Acute and sustained effects of a periodized carbohydrate intake using the sleep-low model in endurance-trained males.

Repeated periodization of carbohydrate (CHO) intake using a diet-exercise strategy called the sleep-low model can potentially induce mitochondrial biogenesis and improve endurance performance in endurance-trained individuals. However, more studies are needed to confirm the performance-related effects and to investigate the sustained effects on maximal fat oxidation (MFO) rate and proteins involved in intramuscular lipid metabolism. Thirteen endurance-trained males (age 23-44 years; V ˙ O2 -max, 63.9 ± 4.6 mL·kg-1 ·min-1 ) were randomized into two groups: sleep-low (LOW-CHO) or high CHO availability (HIGH-CHO) in three weekly training blocks over 4 weeks. The acute metabolic response was investigated during 60 minutes of exercise within the last 3 weeks of the intervention. Pre- and post-intervention, 30-minute time-trial performance was investigated after a 90-minute pre-load, which as a novel approach included nine intense intervals (and estimation of MFO). Additionally, muscle biopsies (v. lateralis) were obtained to investigate expression of proteins involved in intramuscular lipid metabolism using Western blotting. During acute exercise, average fat oxidation rate was ~36% higher in LOW-CHO compared to HIGH-CHO (P = .03). This did not translate into sustained effects on MFO. Time-trial performance increased equally in both groups (overall time effect: P = .005). We observed no effect on intramuscular proteins involved in lipolysis (ATGL, G0S2, CGI-58, HSL) or fatty acid transport and ß-oxidation (CD-36 and HAD, respectively). In conclusion, the sleep-low model did not induce sustained effects on MFO, endurance performance, or proteins involved in intramuscular lipid metabolism when compared to HIGH-CHO. Our study therefore questions the transferability of acute effects of the sleep-low model to superior sustained adaptations.

Metabolism and Whole-Body Fat Oxidation Following Postexercise Carbohydrate or Protein Intake.

PURPOSE: This study investigated how postexercise intake of placebo (PLA), protein (PRO), or carbohydrate (CHO) affected fat oxidation (FO) and metabolic parameters during recovery and subsequent exercise. METHODS: In a cross-over design, 12 moderately trained women (VO2max 45 ± 6 ml·min-1·kg-1) performed three days of testing. A 23-min control (CON) incremental FO bike test (30-80% VO2max) was followed by 60 min exercise at 75% VO2max. Immediately postexercise, subjects ingested PLA, 20 g PRO, or 40 g CHO followed by a second FO bike test 2 h later. RESULTS: Maximal fat oxidation (MFO) and the intensity at which MFO occurs (Fatmax) increased at the second FO test compared to the first following all three postexercise drinks (MFO for CON = 0.28 ± 0.08, PLA = 0.57 ± 0.13, PRO = 0.52 ± 0.08, CHO = 0.44 ± 0.12 g fat·min-1; Fatmax for CON = 41 ± 7, PLA = 54 ± 4, PRO = 55 ± 6, CHO = 50 ± 8 %VO2max, p < 0.01 for all values compared to CON). Resting FO, MFO, and Fatmax were not significantly different between PLA and PRO, but lower for CHO. PRO and CHO increased insulin levels at 1 h postexercise, though both glucose and insulin were equal with PLA at 2 h postexercise. Increased postexercise ketone levels only occurred with PLA. CONCLUSION: Protein supplementation immediately postexercise did not affect the doubling in whole body fat oxidation seen during a subsequent exercise trial 2 h later. Neither did it affect resting fat oxidation during the postexercise period despite increased insulin levels and attenuated ketosis. Carbohydrate intake dampened the increase in fat oxidation during the second test, though a significant increase was still observed compared to the first test.

Skeletal muscle glycogen content and particle size of distinct subcellular localizations in the recovery period after a high-level soccer match.

Whole muscle glycogen levels remain low for a prolonged period following a soccer match. The present study was conducted to investigate how this relates to glycogen content and particle size in distinct subcellular localizations. Seven high-level male soccer players had a vastus lateralis muscle biopsy collected immediately after and 24, 48, 72 and 120 h after a competitive soccer match. Transmission electron microscopy was used to estimate the subcellular distribution of glycogen and individual particle size. During the first day of recovery, glycogen content increased by ~60% in all subcellular localizations, but during the subsequent second day of recovery glycogen content located within the myofibrils (Intramyofibrillar glycogen, a minor deposition constituting 10-15% of total glycogen) did not increase further compared with an increase in subsarcolemmal glycogen (-7 vs. +25%, respectively, P = 0.047). Conversely, from the second to the fifth day of recovery, glycogen content increased (53%) within the myofibrils compared to no change in subsarcolemmal or intermyofibrillar glycogen (P < 0.005). Independent of location, increment in particle size preceded increment in number of particles. Intriguingly, average particle size decreased; however, in the period from 3 to 5 days after the match. These findings suggest that glycogen storage in skeletal muscle is influenced by subcellular localization-specific mechanisms, which account for an increase in number of glycogen particles located within the myofibrils in the period from 2 to 5 days after the soccer match.

Maximal voluntary contraction force, SR function and glycogen resynthesis during the first 72 h after a high-level competitive soccer game.

The aim of this study was to examine maximal voluntary knee-extensor contraction force (MVC force), sarcoplasmic reticulum (SR) function and muscle glycogen levels in the days after a high-level soccer game when players ingested an optimised diet. Seven high-level male soccer players had a vastus lateralis muscle biopsy and a blood sample collected in a control situation and at 0, 24, 48 and 72 h after a competitive soccer game. MVC force, SR function, muscle glycogen, muscle soreness and plasma myoglobin were measured. MVC force sustained over 1 s was 11 and 10% lower (P < 0.05) after 0 and 24 h, respectively, compared with control. The rate of SR Ca(2+) uptake at 800 nM [Ca(2+)](free) was lower (P < 0.05) after 0 h (2.5 µmol Ca(2+) g prot(-1) min(-1)) than for all other time points (24 h: 5.1 µmol Ca(2+) g prot(-1) min(-1)). However, SR Ca(2+) release rate was not affected. Plasma myoglobin was sixfold higher (P < 0.05) immediately after the game, but normalised 24 h after the game. Quadriceps muscle soreness (0-10 VAS-scale) was higher (P < 0.05) after 0 h (3.6), 24 h (1.8), 48 h (1.1) and 72 h (1.4) compared with control (0.1). Muscle glycogen was 57 and 27% lower (P < 0.001) 0 and 24 h after the game compared with control (193 and 328 vs. 449 mmol kg d w(-1)). In conclusion, maximal voluntary contraction force and SR Ca(2+) uptake were impaired and muscle soreness was elevated after a high-level soccer game, with faster recovery of SR function in comparison with MVC force, soreness and muscle glycogen.

Causes of excitation-induced muscle cell damage in isometric contractions: mechanical stress or calcium overload?

Prolonged or unaccustomed exercise leads to muscle cell membrane damage, detectable as release of the intracellular enzyme lactic acid dehydrogenase (LDH). This is correlated to excitation-induced influx of Ca2+, but it cannot be excluded that mechanical stress contributes to the damage. We here explore this question using N-benzyl-p-toluene sulfonamide (BTS), which specifically blocks muscle contraction. Extensor digitorum longus muscles were prepared from 4-wk-old rats and mounted on holders for isometric contractions. Muscles were stimulated intermittently at 40 Hz for 15-60 min or exposed to the Ca2+ ionophore A23187. Electrical stimulation increased 45Ca influx 3-5 fold. This was followed by a progressive release of LDH, which was correlated to the influx of Ca2+. BTS (50 microM) caused a 90% inhibition of contractile force but had no effect on the excitation-induced 45Ca influx. After stimulation, ATP and creatine phosphate levels were higher in BTS-treated muscles, most likely due to the cessation of ATP-utilization for cross-bridge cycling, indicating a better energy status of these muscles. No release of LDH was observed in BTS-treated muscles. However, when exposed to anoxia, electrical stimulation caused a marked increase in LDH release that was not suppressed by BTS but associated with a decrease in the content of ATP. Dynamic passive stretching caused no increase in muscle Ca2+ content and only a minor release of LDH, whereas treatment with A23187 markedly increased LDH release both in control and BTS-treated muscles. In conclusion, after isometric contractions, muscle cell membrane damage depends on Ca2+ influx and energy status and not on mechanical stress.

Suppression of testosterone does not blunt mRNA expression of myoD, myogenin, IGF, myostatin or androgen receptor post strength training in humans.

We hypothesized that suppression of endogenous testosterone blunts mRNA expression post strength training (ST). Twenty-two young men were randomized for treatment with the GnRH analogue goserelin (3.6 mg every 4 weeks) or placebo for a period of 12 weeks. The ST period of 8 weeks started at week 4. Strength test, blood sampling, muscle biopsies, and whole-body dual-energy X-ray absorptiometry (DXA) scan were performed at weeks 4 and 12. Muscle biopsies were taken during the final ST session (pre, post 4 h, and post 24 h). Resting serum testosterone decreased significantly (P < 0.01) in the goserelin group from 22.6 +/- 1.6 (mean +/- s.e.m.) to 2.0 +/- 0.1 nmol l(-1) (week 4), whereas it remained unchanged in the placebo group. An acute increase of serum testosterone was observed during the final ST session in the placebo group (P < 0.05), whereas a decreased response was observed in the goserelin group (P < 0.05). mRNA expression of IGF-IE(bc) and myogenin increased, while expression of myostatin decreased (P < 0.01); however, no differences were observed between the groups. Muscle strength and muscle mass showed a tendency to increase more in the placebo group than in the goserelin group (P = 0.05). In conclusion, despite blocked acute responses of testosterone and 10- to 20-fold lower resting levels in the goserelin group, ST resulted in a similar mRNA expression of myoD, myogenin, IGF-IE(abc), myostatin and androgen receptor as observed in the placebo group. Therefore, in the present study, the molecular events were the same, despite divergent muscle hypertrophy and strength gains.

Suppression of endogenous testosterone production attenuates the response to strength training: a randomized, placebo-controlled, and blinded intervention study.

We hypothesized that suppression of endogenous testosterone would inhibit the adaptations to strength training in otherwise healthy men. Twenty-two young men with minor experience with strength training participated in this randomized, placebo-controlled, double-blinded intervention study. The subjects were randomized to treatment with the GnRH analog goserelin (3.6 mg) or placebo (saline) subcutaneously every 4 wk for 12 wk. The strength training period of 8 wk, starting at week 4, included exercises for all major muscles [3-4 sets per exercise x 6-10 repetitions with corresponding 6- to 10-repetition maximum (RM) loads, 3/wk]. A strength test, blood sampling, and whole body DEXA scan were performed at weeks 4 and 12. Endogenous testosterone decreased significantly (P < 0.01) in the goserelin group from 22.6 +/- 5.5 (mean +/- SD) nmol/l to 2.0 +/- 0.5 (week 4) and 1.1 +/- 0.6 nmol/l (week 12), whereas it remained constant in the placebo group. The goserelin group showed no changes in isometric knee extension strength after training, whereas the placebo group increased from 240.2 +/- 41.3 to 264.1 +/- 35.3 Nm (P < 0.05 within and P = 0.05 between groups). Lean mass of the legs increased 0.37 +/- 0.13 and 0.57 +/- 0.30 kg in the goserelin and placebo groups, respectively (P < 0.05 within and P = 0.05 between groups). Body fat mass increased 1.4 +/- 1.0 kg and decreased 0.6 +/- 1.2 kg in the goserelin and placebo groups, respectively (P < 0.05 within and between groups). We conclude that endogenous testosterone is of paramount importance to the adaptation to strength training.

Effect of high-fat diet on sarcoplasmic reticulum Ca(++)-ATPase activity in different types of rat skeletal muscle.

The aim of the present study was to examine the effect of a high-fat diet on the Ca(2+)-ATPase activity in the sarcoplasmic reticulum of the flexor digitorum longus (fast-twitch, glycolytic muscle) and the soleus (slow-twitch, oxidative muscle). The enzyme activity in the extensor digitorum longus was several-fold higher than in the soleus. The high-fat diet increased the enzyme activity by 22% (p < 0.05) in the soleus but it had no effect in the flexor digitorum longus. It is concluded that a high-fat diet increases the activity of only one isoform of the enzyme, namely the one which is present in the slow-twitch oxidative fibers.