising leg was studied in seven subjects walking uphill (12-17%) at 5 km/h on a treadmill for 90 min or until exhaustion. The first 30 min of exercise were performed in a cool environment (18-21 degrees C); then subjects moved to an adjacent room at 40 degrees C and continued to exercise at the same speed and inclination for a further 60 min or to exhaustion, whichever occurred first. The rate of O2 consumption, 2.6 l/min (1.8-3.3) (average from cool and hot conditions), corresponded to 55-77% of their individual maximums. In the cool environment a steady state was reached at 30 min. When the subjects were shifted to the hot room, the core temperature and heart rate started to rise and reached values greater than 39 degrees C and near-maximal values, respectively, at the termination of the exercise. The leg blood flow (thermodilution method), femoral arteriovenous O2 difference, and consequently leg O2 consumption were unchanged in the hot compared with the cool condition. There was no increase in release of lactate and no reduction in glucose and free net fatty acid uptake in the exercising leg in the heat. Furthermore, the rate of glycogen utilization in the gastrocnemius muscle was not elevated in the hot environment. There was a tendency for cardiac output to increase in the heat (mean 15.2 to 18.4 l/min), which may have contributed to the increase in skin circulation, together with a possible further reduction in flow to other vascular beds, because muscle blood flow was not reduced.(ABSTRACT TRUNCATED AT 250 WORDS)

The purpose of this study was to determine the effect of increasing muscle mass involvement in dynamic exercise on both sympathetic nervous activation and local hemodynamic variables of individual active and inactive skeletal muscle groups. Six male subjects performed 15-min bouts of one-legged knee extension either alone or in combination with the knee extensors of the other leg and/or with the arms. The range of work intensities varied between 24 and 71% (mean) of subjects' maximal aerobic capacity (% VO2max). Leg blood flow, measured in the femoral vein by thermodilution, was determined in both legs. Arterial and venous plasma concentrations of norepinephrine (NE) and epinephrine were analyzed, and the calculated NE spillover was used as an index of sympathetic nervous activity to the limb. NE spillover increased gradually both in the resting, and to a larger extent in the exercising legs, with a steeper rise occurring approximately 70% VO2max. These increases were not associated with any significant changes in leg blood flow or leg vascular conductance at the exercise intensities examined. These results suggest that, as the total active muscle mass increases, the rise in sympathetic nervous activity to skeletal muscle, either resting or working at a constant load, is not associated with any significant neurogenic vasoconstriction and reduction in flow or conductance through the muscle vascular bed, during whole body exercise demanding up to 71% VO2max.

To study the role of muscle mass in glucoregulation, six subjects worked with the knee extensors of one leg on a specially constructed cycle ergometer. The knee extensors of one leg worked either alone or in combination with the knee extensors of the other leg and/or with the arms. Substrate usage was measured across both knee extensors by femoral arterial and venous catheterization and measurement of femoral venous blood flow. Glucose uptake by the working knee extensors was absolutely (by approximately 20%) or relatively decreased when arm cranking was added to knee extensions. The decrease in glucose uptake was not compensated for by increased uptake of free fatty acids but was accompanied by decreases in plasma insulin and increases in plasma epinephrine and norepinephrine. During work with large muscle masses, arterial lactate increased to approximately 6 mM, and net leg lactate release reverted to net lactate uptake. Decreased glucose uptake could not be explained by decreased perfusion. It is concluded that thigh muscle glucose uptake is affected by the size of the total muscle mass engaged in exercise. The decrease in thigh glucose uptake, when arm cranking was added and O2 uptake was increased above 50% of maximum aerobic capacity, may be elicited by neuroendocrine adjustments or lactate-induced inhibition of glycolysis and may represent a mechanism for protecting against premature hypoglycemia during prolonged exercise.

The effect of heat stress on circulation in an exercising leg was determined using one-legged knee extension and two-legged bicycle exercise, both seated and upright. Subjects exercised for three successive 25-min periods wearing a water-perfused suit: control [CT, mean skin temperature (Tsk) = 35 degrees C], hot (H, Tsk = 38 degrees C), and cold (C, Tsk = 31 degrees C). During the heating period, esophageal temperature increased to a maximum of 37.91, 39.35, and 39.05 degrees C in the three types of exercise, respectively. There were no significant changes in pulmonary O2 uptake (VO2) throughout the entire exercise period with either one or two legs. Leg blood flow (LBF), measured in the femoral vein of one leg by thermodilution, remained unchanged between CT, H, and C periods. Venous plasma lactate concentration gradually declined over time, and no trend for an increased lactate release during the heating period was found. Similarly, femoral arteriovenous O2 difference and leg VO2 remained unchanged between the three exercise periods. Although cardiac output (acetylene rebreathing) was not significantly higher during H, there was a tendency for an increase of 1 and 2 l/min in one- and two-legged exercise, respectively, which could account for part of the increase in total skin blood flow during heating (gauged by changes in forearm blood flow). Because LBF was not reduced during exercise and heat stress in these experiments, the additional increase in skin blood flow must have been met by redistribution of blood away from vascular beds other than active skeletal muscle.

This study investigated skeletal muscle adaptations to high altitude and a possible role of physical activity levels. Biopsies were obtained from the m. quadriceps femoris (vastus) and m. biceps brachii (biceps) in 15 male subjects, 7 active and 8 less active. Samples were obtained at sea level and after 75 days altitude exposure at 5250 m or higher. The muscle fiber size decreased at an average of 15% in the vastus and biceps, respectively, and to the same extent in both groups. In both muscles, the mean number of capillaries was 2.1-2.2 cap.fiber(-1) before and after the exposure. As mean fiber area was reduced, the mean number of capillaries per unit area increased in all subjects (from 320 to 405 cap/mm2) with no difference between the active and less active groups. The two enzymes selected to reflect mitochondrial capacity, citrate synthase (CS) and 3-hydroxyl-CoA-dehydrogenase (HAD), did not change in the leg muscles with altitude exposure, CS: 28.7 (20.7-37.8) vs. 27.8 (23.8-29.4); HAD: 35.2 (20.3-43.1) vs. 30.6 (20.7-39.7) micromol.min(-1).g(-1) d.w, pre- and post-altitude, respectively. The muscle buffer capacity was elevated in both the vastus; 220 (194-240) vs. 232 (200-277) and the biceps muscles; 233 (190-301) vs. 253 (193-320) after the acclimatization period. In conclusion, mean fiber area was reduced in response to altitude exposure regardless of physical activity which in turn meant that with an unaltered capillary to fiber ratio there was an elevation in capillaries per unit of muscle area. Muscle enzyme activity was unaffected with altitude exposure in both groups, whereas muscle buffer capacity was increased.

In subduction zones, landward dipping regions of low shear wave velocity and elevated Poisson’s ratio, which can extend to at least 120 km depth, are interpreted to be all or part of the subducting igneous oceanic crust. This crust is considered to be overpressured, because fluids within it are trapped beneath an impermeable seal along the overlying inter-plate boundary. Here we show that during slow slip on the plate boundary beneath southern Vancouver Island, low frequency earthquakes occur immediately below both the landward dipping region of high Poisson’s ratio and a 6–10 km thick shear zone revealed by seismic reflections. The plate boundary here either corresponds to the low frequency earthquakes or to the anomalous elastic properties in the lower 3–5 km of the shear zone immediately above them. This zone of high Poisson’s ratio, which approximately coincides with an electrically conductive layer, can be explained by slab-derived fluids trapped at near-lithostatic pore pressures.