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The Productivity of Care
Published in Christine M. Koggel, Joan Orme, Care Ethics, 2019
Contrary to common belief, care does not necessarily produce stress or make people less productive—at least not always and not under all circumstances. Even in its most draining aspects, care seems to make people find their ‘second wind’, as William James used to call it: an unexpected strength and energy allowing them to overcome challenges and difficulties that stem from their caring about their beloved ones.6 Far more than we are willing to admit, being caring also means being productive. For some, this might mean giving more attention to quality than to quantity; for others, it might mean keeping the same standards in terms of quantity and paying less attention to the quality of the end products. What emerges as quite evident from all the interview accounts is that caring activities, under certain conditions, make people more efficient and increase their capacities to get more things done in a more focused way.
Dictionary
Published in Mario P. Iturralde, Dictionary and Handbook of Nuclear Medicine and Clinical Imaging, 1990
Second-wind angina. This term describes a phenomenon in which an exertion that initially provoked pain is tolerated later on. The pathophysiological explanation must be that at the beginning of the effort the tachycardia and the blood pressure rise produce an oxygen debt which causes pain. Diminution of the peripheral resistance with continuing exertion results in a decrease of cardiac work so that the stress is subsequently tolerated.
Exercise testing patients with metabolic myopathies
Published in Robert B. Schoene, H. Thomas Robertson, Making Sense of Exercise Testing, 2018
Robert B. Schoene, H. Thomas Robertson
McArdle disease is the best-recognized muscle metabolic abnormality that produces a severe limitation in sustained exercise performance. These patients are characterized by an inability to generate the normal increase in arterial lactate during a sustained maximal muscular effort. The metabolic defect is in an intramuscular enzyme that is required to initiate the mobilization of skeletal muscle glycogen during heavy exercise. Without the muscle glycogen mobilization needed to increase pyruvate generation and ultimately fuel mitochondrial ATP generation during moderate and heavy exercise, these patients have only fatty acids as mitochondrial fuel sources and are accordingly quite limited in their maximal exercise performance, with maximal oxygen uptakes less than 50% of predicted normal values. Despite the absence of lactate and acidosis with heavy exercise, these patients do demonstrate an appropriate ventilatory threshold, suggesting that the norepinephrine washing out from muscles during heavy exercise also acts to trigger the ventilatory threshold. In addition to showing no significant increase in arterial lactate during a standard CPET, these patients also show an atypical heart rate response that has been termed a “second wind” phenomenon. While undergoing a long-duration CPET (using very small exercise increments), McArdle patients will approach a maximal heart rate within the initial five minutes and then demonstrate a reduction in exercise heart rate as the load progresses until they once again reach a maximal heart rate at 15–20 minutes of exercise. This recovery of exercise capacity during sustained exercise has been attributed to slower onset glycogen mobilization from the liver (instead of exercising muscle) providing a systemic source of glucose for the exercising muscle.
Pre- and peripartal management of a woman with McArdle disease: a case report
Published in Gynecological Endocrinology, 2018
Tina Stopp, Michael Feichtinger, Wolfgang Eppel, Thomas M. Stulnig, Peter Husslein, Christian Göbl
Glycogen storage disease type 5, also called McArdle disease, is an autosomal recessive inherited disorder in muscle metabolism caused by the lack or dysfunction of muscle glycogen phosphorylase (myophosphorylase). Due to this condition the ability to break down glycogen into glucose subunits within the skeletal muscle during muscle activity is inhibited. This results in intolerance to strenuous exercise which manifests as fatigue, muscle stiffness and myalgia, in some cases accompanied by myoglobinuria and in severe instances renal failure due to muscle breakdown and rhabdomyolysis [1]. Most Patients experience a period of less painful and more effective exercise after an initial period of muscle cramps. The so-called ‘second wind phenomenon’ is typical of McArdle disease [2]. This phenomenon is believed to be caused by a switch to alternative sources of energy such as fatty acid oxidation and an increased blood flow to the muscle [3]. The metabolic shift is more effective when the patient’s muscles are conditioned through regular aerobic exercise [4].
An update on diagnosis and therapy of metabolic myopathies
Published in Expert Review of Neurotherapeutics, 2018
In case the patient presents a history of exercise-induced fatigue, myalgia, and myoglobinurea, it is important to identify the particular type of exercise. Symptoms precipitated by short bursts of high-intensity exercise over about 5 min should raise the suspicion of a GSD [1]. After 5 min of exercise, the second wind phenomenon may arise, characterized by resolution of muscle contractions, myalgias, and exercise intolerance after finishing the short exercise and by regaining normal muscle strength after resting for about 10 min [1]. The second wind phenomenon is not specific for GSD-V but occurs also in other GSDs (e.g. GSD-XIV) [11]. In some GSDs (e.g. GSD-VII) the ‘out-of-wind phenomenon’ can be observed, characterized by worsening of the physical condition with ingestion of glucose [1]. Since such patients do not tolerate glucose, hyperglycemia ensues, preventing the mobilization of fat and ketones. Functional damage due to GSD may manifest as exercise intolerance, muscle pain, contractures, or creatine-kinase (CK)-elevation. Functional damage due to FAODs may manifest as myalgia, fatigue, rhabdomyolysis, or pigmenturia [5]. Triggers of muscular episodes in FAODs include infectious diseases, fat-rich diet, emotional stress, long-duration, vigorous exercise, general anesthesia, fasting, or drugs, such as non-steroidal anti-rheumatic drugs (NSAR) (ibuprofen, diazepam). Symptoms precipitated by prolonged periods of low-intensity or endurance exercise (e.g. hiking, playing football), fasting, fever, or surgery, are indicative of a FAOD or mitochondrial disorder [1,5]. For treating physicians it is important to carefully review previous investigations for temporary abnormalities (e.g. CK fluctuations, elevated myoglobin, elevated serum lactate/pyruvate). In patients with a mitochondrial disorder, the association of exercise intolerance, myalgia, and rhabdomyolysis after physical exertion is less frequently reported than in GSDs or FAODs.
Longitudinal case study and phenotypic multimodal characterization of McArdle disease-linked retinopathy: insight into pathomechanisms
Published in Ophthalmic Genetics, 2020
Veronika Vaclavik, Francine Naderi, André Schaller, Pascal Escher
McArdle disease, also called glycogen storage disease V (MIM# 232600), is a rare recessively inherited myopathy caused by homozygous or compound heterozygous pathogenic variants in the PYGM gene located on chromosome 11 (MIM# 608455) (1–3). The PYGM gene encodes the muscle form of glycogen phosphorylase or myophosphorylase that catalyzes the first reaction in the catabolism of muscle glycogen by transforming glycogen into glucose-1-phosphate (4). The absence of glycogen phosphorylase activity in patients with McArdle disease causes exercise intolerance, with dynamic exercise-induced symptoms mainly in the form of acute fatigue and painful contractures, because the patients are unable to obtain energy from their muscle glycogen stores (5). Myoglobinuria, rhabdomyolysis, and acute renal failure can develop in severe cases (5,6). Patients develop a pathognomonic so-called second-wind phenomenon during aerobic exercise of moderate intensity: about 10 min after the start of exercise, the enhanced uptake of blood glucose and enhanced fat oxidation in contracting muscles decrease the fatigue and tachycardia initially triggered by exercise (7). Symptoms start during childhood, but proper diagnosis is often delayed until the forth decade, also because exercise-triggered pain is often considered as growing pain during teen years (5). The characteristic laboratory findings are elevated creatine kinase levels, even between peaks in disease activity. The clinical diagnosis can be established by a muscle biopsy in which an increase in glycogen content and a decrease or an absence in enzyme activity is typically assessed (5). Because it is less invasive, molecular analysis of the PYGM gene is now the preferred diagnostic method (8). The most frequent pathogenic PYGM variant in populations of European origin is the c.148C>T p.(Arg50*) variant, accounting for up to 55% of disease-causing alleles in Spain (5), to 68–72% in France (9,10) and to 60–63% in the USA (11).