High-fat diet overrules the effects of training on fiber-specific intramyocellular lipid utilization during exercise

In this study, we compared the effects of endurance training in the fasted state (F) vs. the fed state [ample carbohydrate intake (CHO)] on exercise-induced intramyocellular lipid (IMCL) and glycogen utilization during a 6-wk period of a hypercaloric (～+30% kcal/day) fat-rich diet (HFD; 50% of kcal). Healthy male volunteers (18-25 yrs) received a HFD in conjunction with endurance training (four times, 60-90 min/wk) either in F (n = 10) or with CHO before and during exercise sessions (n = 10). The control group (n = 7) received a HFD without training and increased body weight by ～3 kg (P < 0.001). Before and after a HFD, the subjects performed a 2-h constant-load bicycle exercise test in F at ～70% maximal oxygen uptake rate. A HFD, both in the absence (F) or presence (CHO) of training, elevated basal IMCL content by ～50% in type I and by ～75% in type IIa fibers (P < 0.05). Independent of training in F or CHO, a HFD, as such, stimulated exercise-induced net IMCL breakdown by approximately twofold in type I and by approximately fourfold in type IIa fibers. Furthermore, exercise-induced net muscle glycogen breakdown was not significantly affected by a HFD. It is concluded that a HFD stimulates net IMCL degradation by increasing basal IMCL content during exercise in type I and especially IIa fibers. Furthermore, a hypercaloric HFD provides adequate amounts of carbohydrates to maintain high muscle glycogen content during training and does not impair exercise-induced muscle glycogen breakdown.     

Partial restoration of dietary fat induced metabolic adaptations to training by 7 days of carbohydrate diet.

We tested the hypothesis that a shift to carbohydrate diet after prolonged adaptation to fat diet would lead to decreased glucose uptake and impaired muscle glycogen breakdown during exercise compared with ingestion of a carbohydrate diet all along. We studied 13 untrained men; 7 consumed a high-fat (Fat-CHO; 62% fat, 21% carbohydrate) and 6 a high-carbohydrate diet (CHO; 20% fat, 65% carbohydrate) for 7 wk, and thereafter both groups consumed the carbohydrate diet for an eighth week. Training was performed throughout. After 8 wk, during 60 min of exercise (71 +/- 1% pretraining maximal oxygen uptake) average leg glucose uptake (1.00 +/- 0.07 vs. 1.55 +/- 0.21 mmol/min) was lower (P < 0.05) in Fat-CHO than in CHO. The rate of muscle glycogen breakdown was similar (4.4 +/- 0.5 vs. 4.2 +/- 0.7 mmol. min(-1). kg dry wt(-1)) despite a significantly higher preexercise glycogen concentration (872 +/- 59 vs. 688 +/- 43 mmol/kg dry wt) in Fat-CHO than in CHO. In conclusion, shift to carbohydrate diet after prolonged adaptation to fat diet and training causes increased resting muscle glycogen levels but impaired leg glucose uptake and similar muscle glycogen breakdown, despite higher resting levels, compared with when the carbohydrate diet is consumed throughout training.     

Fiber type-specific muscle glycogen sparing due to carbohydrate intake before and during exercise.

The effect of carbohydrate intake before and during exercise on muscle glycogen content was investigated. According to a randomized crossover study design, eight young healthy volunteers (n = 8) participated in two experimental sessions with an interval of 3 wk. In each session subjects performed 2 h of constant-load bicycle exercise ( approximately 75% maximal oxygen uptake). On one occasion (CHO), they received carbohydrates before ( approximately 150 g) and during (1 g.kg body weight(-1).h(-1)) exercise. On the other occasion they exercised after an overnight fast (F). Fiber type-specific relative glycogen content was determined by periodic acid Schiff staining combined with immunofluorescence in needle biopsies from the vastus lateralis muscle before and immediately after exercise. Preexercise glycogen content was higher in type IIa fibers [9.1 +/- 1 x 10(-2) optical density (OD)/microm(2)] than in type I fibers (8.0 +/- 1 x 10(-2) OD/microm(2); P < 0.0001). Type IIa fiber glycogen content decreased during F from 9.6 +/- 1 x 10(-2) OD/microm(2) to 4.5 +/- 1 x 10(-2) OD/microm(2) (P = 0.001), but it did not significantly change during CHO (P = 0.29). Conversely, in type I fibers during CHO and F the exercise bout decreased glycogen content to the same degree. We conclude that the combination of carbohydrate intake both before and during moderate- to high-intensity endurance exercise results in glycogen sparing in type IIa muscle fibers.     

Effect of short-term exercise training on muscle glycogen in resting conditions in rats fed a high fat diet.

It has been reported that exercise training increases muscle glycogen storage in rats fed a high carbohydrate (CHO) diet in resting conditions. The purpose of this study was to examine whether a 3-week swimming training programme would increase muscle glycogen stores in rats fed a high-fat (FAT) diet in resting conditions. Rats were fed either the FAT or CHO diet for 7 days ad libitum, and then were fed regularly twice a day (between 0800 and 0830 hours and 1800 and 1830 hours) for 32 days. During this period of regular feeding, half of the rats in both dietary groups had swimming training for 3 weeks and the other half were sedentary. The rats were not exercised for 48 h before sacrifice. All rats were killed 2 h after their final meal (2030 hours). The glycogen contents in red gastrocnemius muscle, heart and liver were significantly higher in sedentary rats fed the CHO diet than in those fed the FAT diet. Exercise training clearly increased glycogen content in soleus, red gastrocnemius and heart muscle in rats fed the CHO diet. In rats fed the FAT diet, however, training did not increase glycogen content in these muscles or the heart. Exercise training resulted in an 87% increase of total glycogen synthase activity in the gastrocnemius muscle of rats fed the CHO diet. However, this was not observed in rats fed the FAT diet. The total glycogen phosphorylase activity in the gastrocnemius muscle of the rats of both dietary groups was increased approximately twofold by training.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effects of dietary manipulation on blood acid-base status and the performance of high intensity exercise

The effect of a pattern of exercise and dietary modification, which is normally used to alter muscle glycogen content, upon the acid-base status of the blood and the ability to perform high intensity exercise was studied. Eleven healthy male subjects cycled to exhaustion on an electrically braked cycle ergometer at a workload equivalent to 100% of their maximal oxygen uptake (VO2max) on three separate occasions. The first exercise test took place after a normal diet (46.2 +/- 6.7% carbohydrate (CHO)), and was followed by prolonged exercise to exhaustion to deplete muscle glycogen stores. The second test was performed after three days of a low carbohydrate diet (10.1 +/- 6.8% CHO) and subsequently after three days of a high CHO diet (65.5 +/- 9.8% CHO) the final test took place. Acid-base status and selected metabolites were measured on arterialised venous blood at rest prior to exercise and during the post-exercise period. Exercise time to exhaustion was longer after the normal (p less than 0.05) and high (p less than 0.05). CHO dietary phases compared with the low CHO phase. Resting pre-exercise pH was higher after the high CHO diet (p less than 0.05) compared with the low CHO diet. Pre-exercise bicarbonate, PCO2 and base excess measurements were higher after the high CHO treatment compared with both the normal (p less than 0.01, p less than 0.05, p less than 0.01 respectively) and low CHO phases (p less than 0.001, p less than 0.01, p less than 0.001 respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Gender differences in carbohydrate loading are related to energy intake.

We demonstrated that female endurance athletes did not increase their muscle glycogen concentration after an increase in the dietary carbohydrate intake (58 --> 74%), whereas men did (Tarnopolsky MA, SA Atkinson, SM Phillips, and JD McDougall, J Appl Physiol 78: 1360-1368, 1995). This may have been related to a lower energy or carbohydrate intake by the women or due to an inherent gender difference in glycogen storage capacity. We examined whether well-trained men (n = 6) and women (n = 6) increased muscle glycogen concentration after an increase in both the relative (58 --> 75%) and absolute energy and carbohydrate intake and whether potential gender differences were related to muscle hexokinase enzyme activity. Subjects were randomly allocated to three diets [Hab, habitual; CHO, high carbohydrate (75%); and CHO + E, extra energy + CHO ( upward arrow~34%)] for a 4-day period before a muscle biopsy for analysis of total and pro- and macroglycogen and hexokinase activity. Total glycogen concentration was higher for the men on the CHO and CHO + E trials compared with Hab (P < 0.05), whereas women increased only on the CHO + E trial compared with Hab (P < 0.05). There were no gender differences in the proportion of pro- and macroglycogen or hexokinase activity. A low energy intake may explain the previously reported lower capacity for women to glycogen load compared with men.     

Carbohydrate supercompensation and muscle glycogen utilization during exhaustive running in highly trained athletes

Three female and three male highly trained endurance runners with mean maximal oxygen uptake (VO2max) values of 60.5 and 71.5 ml.kg-1.min-1, respectively, ran to exhaustion at 75%-80% of VO2max on two occasions after an overnight fast. One experiment was performed after a normal diet and training regimen (Norm), the other after a diet and training programme intended to increase muscle glycogen levels (Carb). Muscle glycogen concentration in the gastrocnemius muscle increased by 25% (P less than 0.05) from 581 mmol.kg-1 dry weight, SEM 50 to 722 mmol.kg-1 dry weight, SEM 34 after Carb. Running time to exhaustion, however, was not significantly different in Carb and Norm, 77 min, SEM 13 vs 70 min, SEM 8, respectively. The average glycogen concentration following exhaustive running was 553 mmol.kg-1 dry weight, SEM 70 in Carb and 434 mmol.kg-1 dry weight, SEM 57 in Norm, indicating that in both tests muscle glycogen stores were decreased by about 25%. Periodic acid-Schiff staining for semi-quantitative glycogen determination in individual fibres confirmed that none of the fibres appeared to be glycogen-empty after exhaustive running. The steady-state respiratory exchange ratio was higher in Carb than in Norm (0.92, SEM 0.01 vs 0.89, SEM 0.01; P less than 0.05). Since muscle glycogen utilization was identical in the two tests, the indication of higher utilization of total carbohydrate appears to be related to a higher utilization of liver glycogen. We have concluded that glycogen depletion of the gastrocnemius muscle is unlikely to be the cause of fatigue during exhaustive running at 75%-80% of VO2max in highly trained endurance runners. Furthermore, diet- and training-induced carbohydrate super-compensation does not appear to improve endurance capacity in such individuals.     

Simple and complex carbohydrate-rich diets and muscle glycogen content of marathon runners

The effects of simple-carbohydrate (CHO)- and complex-CHO-rich diets on skeletal muscle glycogen content were compared. Twenty male marathon runners were divided into four equal groups with reference to dietary consumption: depletion/simple, depletion/complex, nondepletion/simple, and nondepletion/complex. Subjects consumed either a low-CHO (15% energy [E] intake), or a mixed diet (50% CHO) for 3 days, immediately followed by a high-CHO diet (70% E intake) predominant in either simple-CHO or in complex-CHO (85% of total CHO intake) for another 3 days. Skeletal muscle biopsies and venous blood samples were obtained one day prior to the start of the low-CHO diet or mixed diet (PRE), and then again one day after the completion of the high-CHO diet (POST). The samples were analysed for skeletal muscle glycogen, serum free fatty acids (FFA), insulin, and lactate and blood glucose. Skeletal muscle glycogen content increased significantly (p less than 0.05) only in the nondepletion/simple group. When groups were combined, according to the type of CHO ingested and/or utilization of a depletion diet, significant increases were observed in glycogen content. Serum FFA decreased significantly (p less than 0.05) for the nondepletion/complex group only, while serum insulin, blood glucose, and serum lactate were not altered. It is concluded that significant increases in skeletal muscle glycogen content can be achieved with a diet high in simple-CHO or complex-CHO, with or without initial consumption of a low-CHO diet.     

The influence of dietary manipulation on plasma ammonia accumulation during incremental exercise in man

The influence of a pattern of exercise and dietary manipulation, intended to alter carbohydrate (CHO) availability, on pre-exercise acid-base status and plasma ammonia and blood lactate accumulation during incremental exercise was investigated. On three separate occasions, five healthy male subjects underwent a pre-determined incremental exercise test (IET) on an electrically braked cycle ergometer. Each IET involved subjects exercising for 5 min at 30%, 50%, 70% and 95% of their maximal oxygen uptake (VO2max) and workloads were separated by 5 min rest. The first IET took place after 3 days of normal dietary CHO intake. The second and third tests followed 3 days of low or high CHO intake, which was preceded by prolonged exercise to exhaustion in an attempt to deplete muscle and liver glycogen stores. Acid-base status and plasma ammonia and blood lactate levels were measured on arterialised venous blood samples immediately prior to and during the final 15 s of exercise at each workload and for 40 min following the completion of each IET. Three days of low CHO intake resulted in the development of a mild metabolic acidosis in all subjects. Plasma ammonia (NH3) accumulation on the low-CHO diet tended to be greater than normal at each exercise workload. Values returned towards resting levels during each recovery period. After the normal and high-CHO diets plasma NH3 levels did not markedly increase above resting values until after exercise at 95% VO2max. Plasma NH3 levels after the high-CHO diet were similar to those after the normal CHO diet.(ABSTRACT TRUNCATED AT 250 WORDS)     

Dietary carbohydrate, muscle glycogen content, and endurance performance in well-trained women.

This study examined the ability of well-trained eumenorrheic women to increase muscle glycogen content and endurance performance in response to a high-carbohydrate diet (HCD; approximately 78% carbohydrate) compared with a moderate-carbohydrate diet (MD; approximately 48% carbohydrate) when tested during the luteal phase of the menstrual cycle. Six women cycled to exhaustion at approximately 80% maximal oxygen uptake (VO(2 max)) after each of the randomly assigned diet and exercise-tapering regimens. A biopsy was taken from the vastus lateralis before and after exercise in each trial. Preexercise muscle glycogen content was high after the MD (625.2 +/- 50.1 mmol/kg dry muscle) and 13% greater after the HCD (709.0 +/- 44.8 mmol/kg dry muscle). Postexercise muscle glycogen was low after both trials (MD, 91.4 +/- 34.5; HCD, 80.3 +/- 19.5 mmol/kg dry muscle), and net glycogen utilization during exercise was greater after the HCD. The subjects also cycled longer at approximately 80% VO(2 max) after the HCD vs. MD (115:31 +/- 10:47 vs. 106:35 +/- 8:36 min:s, respectively). In conclusion, aerobically trained women increased muscle glycogen content in response to a high-dietary carbohydrate intake during the luteal phase of the menstrual cycle, but the magnitude was smaller than previously observed in men. The increase in muscle glycogen, and possibly liver glycogen, after the HCD was associated with increased cycling performance to volitional exhaustion at approximately 80% VO(2 max).     

Beneficial metabolic adaptations due to endurance exercise training in the fasted state

Training with limited carbohydrate availability can stimulate adaptations in muscle cells to facilitate energy production via fat oxidation. Here we investigated the effect of consistent training in the fasted state, vs. training in the fed state, on muscle metabolism and substrate selection during fasted exercise. Twenty young male volunteers participated in a 6-wk endurance training program (1-1.5 h cycling at ～70% Vo(?max), 4 days/wk) while receiving isocaloric carbohydrate-rich diets. Half of the subjects trained in the fasted state (F; n = 10), while the others ingested ample carbohydrates before (～160 g) and during (1 g·kg body wt?1·h?1) the training sessions (CHO; n = 10). The training similarly increased Vo(?max) (+9%) and performance in a 60-min simulated time trial (+8%) in both groups (P < 0.01). Metabolic measurements were made during a 2-h constant-load exercise bout in the fasted state at ～65% pretraining Vo(?max). In F, exercise-induced intramyocellular lipid (IMCL) breakdown was enhanced in type I fibers (P < 0.05) and tended to be increased in type IIa fibers (P = 0.07). Training did not affect IMCL breakdown in CHO. In addition, F (+21%) increased the exercise intensity corresponding to the maximal rate of fat oxidation more than did CHO (+6%) (P < 0.05). Furthermore, maximal citrate synthase (+47%) and β-hydroxyacyl coenzyme A dehydrogenase (+34%) activity was significantly upregulated in F (P < 0.05) but not in CHO. Also, only F prevented the development exercise-induced drop in blood glucose concentration (P < 0.05). In conclusion, F is more effective than CHO to increase muscular oxidative capacity and at the same time enhances exercise-induced net IMCL degradation. In addition, F but not CHO prevented drop of blood glucose concentration during fasting exercise.     

An Optimized Histochemical Method to Assess Skeletal Muscle Glycogen and Lipid Stores Reveals Two Metabolically Distinct Populations of Type I Muscle Fibers

Skeletal muscle energy metabolism has been a research focus of physiologists for more than a century. Yet, how the use of intramuscular carbohydrate and lipid energy stores are coordinated during different types of exercise remains a subject of debate. Controversy arises from contradicting data from numerous studies, which used different methodological approaches. Here we review the “pros and cons” of previously used histochemical methods and describe an optimized method to ensure the preservation and specificity of detection of both intramyocellular carbohydrate and lipid stores. For optimal preservation of muscle energy stores, air drying cryosections or cycles of freezing-thawing need to be avoided. Furthermore, optimization of the imaging settings in order to specifically image intracellular lipid droplets stained with oil red O or Bodipy-493/503 is shown. When co-staining lipid droplets with associated proteins, Bodipy-493/503 should be the dye of choice, since oil red O creates precipitates on the lipid droplets blocking the light. In order to increase the specificity of glycogen stain, an antibody against glycogen is used. The resulting method reveals the existence of two metabolically distinct myosin heavy chain I expressing fibers: I-1 fibers have a smaller crossectional area, a higher density of lipid droplets, and a tendency to lower glycogen content compared to I-2 fibers. Type I-2 fibers have similar lipid content than IIA. Exhaustive exercise lead to glycogen depletion in type IIA and IIX fibers, a reduction in lipid droplets density in both type I-1 and I-2 fibers, and a decrease in the size of lipid droplets exclusively in type I-1 fibers.     

Dietary carbohydrate, muscle glycogen, and power output during rowing training

The belief that high-carbohydrate diets enhance training capacity (mean power output) has been extrapolated from studies that have varied dietary carbohydrate over a few days and measured muscle glycogen but did not assess power output during training. We hypothesized that a high-carbohydrate (HI) diet (10 g.kg body mass-1.day-1) would promote greater muscle glycogen content and greater mean power output during training than a moderate-carbohydrate (MOD) diet (5 g.kg body mass-1.day-1) over 4 wk of intense twice-daily rowing training. Dietary protein intake was 2 g.kg body mass-1.day-1, and fat intake was adjusted to maintain body mass. Twelve male and 10 female collegiate rowers were randomly assigned to the treatment groups. Training was 40 min at 70% peak O2 consumption (VO2) (A.M.) and either three 2,500-m time trials to assess power output or interval training at 70-90% peak VO2 (P.M.). Mean daily training was 65 min at 70% peak VO2 and 38 min at greater than or equal to 90% peak VO2. Mean muscle glycogen content increased 65% in the HI group (P less than 0.05) but remained constant at 119 mmol/kg in the MOD group over the 4 wk. Mean power output in time trials increased 10.7 and 1.6% after 4 wk in the HI and MOD groups, respectively (P less than 0.05). We conclude that a diet with 10 g carbohydrate.kg body mass-1.day-1 promotes greater muscle glycogen content and greater power output during training than a diet containing 5 g carbohydrate.kg body mass-1.day-1 over 4 wk of intense twice-daily rowing training.(ABSTRACT TRUNCATED AT 250 WORDS)     

Carbohydrate ingestion and muscle glycogen depletion during marathon and ultramarathon racing

Two studies were undertaken to characterize the effects of carbohydrate ingestion on fuel/hormone response to exercise and muscle glycogen utilization during prolonged competitive exercise. In study 1, eighteen subjects were divided into three groups, matched for maximum oxygen consumption (VO2max) and blood lactate turnpoint. All subjects underwent a 3-day carbohydrate (CHO) depletion phase, followed by 3 days of CHO loading (500-600 g.day-1). During the race, the groups drank either 2% glucose (G), 8% glucose polymer (GP), or 8% fructose (F). Muscle biopsies were performed before and after the race and venous blood was sampled before and at regular intervals during the race. In study 2, eighteen subjects divided into 2 matched groups ingested either a 4% G or 10% GP solution during a 56 km race. Despite significantly greater CHO ingestion by GP and F in study 1 and by GP in study 2, blood glucose, free fatty acids and insulin concentrations, muscle glycogen utilization and running performance were not different between groups. These studies show (i) that hypoglycaemia is uncommon in athletes competing in races of up to 56 km provided they CHO-load before and ingest a minimum of 10 g CHO.h-1 during competition; (ii) that neither the amount (10 g vs 40 g.h-1) nor the type of carbohydrate (G vs GP vs F) has any effect on the extent of muscle glycogen depletion or running performance in matched subjects racing over distances up to 56 km.     

Effect of carbohydrate ingestion on metabolism during running and cycling.

The effects of carbohydrate or water ingestion on metabolism were investigated in seven male subjects during two running and two cycling trials lasting 60 min at individual lactate threshold using indirect calorimetry, U-14C-labeled tracer-derived measures of the rates of oxidation of plasma glucose, and direct determination of mixed muscle glycogen content from the vastus lateralis before and after exercise. Subjects ingested 8 ml/kg body mass of either a 6.4% carbohydrate-electrolyte solution (CHO) or water 10 min before exercise and an additional 2 ml/kg body mass of the same fluid after 20 and 40 min of exercise. Plasma glucose oxidation was greater with CHO than with water during both running (65 +/- 20 vs. 42 +/- 16 g/h; P < 0.01) and cycling (57 +/- 16 vs. 35 +/- 12 g/h; P < 0.01). Accordingly, the contribution from plasma glucose oxidation to total carbohydrate oxidation was greater during both running (33 +/- 4 vs. 23 +/- 3%; P < 0.01) and cycling (36 +/- 5 vs. 22 +/- 3%; P < 0.01) with CHO ingestion. However, muscle glycogen utilization was not reduced by the ingestion of CHO compared with water during either running (112 +/- 32 vs. 141 +/- 34 mmol/kg dry mass) or cycling (227 +/- 36 vs. 216 +/- 39 mmol/kg dry mass). We conclude that, compared with water, 1) the ingestion of carbohydrate during running and cycling enhanced the contribution of plasma glucose oxidation to total carbohydrate oxidation but 2) did not attenuate mixed muscle glycogen utilization during 1 h of continuous submaximal exercise at individual lactate threshold.     

Training-induced alterations in muscle glycogen utilization in fibre-specific types during prolonged exercise

Using the glycogen depletion technique, we have examined utilization of specific fibre types during prolonged submaximal exercise to investigate the recruitment pattern employed by the central nervous system to sustain force generation in the face of a progressive glycogen depletion. Six male subjects (Vo2 max, 52.8 +/- 2.5 mL.kg-1.min-1, mean +/- SE) cycled at 59% of pretraining Vo2 max (the same absolute power output) for 99.5 +/- 6 min on two occasions, before training and after 10-12 days of intensive training, involving 2 h of cycling per day. Prior to the training, glycogen concentration during exercise in the type I and type IIA fibres of the vastus lateralis muscle as measured by microphotometric techniques was progressively reduced during exercise. The pattern of depletion in both of these fibre types was parallel and showed an early marked depletion amounting to 51 (p less than 0.05) and 35% (p less than 0.05) in the type I and type IIA fibres, respectively, during the first 15 min of exercise. At the end of exercise, glycogen levels in type I and type IIA fibres were reduced to 9 and 44% of initial levels, respectively. In contrast, glycogen concentration in type IIB fibres was not significantly (p less than 0.05) altered throughout the exercise. Following training, a pronounced glycogen sparing occurred that was conspicuous in only the type I and type IIA fibres, which was most pronounced during the first 15 min of the exercise. Similar to pretraining, glycogen concentrations in type IIB fibres were unaffected by either exercise or training.(ABSTRACT TRUNCATED AT 250 WORDS)     

Eccentric exercise-induced muscle damage impairs muscle glycogen repletion

Five healthy untrained young male subjects were studied before, immediately after, and 10 days after a 45-min bout of eccentric exercise on a cycle ergometer (201 W). The subjects were sedentary at all other times and consumed a eucaloric meat-free diet. Needle biopsies of the vastus lateralis muscle were examined for intracellular damage and glycogen content. Immediately after exercise, muscle samples showed myofibrillar tearing and edema. At 10 days, there was myofibrillar necrosis, inflammatory cell infiltration, and no evidence of myofibrillar regeneration. Glycogen utilization during the exercise bout was 33 mmol glycosyl units/kg muscle, consistent with the metabolic intensity of 44% of maximal O2 uptake; however, the significant glycogen use by type II fibers contrasted with concentric exercise performed at this intensity. At 10 days after exercise, muscle glycogen was still depleted, in both type I and II fibers. It is possible that the alterations in muscle ultrastructures were related to the lack of repletion of muscle glycogen. Damage produced by eccentric exercise was more persistent than previously reported, indicating that more than 10 days may be necessary for recovery of muscle ultrastructure and carbohydrate reserves.     

Decreased PDH activation and glycogenolysis during exercise following fat adaptation with carbohydrate restoration

Five days of a high-fat diet while training, followed by 1 day of carbohydrate (CHO) restoration, increases rates of whole body fat oxidation and decreases CHO oxidation during aerobic cycling. The mechanisms responsible for these shifts in fuel oxidation are unknown but involve up- and downregulation of key regulatory enzymes in the pathways of skeletal muscle fat and CHO metabolism, respectively. This study measured muscle PDH and HSL activities before and after 20 min of cycling at 70% VO2peak and 1 min of sprinting at 150% peak power output (PPO). Estimations of muscle glycogenolysis were made during the initial minute of exercise at 70% VO2peak and during the 1-min sprint. Seven male cyclists undertook this exercise protocol on two occasions. For 5 days, subjects consumed in random order either a high-CHO (HCHO) diet (10.3 g x kg(-1) x day(-1) CHO, or approximately 70% of total energy intake) or an isoenergetic high-fat (FAT-adapt) diet (4.6 g x kg(-1) x day(-1) FAT, or 67% of total energy) while undertaking supervised aerobic endurance training. On day 6 for both treatments, subjects ingested an HCHO diet and rested before their experimental trials on day 7. This CHO restoration resulted in similar resting glycogen contents (FAT-adapt 873 +/- 121 vs. HCHO 868 +/- 120 micromol glucosyl units/g dry wt). However, the respiratory exchange ratio was lower during cycling at 70% VO2peak in the FAT-adapt trial, which resulted in an approximately 45% increase and an approximately 30% decrease in fat and CHO oxidation, respectively. PDH activity was lower at rest and throughout exercise at 70% VO2peak (1.69 +/- 0.25 vs. 2.39 +/- 0.19 mmol x kg wet wt(-1) x min(-1)) and the 1-min sprint in the FAT-adapt vs. the HCHO trial. Estimates of glycogenolysis during the 1st min of exercise at 70% VO2peak and the 1-min sprint were also lower after FAT-adapt (9.1 +/- 1.1 vs. 13.4 +/- 2.1 and 37.3 +/- 5.1 vs. 50.5 +/- 2.7 glucosyl units x kg dry wt(-1) x min(-1)). HSL activity was approximately 20% higher (P = 0.12) during exercise at 70% VO2peak after FAT-adapt. Results indicate that previously reported decreases in whole body CHO oxidation and increases in fat oxidation after the FAT-adapt protocol are a function of metabolic changes within skeletal muscle. The metabolic signals responsible for the shift in muscle substrate use during cycling at 70% VO2peak remain unclear, but lower accumulation of free ADP and AMP after the FAT-adapt trial may be responsible for the decreased glycogenolysis and PDH activation during sprinting.     

Post-exercise ketosis and the glycogen content of liver and muscle in rats on a high carbohydrate diet

Post-exercise ketosis is known to be suppressed by physical training and by a high carbohydrate diet. As a result it has often been presumed, but not proven, that the development of post-exercise ketosis is closely related to the glycogen content of the liver. We therefore studied the effect of 1 h of treadmill running on the blood 3-hydroxybutyrate and liver and muscle glycogen concentrations of carbohydrate-loaded trained (n = 72) and untrained rats (n = 72). Resting liver and muscle glycogen levels were 25%-30% higher in the trained than in the untrained animals. The resting 3-hydroxybutyrate concentrations of both groups of rats were very low: less than 0.08 mmol.l-1. Exercise did not significantly influence the blood 3-hydroxybutyrate concentrations of trained rats, but caused a marked post-exercise ketosis (1.40 +/- 0.40 mmol.l-1 h after exercise) in the untrained animals, the time-course of which was the approximate inverse of the changes in liver glycogen concentration. Interpreting the results in the light of similar data obtained after a normal and low carbohydrate diet it has been concluded that trained animals probably owe their relative resistance to post-exercise ketosis to their higher liver glycogen concentrations as well as to greater peripheral stores of mobilizable carbohydrate.