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 ≤ 0.01) and plasma lactate concentration higher (P ≤ 0.01). Muscle glycogen was lower post‐exercise with 24 : 36 s (P ≤ 0.05). Muscle free carnitine decreased (P ≤ 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 ≤ 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.     

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.     

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.     

The effect of high-intensity exercise on the respiratory capacity of sceletal muscle

The effect of high-intensity exercise on the respiratory capacity of skeletal muscle was studied in horses which ran five 600-m bouts on a track with 2 min of rest between exercise bouts, or once to fatigue on a treadmill at an intensity that elicited the maximal oxygen uptake. Venous blood and biopsy samples of the middle gluteal muscle were collected at rest, after each exercise bout, and 30 and 60 min post-exercise. Blood samples were analyzed for lactate concentration and pH and muscle samples for metabolites, pH, and respiratory capacity. Venous blood and muscle pH declined to 6.91±0.02 and 6.57±0.02, respectively, after the fifth track run and to 6.98±0.02 and 6.71±0.07, respectively, after treadmill running. Muscle metabolite changes were consistent with the metabolic response to high-intensity exercise. Muscle respiratory capacity declined >20% (P<0.05) after a single exercise bout and was 45% of the control value after the fifth track run. Tissue respiration was depressed 60 min post-exercise but was normal 24 h later. These observations suggest that high-intensity exercise impairs the respiratory capacity of the working muscle. Although this occurred in parallel with reductions in pH, other factors could be responsible for this response.     

Glycogen depletion of different fibre types in human skeletal muscle during intermittent and continuous exercise

Muscle biopsies from the vastus lateralis were obtained from thirteen healthy subjects at rest and at intervals during continuous and intermittent exercise. After freeze-drying of the muscle sample, fragments of single fibres were dissected out and stained for myofibrillar ATPase with preincubation at pH 10.3, 4.6 or 4.3 to identify type 1, II A and II B fibres respectively. The remaining part of each fragment was used for quantitative glycogen analyses. At rest, mean glycogen content was significantly higher in type II fibres (402 mmol/kg dry weight) than in type 1 (344 mmol/kg dry weight). After 60 min continuous exercise at moderate work load a more pronounced glycogen depletion had occurred in type I (277 mmol/kg dry weight) than in type II (A-r B) fibres (113 mmol/kg dry weight). With 60 min intense intermittent exercise a significant and similar depletion occurred in both type I (213 mmol/kg dry weight) and type II (A + B) fibres (203 mmol/kg dry weight). With continuous intense exercise to exhaustion (4–6 min), glycogen depletion was more marked in type II (A- B) (1 !8 mmol/kg dry weight) than type I fibres (74 mmol/kg dry weight). These data imply that the glycogen depletion pattern in muscle fibres is determined mainly by the work intensity but the lower glycogen depletion per unit time in intermittent compared with continuous intense exercise indicates that the mode and duration of exercise is important, too.     

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.     

Ultrastructural changes and sarcoplasmic reticulum Ca2+ regulation in red vastus muscle following eccentric exercise in the rat

This study examined the effects of a bout of low-intensity, prolonged downhill exercise on sarcoplasmic reticulum (SR) Ca(2+)-ATPase activity, Ca(2+) uptake and release in rat red vastus muscle. Ionophore stimulation was determined to assess vesicle integrity by measuring the ratio of Ca(2+)-ATPase activities in the presence and absence of A23187. Observations of the muscle ultrastructure were made to evaluate muscle damage at the level of the myofibrils and SR. Adult male Sprague-Dawley rats (weight, 395 +/- 5.9 g) were either assigned as non-exercise controls or subjected to 90 min of downhill treadmill exercise (-16 deg; 15 m min(-1)), and then killed immediately, 4, 24, 48, 72 or 144 h after exercise (n = 7). Calcium uptake was significantly lower (P < 0.05) compared with control values (19.25 +/- 1.38 nmol min(-1) (mg protein)(-1)), by 29 and 36% immediately and 4 h postexercise, respectively, and remained depressed (P < 0.05) 24 h postexercise. Calcium release was also significantly lower (P < 0.05) compared with control values (31.06 +/- 2.36 nmol min(-1) (mg protein)(-1)), by 37 and 39% immediately and 4 h postexercise, respectively, and remained depressed (P < 0.05) 24 h postexercise. Ca(2+)-ATPase activity measured with ionophore was 31% lower (P < 0.05) 4 h postexercise, and remained lower (P < 0.05) 24 h postexercise. The ratio of Ca(2+)-ATPase activities in the presence and absence of A23187 was not significantly changed after exercise, indicating that membrane integrity was not altered by the exercise. Focal dilatations of the SR were observed immediately and 4 h following exercise, implying that SR may be susceptible to damage in the localized regions of overstretched sarcomeres. The results demonstrate that a bout of low-intensity, prolonged downhill exercise results in a long-lasting depression of SR function that is not fully restored after 2 days of recovery, which may underlie some functional impairments induced by eccentric exercise.     

Glycogen synthase activation in human skeletal muscle: effects of diet and exercise.

We investigated the role of glycogen synthase in supranormal resynthesis (supercompensation) of skeletal muscle glycogen after exhaustive exercise. Six healthy men exercised 60 min by cycling with one leg at 75% VO2max, recovered 3 days on a low-carbohydrate diet, exercised again, and recovered 4 days on high-carbohydrate diet. Glycogen and glycogen synthase activities at several glucose-6-phosphate (G6P) concentrations were measured in biopsy samples of m. vastus lateralis. Dietary alterations alone did not affect glycogen, whereas exercise depleted glycogen stores. After the second exercise bout, glycogen returned to normal within 24 h and reached supercompensated levels by 48 h of recovery. Glycogen synthase activation state strikingly increased after exercise in exercised muscle and remained somewhat elevated for the first 48 h of recovery in both muscles. We suggest that 1) forms of glycogen synthase intermediate to I (G6P-independent) and D (G6P-dependent) forms are present in vivo, and 2) glycogen supercompensation can in part be explained by the formation of intermediate forms of glycogen synthase that exhibit relatively low activity ratios, but an increased sensitivity to activation by G6P.     

A single bout of exercise activates skeletal muscle satellite cells during subsequent overnight recovery

Skeletal muscle satellite cell (SC) content has been reported to increase following a single bout of exercise. Data on muscle fibre type-specific SC content and/or SC activation status are presently lacking. The objective of the study was to determine the impact of a single bout of exercise on muscle fibre type-specific SC content and activation status following subsequent overnight recovery. Eight healthy men (age, 20 ± 1 years) performed a single bout of combined endurance- and resistance-type exercise. Muscle biopsies were collected before and immediately after exercise, and following 9 h of postexercise, overnight recovery. Muscle fibre type-specific SC and myonuclear content and SC activation status were determined by immunohistochemical analyses. Satellite cell activation status was assessed by immunohistochemical staining for both Delta-like homologue 1 (DLK1) and Ki-67. Muscle fibre size and fibre area per nucleus were greater in type II compared with type I muscle fibres (P < 0.05). At baseline, no differences were observed in the percentage of SCs staining positive for DLK1 and/or Ki67 between fibre types. No significant changes were observed in SC content following 9 h of postexercise, overnight recovery; however, the percentage of DLK1-positive SCs increased significantly during overnight recovery, from 22 ± 5 to 41 ± 5% and from 24 ± 6 to 51 ± 9% in the type I and II muscle fibres, respectively. No changes were observed in the percentage of Ki-67-positive SCs. A single bout of exercise activates both type I and II skeletal muscle fibre SCs within a single night of postexercise recovery, preceding the subsequent increase in SC content.     

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     

Intramyocellular lipid and glycogen content are reduced following resistance exercise in untrained healthy males

Resistance exercise has recently been shown to improve whole-body insulin sensitivity in healthy males. Whether this is accompanied by an exercise-induced decline in skeletal muscle glycogen and/or lipid content remains to be established. In the present study, we determined fibre-type-specific changes in skeletal muscle substrate content following a single resistance exercise session. After an overnight fast, eight untrained healthy lean males participated in a ~45 min resistance exercise session. Muscle biopsies were collected before, following cessation of exercise, and after 30 and 120 min of post-exercise recovery. Subjects remained fasted throughout the test. Conventional light and (immuno)fluorescence microscopy were applied to assess fibre-type-specific changes in intramyocellular triacylglycerol (IMTG) and glycogen content. A significant 27±7% net decline in IMTG content was observed in the type I muscle fibres (P<0.05), with no net changes in the type IIa and IIx fibres. Muscle glycogen content decreased with 23±6, 40±7 and 44±7% in the type I, IIa and IIx muscle fibres, respectively (P<0.05). Fibre-type-specific changes in intramyocellular lipid and/or glycogen content correlated well with muscle fibre-type oxidative capacity. During post-exercise recovery, type I muscle fibre lipid content returned to pre-exercise levels within 120 min. No changes in muscle glycogen content were observed during recovery. We conclude that intramyocellular lipid and glycogen stores are readily used during resistance exercise and this is likely associated with the reported increase in whole-body insulin sensitivity following resistance exercise.     

Substrate oxidation during acute exercise and with exercise training in lean and obese women

The purpose of this study was to examine the rates of substrate oxidation in lean and obese women during short-duration, high-intensity exercise and to examine the effects of a 16-week exercise training program on substrate oxidation during 30 min of exercise in lean and obese individuals. Fat and carbohydrate oxidation were measured in 8 non-obese (Non-Ob), 11 lower-body obese (LBO) and 12 upper-body obese (UBO) women at rest and during 30 min of treadmill exercise at 70% of peak oxygen uptake. The obese women participated in 16 weeks of aerobic training (3 times per week at 70% of maximum oxygen uptake). Total fat and carbohydrate oxidation were measured using indirect calorimetry. The respiratory exchange ratio (R) was similar between groups at rest and was found to decrease throughout the exercise session (P<0.01). Fat oxidation was greater at 15 min of exercise than at rest (P<0.01) but did not increase significantly more at 30 min of exercise. Obese women had significantly greater fat oxidation (both absolute concentrations and when expressed per kg of fat free mass, FFM) at 30 min of exercise than the Non-Ob women [Non-Ob 23.5 (3.7) μmol·kg FFM^–1·min^–1, LBO 35.2 (3.1) μmol·kg FFM^–1·min^–1, UBO 33.2 (2.6) μmol·kg FFM^–1·min^–1; P<0.01]. Carbohydrate oxidation also increased (P<0.01) in response to exercise, but no group differences were found. The pattern of fat distribution (LBO vs UBO) did not affect the resting or exercise fat oxidation (P=NS). Sixteen weeks of aerobic exercise did not result in significant changes in resting or exercise fat oxidation in the obese women (n=10; P=NS), but did significantly increase carbohydrate oxidation [pre-training 8.6 (1.4) μmol·kg FFM^–1, post-training 13.6 (2.1) μmol·kg FFM^–1·min^–1; P<0.01]. Unlike earlier studies, this shorter-duration, higher-intensity exercise resulted in a greater whole-body fat oxidation in the obese women than in the Non-Ob women, and exercise training did not result in any changes in fat oxidation, but did increase exercise carbohydrate oxidation. Electronic Publication     

Relationship of recovery from intensive exercise to the oxidative potential of skeletal muscle

This study examined if there was a relationship between the aerobic-oxidative potential of skeletal muscle and the metabolic and force recovery after intense exercise. Eleven male subjects performed three bouts of unilateral knee extensions using an isokinetic device. Sixty seconds of rest separated bouts. Muscle biopsies were taken from the vastus lateralis prior to exercise, immediately after bout 2 and before bout 3. Samples were analysed for adenosine triphosphate (ATP), adenosine diphosphate (ADP), inosine monophosphate (IMP), creatine phosphate (CP) and lactate contents and citrate synthase (CS) activity. Peak torque at the end of bout 2 was 45% of initial peak torque of bout 1 (IPT1). With recovery, initial peak torque of bout 3 (IPT3) was 81% of IPT1. Peak torque after recovery (IPT3/IPT1) was related to CS activity (r = 0.69). ATP, CP and ATP/ADP decreased with exercise. ADP, IMP and lactate increased. With recovery, ATP and CP remained depressed. IMP and lactate remained elevated. ATP/ADP and ADP returned towards 'normal', but only the latter attained resting levels. When analysing the individual responses the following correlations were found. After recovery, ATP/ADP (r = 0.57), ATP/ADP relative to rest (r = 0.71), lactate (r = -0.62), CP (r = 0.75) and CP relative to rest (r = 0.83) were related to CS activity. The changes in lactate (r = -0.76) and CP (r = 0.79) during recovery (bout 3-bout 2) were also related to CS activity. The results suggest that the recovery of force and the 'normalization' of metabolite contents after short-term, intense exercise are dependent on the aerobic-oxidative potential of skeletal muscle.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of exercise training on glycogen,glycogen synthase and phosphorylase in muscle and liver

Summary It is thought that exercise training in both man and the rat results in a protective effect against the depletion of carbohydrate stores during exercise (glycogen-sparing). However there has been no comprehensive study of the effects of training on glycogen anabolic and catabolic enzymes with liver or muscle. The aim of this study was to examine whether changes in these enzymes occur and whether these changes may provide an explanation for the glycogen-sparing which results from exercise training.Male rats were trained by a treadmill running program at three different workloads. In addition, there were three control groups: free eating (SF), food restricted (SR), and one SF with a single bout of exercise prior to sacrifice.Exercise training was associated with a 60–150% increase in glycogen synthase and phosphorylase and a 50–70% increase in glycogen content in soleus, an intermediate muscle, but not in extensor digitorum longus (EDL), a white muscle nor in liver. The increase in glycogen synthase and phosphorylase in intermediate muscle was proportional to the degree of training and there was a significant correlation between glycogen content, glycogen synthase, and phosphorylase activity in intermediate muscle. Cytochrome c oxidase activity, an indicator of respiratory capacity, increased 50% in gastrocnemius of trained rats and was significantly correlated with glycogen synthase and phosphorylase in soleus.These results indicate a significant effect of exercise training on glycogen anabolic and catabolic enzymes in intermediate muscle, with no significant effects in white muscle or liver. The changes do not provide an explanation for glycogen-sparing, but are consistent with improved capacity of intermediate muscle for rapid glycogen mobilisation and repletion.     

The decrease in electrically evoked force production is delayed by a previous bout of stretch–shortening cycle exercise

Aim: Unaccustomed physical exercise with a large eccentric component is accompanied by muscle damage and impaired contractile function, especially at low stimulation frequencies. A repeated bout of eccentric exercise results in less damage and improved recovery of contractile function. Here we test the hypotheses that (1) a prior stretch–shortening cycle (SSC) exercise protects against impaired muscle function during a subsequent bout of SSC exercise and (2) the protection during exercise is transient and becomes less effective as the exercise progresses. Methods: Healthy untrained men (n = 7) performed SSC exercise consisting of 100 maximal drop jumps at 30 s intervals. The same exercise was repeated 4 weeks later. Peak quadriceps muscle force evoked by electrical stimulation at 15 (P15) and 50 (P50) Hz was measured before exercise, after 10, 25, 50 and 100 jumps as well as 1 and 24 h after exercise. Results: P15 and P50 were higher during the initial phase of the repeated bout compared with the first exercise bout, but there was no difference between the bouts at the end of the exercise periods. P15 and P50 were again larger 24 h after the repeated bout. The P15/P50 ratio during exercise was not different between the two bouts, but it was higher after the repeated bout. Conclusion: A prior bout of SSC exercise temporarily protects against impaired contractile function during a repeated exercise bout. The protection can again be seen after exercise, but the underlying mechanism then seems to be different.     

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-1 dry 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 less than 35 min (n = 3) had GSF values in muscle which were lower than at rest, whereas those subjects who cycled for greater than 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 less than 0.001) and negatively related to the glycogen content at the end of exercise (r = -0.82; y = 516-2x + 0.001x2; P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Human soleus muscle protein synthesis following resistance exercise

AIM: It is generally believed the calf muscles in humans are relatively unresponsive to resistance training when compared with other muscles of the body. The purpose of this investigation was to determine the muscle protein synthesis response of the soleus muscle following a standard high intensity bout of resistance exercise. METHODS: Eight recreationally active males (27 +/- 4 years) completed three unilateral calf muscle exercises: standing calf press/heel raise, bent-knee calf press/heel raise, and seated calf press/heel raise. Each exercise consisted of four sets of 15 repetitions (approximately 15 repetition maximum, RM, or approximately 70% 1RM). Fractional rate of muscle protein synthesis (FSR) was determined with a primed constant infusion of [2H5]phenylalanine coupled with muscle biopsies immediately and 3 h following the exercise in both the exercise and non-exercise (resting control) leg. RESULTS: FSR was elevated (P < 0.05) in the exercise (0.069 +/- 0.010) vs. the control (0.051 +/- 0.012) leg. Muscle glycogen concentration was lower (P < 0.05) in the exercise compared with the control leg (Decrease from control; immediate post-exercise: 54 +/- 5; 3 h post-exercise: 36 +/- 4 mmol kg(-1) wet wt.). This relatively high amount of glycogen use is comparable with previous studies of resistance exercise of the thigh (i.e. vastus lateralis; approximately 41-49 mmol kg(-1) wet wt.). However, the exercise-induced increase in FSR that has been consistently reported for the vastus lateralis (approximately 0.045-0.060% h(-1)) is on average approximately 200% higher than reported here for the soleus (0.019 +/- 0.003% h(-1)). CONCLUSIONS: These results suggest the relatively poor response of soleus muscle protein synthesis to an acute bout of resistance exercise may be the basis for the relative inability of the calf muscles to respond to resistance training programs.     

Heat shock protein translocation and expression response is attenuated in response to repeated eccentric exercise

Aim: This study hypothesized that heat shock protein (HSP) translocation and upregulation is more probable to occur after eccentric exercise than after concentric exercise or repeated eccentric exercise. Methods: Fourteen young, healthy, untrained male subjects completed two bench‐stepping exercise bouts with 8 weeks between bouts, and were compared with a control group (n = 6). Muscle biopsies collected from m. vastus lateralis of both legs prior to and at 3 h, 24 h and 7 days after exercise were quantified for mRNA levels and/or for HSP27, αβ‐crystallin and inducible HSP70 content in cytosolic and cytoskeletal protein fractions. Results: The first bout of exercise reduced muscle strength and increased muscle soreness predominantly in the eccentric leg (P < 0.05). These responses were attenuated after the repeated eccentric exercise bout (P < 0.05), suggesting a repeated bout adaptation. Increases in inducible HSP70 and HSP27 protein content in cytoskeletal fractions were observed exclusively after eccentric exercise (P < 0.05). For HSP27, an approx. 10‐fold upregulation after first‐bout eccentric exercise was attenuated to a an approximately fourfold upregulation after the repeated eccentric exercise bout. mRNA levels for HSP70, HSP27 and αβ‐crystallin were upregulated within approximately two to fourfold ranges at time points 3 and 24 h post‐exercise (P < 0.05). This upregulation was induced exclusively by eccentric exercise but with a tendency to attenuated expression 3 h after the repeated eccentric exercise bout. Conclusion: Our results show that HSP translocation and expression responses are induced by muscle damaging exercise, and suggest that such HSP responses are closely related to the extent of muscle damage.     

Formation of acetylcarnitine in muscle of horse during high intensity exercise

Summary To study the changes in carnitine in muscle with sprint exercise, two Thoroughbred horses performed two treadmill exercise tests. Biopsies of the middle gluteal were taken before, after exercise and after 12 min recovery. Resting mean muscle total carnitine content was 29.5 mmol · kg⁻¹ dry muscle (d. m.). Approximately 88% was free carnitine, 7% acetylcarnitine and acylcarnitine was estimated at 5%. Exercise did not affect total carnitine, but resulted in a marked fall in free carnitine and almost equivalent rise in acetylcarnitine. The results are consistent with a role for carnitine in the regulation of the acetyl-CoA/CoA ratio during sprint exercise in the Thoroughbred horse by buffering excess production of acetyl units.