Machine learning algorithms can classify outdoor terrain types during running using accelerometry data.

BACKGROUND: Running is a popular physical activity that benefits health; however, running surface characteristics may influence loading impact and injury risk. Machine learning algorithms could automatically identify running surface from wearable motion sensors to quantify running exposures, and perhaps loading and injury risk for a runner. RESEARCH QUESTION: (1) How accurately can machine learning algorithms identify surface type from three-dimensional accelerometer sensors? (2) Does the sensor count (single or two-sensor setup) affect model accuracy? METHODS: Twenty-nine healthy adults (23.3 ±â€¯3.6 years, 1.8 ±â€¯0.1 m, and 63.6 ±â€¯8.5 kg) participated in this study. Participants ran on three different surfaces (concrete, synthetic, woodchip) while fit with two three-dimensional accelerometers (lower-back and right tibia). Summary features (n = 208) were extracted from the accelerometer signals. Feature-based Gradient Boosting (GB) and signal-based deep learning Convolutional Neural Network (CNN) models were developed. Models were trained on 90% of the data and tested on the remaining 10%. The process was repeated five times, with data randomly shuffled between train-test splits, to quantify model performance variability. RESULTS: All models and configurations achieved greater than 90% average accuracy. The highest performing models were the two-sensor GB and tibia-sensor CNN (average accuracy of 97.0 ±â€¯0.7 and 96.1 ±â€¯2.6%, respectively). SIGNIFICANCE: Machine learning algorithms trained on running data from a single- or dual-sensor accelerometer setup can accurately distinguish between surfaces types. Automatic identification of surfaces encountered during running activities could help runners and coaches better monitor training load, improve performance, and reduce injury rates.

Effect of combining pre-exercise carbohydrate intake and repeated short sprints on the blood glucose response to moderate-intensity exercise in young individuals with Type 1 diabetes.

AIMS: To determine whether pre-exercise ingestion of carbohydrates to maintain stable glycaemia during moderate-intensity exercise results in excessive hyperglycaemia if combined with repeated sprints in individuals with Type 1 diabetes. METHODS: Eight overnight-fasted people with Type 1 diabetes completed the following four 40-min exercise sessions on separate days in a randomized counterbalanced order under basal insulinaemic conditions: continuous moderate-intensity exercise at 50% V ˙ O 2 peak; intermittent high-intensity exercise (moderate-intensity exercise interspersed with 4-s sprints every 2 min and a final 10-s sprint); continuous moderate-intensity exercise with prior carbohydrate intake (~10 g per person); and intermittent high-intensity exercise with prior carbohydrate intake. Venous blood was sampled during and 2 h after exercise to measure glucose and lactate levels. RESULTS: The difference in marginal mean time-averaged area under the blood glucose curve between continuous moderate-intensity exercise + prior carbohydrate and intermittent high-intensity exercise + prior carbohydrate during exercise and recovery was not significant [0.2 mmol/l (95% CI -0.7, 1.1); P = 0.635], nor was the difference in peak blood glucose level after adjusting for baseline level [0.2 mmol/l (95% CI -0.7, 1.1); P = 0.695]. The difference in marginal mean time-averaged area under the blood glucose curve between continuous moderate-intensity and intermittent high-intensity exercise during exercise and recovery was also not significant [-0.2 mmol/l (95% CI -1.2, 0.8); P = 0.651]. CONCLUSIONS: When carbohydrates are ingested prior to moderate-intensity exercise, adding repeated sprints is not significantly detrimental to glycaemic management in overnight fasted people with Type 1 diabetes under basal insulin conditions.

The time lag prior to the rise in glucose requirements to maintain stable glycaemia during moderate exercise in a fasted insulinaemic state is of short duration and unaffected by the level at which glycaemia is maintained in Type 1 diabetes.

AIMS: To determine the duration of the low hypoglycaemia risk period after the start of moderate-intensity exercise performed under basal insulinaemic conditions and whether this period is affected by the level at which glycaemia is maintained under these conditions. METHODS: This was a prospective, randomized counterbalanced study. Eight participants with Type 1 diabetes (mean ± sd age 21.5 ± 4.0 years) underwent either a euglycaemic (5-6 mmol/l) or hyperglycaemic clamp (9-10 mmol/l) on separate days and were infused with insulin at basal rates and [6,6-2 H]glucose while cycling for 40 min at 50% maximum oxygen consumption rate. The main outcome measures were the glucose infusion rates required to maintain stable glycaemia and glucoregulatory hormone levels, and rates of glucose appearance and disappearance. RESULTS: During the first 20 min of exercise, the glucose infusion rate did not increase significantly, irrespective of the level at which glycaemia was maintained, but increased acutely between 20 and 25 min under both conditions. Maintaining higher glycaemia resulted in higher glucose infusion rate during, but not early post-exercise. With the exception of epinephrine, the glucoregulatory hormone levels and rates of glucose appearance and disappearance were similar between conditions. CONCLUSION: Irrespective of the levels at which glycaemia is maintained, there is a 20-min low exogenous glucose demand period during which the exogenous glucose requirements to maintain stable glycaemia do not increase during moderate exercise performed at basal insulin level.

The glycaemic benefits of a very-low-carbohydrate ketogenic diet in adults with Type 1 diabetes mellitus may be opposed by increased hypoglycaemia risk and dyslipidaemia.

AIMS: To investigate whether very-low-carbohydrate high-fat diets, typical of ketogenic diets, can improve glycaemic control without causing any ill health effects in adults with Type 1 diabetes. METHODS: In this observational study, 11 adults with Type 1 diabetes (seven men, four women, mean ± sd age 36.1± 6.8 years, mean ± sd duration of diabetes 12.8 ± 10.3 years), who followed a ketogenic diet (< 55 g carbohydrate per day) for a mean ± sd of 2.6 ± 3.3 years (ß-hydroxybutyrate 1.6 ± 1.3 mmol/l), underwent sampling and analysis of fasting blood, and were fitted with a blinded continuous glucose monitor for 7 days to measure glycaemic variability. RESULTS: The mean ± sd HbA1c levels were 35±4 mmol/mol (5.3±0.4%), and participants spent 74±20 and 3±8% of their time in the euglycaemic (4-8 mmol/l) and hyperglycaemic (>10 mmol/l) ranges, respectively, with little daily glycaemic variability (sd 1.5±0.7 mmol/l; coefficient of variation 26±8%). Blood glucose levels were <3.0 mmol/l for 3.6% of the time, and participants experienced a median (range) of 0.9 (0.0-2.0) daily episodes of hypoglycaemia. Total cholesterol, LDL cholesterol, total cholesterol/HDL cholesterol ratio, and triglycerides were above the recommended range in 82%, 82%, 64% and 27% of participants, respectively; however, HDL cholesterol levels were within the recommended range for all participants. Participants displayed no or little evidence of hepatic or renal dysfunction. CONCLUSION: This study provides the first evidence that, ketogenic diets in adults with Type 1 diabetes are associated with excellent HbA1c levels and little glycaemic variability, but may also be associated with dyslipidaemia and a high number of hypoglycaemic episodes.

A 10-second sprint does not blunt hormonal counter-regulation to subsequent hypoglycaemia.

AIM: To investigate whether a 10-second (s) sprint impairs the counter-regulatory response to subsequent hypoglycaemia. METHODS: Nine people (five male, four female) with Type 1 diabetes, aged 21.1 ± 4.5 years, performed a 10-s rest or a 10-s maximum-effort sprint in random order on different days, while subjected to an euinsulinaemic-euglycaemic clamp. This was followed by a hyperinsulinaemic-hypoglycaemic glucose clamp 2.5 h later to induce hypoglycaemia for 40 min. At timed intervals, the counter-regulatory hormonal responses to hypoglycaemia were measured. Blood pressure, heart rate and hypoglycaemic symptoms were also assessed. RESULTS: During the hypoglycaemic clamp, epinephrine, norepinephrine, growth hormone and cortisol levels increased significantly from baseline, and their responses were similar after both rest and sprint conditions. In particular, plasma epinephrine rose eightfold, from 197 ± 103 pmol/l to 1582 ± 1118 pmol/l after the rest condition, and from 219 ± 119 pmol/l to 1900 ± 898 pmol/l after the sprint condition. CONCLUSION: A 10-s sprint is unlikely to blunt the subsequent hormonal counter-regulation to hypoglycaemia in individuals with Type 1 diabetes.

Reproducibility of the plasma glucose response to moderate-intensity exercise in adolescents with Type 1 diabetes.

AIMS: The aim of the study was to evaluate the reproducibility of the plasma glucose response to moderate-intensity exercise performed on different days under controlled conditions in adolescents with Type 1 diabetes. METHODS: Eight adolescents with Type 1 diabetes on continuous subcutaneous insulin infusion completed two exercise sessions, each on two separate days, under basal insulin and fasting conditions. On each day, participants cycled twice for 30 min at 55% of their peak rate of oxygen consumption, with each exercise session separated by a 30-min rest. RESULTS: Plasma insulin levels were similar between testing days and exercise sessions. The mean absolute drop in plasma glucose from the commencement to the end of exercise was 1.6 ± 0.5 mmol/l on day 1 and 1.9 ± 0.7 mmol/l on day 2 (P = 0.3). In response to the first exercise session, plasma glucose levels relative to baseline did not change significantly (0.2 ± 0.6 and -0.2 ± 0.5 mmol/l on days 1 and 2). By contrast, the change in plasma glucose during the second exercise session was -1.1 ± 0.7 and -1.3 ± 0.7mmol/l on days 1 and 2, respectively. The mean absolute intra-individual difference in the change in plasma glucose between testing days were 0.7 ± 0.5 [95% confidence interval (CI) 0.4-1.0] and 0.7 ± 0.4 (95% CI 0.4-1.0) mmol/l, at the end of the first and second exercise sessions respectively. CONCLUSIONS: The plasma glucose response to moderate-intensity exercise under similar glycaemic and basal insulin conditions can be reproducible in adolescents with Type 1 diabetes.

The effect of a short sprint on postexercise whole-body glucose production and utilization rates in individuals with type 1 diabetes mellitus.

CONTEXT: Recently we showed that a 10-sec maximal sprint effort performed before or after moderate intensity exercise can prevent early hypoglycemia during recovery in individuals with type 1 diabetes mellitus (T1DM). However, the mechanisms underlying this protective effect of sprinting are still unknown. OBJECTIVE: The objective of the study was to test the hypothesis that short duration sprinting increases blood glucose levels via a disproportionate increase in glucose rate of appearance (Ra) relative to glucose rate of disappearance (Rd). SUBJECTS AND EXPERIMENTAL DESIGN: Eight T1DM participants were subjected to a euglycemic-euinsulinemic clamp and, together with nondiabetic participants, were infused with [6,6-(2)H]glucose before sprinting for 10 sec and allowed to recover for 2 h. RESULTS: In response to sprinting, blood glucose levels increased by 1.2 ± 0.2 mmol/liter (P < 0.05) within 30 min of recovery in T1DM participants and remained stable afterward, whereas glycemia rose by only 0.40 ± 0.05 mmol/liter in the nondiabetic group. During recovery, glucose Ra did not change in both groups (P > 0.05), but glucose Rd in the nondiabetic and diabetic participants fell rapidly after exercise before returning within 30 min to preexercise levels. After sprinting, the levels of plasma epinephrine, norepinephrine, and GH rose transiently in both experimental groups (P < 0.05). CONCLUSION: A sprint as short as 10 sec can increase plasma glucose levels in nondiabetic and T1DM individuals, with this rise resulting from a transient decline in glucose Rd rather than from a disproportionate rise in glucose Ra relative to glucose Rd as reported with intense aerobic exercise.

Effect of a carbohydrate mouth rinse on maximal sprint performance in competitive male cyclists.

There is evidence that rinsing the mouth with a carbohydrate (CHO) solution can improve endurance performance. The goal of this study was to investigate whether a CHO mouth rinse can improve the performance of a maximal sprint effort. Fourteen competitive male cyclists (64.0±5.6 mL kg(-1) min(-1) (mean±SD)) each completed the following 5-s mouth rinse trials in a randomised counter-balanced order; (a) 6.4% maltodextrin solution [Mal], (b) 7.1% glucose solution [Glu], (c) water [Wa] and (d) a control trial with no rinse [Con]. Each participant then performed a 30-s maximal sprint effort on a cycle ergometer. Glu, Mal and Wa trials were not significantly different from Con across all indicators of sprint performance (maximal power output, mean power output over 0-30, 0-10, 10-20, and 20-30s), nausea or fatigue level (p>0.05). These findings suggest that the use of a 5-s mouth rinse with an isoenergetic amount of either maltodextrin or glucose is not beneficial for maximal sprint performance.

Supervised home-based exercise may attenuate the decline of glucose tolerance in obese pregnant women.

AIM: The significant deterioration of insulin sensitivity and glucose tolerance during pregnancy can have serious health implications for both the pregnant woman and her baby. Although it is well established that regular exercise benefits insulin sensitivity in the nonpregnant population, the effect on glucose tolerance in obese pregnant women is not known. The purpose of this study was to investigate the effect of a supervised 10-week, home-based, exercise programme, beginning at week 18 of gestation, on glucose tolerance and aerobic fitness in previously sedentary obese women. METHODS: Twelve sedentary obese women were randomized into an exercise (EX; n=6) or control (CON; n=6) group at 18 weeks of gestation. Those randomized to EX engaged in 10 weeks of supervised home-based exercise (three sessions a week of stationary cycling), while those in the CON group maintained their usual daily activity. Their glucose and insulin responses to an oral glucose tolerance test (OGTT), as well as their aerobic fitness, were assessed both pre- and postintervention. RESULTS: Reduced glucose tolerance in the CON, but not EX, group was indicated by a tendency postintervention towards higher blood glucose levels at 1h of the OGTT (P=0.072). Furthermore, at 2h of the postintervention OGTT, blood glucose tended to remain elevated from baseline in the CON (P=0.077). There was also a trend towards increased fitness in the EX (P=0.064), but not the CON group. CONCLUSION: Regular aerobic exercise begun during pregnancy may have favourable effects on glucose tolerance and fitness in obese women, and warrants further investigation in a larger sample population.

Fiber-specific responses of muscle glycogen repletion in fasted rats physically active during recovery from high-intensity physical exertion.

Mild physical activity performed immediately after a bout of intense exercise in fasting humans results in net glycogen breakdown in their slow oxidative (SO) muscle fibers and glycogen repletion in their fast twitch (FT) fibers. Because several animal species carry a low proportion of SO fibers, it is unclear whether they can also replenish glycogen in their FT fibers under these conditions. Given that most skeletal muscles in rats are poor in SO fibers (<5%), this issue was examined using groups of 24-h fasted Wistar rats (n=10) that swam for 3 min at high intensity with a 10% weight followed by either a 60-min rest (passive recovery, PR) or a 30-min swim with a 0.5% weight (active recovery, AR) preceding a 30-min rest. The 3-min sprint caused 61-79% glycogen fall across the muscles examined, but not in the soleus (SOL). Glycogen repletion during AR without food was similar to PR in the white gastrocnemius (WG), where glycogen increased by 71%, and less than PR in both the red and mixed gastrocnemius (RG, MG). Glycogen fell by 26% during AR in the SOL. Following AR, glycogen increased by 36%, 87%, and 37% in the SOL, RG, and MG, respectively, and this was accompanied by the sustained activation of glycogen synthase and inhibition of glycogen phosphorylase in the RG and MG. These results suggest that mammals with a low proportion of SO fibers can also replenish the glycogen stores of their FT fibers under extreme conditions combining physical activity and fasting.

A 10-s sprint performed prior to moderate-intensity exercise prevents early post-exercise fall in glycaemia in individuals with type 1 diabetes.

AIMS/HYPOTHESIS: We investigated whether a 10-s maximal sprint effort performed immediately prior to moderate-intensity exercise provides another means to counter the rapid fall in glycaemia associated with moderate-intensity exercise in individuals with type 1 diabetes. MATERIALS AND METHODS: Seven complication-free type 1 diabetic males (21.6 +/- 3.6 years; mean+/-SD) with HbA(1c) levels of 7.4 +/- 0.7% injected their normal morning insulin dose and ate their usual breakfast. When post-meal glycaemia fell to approximately 11 mmol/l, participants were asked to perform a 10-s all-out sprint (sprint trial) or to rest (control trial) immediately before cycling at 40% of peak rate of oxygen consumption for 20 min, with both trials conducted in a random counterbalanced order. RESULTS: Sprinting did not affect the rapid fall in glycaemia during the subsequent bout of moderate-intensity exercise (2.9 +/- 0.4 mmol/l in 20 min; p = 0.00; mean+/-SE). However, during the following 45 min of recovery, glycaemia in the control trial decreased by 1.23 +/- 0.60 mmol/l (p = 0.04) while remaining stable in the sprint trial, subsequently decreasing in this latter trial at a rate similar to that in the control trial. The large increase in noradrenaline (norepinephrine) (p = 0.005) and lactate levels (p = 0.0005) may have contributed to the early post-exercise stabilisation of glycaemia in the sprint trial. During recovery, adrenaline (epinephrine) and NEFA levels increased marginally in the sprint trial, but other counter-regulatory hormones did not change significantly (p < 0.05). CONCLUSIONS/INTERPRETATION: A 10-s sprint performed immediately prior to moderate-intensity exercise prevents glycaemia from falling during early recovery from moderate-intensity exercise in individuals with type 1 diabetes.

Effect of intermittent high-intensity compared with continuous moderate exercise on glucose production and utilization in individuals with type 1 diabetes.

Previously, the decline in glycemia in individuals with type 1 diabetes has been shown to be less with intermittent high-intensity exercise (IHE) compared with continuous moderate-intensity exercise (MOD) despite the performance of a greater amount of total work. The purpose of the present study was to determine whether this lesser decline in glycemia can be attributed to a greater increment in endogenous glucose production (Ra) or attenuated glucose utilization (Rd). Nine individuals with type 1 diabetes were tested on two separate occasions, during which either a 30-min MOD or IHE protocol was performed under conditions of a euglycemic clamp in combination with the infusion of [6,6-(2)H]glucose. MOD consisted of continuous cycling at 40% VO2 peak, whereas IHE involved a combination of continuous exercise at 40% VO2 peak interspersed with additional 4-s maximal sprint efforts performed every 2 min to simulate the activity patterns of intermittent sports. During IHE, glucose Ra increased earlier and to a greater extent compared with MOD. Similarly, glucose Rd increased sooner during IHE, but the increase by the end of exercise was comparable with that elicited by MOD. During early recovery from IHE, Rd rapidly declined, whereas it remained elevated after MOD, a finding consistent with a lower glucose infusion rate during early recovery from IHE compared with MOD (P<0.05). The results suggest that the lesser decline in glycemia with IHE may be attributed to a greater increment in Ra during exercise and attenuated Rd during exercise and early recovery.

Glycogen resynthesis in the absence of food ingestion during recovery from moderate or high intensity physical activity: novel insights from rat and human studies.

The finding that during recovery from high intensity exercise, rats have the capacity to replenish their muscle glycogen stores even in the absence of food intake has provided us with an experimental model of choice to explore further this process. Our objective here is to share those questions arising from research carried out by others and ourselves on rats and humans that are likely to be of interest to comparative biochemists/physiologists. On the basis of our findings and those of others, it is proposed that across vertebrate species: (1). the capacity of muscles to replenish their glycogen stores from endogenous carbon sources is dependent on the type of physical activity and animal species; (2). lactate and amino acids are the major endogenous carbon sources mobilized for the resynthesis of muscle glycogen during recovery from exercise, their relative contributions depending on the duration of recovery and type of exercise; (3). the relative contributions of lactate glyconeogenesis and hepatic/renal gluconeogenesis to muscle glycogen synthesis is species- and muscle fiber-dependent; and (4). glycogen synthase and phosphorylase play an important role in the control of the rate of glycogen synthesis post-exercise, with the role of glucose transport being species-dependent.

Muscle glycogen supercompensation: absence of a gender-related difference.

Recently it has been reported that women do not have the capacity to accumulate supranormal levels of muscle glycogen when subjected to a carbohydrate (CHO) loading regimen [Tarnopolsky et al. (1995) J Appl Physiol 78:1360-1368]. Since, in this study, CHO intake relative to body mass in the female subjects was much lower than that in males, our primary aim was to re-examine this issue using subjects fed comparable amounts of CHO. Endurance-trained female and male subjects ingested 12 g CHO x kg(-1) lean body mass day(-1) in conjunction with the cessation of their daily physical training. A 3-day exposure to this diet resulted in a marked rise in muscle glycogen levels from [mean (SD)] 108 (15) mmol x kg(-1) wet weight to 193 (14) mmol x kg(-1) wet weight and 111 (16) m mol x kg(-1) wet weight to 202 (20) mmol x kg(-1) wet weight in the female participants during the post-menstrual and pre-menstrual phases of their menstrual cycle, respectively, and from 109 (27) mmol x kg(-1) wet weight to 183 (25) mmol x kg(-1) wet weight in males. We conclude that (1) female athletes have the capacity to accumulate supranormal levels of muscle glycogen, and (2) when exercise-trained males and females are fed comparable amounts of CHO relative to lean body mass, there is no gender-related difference in their ability to accumulate supranormal levels of muscle glycogen.

Effect of streptozotocin-induced diabetes on glycogen resynthesis in fasted rats post-high-intensity exercise.

It has recently been shown that food intake is not essential for the resynthesis of the stores of muscle glycogen in fasted animals recovering from high-intensity exercise. Because the effect of diabetes on this process has never been examined before, we undertook to explore this issue. To this end, groups of rats were treated with streptozotocin (60 mg/kg body mass ip) to induce mild diabetes. After 11 days, each animal was fasted for 24 h before swimming with a lead weight equivalent to 9% body mass attached to the tail. After exercise, the rate and the extent of glycogen repletion in muscles were not affected by diabetes, irrespective of muscle fiber composition. Consistent with these findings, the effect of exercise on the phosphorylation state of glycogen synthase in muscles was only minimally affected by diabetes. In contrast to its effects on nondiabetic animals, exercise in fasted diabetic rats was accompanied by a marked fall in hepatic glycogen levels, which, surprisingly, increased to preexercise levels during recovery despite the absence of food intake.

Characterization of mouse glycogenin-1 cDNA and promoter region.

Glycogenin-1 is an autocatalytic, self-glucosylating protein which acts as the primer for glycogen synthesis in mammalian skeletal muscle. In this study, we have cloned the glycogenin-1 cDNA from mouse skeletal muscle. Mouse glycogenin-1 has a predicted molecular mass of 37¿ omitted¿399 Da, and the deduced amino acid sequence exhibited 87% homology with human glycogenin-1. Northern blot analysis specifically detected mouse glycogenin-1 transcript in skeletal muscle and heart, and to a lesser extent in kidney, lung and brain. 5'-RACE analysis revealed the major transcription start site to be localized 47 bp upstream of the initiation of translation codon. Sequence analysis of approximately 2 kb of the 5'-flanking region revealed potentially important regions of homology between the mouse and human glycogenin-1 promoters. Several conserved but putative elements, including a TATA box, Sp1 site, and a cyclic AMP responsive element, were observed proximal to the transcription start site. Significantly, Northern blot analysis revealed dibutyryl-cAMP treatment of cultured mouse C2C12 myotubes markedly reduced the levels of glycogenin-1 mRNA in a dose-dependent manner.

Characterization of the human glycogenin-1 gene: identification of a muscle-specific regulatory domain.

The de-novo synthesis of glycogen is now known to involve a novel class of self-glucosylating protein primers. In mammalian skeletal muscle, glycogenin-1 is the protein responsible for this initiation step. Northern blot analysis revealed that glycogenin-1 gene transcription is differentially regulated in the C2C12 mouse muscle cell line. To define the regulatory elements that control expression of the glycogenin-1 gene, we have cloned and characterized the genomic structure of the human glycogenin-1 gene and its promoter region. This gene consists of seven exons and six introns, and spans over 13kb. Transcription of human glycogenin-1 is initiated at two major sites, 80 and 86bp upstream from the initiation of translation codon. Nucleotide sequence analysis of 2.1kb of the 5'-flanking region revealed the proximal promoter contains both a TATA box and two putative Sp1 binding sites located in a CpG island. There are numerous binding sites for developmental and cell-type-specific transcription factors, including AP-1, AP-2, GATA, and several potential Oct 1 binding domains. There are also nine consensus E-boxes that bind the basic helix-loop-helix family of muscle-specific transcription factors. The transcriptional activity of the glycogenin-1 gene was investigated by transient transfection of the 5'-flanking region in HepG2 cells and C2C12 myoblasts and myotubes. These results permitted the definition of a minimal 232bp promoter fragment that is responsible for basal level transcription in a cell-type-independent manner. Furthermore, we have identified a regulatory region located between -2076 and -1736 of the 5'-flanking region of the human glycogenin-1 gene that allows myotube-specific expression in C2C12 cells.

Glycogen repletion following burst activity: a carbohydrate-sparing mechanism in animals adapted to arid environments?

The Western chestnut mouse (Pseudomys nanus ferculinus) is one of several native rodent species adapted to the arid environments of Australia. Since these environments are often associated with a paucity in dietary carbohydrate, the problem arises as to the mechanism whereby these rodents replete their stores of muscle glycogen when recovering from high intensity physical activity. This is an important issue since the maintenance of adequate stores of muscle glycogen is crucial to support the energy demands associated with 'flight or fight' responses. Whilst it is known that food ingestion post-exercise is required for the total repletion of muscle glycogen in rats and humans, our findings indicate that the Western chestnut mouse has the impressive capacity to replete completely its stores of muscle glycogen, even in the absence of food intake. Indeed during recovery from burst activity which results in the massive breakdown of the stores of muscle glycogen, the levels of glycogen return back to pre-exercise levels within only 50 minutes despite the absence of food intake. This capacity is important in the broader context of nutritional adaptation to arid/seasonally-arid regions since it allows muscles to replete their fuel stores even when food is not available. How common is this strategy among desert-adapted mammal species is a question yet to be answered.

Prolonged exposure to halothane and associated changes in carbohydrate metabolism in rat muscles in vivo.

Halothane, an anesthetic presently used in animal experimentation, is reported to stimulate glycogen breakdown in isolated preparations of rat skeletal muscles, suggesting that it may not be a suitable anesthetic for the study of glycogen metabolism in rats in vivo. The purpose of this study was to establish whether prolonged exposure to halothane in rats in vivo is associated with accelerated glycogenolysis. Exposure of rats to halothane for up to 1 h was not accompanied by either any change in the levels of glycogen or increase in activity ratios of glycogen phosphorylase in muscles, irrespective of their fiber compositions. In marked contrast, the levels of lactate, inorganic phosphate, glucose 1-phosphate, glucose 6-phosphate, fructose 1,6-bisphosphate, and fructose 2, 6-bisphosphate changed progressively during anesthesia. Accordingly, the interpretation of muscle metabolite levels must be performed with caution in experiments involving prolonged exposure to halothane. Overall, our findings indicate that the reported halothane-mediated stimulation of glycogen breakdown in vitro is likely to be an artifact and that halothane is a suitable anesthetic for experiments concerned with glycogen metabolism in rats.