In an attempt to approach a system of isolated exercising muscle in humans, a model has been developed that enables the study of muscle activity and metabolism over the quadriceps femoris (QF) muscles while the rest of the body remains relaxed. The simplest version includes the subject sitting on a table with a rod connecting the ankle and the pedal arm of a bicycle ergometer placed behind the subject. Exercise is performed by knee extension from a knee angle of 90 to approximately 170 degrees while flywheel momentum repositions the relaxed leg during flexion. Experiments where electromyographic recordings have been taken from biceps femoris, gastrocnemius, tibialis anterior, and other muscles in addition to QF indicate that only the QF is active and that there is an equal activation of the lateral, medial, and rectus femoris heads relative to maximum. Furthermore, virtually identical pulmonary O2 uptake (Vo2) during and without application of a pressure cuff below the knee emphasizes the inactivity of the lower leg muscles. The advantages of the model are that all external work can be localized to a single muscle group suitable for taking biopsies and that the blood flow in and sampling from the femoral vein are representative of the active muscles. Thus all measurements can be closely related to changes in the working muscle. Using this model we find that a linear relationship exists between external work and pulmonary Vo2 over the submaximal range and the maximal Vo2 per kilogram of muscle may be as much as twice as high as previously estimated.
Six subjects performed one-legged dynamic knee-extension. Blood samples were drawn from the femoral artery and vein, and muscle biopsies were obtained from the quadriceps muscle. Leg blood flow was measured by the thermodilution technique, and 3H-inulin was infused for determination of extra- and intracellular muscle water shifts. During the submaximal work load (S) muscle lactate increased, whereas muscle pH remained almost constant; after maximal exercise (M) the values markedly increased for lactate and decreased for pH. Except for a release of lactate from the exercising muscles, K was continuously released throughout S, and this release increased during M. Immediately when the muscles relaxed, the K release was converted to a K re-uptake. The calculated K loss, based on v- a and flow values, agreed with the decrease in muscle K content from 458 mmol/kg dw at rest to 414 mmol/kg dw at exhaustion (P less than 0.05), as analyzed on the muscle biopsies. Muscle water content increased during S mainly because of an increased extracellular H2O, whereas during M the largest increase occurred in intracellular H2O (H2Oi). Because of the simultaneous K loss and H2Oi increase in the exercising muscle the intracellular [K] was calculated to decrease from 165 mM at rest to 129 mM at exhaustion. This decrease and an increase in extracellular [K] from 4.5 mM at rest to greater than 6.0 mM at exhaustion affects the muscle membrane excitability. Muscle fatigue may thus not only be caused by changes within the cell, affecting energy metabolism or actin-myosin reaction, but may be located at the membrane protecting the cell against overload.
Six subjects rode a bicycle ergometer on three occasions breathing 17, 21, or 60% oxygen. In addition to rest and recovery periods, each subject worked for 10 min at 55% of maximal oxygen uptake (VO2 max) and then to exhaustion at approximately 90% VO2 max. Performance time, inspired and expired gas fractions, ventilation, and arterialized venous oxygen tension (PO2), carbon dioxide tension (PCO2), lactate, and pH were measured. VO2, carbon dioxide output, [H+]a, and [HCO3-]a were calculated. Performance times were longer in hyperoxia than in normoxia or hypoxia. However, VO2 was not different at exhaustion in normoxia compared with hypoxia or hyperoxia. During exercise, hypoxia was associated with increased lactate levels and decreased [H+]a, PCO2, and [HCO3-]a. The opposite trends were generally associated with hyperoxia. At exhaustion, [H+]a was not different under any inspired oxygen fraction. These results support the contention that oxygen is not limiting for exercise of this intensity and duration. The results also suggest that [H+] is a possible limiting factor and that the effect of oxygen on performance is perhaps related to control of [H+].
Prediabetes is a state of glycaemic dysregulation below the diagnostic threshold of type 2 diabetes (T2D). Globally, ~352 million people have prediabetes, of which 35–50% develop full-blown diabetes within five years. T2D and its complications are costly to treat, causing considerable morbidity and early mortality. Whether prediabetes is causally related to diabetes complications is unclear. Here we report a causal inference analysis investigating the effects of prediabetes in coronary artery disease, stroke and chronic kidney disease, complemented by a systematic review of relevant observational studies. Although the observational studies suggest that prediabetes is broadly associated with diabetes complications, the causal inference analysis revealed that prediabetes is only causally related with coronary artery disease, with no evidence of causal effects on other diabetes complications. In conclusion, prediabetes likely causes coronary artery disease and its prevention is likely to be most effective if initiated prior to the onset of diabetes.
SummaryBackground: Exacerbations are now an important clinical variable for research into, and management of, chronic obstructive pulmonary disease (COPD). Emphasis is usually on reductions in the incidence of exacerbations and their impact on quality of life. For such research to be useful and comparable there needs to be a clearly defined understanding of what is meant by the term 'exacerbation'. The aim of this study was to explore the notion of COPD exacerbations from the viewpoint of patients who had recently suffered an exacerbation. Methods: Using principles from grounded theory we conducted semi-structured, in-depth interviews with 23 volunteers from Denmark, the Netherlands and the UK who were identified as having had a COPD exacerbation. Interviews were recorded locally and translated into English for analysis. Notable themes were identified for each informant and their occurrences compared. Results: Patients' reasons for consulting fell into four categories: 'frightening change'; 'change in sputum colour'; 'gradual deterioration'; and 'opportunistic diagnosis'. Most patients consulted frequently about their COPD, but did not afford their exacerbations the same degree of prominence as healthcare professionals (HCPs). Conclusions: These data provide a new way of thinking about COPD exacerbations, offering a greater understanding and classification of the reasons underlying the decision of COPD patients to consult with HCPs. They suggest that the patient perspective of exacerbations is more complex than previously thought. These findings could be applied to clinical practice and research, facilitating focussed decisions on COPD management.
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