Brief intense exercise followed by passive recovery modifies the pattern of fuel use in humans during subsequent sustained intermittent exercise.

The role of work period duration as the principal factor influencing carbohydrate metabolism during intermittent exercise has been investigated. Fuel oxidation rates and muscle glycogen and free carnitine content were compared between two protocols of sustained intermittent intense exercise with identical treadmill speed and total work duration. In the first experiment subjects (n=6) completed 40 min of intermittent treadmill running involving a work : recovery cycle of 6 : 9 s or 24 : 36 s on separate days. With 24 : 36 s exercise a higher rate of carbohydrate oxidation approached significance (P=0.057), whilst fat oxidation rate was lower (P < or = 0.01) and plasma lactate concentration higher (P < or = 0.01). Muscle glycogen was lower post-exercise with 24 : 36 s (P < or = 0.05). Muscle free carnitine decreased (P < or = 0.05), but there was no difference between protocols. In the second experiment a separate group of subjects (n=5) repeated the intermittent exercise protocols with the addition of a 10-min bout of intense exercise, followed by 43 +/- 5 min passive recovery, prior to sustained (40 min) intermittent exercise. For this experiment the difference in fuel use observed previously between 6 : 9 s and 24 : 36 s was abolished. Carbohydrate and fat oxidation, plasma lactate and muscle glycogen levels were similar in 6 : 9 s and 24 : 36 s. When compared with the first experiment, this result was because of reduced carbohydrate oxidation in 24 : 36 s (P < or = 0.05). There was no difference, and no change, in muscle free carnitine between protocols. A 10-min bout of intense exercise, followed by 43 +/- 5 min of passive recovery, substantially modifies fuel use during subsequent intermittent intense exercise.     

A comparison of skeletal muscle oxygenation and fuel use in sustained continuous and intermittent exercise

In this study we compared substrate oxidation and muscle oxygen availability during sustained intermittent intense and continuous submaximal exercise with similar overall (i.e. work and recovery) oxygen consumption (V˙O₂). Physically active subjects (n?=?7) completed 90?min of an intermittent intense (12?s work:18?s recovery) and a continuous submaximal treadmill running protocol on separate days. In another experiment (n?=?5) we compared oxygen availability in the vastus lateralis muscle between these two exercise protocols using near-infrared spectroscopy. Initially, overall V˙O₂ (i.e. work and recovery) was matched, and from 37.5?min to 67.5?min of exercise was similar, although slightly higher during continuous exercise (8%; P??1?·?kg^?1] and continuous submaximal [0.85 (0.01)?kJ?·?min^?1?·?kg^?1] exercise. Overall exercise intensity, represented as a proportion of peak aerobic power (V˙O_2peak), was 68.1 (2.5)% V˙O_2peak and 71.8 (1.8)% V˙O_2peak for intermittent and continuous exercise protocols, respectively. Fat oxidation was almost 3 times lower (P?P?P?P?P?r?=?0.72; P?V˙O₂ and identical energy expenditure.     

Effect of work and recovery duration on skeletal muscle oxygenation and fuel use during sustained intermittent exercise

The purpose of this study was to compare rates of substrate oxidation in two protocols of intermittent exercise, with identical treadmill speed and total work duration, to reduce the effect of differences in factors such as muscle fibre type activation, hormonal responses, muscle glucose uptake and non-esterified fatty acid (NEFA) availability on the comparison of substrate utilisation. Subjects (n?=?7) completed 40?min of intermittent intense running requiring a work:recovery ratio of either 6?s:9?s (short-interval exercise, SE) or 24?s:36?s (long-interval exercise, LE), on separate days. Another experiment compared O₂ availability in the vastus lateralis muscle across SE (10?min) and LE (10?min) exercise using near-infrared spectroscopy (RunMan, NIM. Philadelphia, USA). Overall (i.e. work and recovery) O₂ consumption (V˙O₂) and energy expenditure were lower during LE (P?P?V˙O_2peak), was [mean (SEM)] 64.9?(2.7)% V˙O_2peak (LE) and 71.4?(2.4)% V˙O_2peak (SE). Fat oxidation was three times lower (P?P?P?P?P?n?=?4) or plasma noradrenaline and adrenaline. Muscle oxygenation declined in both protocols (P?P?r?=?0.68; P?n?=?12). Lower levels of fat oxidation occurred concurrent with accelerated carbohydrate metabolism, increases in lactate and pyruvate and reduced muscle O₂ availability. These changes were associated with proportionately longer work and recovery periods, despite identical treadmill speed and total work duration. The proposal that a metabolic regulatory factor within the muscle fibre retards fat oxidation under these conditions is supported by the current findings.     

Short-term exercise training in humans reduces AMPK signalling during prolonged exercise independent of muscle glycogen

We examined the effect of short-term exercise training on skeletal muscle AMP-activated protein kinase (AMPK) signalling and muscle metabolism during prolonged exercise in humans. Eight sedentary males completed 120 min of cycling at 66 ± 1%     , then exercise trained for 10 days, before repeating the exercise bout at the same absolute workload. Participants rested for 72 h before each trial while ingesting a high carbohydrate diet (HCHO). Exercise training significantly ( P < 0.05) attenuated exercise-induced increases in skeletal muscle free AMP: ATP ratio and glucose disposal and increased fat oxidation. Exercise training abolished the 9-fold increase in AMPK α2 activity observed during pretraining exercise. Since training increased muscle glycogen content by 93 ± 12% ( P < 0.01), we conducted a second experiment in seven sedentary male participants where muscle glycogen content was essentially matched pre- and post-training by exercise and a low CHO diet (LCHO; post-training muscle glycogen 52 ± 7% less than in HCHO, P < 0.001). Despite the difference in muscle glycogen levels in the two studies we obtained very similar results. In both studies the increase in ACCβ Ser²²¹ phosphorylation was reduced during exercise after training. In conclusion, there is little activation of AMPK signalling during prolonged exercise following short-term exercise training suggesting that other factors are important in the regulation of glucose disposal and fat oxidation under these circumstances. It appears that muscle glycogen is not an important regulator of AMPK activation during exercise in humans when exercise is begun with normal or high muscle glycogen levels.     

Effects of continuous and intermittent exercise on executive function in children aged 8–10 years

Understanding the effects of acute exercise on executive function in prepubescent children may be important for the enhancement of school performance. This study assessed the effect of an acute bout of continuous (CONT) or intermittent (INT), moderate‐intensity treadmill exercise on executive function in young children. Twenty healthy children, mean (SD); age: 8.8 (0.8) years; height: 140 (9) cm; weight: 36 (11) kg; boys: n = 9, performed a graded‐exercise test to determine maximal oxygen uptake, and two 15‐min submaximal bouts of treadmill exercise; protocols were either CONT or INT. During CONT, participants ran at 90% of gas exchange threshold. During INT, participants performed six consecutive 2.5 min blocks of exercise, which were designed to reflect children's typical activity patterns, comprising 45 s at a heavy intensity, 33 s at a moderate intensity, 10 s at a severe intensity, and 62 s at a low intensity. Participants performed the Stroop task before the submaximal exercise bouts and after, at 1‐, 15‐, and 30‐min intervals. Near‐infrared spectroscopy (NIRS) measured cerebral perfusion and oxygenation. Regardless of condition, Stroop performance was improved at 1 min after compared to before, 54.9 (9.8) s versus 57.9 (11) s, respectively, p < .01, and improvements were maintained until 30 min after. NIRS (oxyhemoglobin, total hemoglobin) explained a significant amount of variance in the change in Stroop performance for INT only (49%, p < .05). An acute bout of exercise, of either an intermittent or continuous nature, improves executive function in children, and effects are maintained for ≤ 30 min following exercise cessation. Accordingly, it is recommended that children should engage in physical activity during periods of school recess.     

Fuel metabolism during ultra-endurance exercise

 Cyclists either ingested 300 ml 100 g/l U-[¹⁴C] glucose solution every 30 min during 6 h rides at 55% of VO_2max (n=6) or they consumed unlabelled glucose and were infused with U-[¹⁴C] lactate (n=5). Maintenance of euglycaemia limited rises in circulating free fatty acids, noradrenaline and adrenaline concentrations to 0.9±0.1 mM, 27±4 nM and 2.0±0.5 nM, respectively, and sustained the oxidation of glucose and lactate. As muscle glycogen oxidation declined from 100±13 to 71±9 μmol/min/kg in the last 3 h of exercise, glucose and lactate oxidation and interconversion rates remained at approximately 60 and 50 and at about 4 and 5 μmol/min/kg, respectively. Continued high rates of carbohydrate oxidation led to a total oxidation of around 270 g glucose, 130 g plasma lactate and 530 g muscle glycogen. Oxidation of some 530 g of muscle glycogen far exceeded the predicted (about 250 g) initial glycogen content of the active muscles and suggested that there must have been a considerable diffusion of unlabelled lactate from glycogen breakdown in inactive muscle fibres to adjacent active muscle fibres via the interstitial fluid that did not equilibrate with ¹⁴C lactate in the circulation. Received: 19 September 1997 / Received after revision: 15 December 1997 / Accepted: 22 January 1998     

Non-exercising muscle metabolism during exercise

Glycogen decrements have been observed in non-exercising muscles during exercise. We therefore investigated whether the degraded glycogen was retained within the muscle in the form of glycolytic intermediates, or whether it was effluxed from the non-exercising muscles. For these studies a suspension harness was used to unload the hindlimb muscles at rest and during exercise [McDermott et al. (1987) J Appl Physiol 63:1275–1283]. Concentrations of glycogen and glycolytic intermediates glucose 6-phosphate, fructose 6-phosphate, fructose 1,6-bisphosphate, glycerol 3-phosphate, and lactate) were measured in non-exercising and exercising muscles (soleus, plantaris, red and white gastrocnemius) during a 90-min exercise bout 15 m/min, 8% grade). On-line electromyographic analysis showed that the contractile activity in the non-exercising muscles was markedly lower than in the exercising muscles. Similar decrements in muscle glycogen levels were observed in both the non-exercising and exercising muscles at the end of the 90-min, exercise bout (P<0.05), despite significantly different activity profiles. An increase in tissue lactate concentrations occurred in both non-exercising and exercising muscle (P<0.05), although only slight changes in the glycolytic intermediates occurred. The sum total of all the accumulated glycolytic intermediates and lactate (converted to glucosyl units) in the non-exercising muscles only accounted for a small fraction of the glycogen degraded ( 15%–28%). We conclude that the metabolism of glycogen is enhanced in non-exercising muscle, and that glycogen utilization is uncoupled from the energetic demands of the muscle. Furthermore, the glycogen mobilized in non-exercising muscle is not retained within the muscle in other metabolite pools. We speculate that the carbon units derived from glycogen may be effluxed into the circulation to join the oxidizable/gluconeogenic carbon pool.     

Effect of low glycogen on glycogen synthase in human muscle during and after exercise

Subjects cycled at a work load calculated to elicit 75% of maximal oxygen uptake on two occasions: the first to fatigue (34.5 ± 5.3 min; mean ± SE), and the second at the same workload and for the same duration as the first. Biopsies were obtained from the quadriceps femoris muscle before and immediately after exercise, and 5 min post-exercise. Before the first experiment, muscle glycogen was lowered by a combination of exercise and diet, and before the second, experiment muscle glycogen was elevated. In the low glycogen condition (LG), muscle glycogen decreased from 169 ± 15 mmol glucosyl units kg^-1dry wt at to rest to 13 ± 6 after exercise. In the high glycogen condition (HG) glycogen decreased from 706 ± 52 at rest to 405 ± 68 after exercise. Glycogen synthase fractional activity (GSF) was always higher during the LG treatment. During exercise in the HG condition, those subjects who cycled for < 35 min (n= 3) had GSF values in muscle which were lower than at rest, whereas those subjects who cycled for > 35 min (n= 4) had values which were similar to or higher than at rest. Thus the change in GSF in muscle during HG was positively related to the exercise duration (r= 0.94; y = 254–17x + 0.3x²; P < 0.001) and negatively related to the glycogen content at the end of exercise (r=–0.82; y= 516–2x + 0.001x²; P < 0.05). During LG exercise GSF remained constant. GSF increased markedly after 5 min post-exercise in both HG and LG conditions. cAMP dependent protein kinase activity increased similarly during both LG and HG exercise and reverted to the preexercise values 5 min post-exercise. It is concluded that muscle contraction decreases GSF, but low glycogen levels can attenuate or abolish the decrease in GSF. The rapid increase of GSF during recovery from exercise does not require glycogen depletion during the exercise.     

Responses of plasma glutamine, free tryptophan and branched-chain amino acids to prolonged exercise after a regime designed to reduce muscle glycogen

Prolonged exercise can elicit a reduction in the plasma glutamine concentration and an increase in the plasma concentration ratio of free tryptophan (FTrp) to branched-chain amino acids (BCAA). The purpose of this investigation was to study the effects of a 60-min bout of vigorous treadmill running with dietary manipulation on plasma concentrations of glutamine, FTrp and BCAA after an exercise and diet regime designed to reduce muscle glycogen. Seven male distance runners [mean (SD) age: 29.3?(2.1) years; ˙VO _2max : 62.7?(3.3) ml?·?kg^?1?·?min^?1] acted as subjects. Each undertook a regime designed to reduce muscle glycogen, then performed a 60-min treadmill run (75% ˙VO _2max ) under two dietary conditions: after a 14-h fast (?fasted) and after ingestion of a high carbohydrate meal (30?kJ?·?kg^?1: 80% carbohydrate, 10% protein, 10% fat) 3?h before running (?fed). Plasma concentrations of glutamine, FTrp, BCAA, free fatty acids (FFA), glycerol and glucose were measured 5?min before and 5?min after the run, under each dietary condition. Plasma glutamine did not change in response to exercise when fasted (P > 0.05), but increased when fed (P = 0.007). Plasma FTrp increased under both dietary conditions (P < 0.001), but the magnitude of this increase was greater when fasted than when fed (P < 0.001). Plasma BCAA did not change under either dietary condition (P < 0.05). Increases in the plasma FTrp/BCAA ratio reflected increases in plasma FFA and glycerol concentrations (P < 0.001; both dietary conditions) and these changes were all greater under fasted conditions when a fall in blood glucose concentration was observed (P = 0.007). These data emphasise the importance of dietary carbohydrate intake between repeated bouts of prolonged exercise on responses of plasma glutamine, FTrp and BCAA during subsequent exercise.     

Effects of moderate dietary manipulation on intermittent exercise performance and metabolism in women

The aim of the current study was to examine the effect of a moderate alteration in pre-exercise diet composition on the performance of, and metabolic response to, intermittent treadmill exercise in a group of normally menstruating females. Eight recreationally active women performed two intermittent, incremental exercise trials, one preceded by 2 days of a high [61 (1)%] carbohydrate (CHO) diet and the other by 2 days of a low [31 (1)%] CHO diet. Oxygen uptake (VO₂) was measured during, and blood samples were obtained immediately after, each bout for the determination of blood lactate, glucose, glycerol, plasma free fatty acids and plasma ammonia. Performance, as assessed by time to exhaustion in the final bout, was found to be similar whether preceded by a high- or low-CHO diet [median (range): 28.0 (18–54) s, 29 (18–54) s, respectively]. No significant between trial differences were found in VO₂, heart rate, or any of the blood metabolites. The results of the current study indicate that moderate alterations of pre-exercise diet do not affect intermittent, high-intensity exercise performance in women, despite some evidence of an alteration in the pattern of the metabolic response to exercise. Accepted: 7 September 1999     

The effect of glycogen availability on power output and the metabolic response to repeated bouts of maximal,isokinetic exercise in man

The relationship of glycogen availability to performance and blood metabolite accumulation during repeated bouts of maximal exercise was examined in 11 healthy males. Subjects performed four bouts of 30 s maximal, isokinetic cycling exercise at 100 rev · min^–1, each bout being separated by 4 min of recovery. Four days later, all subjects cycled intermittently to exhaustion [mean (SEM) 106 (6) min] at 75% maximum oxygen uptake Subjects were then randomly assigned to an isoenergetic low-carbohydrate (CHO) diet [7.8 (0.6)% total energy intake,n = 6] or an isoenergetic high-CHO diet [81.5 (0.4)%,n = 5], for 3 days. On the following day, all subjects performed 30 min cycling at 75% and, after an interval of 2 h, repeated the four bouts of 30 s maximal exercise. No difference was seen when comparing total work production during each bout of exercise before and after a high-CHO diet. After a low-CHO diet, total work decreased from 449 (20) to 408 (31) J · kg^–1 body mass in bout 1 (P < 0.05), from 372 (15) to 340 (18) J · kg^–1 body mass in bout 2 (P < 0.05), and from 319 (12) to 306 (16) J · kg^t-1 body mass in bout 3 (P < 0.05), but was unchanged in bout 4. Blood lactate and plasma ammonia accumulation during maximal exercise was lower after a low-CHO diet (P < 0.001), but unchanged after a high-CHO diet. In conclusion, muscle glycogen depletion impaired performance during the initial three, but not a fourth bout of maximal, isokinetic cycling exercise. Irrespective of glycogen availability, prolonged submaximal exercise appeared to have no direct effect on subsequent maximal exercise performance.     

The effect of acute exercise on glycogen synthesis rate in obese subjects studied by 13C MRS

In obesity, insulin-stimulated glucose uptake in skeletal muscle is decreased. We investigated whether the stimulatory effect of acute exercise on glucose uptake and subsequent glycogen synthesis was normal. The study was performed on 18 healthy volunteers, 9 obese (BMI?=?32.6?±?1.2?kg/m², mean?±?SEM) and 9 lean (BMI?=?22.0?±?0.9?kg/m²), matched for age and gender. All participants underwent a euglycemic hyperinsulinemic clamp, showing reduced glucose uptake in the obese group (P?=?0.01), during which they performed a short intense local exercise (single-legged toe lifting). Dynamic glucose incorporation into glycogen in the gastrocnemius muscle before and after exercise was assessed by ¹³C magnetic resonance spectroscopy combined with infusion of [1-¹³C]glucose. Blood flow was measured to investigate its potential contribution to glucose uptake. Before exercise, glycogen synthesis rate tended to be lower in obese subjects compared with lean (78?±?14 vs. 132?±?24???mol/kg muscle/min; P?=?0.07). Exercise induced highly significant rises in glycogen synthesis rates in both groups, but the increase in obese subjects was reduced compared with lean (112?±?15 vs. 186?±?27???mol/kg muscle/min; P?=?0.03), although the relative increase was similar (184?±?35 vs. 202?±?51%; P?=?0.78). After exercise, blood flow increased equally in both groups, without a temporal relationship with the rate of glycogen synthesis. In conclusion, this study shows a stimulatory effect of a short bout of acute exercise on insulin-induced glycogen synthesis rate that is reduced in absolute values but similar in percentages in obese subjects. These results suggest a shared pathway between insulin- and exercise-induced glucose uptake and subsequent glycogen synthesis.     

Availability of glucose ingested during muscle exercise performed under acipimox-induced lipolysis blockade

This study investigated the percentage of carbohydrate utilization than can be accounted for by glucose ingested during exercise performed after the ingestion of the potent lipolysis inhibitor Acipimox. Six healthy male volunteers exercised for 3 h on a treadmill at about 45% of their maximal oxygen uptake, 75 min after having ingested 250 mg of Acipimox. After 15-min adaptation to exercise, they ingested either glucose dissolved in water, 50 g at time 0 min and 25 g at time 60 and 120 min (glucose, G) or sweetened water (control, C). Naturally labelled [¹³C]glucose was used to follow the conversion of the ingested glucose to expired-air CO₂. Acipimox inhibited lipolysis in a similar manner in both experimental conditions. This was reflected by an almost complete suppression of the exercise-induced increase in plasma free fatty acid and glycerol and by an almost constant rate of lipid oxidation. Total carbohydrate oxidation evaluated by indirect calorimetry, was similar in both experimental conditions [C, 182, (SEM 21); G, 194 (SEM 16) g · 3 h^–1], as was lipid oxidation [C, 57 (SEM 6); G, 61 (SEM 3) g · 3 h^–1]. Exogenous glucose oxidation during exercise G, calculated by the changes in¹³C:¹²C ratio of expired air CO₂, averaged 66 (SEM 5) g · 3 h^–1 (19% of the total energy requirement). Consequently, endogenous carbohydrate utilization was significantly smaller after glucose than after placebo ingestion: 128 (SEM 18) versus 182 (SEM 21) g · 3 h^–1, respectively (P < 0.05). Symptoms of intense fatigue and leg cramps observed with intake of sweet placebo were absent with glucose ingestion.In conclusion, we found glucose ingestion during 3-h exercise with lipolysis blockade could provide metabolic substrate permitting a significant sparing of endogenous carbohydrate and consequently an improvement in performance.     

High-intensity exercise and muscle glycogen availability in humans

This study investigated the effects of muscle glycogen availability on performance and selected physiological and metabolic responses during high-intensity intermittent exercise. Seven male subjects completed a regimen of exercise and dietary intake (48 h) to either lower and keep low (LOW-CHO) or lower and then increase (HIGH-CHO) muscle glycogen stores, on two separate occasions at least a week apart. On each occasion the subjects completed a short-term (<10 min) and prolonged (>30 min) intermittent exercise (IEX) protocol, 24 h apart, which consisted of 6-s bouts of high-intensity exercise performed at 30-s intervals on a cycle ergometer. Glycogen concentration (mean ± SEM) in m. vastus lateralis before both IEx_short and IEx_long was significantly lower following LOW-CHO [180 (14), 181 (17) mmol kg (dw)^–1] compared with HIGH-CHO [397 (35), 540 (25) mmol kg (dw)^–1]. In both IEx_short and IEx_long, significantly less work was performed following LOW-CHO compared with HIGH-CHO. In IEx_long, the number of exercise bouts that could be completed at a pre-determined target exercise intensity increased by 265% from 111 (14) following LOW-CHO to 294 (29) following HIGH-CHO (P < 0.05). At the point of fatigue in IEx_long, glycogen concentration was significantly lower with the LOW-CHO compared with HIGH-CHO [58 (25) vs. 181 (46) mmol kg (dw)^–1, respectively]. The plasma concentrations of adrenaline and nor-adrenaline (in IEx_short and IEx_long), and FFA and glycerol (in IEx_long), increased several-fold above resting values with both experimental conditions. Oxygen uptake during the exercise periods in IEx_long approached 70% of V o_2max. These results suggest that muscle glycogen availability can affect performance during both short-term and more prolonged high-intensity intermittent exercise and that with repeated exercise periods as short as 6 s, there can be a relatively high aerobic contribution.     

Enhanced endurance in trained cyclists during moderate intensity exercise following 2 weeks adaptation to a high fat diet

These studies investigated the effects of 2 weeks of either a high-fat (HIGH-FAT: 70% fat, 7% CHO) or a high-carbohydrate (HIGH-CHO: 74% CHO, 12% fat) diet on exercise performance in trained cyclists (n = 5) during consecutive periods of cycle exercise including a Wingate test of muscle power, cycle exercise to exhaustion at 85% of peak power output [90% maximal oxygen uptake ( O_2max), high-intensity exercise (HIE)] and 50% of peak power output [60% O_2max, moderate intensity exercise (MIE)]. Exercise time to exhaustion during HIE was not significantly different between trials: nor were the rates of muscle glycogen utilization during HIE different between trials, although starting muscle glycogen content was lower [68.1 (SEM 3.9) vs 120.6 (SEM 3.8) mmol · kg ^–1 wet mass, P < 0.01] after the HIGH-FAT diet. Despite a lower muscle glycogen content at the onset of MIE [32 (SEM 7) vs 73 (SEM 6) mmol · kg ^–1 wet mass, HIGH-FAT vs HIGH-CHO, P < 0.01], exercise time to exhaustion during subsequent MIE was significantly longer after the HIGH-FAT diet [79.7 (SEM 7.6) vs 42.5 (SEM 6.8) min, HIGH-FAT vs HIGH-CHO, P<0.01]. Enhanced endurance during MIE after the HIGH-FAT diet was associated with a lower respiratory exchange ratio [0.87 (SEM 0.03) vs 0.92 (SEM 0.02), P<0.05], and a decreased rate of carbohydrate oxidation [1.41 (SEM 0.70) vs 2.23 (SEM 0.40) g CHO · min^–1, P<0.05]. These results would suggest that 2 weeks of adaptation to a high-fat diet would result in an enhanced resistance to fatigue and a significant sparing of endogenous carbohydrate during low to moderate intensity exercise in a relatively glycogen-depleted state and unimpaired performance during high intensity exercise.     

Fuel substrate turnover and oxidation and glycogen sparing with carbohydrate ingestion in non-carbohydrate-loaded cyclists

This study examined the effects of ingesting 500 ml/h of either a 10% carbohydrate (CHO) drink (CI) or placebo (PI) on splanchnic glucose appearance rate (endogenous + exogenous) (R _a), plasma glucose oxidation and muscle glycogen utilisation in 17, non-carbohydrate-loaded, male, endurance-trained cyclists who rode for 180 min at 70% of maximum oxygen uptake. Mean muscle glycogen content at the start of exercise was 130 ± 6 mmol/kg ww; (mean ± SEM). Total CHO oxidation was similar in CI and PI subjects and declined during the trial. R _a increased significantly during the trial (P < 0.05) in both groups. Plasma glucose oxidation also increased significantly during the trial, reaching a plateau in the PI subjects, but was significantly (P < 0.05) higher in CI than PI subjects at the end of exercise [(98 ± 14 vs. 72 ± 10 μmol/min/kg fat-free mass) (FFM) (1.34 ± 0.19 vs. 0.93 ± 0.13 g/min)]. However, mean endogenous R _a was significantly (P < 0.05) lower in the CI than PI subjects throughout exercise (35 ± 7 vs. 54 ± 6 μmol/min/kg FFM), as was the oxidation of endogenous plasma glucose, which remained almost constant in CI subjects, and reached values at the end of exercise of 42 ± 13 and 72 ± 10 μmol/min/kg FFM in the CI and PI groups respectively. Of the 150 g CHO ingested during the trial, 50% was oxidised. Muscle glycogen disappearance was identical during the first 2 h of exercise in both groups and continued at the same rate in PI subjects, however no net muscle glycogen disappearance occurred during the final hour in CI subjects. We conclude that ingestion of 500 ml/h of a 10% CHO solution during prolonged exercise in non carbohydrate loaded subjects has a marked liver glycogen-sparing effect or causes a reduction in gluconeogenesis, or both, maintains plasma glucose concentration and has a muscle glycogen-sparing effect. Received: 25 August 1995/Received after revision: 25 March 1996/Accepted: 29 April 1996     

Effect of various types of acute exercise and exercise training on the insulin sensitivity of rat soleus muscle measured in vitro

Effects of acute exercise varying in duration and intensity, as well as of two training regimes (endurance and sprint training) on the sensitivity of the soleus muscle of rat to insulin was measured in vitro and compared in rats. As an index of the muscle insulin sensitivity the hormone concentration in the incubation medium which would produce half maximum stimulation of lactate production (LA) and glycogen synthesis was determined. A single bout of moderate endurance exercise (60 min treadmill running at 20 m×min^–1, 0° inclination) increased the rate of LA production at the hormone concentrations used and increased the sensitivity of the process to insulin at 0.25 and 2 h but not 24 h after termination of exercise. Similar though less pronounced effects were found after heavy endurance exercise (30 min at 25 m×min^–1, 10°), but sprint exercise (6×10 s bouts at 43 m×min^–1, 0°) had no influence on the insulin sensitivity of the soleus muscle. The rate of glycogen synthesis in vitro was accelerated after endurance exercise, but the sensitivity of this process to insulin was unaffected by the preceding exercise. Endurance training for 5 weeks caused marked enhancement of sensitivity of both LA production and glycogen synthesis to insulin, which persisted for at least 48 h after the last training session. No changes in the soleus muscle sensitivity to insulin were found after sprint training. It is concluded that the increased insulin sensitivity of glucose utilization by skeletal muscle which occurs after endurance exercise and particularly during endurance training can substantially contribute to improved carbohydrate tolerance. Sprint exercise does not produce any changes in muscle insulin sensitivity, at least in the soleus muscle of the rat.Dedicated to the late Professor Stanislaw Kozlowski     

Non-invasive techniques for assessing carbohydrate flux:

Glycogen forms the smallest yet most labile energy substrate store. Therefore studying carbohydrate flux may be crucial to understanding the regulation of energy balance. Indirect calorimetry has been used to measure carbohydrate oxidation overnight and during exercise in nine fasted subjects. Overnight carbohydrate oxidation (averaging 2.85 ± 0.8 g h^-1) was assumed to be derived primarily from hepatic glycogen since subjects were inactive or asleep, and since glucose oxidized after gluconeogenesis from protein is measured as protein oxidation. Lower-limb muscle glycogen stores were depleted by repeated 30-min periods of cycle ergometry at 45%Vo_2max until exhaustion (8 ± 1 periods). The carbohydrate oxidation rate decreased as exercise progressed. Quadratic curves yielded a close fit to each individual's exercise carbohydrate depletion data (mean multiple correlation r= 0.9996) and provided excellent inter-subject discrimination. Total (muscle plus liver) glycogen stores prior to exercise were estimated by extrapolation of the depletion curves to zero oxidation rate. This produced an estimate (174 ± 61 g) which compared well with predictions (208 ± 43 g) based on reference values for muscle mass and initial glycogen content. The results demonstrate that non-invasive estimates of glycogen status can be obtained from accurate respiratory exchange data.     

Carbohydrate supplementation during prolonged cycling exercise spares muscle glycogen but does not affect intramyocellular lipid use

Using contemporary stable-isotope methodology and fluorescence microscopy, we assessed the impact of carbohydrate supplementation on whole-body and fiber-type-specific intramyocellular triacylglycerol (IMTG) and glycogen use during prolonged endurance exercise. Ten endurance-trained male subjects were studied twice during 3 h of cycling at 63 ± 4% of maximal O₂ uptake with either glucose ingestion (CHO trial; 0.7 g CHO kg⁻¹ h⁻¹) or without (CON placebo trial; water only). Continuous infusions with [U-¹³C] palmitate and [6,6-²H₂] glucose were applied to quantify plasma free fatty acids (FFA) and glucose oxidation rates and to estimate intramyocellular lipid and glycogen use. Before and after exercise, muscle biopsy samples were taken to quantify fiber-type-specific IMTG and glycogen content. Plasma glucose rate of appearance (R _a) and carbohydrate oxidation rates were substantially greater in the CHO vs CON trial. Carbohydrate supplementation resulted in a lower muscle glycogen use during the first hour of exercise in the CHO vs CON trial, resulting in a 38 ± 19 and 57 ± 22% decreased utilization in type I and II muscle-fiber glycogen content, respectively. In the CHO trial, both plasma FFA R _a and subsequent plasma FFA concentrations were lower, resulting in a 34 ± 12% reduction in plasma FFA oxidation rates during exercise (P < 0.05). Carbohydrate intake did not augment IMTG utilization, as fluorescence microscopy revealed a 76 ± 21 and 78 ± 22% reduction in type I muscle-fiber lipid content in the CHO and CON trial, respectively. We conclude that carbohydrate supplementation during prolonged cycling exercise does not modulate IMTG use but spares muscle glycogen use during the initial stages of exercise in endurance-trained men.     

Effects of high-intensity training and acute exercise on in vitro function of rat sarcoplasmic reticulum

To evaluate the effects of high-intensity training and/or a single bout of exercise on in vitro function of the sarcoplasmic reticulum (SR), the rats were subjected to 8 weeks of interval running program (final training: 2.5-min running × 4 sets per day, 50 m/min at 10% incline). Following training, SR function, i.e., Ca²⁺-ATPase activity and Ca²⁺-uptake and release rates, was examined in homogenates of the superficial region of the vastus lateralis muscle from rats subjected to a single bout of treadmill running (50 m/min at 10% incline) for 2.5 min or to exhaustion. Training brought about a 12.4% increase (P < 0.05) in SR Ca²⁺-uptake rate in rested muscles. This change was not accompanied by alterations in Ca²⁺-ATPase activity, Ca²⁺-release rate, Ca²⁺ dependence of enzyme and protein contents of Ca²⁺-ATPase and ryanodine receptor. A single bout of high-intensity exercise to exhaustion evoked significant reductions (P < 0.05) in SR function, irrespective of whether or not the animals were trained. For 2.5-min run and exhausted rats, no differences existed between SR functions of untrained and trained muscles. These data suggest that high-intensity training may be capable of enhancing SR Ca²⁺-sequestering ability, and may not protect against decreasing SR function with high-intensity exercise.