The number of species that merit conservation interventions is increasing daily with ongoing habitat destruction, increased fragmentation and loss of population connectivity. Desertification and climate change reduce suitable conservation areas. Physiological stress is an inevitable part of the capture and translocation process of wild animals. Globally, capture myopathy—a malignant outcome of stress during capture operations—accounts for the highest number of deaths associated with wildlife translocation. These deaths may not only have considerable impacts on conservation efforts but also have direct and indirect financial implications. Such deaths usually are indicative of how well animal welfare was considered and addressed during a translocation exercise. Importantly, devastating consequences on the continued existence of threatened and endangered species succumbing to this known risk during capture and movement may result. Since first recorded in 1964 in Kenya, many cases of capture myopathy have been described, but the exact causes, pathophysiological mechanisms and treatment for this condition remain to be adequately studied and fully elucidated. Capture myopathy is a condition with marked morbidity and mortality that occur predominantly in wild animals around the globe. It arises from inflicted stress and physical exertion that would typically occur with prolonged or short intense pursuit, capture, restraint or transportation of wild animals. The condition carries a grave prognosis, and despite intensive extended and largely non-specific supportive treatment, the success rate is poor. Although not as common as in wildlife, domestic animals and humans are also affected by conditions with similar pathophysiology. This review aims to highlight the current state of knowledge related to the clinical and pathophysiological presentation, potential treatments, preventative measures and, importantly, the hypothetical causes and proposed pathomechanisms by comparing conditions found in domestic animals and humans. Future comparative strategies and research directions are proposed to help better understand the pathophysiology of capture myopathy.

IIx fibers (range 50 -80%), whereas human muscle had more type I and IIa. Oxidative capacity of both felids (CS: 5 -9 µmol/min/g ww and 3HAD: 1.4 -2.6 µmol/min/g ww) was lower than humans, whereas the glycolytic capacity was elevated. LDH activity of caracal (346 ± 81) was higher than lion (227 ± 62 µmol/min/g ww), with human being the lowest (55 ± 17). CK and PHOS activities were also higher in caracal and lion compared to human, but PFK was lower in both felid species. The current data and past research are illustrated graphically showing a strong 2 relationship between type II fibers and sprinting ability in various species. These data on caracal and lion muscle confirm their sprinting behavior.

Key pointsr Blood glucose is an important fuel for endurance exercise. It can be derived from ingested carbohydrate, stored liver glycogen and newly synthesized glucose (gluconeogenesis).r We hypothesized that athletes habitually following a low carbohydrate high fat (LCHF) diet would have higher rates of gluconeogenesis during exercise compared to those who follow a mixed macronutrient diet.r We used stable isotope tracers to study glucose production kinetics during a 2 h ride in cyclists habituated to either a LCHF or mixed macronutrient diet.r The LCHF cyclists had lower rates of total glucose production and hepatic glycogenolysis but similar rates of gluconeogenesis compared to those on the mixed diet.r The LCHF cyclists did not compensate for reduced dietary carbohydrate availability by increasing glucose synthesis during exercise but rather adapted by altering whole body substrate utilization.Abstract Endogenous glucose production (EGP) occurs via hepatic glycogenolysis (GLY) and gluconeogenesis (GNG) and plays an important role in maintaining euglycaemia. Rates of GLY and GNG increase during exercise in athletes following a mixed macronutrient diet; however, these processes have not been investigated in athletes following a low carbohydrate high fat (LCHF) diet. Therefore, we studied seven well-trained male cyclists that were habituated to either a LCHF (7% carbohydrate, 72% fat, 21% protein) or a mixed diet (51% carbohydrate, 33% fat, 16% protein) for longer than 8 months. After an overnight fast, participants performed a 2 h laboratory ride at 72% of maximal oxygen consumption. Glucose kinetics were measured at rest and during the final 30 min of exercise by infusion of [6,6-2 H 2 ]-glucose and the ingestion of 2 H 2 O tracers. Rates of EGP and GLY both at rest and during exercise were significantly lower in the LCHF group than the mixed diet group (Exercise EGP: LCHF, 6.0 ± 0.9 mg kg −1 min −1 , Mixed, 7.8 ± 1.1 mg kg −1 min −1 , P < 0.01; Exercise GLY: LCHF, 3.2 ± 0.7 mg kg −1 min −1 , Mixed, 5.3 ± 0.9 mg kg −1 min −1 , P < 0.01). Conversely, no difference was detected in rates of GNG between groups at rest or during exercise (Exercise: LCHF, 2.8 ± 0.4 mg kg −1 min −1 , Mixed, 2.5 ± 0.3 mg kg −1 min −1 , P = 0.15). We conclude that athletes on a LCHF diet do not compensate for reduced glucose availability via higher rates of glucose synthesis compared to athletes on a mixed diet. Instead, GNG remains relatively stable, whereas glucose oxidation and GLY are influenced by dietary factors. Abbreviations ASA24, automated self-administered 24 h recall; βHB, β-hydroxybutyrate; BMI, body mass index; CV, coefficient of variation; EGP, endogenous glucose production; FFA, free fatty acids; GLY, glycogenolysis; GNG, gluconeogenesis; HR, heart rate; HR max , maximum heart rate; LCHF, low carbohydrate high fat; MIDA, mass isotopomer distribution analysis; MUFA, monounsaturated fatty acids; PPO, peak power output; PUFA, polyunsaturated fatty acids; R a , rate of appearance; R d , rate of disappearance; RER, respira...