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.     

Diet-induced modulation of mitochondrial activity in rat muscle

Growing evidence supports the theory that mitochondrial dysfunction is an underlying cause of intramyocellular lipid (IMCL) accumulation and insulin resistance. Here, we hypothesized that high dietary fat (HF) intake could trigger changes in mitochondrial activity such that fatty acid oxidation is impaired in muscle and contributes to an elevation in intramyocellular lipid (IMCL) levels. Muscle mitochondrial activity was determined in vivo through measurement of the F(1)F(0) ATP synthase flux, the terminal step in the oxidative phosphorylation process. An initial study comparing rats on normal chow diet with rats on an HF diet revealed strong correlations between muscle ATP synthesis rates, IMCL levels and whole body glucose tolerance. Results obtained from two latter studies showed multiphasic responses to dietary intervention. Initially, the ATP synthesis rates decreased as much as 50% within 24 h of raising the fat content in the diet to 60% of the caloric intake. These rates eventually returned to normal values after 2-3 wk on the HF regimen, seemingly to prevent further IMCL accumulation. Only beyond 1 mo on the HF diet did results consistently show ATP synthesis rates to diminish by 30-50% accompanied by steadily augmenting IMCL levels. Interestingly, switching back to a chow diet after 3 wk of HF feeding reversed the initial diet-induced changes. Although the muscle mitochondrial system may initially offer enough compliance to counteract lipid surplus, these in vivo data suggest a vicious long-term cycle among mitochondrial dysfunction, IMCL accumulation, and glucose intolerance in the rat.     

Dietary fat increases energy intake across the range of typical consumption in the United States

Objective: The fat content of a diet has been shown to affect total energy intake, but controlled feeding trials have only compared very high (40% of total calories) fat diets with very low (20% of total calories) fat diets. This study was designed to measure accurately the voluntary food and energy intake over a range of typical intake for dietary fat. Methods and Procedures: Twenty‐two non‐obese subjects were studied for 4 days on each of three diets, which included core foods designed to contain 26, 34, and 40% fat, respectively of total calories and ad lib buffet foods of similar fat content. All diets were matched for determinants of energy density except dietary fat. Subjects consumed two meals/day in an inpatient unit and were provided the third meal and snack foods while on each diet. All food provided and not eaten was measured by research staff. Results: Voluntary energy intake increased significantly as dietary fat content increased (P = 0.008). On the 26% dietary fat treatment, subjects consumed 23.8% dietary fat (core and ad lib foods combined) and 2,748 ± 741 kcal/day (mean ± s.d.); at 34% dietary fat, subjects consumed 32.7% fat and 2,983 ± 886 kcal/day; and at 40% dietary fat subjects consumed 38.1% fat and 3,018 ± 963 kcal/day. Discussion: These results show that energy intake increases as dietary fat content increases across the usual range of dietary fat consumed in the United States. Even small reductions in dietary fat could help in lowering total energy intake and reducing weight gain in the population.     

Determination of the optimum dose of fats in the food of rats of different ages

Over a 14-day period, male SPF Wistar rats with an initial weight of 60, 200 and 250 g (ages 30, 75 and 90 days) were given diets with a constant protein content (10% casein) and a mounting fat content (10, 15, 20, 25, 30, 40 and 50% margarine, at the expense of the saccharides in the standard diet). The utilization parameter of protein biological value (NPU) for the various diets was determined from protein intake and the body nitrogen values. The reciprocal relation of the intake of the two nutrients was determined on the basis of linearity between th growth parameter NPR and protein and fat intake and, after substituting the optimum protein intake, was used to compute the optimum fat content of the diet. From the aspect of the maximum NPU value the optimum fat contents were 30% for 30-day-old, 15% for 75-day-old and 10% for 90-day-old animals. In all three age groups (according to the growth curve for the standard Larsen diet animals with an equal growth rate of 3 g/day), protein utilization under optimum nutritional conditions was the same. The optimum fat content of the diet computed from the reciprocal relationship of fat and protein intake is in agreement with the value obtained by the biological method - 29.4% (49.5 energy %) for 30-day-old animals, 15,8% (30.4% of the total energy value of the diet) for 75-day-old animals and 11.83% (23.7% of total energy) for 90-day-old rats. By using a biological and a mathematical method, this study contributes to the determination of optimum physiological doses of nutrients.     

Early postexercise muscle glycogen recovery is enhanced with a carbohydrate-protein supplement.

In the present study, we tested the hypothesis that a carbohydrate-protein (CHO-Pro) supplement would be more effective in the replenishment of muscle glycogen after exercise compared with a carbohydrate supplement of equal carbohydrate content (LCHO) or caloric equivalency (HCHO). After 2.5 +/- 0.1 h of intense cycling to deplete the muscle glycogen stores, subjects (n = 7) received, using a rank-ordered design, a CHO-Pro (80 g CHO, 28 g Pro, 6 g fat), LCHO (80 g CHO, 6 g fat), or HCHO (108 g CHO, 6 g fat) supplement immediately after exercise (10 min) and 2 h postexercise. Before exercise and during 4 h of recovery, muscle glycogen of the vastus lateralis was determined periodically by nuclear magnetic resonance spectroscopy. Exercise significantly reduced the muscle glycogen stores (final concentrations: 40.9 +/- 5.9 mmol/l CHO-Pro, 41.9 +/- 5.7 mmol/l HCHO, 40.7 +/- 5.0 mmol/l LCHO). After 240 min of recovery, muscle glycogen was significantly greater for the CHO-Pro treatment (88.8 +/- 4.4 mmol/l) when compared with the LCHO (70.0 +/- 4.0 mmol/l; P = 0.004) and HCHO (75.5 +/- 2.8 mmol/l; P = 0.013) treatments. Glycogen storage did not differ significantly between the LCHO and HCHO treatments. There were no significant differences in the plasma insulin responses among treatments, although plasma glucose was significantly lower during the CHO-Pro treatment. These results suggest that a CHO-Pro supplement is more effective for the rapid replenishment of muscle glycogen after exercise than a CHO supplement of equal CHO or caloric content.     

Exercise-induced alterations in intramyocellular lipids and insulin resistance: the athlete's paradox revisited

We previously reported an "athlete's paradox" in which endurance-trained athletes, who possess a high oxidative capacity and enhanced insulin sensitivity, also have higher intramyocellular lipid (IMCL) content. The purpose of this study was to determine whether moderate exercise training would increase IMCL, oxidative capacity of muscle, and insulin sensitivity in previously sedentary overweight to obese, insulin-resistant, older subjects. Twenty-five older (66.4 +/- 0.8 yr) obese (BMI = 30.3 +/- 0.7 kg/m2) men (n = 9) and women (n = 16) completed a 16-wk moderate but progressive exercise training program. Body weight and fat mass modestly but significantly (P < 0.01) decreased. Insulin sensitivity, measured using the euglycemic hyperinsulinemic clamp, was increased (21%, P = 0.02), with modest improvements (7%, P = 0.04) in aerobic fitness (Vo2peak). Histochemical analyses of IMCL (Oil Red O staining), oxidative capacity [succinate dehydrogenase activity (SDH)], glycogen content, capillary density, and fiber type were performed on skeletal muscle biopsies. Exercise training increased IMCL by 21%. In contrast, diacylglycerol and ceramide, measured by mass spectroscopy, were decreased (n = 13; -29% and -24%, respectively, P < 0.05) with exercise training. SDH (19%), glycogen content (15%), capillary density (7%), and the percentage of type I slow oxidative fibers (from 50.8 to 55.7%), all P < or = 0.05, were increased after exercise. In summary, these results extend the athlete's paradox by demonstrating that chronic exercise in overweight to obese older adults improves insulin sensitivity in conjunction with favorable alterations in lipid partitioning and an enhanced oxidative capacity within muscle. Therefore, several key deleterious effects of aging and/or obesity on the metabolic profile of skeletal muscle can be reversed with only moderate increases in physical activity.     

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.     

Effect of postexercise carbohydrate supplementation on glucose uptake-associated gene expression in the human skeletal muscle

We previously found that the exercise-induced elevation in GLUT4 mRNA of rat muscle can be rapidly down-regulated when glucose is given immediately following exercise. The purpose of this study was to determine the effect of postexercise carbohydrate diet on GLUT4 and hexokinase (HK) II mRNA levels in the human skeletal muscle. Eight untrained male subjects (age, 20.7+/-3.1 years) exercised for 60 min on a cycle ergometer at a 70-75% maximal oxygen consumption. The postexercise dietary treatment was performed in a crossover design. Immediately after the exercise, a diet with 70% carbohydrate content (1 g per kilogram of body weight; 356+/-19.8 kcal) was given to half of the subjects (eaten in 10 min) followed by a 3-h recovery, while the control subjects remained unfed for 3 h. Biopsies were performed on the deep portion of the vastus lateralis muscle of all subjects immediately after the exercise and 3 h after the carbohydrate ingestion. Blood glucose and serum insulin concentrations were measured every 30 min for 3 h. At the end of the 3-h recovery, blood glucose and serum insulin levels were not different from control levels, indicating that the oral carbohydrate was mostly disposed in the body within 3 h. In addition, GLUT4 and HK II mRNA levels were significantly lowered in the exercised human skeletal muscle in subjects receiving the carbohydrate diet. In conclusion, the present study demonstrates that GLUT4 mRNA and HK II mRNA in the exercised human skeletal muscle were significantly lowered by a high-carbohydrate diet.     

Intramyocellular Lipid Content and Molecular Adaptations in Response to a 1‐Week High‐Fat Diet

Objective: To investigate molecular adaptations that accompany the elevation of intramyocellular lipid (IMCL) content on a high‐fat (HF) diet for 1 week. Research Methods and Procedures: Ten subjects consumed a normal‐fat (NF) diet for 1 week, followed by an HF diet for another week. After both dietary periods, we determined the IMCL content by proton magnetic resonance spectroscopy in the vastus lateralis muscle and quantified changes in gene expression, protein content, and activity in biopsy samples. We investigated genes involved in carbohydrate and fatty acid handling [lipoprotein lipase, acetyl‐coenzyme A carboxylase (ACC) 2, hormone‐sensitive lipase, hexokinase II, and glucose transporter 4] and measured protein levels of CD36 and phosphorylated and unphosphorylated ACC2 and the activity of adenosine monophosphate‐activated kinase. Results: IMCL content was increased by 54% after the HF period. Lipoprotein lipase mRNA concentration was increased by 33%, whereas ACC2 mRNA concentration tended to be increased after the HF diet. Hexokinase II, glucose transporter 4, and hormone‐sensitive lipase mRNA were unchanged after the HF diet. ACC2 and CD36 protein levels, phosphorylation status of ACC2, and adenosine monophosphate‐activated kinase activity did not change in response to the HF diet. Discussion: We found that IMCL content in skeletal muscle increased after 1 week of HF feeding, accompanied by molecular adaptations that favor fat storage in muscle rather than oxidation.     

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.     

Dietary Fat Dose Dependently Increases Spontaneous Caloric Intake in Rat

Objective: To characterize the dose‐response relationship between dietary fat to carbohydrate ratio and spontaneous caloric intake. Research Methods and Procedures: Male Long‐Evans rats consumed milk‐based liquid diets that differed in fat content (17% to 60% of kilocalories) but had equivalent protein content and energy density. In Experiment 1, rats consumed one of the diets (n = 9/diet group) as the sole source of nutrition for 16 days. In Experiment 2, diets were offered as an option to nutritionally complete chow for 4 days followed by a 3‐day chow‐only washout in a randomized within‐subjects design (n = 30). In Experiment 3, nine rats received isocaloric intragastric infusions of diet overnight, with chow available ad libitum. At least two no‐infusion days separated the different diet infusions, which were given in random order. Food intake was measured daily Results: Dietary fat dose dependently increased total daily kilocalories in each of the three paradigms. Discussion: These data imply that the postingestive effects of carbohydrate and fat differentially engage the physiological substrates that regulate daily caloric intake. These findings reiterate the importance of investigating macronutrient‐specific controls of feeding, rather than prematurely concluding that dietary attributes that covary with fat content (e.g., caloric density and palatability) drive the overeating associated with a high‐fat diet.     

Influence of diet on the storage, mobilization and utilization of energy reserves in trained and untrained rats

The effect of the major dietary energy source (fat or carbohydrate) on some of the adaptations to physical training, particularly body composition and tissue glycogen concentrations, were studied in growing male Wistar rats. Resting liver glycogen concentrations were lower in both trained and sedentary rats fed a high fat diet compared to corresponding rats fed a high carbohydrate (low fat) diet. Trained rats on both diets had higher liver glycogen levels than corresponding sedentary controls. Resting gastrocnemius muscle glycogen concentrations were not influenced by diet or training. Rates of liver and muscle glycogen depletion during a 60-min swim were lower in trained rats but were not influenced by diet. Significant interactions were noted between the dietary energy source and exercise training with respect to body weight gain, body fat content, liver weight and liver glycogen concentrations.     

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)     

Serum and urinary markers of skeletal muscle tissue damage after weight lifting exercise

The purpose of this study was to determine whether high intensity weight lifting exercise produces elevations of urinary 3-methylhistidine (3-MH), serum creatine kinase activity (CK), and serum myoglobin concentration (MY), and whether trained weight lifters differed in such responses when compared to a group of untrained subjects. Ten experienced male weight lifters (EWL) and seven untrained male subjects (IWL) performed three sets of six weight lifting exercises at 70%-80% of 1 RM. All subjects consumed a meat-free diet. The 3-MH:creatinine (3-MH:CR) values decreased 24 h and 48 h following exercise (P less than 0.05). The 12-h and 24-h postexercise CK response and the 12-h postexercise MY response increased for both EWL and IWL (P less than 0.05). However, EWL had a lower 24-h postexercise CK response and lower 12-h and 24-h postexercise MY responses compared to IWL (P less than 0.05). Within 48 h following weight lifting exercise, skeletal muscle protein degradation (as assessed by 3-MH:CR values) decreased regardless of prior training experience whereas skeletal muscle tissue damage (as assessed by CK and MY responses) increased. However, prior weight lifting training appeared to diminish the extent of muscle tissue damage.     

A high-fat diet raises fasting plasma CCK but does not affect upper gut motility, PYY, and ghrelin, or energy intake during CCK-8 infusion in lean men

There is evidence from studies in animals that the effects of both fat and CCK on gastrointestinal function and energy intake are attenuated by consumption of a high-fat diet. In humans, the effects of exogenous CCK-8 on antropyloroduodenal motility, plasma CCK, peptide YY (PYY), and ghrelin concentrations, appetite, and energy intake are attenuated by a high-fat diet. Ten healthy lean males consumed isocaloric diets (~15,400 kJ per day), containing either 44% (high-fat, HF) or 9% (low-fat, LF) fat, for 21 days in single-blind, randomized, cross-over fashion. Immediately following each diet (i.e., on day 22), subjects received a 45-min intravenous infusion of CCK-8 (2 ng.kg(-1).min(-1)), and effects on antropyloroduodenal motility, plasma CCK, PYY, ghrelin concentrations, hunger, and fullness were determined. Thirty minutes after commencement of the infusion, subjects were offered a buffet-style meal, from which energy intake (in kilojoules) was quantified. Body weight was unaffected by the diets. Fasting CCK (P < 0.05), but not PYY and ghrelin, concentrations were greater following the HF, compared with the LF, diet. Infusion of CCK-8 stimulated pyloric pressures (P < 0.01) and suppressed antral and duodenal pressures (P < 0.05), with no difference between the diets. Energy intake also did not differ between the diets. Short-term consumption of a HF diet increases fasting plasma CCK concentrations but does not affect upper gut motility, PYY and ghrelin, or energy intake during CCK-8 infusion, in a dose of 2 ng.kg(-1).min(-1), in healthy males.     

Effects of endurance exercise training on muscle glycogen accumulation in humans.

The purpose of this investigation was to determine whether endurance exercise training increases the ability of human skeletal muscle to accumulate glycogen after exercise. Subjects (4 women and 2 men, 31 +/- 8 yr old) performed high-intensity stationary cycling 3 days/wk and continuous running 3 days/wk for 10 wk. Muscle glycogen concentration was measured after a glycogen-depleting exercise bout before and after endurance training. Muscle glycogen accumulation rate from 15 min to 6 h after exercise was twofold higher (P < 0.05) in the trained than in the untrained state: 10.5 +/- 0.2 and 4.5 +/- 1.3 mmol. kg wet wt(-1). h(-1), respectively. Muscle glycogen concentration was higher (P < 0.05) in the trained than in the untrained state at 15 min, 6 h, and 48 h after exercise. Muscle GLUT-4 content after exercise was twofold higher (P < 0.05) in the trained than in the untrained state (10.7 +/- 1.2 and 4.7 +/- 0.7 optical density units, respectively) and was correlated with muscle glycogen concentration 6 h after exercise (r = 0.64, P < 0.05). Total glycogen synthase activity and the percentage of glycogen synthase I were not significantly different before and after training at 15 min, 6 h, and 48 h after exercise. We conclude that endurance exercise training enhances the capacity of human skeletal muscle to accumulate glycogen after glycogen-depleting exercise.     

Metabolic Implications of Dietary Trans‐fatty Acids

Dietary trans‐fatty acids are associated with increased risk of cardiovascular disease and have been implicated in the incidence of obesity and type 2 diabetes mellitus (T2DM). It is established that high‐fat saturated diets, relative to low‐fat diets, induce adiposity and whole‐body insulin resistance. Here, we test the hypothesis that markers of an obese, prediabetic state (fatty liver, visceral fat accumulation, insulin resistance) are also worsened with provision of a low‐fat diet containing elaidic acid (18:1t), the predominant trans‐fatty acid isomer found in the human food supply. Male 8‐week‐old Sprague–Dawley rats were fed a 10% trans‐fatty acid enriched (LF‐trans) diet for 8 weeks. At baseline, 3 and 6 weeks, in vivo magnetic resonance spectroscopy (¹H‐MR) assessed intramyocellular lipid (IMCL) and intrahepatic lipid (IHL) content. Euglycemic–hyperinsulinemic clamps (week 8) determined whole‐body and tissue‐specific insulin sensitivity followed by high‐resolution ex vivo ¹H‐NMR to assess tissue biochemistry. Rats fed the LF‐trans diet were in positive energy balance, largely explained by increased energy intake, and showed significantly increased visceral fat and liver lipid accumulation relative to the low‐fat control diet. Net glycogen synthesis was also increased in the LF‐trans group. A reduction in glucose disposal, independent of IMCL accumulation was observed in rats fed the LF‐trans diet, whereas in rats fed a 45% saturated fat (HF‐sat) diet, impaired glucose disposal corresponded to increased IMCL_TA. Neither diet induced an increase in IMCL_soleus. These findings imply that trans‐fatty acids may alter nutrient handling in liver, adipose tissue, and skeletal muscle and that the mechanism by which trans‐fatty acids induce insulin resistance differs from diets enriched with saturated fats.     

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.     

Exercise and diet enhance fat oxidation and reduce insulin resistance in older obese adults.

Older, obese, and sedentary individuals are at high risk of developing diabetes and cardiovascular disease. Exercise training improves metabolic anomalies associated with such diseases, but the effects of caloric restriction in addition to exercise in such a high-risk group are not known. Changes in body composition and metabolism during a lifestyle intervention were investigated in 23 older, obese men and women (aged 66 +/- 1 yr, body mass index 33.2 +/- 1.4 kg/m(2)) with impaired glucose tolerance. All volunteers undertook 12 wk of aerobic exercise training [5 days/wk for 60 min at 75% maximal oxygen consumption (Vo(2max))] with either normal caloric intake (eucaloric group, 1,901 +/- 277 kcal/day, n = 12) or a reduced-calorie diet (hypocaloric group, 1,307 +/- 70 kcal/day, n = 11), as dictated by nutritional counseling. Body composition (decreased fat mass; maintained fat-free mass), aerobic fitness (Vo(2max)), leptinemia, insulin sensitivity, and intramyocellular lipid accumulation (IMCL) in skeletal muscle improved in both groups (P < 0.05). Improvements in body composition, leptin, and basal fat oxidation were greater in the hypocaloric group. Following the intervention, there was a correlation between the increase in basal fat oxidation and the decrease in IMCL (r = -0.53, P = 0.04). In addition, basal fat oxidation was associated with circulating leptin after (r = 0.65, P = 0.0007) but not before the intervention (r = 0.05, P = 0.84). In conclusion, these data show that exercise training improves resting substrate oxidation and creates a metabolic milieu that appears to promote lipid utilization in skeletal muscle, thus facilitating a reversal of insulin resistance. We also demonstrate that leptin sensitivity is improved but that such a trend may rely on reducing caloric intake in addition to exercise training.     

Lifelong training preserves some redox-regulated adaptive responses after an acute exercise stimulus in aged human skeletal muscle

Several redox-regulated responses to an acute exercise bout fail in aged animal skeletal muscle, including the ability to upregulate the expression of antioxidant defense enzymes and heat shock proteins (HSPs). These findings are generally derived from studies on sedentary rodent models and thus may be related to reduced physical activity and/or intraspecies differences as opposed to aging per se. This study, therefore, aimed to determine the influence of age and training status on the expression of HSPs, antioxidant enzymes, and NO synthase isoenzymes in quiescent and exercised human skeletal muscle. Muscle biopsy samples were obtained from the vastus lateralis before and 3 days after an acute high-intensity-interval exercise bout in young trained, young untrained, old trained, and old untrained subjects. Levels of HSP72, PRX5, and eNOS were significantly higher in quiescent muscle of older compared with younger subjects, irrespective of training status. 3-NT levels were elevated in muscles of the old untrained but not the old trained state, suggesting that lifelong training may reduce age-related macromolecule damage. SOD1, CAT, and HSP27 levels were not significantly different between groups. HSP27 content was upregulated in all groups studied postexercise. HSP72 content was upregulated to a greater extent in muscle of trained compared with untrained subjects postexercise, irrespective of age. In contrast to every other group, old untrained subjects failed to upregulate CAT postexercise. Aging was associated with a failure to upregulate SOD2 and a downregulation of PRX5 in muscle postexercise, irrespective of training status. In conclusion, lifelong training is unable to fully prevent the progression toward a more stressed muscular state as evidenced by increased HSP72, PRX5, and eNOS protein levels in quiescent muscle. Moreover, lifelong training preserves some (e.g., CAT) but not all (e.g., SOD2, HSP72, PRX5) of the adaptive redox-regulated responses after an acute exercise bout. Collectively, these data support many but not all of the findings from previous animal studies and suggest parallel aging effects in humans and mice at rest and after exercise that are not modulated by training status in human skeletal muscle.