Contribution Of Glycolysis Research Articles

Physiological adaptations to repeated sprint training in hypoxia induced by voluntary hypoventilation at low lung volume.

This study investigated the effects of repeated-sprint (RS) training in hypoxia induced by voluntary hypoventilation at low lung volume (RSH-VHL) on physiological adaptations, RS ability (RSA) and anaerobic performance. Over a 3-week period, eighteen well-trained cyclists completed six RS sessions in cycling either with RSH-VHL or with normal conditions (RSN). Before (Pre) and after (Post) the training period, the subjects performed an RSA test (10 × 6-s all-out cycling sprints) during which oxygen uptake [Formula: see text] and the change in both muscle deoxyhaemoglobin (Δ[HHb]) and total haemoglobin (Δ[THb]) were measured. A 30-s Wingate test was also performed and maximal blood lactate concentration ([La]max) was assessed. At Post compared to Pre, the mean power output during both the RSA and the Wingate tests was improved in RSH-VHL (846 ± 98 vs 911 ± 117W and 723 ± 112 vs 768 ± 123W, p < 0.05) but not in RSN (834 ± 52 vs 852 ± 69W, p = 0.2; 710 ± 63 vs 713 ± 72W, p = 0.68). The average [Formula: see text] recorded during the RSA test was significantly higher in RSH-VHL at Post but did not change in RSN. No change occurred for Δ[THb] whereas Δ[HHb] increased to the same extent in both groups. [Lamax] after the Wingate test was higher in RSH-VHL at Post (13.9 ± 2.8 vs 16.1 ± 3.2mmolL-1, p < 0.01) and tended to decrease in RSN (p = 0.1). This study showed that RSH-VHL could bring benefits to both RSA and anaerobic performance through increases in oxygen delivery and glycolytic contribution. On the other hand, no additional effect was observed for the indices of muscle blood volume and O2 extraction.

An alternative to oxygen deficit as a way to quantify anaerobic contributions in running

The purpose of this study was to determine if the sum of estimates of the phosphocreatine contribution and the glycolytic contribution (we refer to this sum as PCr+glycolysis ) provides an alternative to oxygen deficit as a way to quantify the anaerobic contribution in running. Thirty university students performed three treadmill tests, each test at one speed individually selected for each participant; one test was terminated after 3 min, one after 7 min, and one at exhaustion (mean ± SD, 10.3 ± 0.4 min). Oxygen deficit was calculated by subtraction of the accumulated oxygen uptake from the total oxygen cost. Phosphocreatine and glycolysis contributions were determined from post-exercise VO 2 responses and blood lactate concentrations, respectively. The mean values for PCr+glycolysis was ~3 mL·kg –1 lower (p < .05) than oxygen deficit across three exercise durations, but well correlated ( r ≥ .80, p < .05) at each. These results confirm the validity of PCr+glycolysis as an alternative to oxygen deficit to quantify the anaerobic contribution in running exercise.

Can Caffeine Intake Improve Neuromuscular and Technical-Tactical Performance During Judo Matches?

Athayde, MSdS, Lima Kons, R, and Detanico, D. Can caffeine intake improve neuromuscular and technical-tactical performance during judo matches? J Strength Cond Res 32(11): 3095-3102, 2018-This study aimed to verify the effect of caffeine intake on blood lactate concentrations and neuromuscular and technical-tactical performance during simulated judo matches. Fourteen male judo athletes received capsules containing caffeine or placebo and were evaluated in both conditions. Before the baseline and 1 hour after the caffeine/placebo intake, athletes performed the countermovement jump (CMJ) test, handgrip strength, judogi grip strength test (JGST), and blood samples were collected. Subsequently, the athletes were submitted to three 5-minute matches with 15-minute intervals. All neuromuscular tests were performed and blood samples were taken during the matches' intervals. Significant interaction between condition and time (p = 0.01) was found for blood lactate concentrations. No interaction between condition and time was verified for CMJ performance (p > 0.05), handgrip strength (p > 0.05), JGST performance (p = 0.32), and number of attacks (p = 0.97). However, for all variables, a significant decrease was observed throughout time (p ≤ 0.05). According to clinical results (magnitude-based inference), we identified that post-match 2 and post-match 3 showed higher effect (most likely positive effect) regarding delta caffeine-placebo than other moments (pre-match and post-match 1) for blood lactate. Caffeine increased the estimated glycolytic contribution over the matches; however, it did not induce improvements in neuromuscular performance or number of attacks.

Effects of β-alanine and sodium bicarbonate supplementation on the estimated energy system contribution during high-intensity intermittent exercise.

The effects of β-alanine (BA) and sodium bicarbonate (SB) on energy metabolism during work-matched high-intensity exercise and cycling time-trial performance were examined in 71 male cyclists. They were randomised to receive BA + placebo (BA, n = 18), placebo + SB (SB, n = 17), BA + SB (BASB, n = 19), or placebo + placebo (PLA, n = 18). BA was supplemented for 28days (6.4gday-1) and SB (0.3gkg-1) ingested 60min before exercise on the post-supplementation trial. Dextrose and calcium carbonate were placebos for BA and SB, respectively. Before (PRE) and after (POST) supplementation, participants performed a high-intensity intermittent cycling test (HICT-110%) consisting of four 60-s bouts at 110% of their maximal power output (60-s rest between bouts). The estimated contribution of the energy systems was calculated for each bout in 39 of the participants (BA: n = 9; SB: n = 10; BASB: n = 10, PLA: n = 10). Ten minutes after HICT-110%, cycling performance was determined in a 30-kJ time-trial test in all participants. Both groups receiving SB increased estimated glycolytic contribution in the overall HICT-110%, which approached significance (SB: + 23%, p = 0.068 vs. PRE; BASB: + 18%, p = 0.059 vs. PRE). No effects of supplementation were observed for the estimated oxidative and ATP-PCr systems. Time to complete 30 kJ was not significantly changed by any of the treatments, although a trend toward significance was shown in the BASB group (p = 0.06). We conclude that SB, but not BA, increases the estimated glycolytic contribution to high-intensity intermittent exercise when total work done is controlled and that BA and SB, either alone or in combination, do not improve short-duration cycling time-trial performance.

Sodium bicarbonate ingestion increases glycolytic contribution and improves performance during simulated taekwondo combat

Purpose: To investigate the effect of sodium bicarbonate (NaHCO3) on performance and estimated energy system contribution during simulated taekwondo combat. Methods: Nine taekwondo athletes completed two experimental sessions separated by at least 48 h. Athletes consumed 300 mg/kg body mass of NaHCO3 or placebo (CaCO3) 90 min before the combat simulation (three rounds of 2 min separated by 1 min passive recovery), in a double-blind, randomized, repeated-measures crossover design. All simulated combat was filmed to quantify the time spent fighting in each round. Lactate concentration [La−] and rating of perceived exertion (RPE) were measured before and after each round, whereas heart rate (HR) and the estimated contribution of the oxidative (WOXI), ATP (adenosine triphosphate)-phosphocreatine (PCr) (WPCR), and glycolytic (W[La−]) systems were calculated during the combat simulation. Results: [La−] increased significantly after NaHCO3 ingestion, when compared with the placebo condition (+14%, P = 0.04, d = 3.70). NaHCO3 ingestion resulted in greater estimated glycolytic energy contribution in the first round when compared with the placebo condition (+31%, P = 0.01, d = 3.48). Total attack time was significantly greater after NaHCO3 when compared with placebo (+13%, P = 0.05, d = 1.15). WOXI, WPCR, VO2, HR and RPE were not different between conditions (P > 0.05). Conclusion: NaHCO3 ingestion was able to increase the contribution of glycolytic metabolism and, therefore, improve performance during simulated taekwondo combat.

Anaerobic Contribution Determined in Swimming Distances: Relation with Performance

Total anaerobic contribution (TAn) can be assessed by accumulated oxygen deficit, and through sum of glycolytic and phosphagen contribution which enable the evaluation of TAn without influences on mechanical parameters. However, little is known about the difference of TAn within swimming distances. Therefore, the objectives of the present study were to determine and compare the TAn in different performances using the backward extrapolation technique and amount of lactate accumulated during exercise, and relate it with swimming performance. Fourteen competitive swimmers performed five maximal front crawl swims of 50, 100, 200, 400, and 800 m. The total phosphagen (AnAl) and glycolytic (AnLa) contributions were assumed as the fast component of post-exercise oxygen consumption (EPOCFAST) and amount of blood lactate accumulated during exercise, respectively. TAn was the sum of AnAl and AnLa. Significantly lower values of AnLa were observed in the 800 m (p < 0.01) than other distances. For AnAl, the 50 m performance presented the lowest values, followed by 100 and 800 m (p < 0.01). The highest values of AnAl were observed in the 200 and 400 m (p > 0.13). The TAn was significantly higher in the 200 and 400 m performances than observed at 50 and 800 m (p < 0.01). Anaerobic contributions were correlated with 50, 100, 200, and 400 m performances (p < 0.01). The AnAl contribution was not correlated with 400 m performance. Anaerobic parameters were not correlated with 800 m performance. In conclusion, the highest values of anaerobic contribution were observed in the 200 and 400 m distances. Moreover, TAn is important to performances below 400 m, and may be used in training routines.

Rewiring of embryonic glucose metabolism via suppression of PFK-1 and aldolase during mouse chorioallantoic branching

Adapting the energy metabolism state to changing bioenergetic demands is essential for mammalian development accompanying massive cell proliferation and cell differentiation. However, it remains unclear how developing embryos meet the changing bioenergetic demands during the chorioallantoic branching (CB) stage, when the maternal-fetal exchange of gases and nutrients is promoted. In this study, using metabolome analysis with mass-labeled glucose, we found that developing embryos redirected glucose carbon flow into the pentose phosphate pathway via suppression of the key glycolytic enzymes PFK-1 and aldolase during CB. Concomitantly, embryos exhibited an increase in lactate pool size and in the fractional contribution of glycolysis to lactate biosynthesis. Imaging mass spectrometry visualized lactate-rich tissues, such as the dorsal or posterior neural tube, somites and head mesenchyme. Furthermore, we found that the heterochronic gene Lin28a could act as a regulator of the metabolic changes observed during CB. Perturbation of glucose metabolism rewiring by suppressing Lin28a downregulation resulted in perinatal lethality. Thus, our work demonstrates that developing embryos rewire glucose metabolism following CB for normal development.

Performance and energy systems contributions during upper-body sprint interval exercise.

The main purpose of this study was to investigate the performance and energy systems contribution during four upper-body Wingate tests interspersed by 3-min intervals. Fourteen well-trained male adult Judo athletes voluntarily took part in the present study. These athletes were from state to national level, were in their competitive period, but not engaged in any weight loss procedure. Energy systems contributions were estimated using oxygen uptake and blood lactate measurements. The main results indicated that there was higher glycolytic contribution compared to oxidative (P<0.001) during bout 1, but lower glycolytic contribution was observed compared to the phosphagen system (adenosine triphosphate-creatine phosphate, ATP-PCr) contribution during bout 3 (P<0.001), lower glycolytic contribution compared to oxidative and ATP-PCr (P<0.001 for both comparisons) contributions during bout 4 and lower oxidative compared to ATP-PCr during bout 4 (P=0.040). For the energy system contribution across Wingate bouts, the ATP-PCr contribution during bout 1 was lower than that observed during bout 4 (P=0.005), and the glycolytic system presented higher percentage contribution in the first bout compared to the third and fourth bouts (P<0.001 for both comparisons), and higher percentage participation in the second compared to the fourth bout (P<0.001). These results suggest that absolute oxidative and ATP-PCr participations were kept constant across Wingate tests, but there was an increase in relative participation of ATP-PCr in bout 4 compared to bout 1, probably due to the partial phosphocreatine resynthesis during intervals and to the decreased glycolytic activity.

Correction: Caffeine Ingestion Increases Estimated Glycolytic Metabolism during Taekwondo Combat Simulation but Does Not Improve Performance or Parasympathetic Reactivation

[This corrects the article DOI: 10.1371/journal.pone.0142078.].

Energy-System Contributions to Simulated Judo Matches.

To estimate the contribution of the 3 energy systems to simulated judo matches. Twelve judo athletes (18 ± 1 y, 175.1 ± 5.3 cm, 74.3 ± 10.5 kg, 11.7% ± 1.5% body fat, 8 ± 2 y of practice) performed 5 combats with different durations (1, 2, 3, 4, and 5 min), against the same opponent, on different days and blinded to the duration. The estimated energy contributions for the oxidative, glycolytic, and ATP-PCr systems were calculated based on oxygen uptake (V̇O2) during activity, Delta of lactate, and the fast phase of excess V ̇ O2, respectively. Analysis of mixed models for repeated measures was used to compare the contribution of the 3 energy systems and different durations of judo matches, followed by a post hoc Bonferroni test. The oxidative system's contribution (70%) was higher than those of the glycolytic (8%; P < .001) and ATP-PCr (21%; P < .001) energy systems (in all durations), and the ATP-PCr contribution was higher than that of the glycolytic energy system (up to 3 min). In addition, during the match there was an increase in the oxidative (from 50% to 81%; P < .001), a decrease in the ATP-PCr (from 40% to 12%; P < .001), and maintenance of the glycolytic contributions (between 6% and 10%). There is a predominance of the oxidative system to supply the energy cost of judo matches from the first minute of combat up to the end, compared with the anaerobic systems.

Measurement and Analysis of Extracellular Acid Production to Determine Glycolytic Rate

Extracellular measurement of oxygen consumption and acid production is a simple and powerful way to monitor rates of respiration and glycolysis1. Both mitochondrial (respiration) and non-mitochondrial (other redox) reactions consume oxygen, but these reactions can be easily distinguished by chemical inhibition of mitochondrial respiration. However, while mitochondrial oxygen consumption is an unambiguous and direct measurement of respiration rate2, the same is not true for extracellular acid production and its relationship to glycolytic rate 3-6. Extracellular acid produced by cells is derived from both lactate, produced by anaerobic glycolysis, and CO2, produced in the citric acid cycle during respiration. For glycolysis, the conversion of glucose to lactate- + H+ and the export of products into the assay medium is the source of glycolytic acidification. For respiration, the export of CO2, hydration to H2CO3 and dissociation to HCO3- + H+ is the source of respiratory acidification. The proportions of glycolytic and respiratory acidification depend on the experimental conditions, including cell type and substrate(s) provided, and can range from nearly 100% glycolytic acidification to nearly 100% respiratory acidification 6. Here, we demonstrate the data collection and calculation methods needed to determine respiratory and glycolytic contributions to total extracellular acidification by whole cells in culture using C2C12 myoblast cells as a model.

Measurement and Analysis of Extracellular Acid Production to Determine Glycolytic Rate.

Extracellular measurement of oxygen consumption and acid production is a simple and powerful way to monitor rates of respiration and glycolysis1. Both mitochondrial (respiration) and non-mitochondrial (other redox) reactions consume oxygen, but these reactions can be easily distinguished by chemical inhibition of mitochondrial respiration. However, while mitochondrial oxygen consumption is an unambiguous and direct measurement of respiration rate2, the same is not true for extracellular acid production and its relationship to glycolytic rate 3-6. Extracellular acid produced by cells is derived from both lactate, produced by anaerobic glycolysis, and CO2, produced in the citric acid cycle during respiration. For glycolysis, the conversion of glucose to lactate- + H+ and the export of products into the assay medium is the source of glycolytic acidification. For respiration, the export of CO2, hydration to H2CO3 and dissociation to HCO3- + H+ is the source of respiratory acidification. The proportions of glycolytic and respiratory acidification depend on the experimental conditions, including cell type and substrate(s) provided, and can range from nearly 100% glycolytic acidification to nearly 100% respiratory acidification 6. Here, we demonstrate the data collection and calculation methods needed to determine respiratory and glycolytic contributions to total extracellular acidification by whole cells in culture using C2C12 myoblast cells as a model.

Caffeine Ingestion Increases Estimated Glycolytic Metabolism during Taekwondo Combat Simulation but Does Not Improve Performance or Parasympathetic Reactivation.

ObjectivesThe aim of this study was to evaluate the effect of caffeine ingestion on performance and estimated energy system contribution during simulated taekwondo combat and on post-exercise parasympathetic reactivation.MethodsTen taekwondo athletes completed two experimental sessions separated by at least 48 hours. Athletes consumed a capsule containing either caffeine (5 mg∙kg-1) or placebo (cellulose) one hour before the combat simulation (3 rounds of 2 min separated by 1 min passive recovery), in a double-blind, randomized, repeated-measures crossover design. All simulated combat was filmed to quantify the time spent fighting in each round. Lactate concentration and rating of perceived exertion were measured before and after each round, while heart rate (HR) and the estimated contribution of the oxidative (WAER), ATP-PCr (WPCR), and glycolytic (W[La-]) systems were calculated during the combat simulation. Furthermore, parasympathetic reactivation after the combat simulation was evaluated through 1) taking absolute difference between the final HR observed at the end of third round and the HR recorded 60-s after (HRR60s), 2) taking the time constant of HR decay obtained by fitting the 6-min post-exercise HRR into a first-order exponential decay curve (HRRτ), or by 3) analyzing the first 30-s via logarithmic regression analysis (T30).ResultsCaffeine ingestion increased estimated glycolytic energy contribution in relation to placebo (12.5 ± 1.7 kJ and 8.9 ± 1.2 kJ, P = 0.04). However, caffeine did not improve performance as measured by attack number (CAF: 26. 7 ± 1.9; PLA: 27.3 ± 2.1, P = 0.48) or attack time (CAF: 33.8 ± 1.9 s; PLA: 36.6 ± 4.5 s, P = 0.58). Similarly, RPE (CAF: 11.7 ± 0.4 a.u.; PLA: 11.5 ± 0.3 a.u., P = 0.62), HR (CAF: 170 ± 3.5 bpm; PLA: 174.2 bpm, P = 0.12), oxidative (CAF: 109.3 ± 4.5 kJ; PLA: 107.9 kJ, P = 0.61) and ATP-PCr energy contributions (CAF: 45.3 ± 3.4 kJ; PLA: 46.8 ± 3.6 kJ, P = 0.72) during the combat simulation were unaffected. Furthermore, T30 (CAF: 869.1 ± 323.2 s; PLA: 735.5 ± 232.2 s, P = 0.58), HRR60s (CAF: 34 ± 8 bpm; PLA: 38 ± 9 bpm, P = 0.44), HRRτ (CAF: 182.9 ± 40.5 s, PLA: 160.3 ± 62.2 s, P = 0.23) and HRRamp (CAF: 70.2 ± 17.4 bpm; PLA: 79.2 ± 17.4 bpm, P = 0.16) were not affected by caffeine ingestion.ConclusionsCaffeine ingestion increased the estimated glycolytic contribution during taekwondo combat simulation, but this did not result in any changes in performance, perceived exertion or parasympathetic reactivation.

Prior low- or high-intensity exercise alters pacing strategy, energy system contribution and performance during a 4-km cycling time trial.

We analyzed the influence of prior exercise designed to reduce predominantly muscle glycogen in either type I or II fibers on pacing and performance during a 4-km cycling time trial (TT). After preliminary and familiarization trials, in a randomized, repeated-measures crossover design, ten amateur cyclists performed: 1) an exercise designed to reduce glycogen of type I muscle fibers, followed by a 4-km TT (EX-FIB I); 2) an exercise designed to reduce glycogen of type II muscle fibers, followed by a 4-km TT (EX-FIB II) and; 3) a 4-km TT, without the prior exercise (CONT). The muscle-glycogen-reducing exercise in both EX-FIB I and EX-FIB II was performed in the evening, ∼12 h before the 4-km TT. Performance time was increased and power output (PO) was reduced in EX-FIB I (432.8±8.3 s and 204.9±10.9 W) and EX-FIB II (428.7±6.7 s and 207.5±9.1 W) compared to CONT (420.8±6.4 s and 218.4±9.3 W; P<0.01), without a difference between EX-FIB I and EX-FIB II (P>0.05). The PO was lower in EX-FIB I than in CONT at the beginning and middle of the trial (P<0.05). The mean aerobic contribution during EX-FIB I was also significantly lower than in CONT (P<0.05), but there was no difference between CONT and EX-FIB II or between EX-FIB I and EX-FIB II (P>0.05). The integrated electromyography was unchanged between conditions (P>0.05). Performance may have been impaired in EX-FIB I due a more conservative pacing at the beginning and middle, which was associated with a reduced aerobic contribution. In turn, the PO profile adopted in EX-FIB II was also reduced throughout the trial, but the impairment in performance may be attributed to a reduced glycolytic contribution (i.e. reduced lactate accumulation).

Discussion of “Effect of plasma donation and blood donation on aerobic and anaerobic responses in exhaustive, severe-intensity exercise”

I readwith interest the paper by Hill and co-workers recently published in Applied Physiology, Nutrition, and Metabolism (Hill et al. 2013), and I would like to discuss some differences with previous work from my lab. Similarly toHill’s study,weexercise testedhealthyuniversity studentsprior, and2h, 2days, and7days after a standardblood-bank donation (450mLextraction;Mora-Rodriguez et al. 2012).We focused on the physiological responses during steady-state submaximal pedaling (60 min at 154 W) while Hill studied O2 kinetics during cycle ergometer short test to exhaustion ( 4 min at 274 W). Our experiments were conducted in different environments (35 °C vs. 22 °C); however, in each study, all trials took place in the same environment and thus the effects of blood donation should have been similar. Hill’s finding of unchanged O2 kinetic during exercise after blood donation expands our findings of unchanged O2 consumption rates upon donation when exercising at submaximal workloads (MoraRodriguez et al. 2012). We found that the relation between oxygen consumption (VO2) and external work intensity was independent of hemoglobin concentration. The maintenance of the rates of oxygen delivery and consumption despite reductions in the main blood oxygencarrier (i.e., hemoglobin) requires a tightly regulated increase in cardiac output, which time course after donation is depicted in our Fig. 4 (Mora-Rodriguez et al. 2012). This cardiovascular adjustment to maintain oxygen rates of consumption after venesection was shown in the classic study of Woodson et al. (1978) and more recently by Beng Saltin’s group (Koskolou et al. 1997). While we agree that blood donation does not affect the VO2 response during submaximal exercise, we found that CO2 production is affected by a standard blood-bank donation. We reported increased carbon dioxide production (VCO2) for the same VO2 and thus increased calculated carbohydrate oxidation when exercising 2 h after blood donation. Furthermore, in contrast to Hill’s data, we found blood lactate concentration elevated when exercising after donation. Ekblom et al. (1976) also found a higher blood lactate concentration during submaximal exercise after venesection of 800 mL of whole blood. Both papers suggest a higher anaerobic energy yield in a situation of reduced O2 availability per liter of blood (i.e., after blood donation). The unchanged end of exercise plasma lactate concentration in Hill’s study andothers (Panebianco et al. 1995;Duda et al. 2003) could be an artifact of the different energy demand in their trials. Two hours after donation subjects exercised for 19% less time than in the trial before donation (218 vs. 268 s), expending less energy. However, final plasma lactate concentration was similar between trials. To me, this suggests that the rates of anaerobic energy utilization were larger to achieve similar lactate concentrationwith 19% less exercise duration. Another factor that could have influenced plasma lactate concentration is blood bicarbonate availability. Blood bicarbonate elevation by dietary supplementation increases blood lactate concentration during exercise (Zinner et al. 2011). In contrast, blood donation lowers plasma bicarbonate concentration (Duda et al. 2003), likely reducing the buffering of the dissociated hydrogen proton of the lactic acid and thus lactate incorporation into blood. Again, similar plasma lactate with lower plasma bicarbonate (Duda et al. 2003) suggests a higher reliance on glycolysis. In summary, our elevations in VCO2 and blood lactate data during submaximal exercise upon a standard blood-bank donation suggest a higher contribution of glycolysis and anaerobicmetabolism in this situation of reduced O2 availability. I realize that Hill’s thesis is that the “capacity” of the anaerobic system to produce energy during short-fatiguing exercise is not undermined by blood donation. Presently, I argue that anaerobic energy contribution to exercise is increased after blood donation based on our submaximal exercise results (Mora-Rodriguez et al. 2012). I amunclear if both findings can co-exist and I would like to know Dr. Hill’s opinion on this issue.

High-Intensity Interval Training, Solutions to the Programming Puzzle

High-intensity interval training (HIT) is a well-known, time-efficient training method for improving cardiorespiratory and metabolic function and, in turn, physical performance in athletes. HIT involves repeated short (<45 s) to long (2-4 min) bouts of rather high-intensity exercise interspersed with recovery periods (refer to the previously published first part of this review). While athletes have used 'classical' HIT formats for nearly a century (e.g. repetitions of 30 s of exercise interspersed with 30 s of rest, or 2-4-min interval repetitions ran at high but still submaximal intensities), there is today a surge of research interest focused on examining the effects of short sprints and all-out efforts, both in the field and in the laboratory. Prescription of HIT consists of the manipulation of at least nine variables (e.g. work interval intensity and duration, relief interval intensity and duration, exercise modality, number of repetitions, number of series, between-series recovery duration and intensity); any of which has a likely effect on the acute physiological response. Manipulating HIT appropriately is important, not only with respect to the expected middle- to long-term physiological and performance adaptations, but also to maximize daily and/or weekly training periodization. Cardiopulmonary responses are typically the first variables to consider when programming HIT (refer to Part I). However, anaerobic glycolytic energy contribution and neuromuscular load should also be considered to maximize the training outcome. Contrasting HIT formats that elicit similar (and maximal) cardiorespiratory responses have been associated with distinctly different anaerobic energy contributions. The high locomotor speed/power requirements of HIT (i.e. ≥95 % of the minimal velocity/power that elicits maximal oxygen uptake [v/p(·)VO(2max)] to 100 % of maximal sprinting speed or power) and the accumulation of high-training volumes at high-exercise intensity (runners can cover up to 6-8 km at v(·)VO(2max) per session) can cause significant strain on the neuromuscular/musculoskeletal system. For athletes training twice a day, and/or in team sport players training a number of metabolic and neuromuscular systems within a weekly microcycle, this added physiological strain should be considered in light of the other physical and technical/tactical sessions, so as to avoid overload and optimize adaptation (i.e. maximize a given training stimulus and minimize musculoskeletal pain and/or injury risk). In this part of the review, the different aspects of HIT programming are discussed, from work/relief interval manipulation to HIT periodization, using different examples of training cycles from different sports, with continued reference to the cardiorespiratory adaptations outlined in Part I, as well as to anaerobic glycolytic contribution and neuromuscular/musculoskeletal load.

Kinetic Modeling of Human Hepatic Glucose Metabolism in Type 2 Diabetes Mellitus Predicts Higher Risk of Hypoglycemic Events in Rigorous Insulin Therapy

A major problem in the insulin therapy of patients with diabetes type 2 (T2DM) is the increased occurrence of hypoglycemic events which, if left untreated, may cause confusion or fainting and in severe cases seizures, coma, and even death. To elucidate the potential contribution of the liver to hypoglycemia in T2DM we applied a detailed kinetic model of human hepatic glucose metabolism to simulate changes in glycolysis, gluconeogenesis, and glycogen metabolism induced by deviations of the hormones insulin, glucagon, and epinephrine from their normal plasma profiles. Our simulations reveal in line with experimental and clinical data from a multitude of studies in T2DM, (i) significant changes in the relative contribution of glycolysis, gluconeogenesis, and glycogen metabolism to hepatic glucose production and hepatic glucose utilization; (ii) decreased postprandial glycogen storage as well as increased glycogen depletion in overnight fasting and short term fasting; and (iii) a shift of the set point defining the switch between hepatic glucose production and hepatic glucose utilization to elevated plasma glucose levels, respectively, in T2DM relative to normal, healthy subjects. Intriguingly, our model simulations predict a restricted gluconeogenic response of the liver under impaired hormonal signals observed in T2DM, resulting in an increased risk of hypoglycemia. The inability of hepatic glucose metabolism to effectively counterbalance a decline of the blood glucose level becomes even more pronounced in case of tightly controlled insulin treatment. Given this Janus face mode of action of insulin, our model simulations underline the great potential that normalization of the plasma glucagon profile may have for the treatment of T2DM.

Increased Glyceride–Glycerol Synthesis in Liver and Brown Adipose Tissue of Rat: In‐Vivo Contribution of Glycolysis and Glyceroneogenesis

We have previously shown that a high-protein, carbohydrate-free diet can decrease the production of glycerol-3-phosphate (G3P) from glucose and increase glyceroneogenesis in both brown (BAT) and epididymal (EAT) adipose tissue. Here, we utilized an in-vivo approach to examine the hypothesis that there is reciprocal regulation in the G3P synthesis from glucose (via glycolysis) and glyceroneogenesis in BAT, EAT and liver of fasted rats and cafeteria diet-fed rats. Glyceroneogenesis played a prominent role in the generation of G3P in the liver (~70%) as well as in BAT and EAT (~80%) in controls rats. The cafeteria diet induced an increase in the total glyceride-glycerol synthesis and G3P synthesis from glucose and a decrease in glyceroneogenesis in BAT; this diet did not affect either the total glyceride-glycerol synthesis or G3P generation from glyceroneogenesis or glycolysis in the liver or EAT. Fasting induced an increase in total glyceride-glycerol synthesis and glyceroneogenesis and a decrease in G3P synthesis from glucose in the liver but did not affect either the total glyceride-glycerol synthesis or G3P synthesis from glyceroneogenesis in BAT and EAT, despite a reduction in glycolysis in these tissues. These data demonstrate that reciprocal changes in the G3P generation from glucose and from glyceroneogenesis in the rat liver and BAT occur only when the synthesis of glycerides-glycerol is increased. Further, our data suggest that this increase may be essential for the systemic recycling of fatty acids by the liver from fasted rats and for the maintenance of the thermogenic capacity of BAT from cafeteria diet-fed rats.

Muscle metabolic status and acid-base balance during 10-s work:5-s recovery intermittent and continuous exercise

Gastrocnemius muscle phosphocreatine ([PCr]) and hydrogen ion ([H(+)]) were measured using (31)P-magnetic resonance spectroscopy during repeated bouts of 10-s heavy-intensity (HI) exercise and 5-s rest compared with continuous (CONT) HI exercise. Recreationally active male subjects (n = 7; 28 yr ± 9 yr) performed on separate occasions 12 min of isotonic plantar flexion (0.75 Hz) CONT and intermittent (INT; 10-s exercise, 5-s rest) exercise. The HI power output in both CONT and INT was set at 50% of the difference between the power output associated with the onset of intracellular acidosis and peak exercise determined from a prior incremental plantar flexion protocol. Intracellular concentrations of [PCr] and [H(+)] were calculated at 4 s and 9 s of the work period and at 4 s of the rest period in INT and during CONT exercise. [PCr] and [H(+)] (mean ± SE) were greater at 4 s of the rest periods vs. 9 s of exercise over the course of the INT exercise bout: [PCr] (20.7 mM ± 0.6 vs. 18.7 mM ± 0.5; P < 0.01); [H(+)] (370 nM ± 13.50 vs. 284 nM ± 13.6; P < 0.05). Average [H(+)] was similar for CONT vs. INT. We therefore suggest that there is a glycolytic contribution to ATP recovery during the very short rest period (<5 s) of INT and that the greater average power output of CONT did not manifest in greater [H(+)] and greater glycolytic contribution compared with INT exercise.

Life of mice - development of cardiac energetics

Life of mice - development of cardiac energetics