Kasper Degn Gejl

Muscle Glycogen Content Modifies SR Ca2 + Release Rate in Elite Endurance Athletes.

PURPOSE The aim of the present study was to investigate the influence of muscle glycogen content on sarcoplasmic reticulum (SR) function and peak power output (Wpeak) in elite endurance athletes. METHODS Fourteen highly trained male triathletes (VO2max = 66.5 ± 1.3 mL O2·kg·min), performed 4 h of glycogen-depleting cycling exercise (HRmean = 73% ± 1% of maximum). During the first 4 h of recovery, athletes received either water (H2O) or carbohydrate (CHO), separating alterations in muscle glycogen content from acute changes affecting SR function and performance. Thereafter, all subjects received CHO-enriched food for the remaining 20-h recovery period. RESULTS Immediately after exercise, muscle glycogen content and SR Ca release rate was reduced to 32% ± 4% (225 ± 28 mmol·kg dw) and 86% ± 2% of initial levels, respectively (P < 0.01). Glycogen markedly recovered after 4 h of recovery with CHO (61% ± 2% of preexercise) and SR Ca release rate returned to preexercise level. However, in the absence of CHO during the first 4 h of recovery, glycogen and SR Ca release rate remained depressed, with the normalization of both parameters at the end of the 24 h of recovery after receiving a CHO-enriched diet. Linear regression demonstrated a significant correlation between SR Ca release rate and muscle glycogen content (P < 0.01, r = 0.30). The 4 h of cycling exercise reduced Wpeak by 5.5%-8.9% at different cadences (P < 0.05), and Wpeak was normalized after 4 h of recovery with CHO, whereas Wpeak remained depressed (P < 0.05) after water provision. Wpeak was fully recovered after 24 h in both the H2O and the CHO group. CONCLUSION In conclusion, the present results suggest that low muscle glycogen depresses muscle SR Ca release rate, which may contribute to fatigue and delayed recovery of Wpeak 4 h postexercise.

Plasticity in mitochondrial cristae density allows metabolic capacity modulation in human skeletal muscle

In human skeletal muscles, the current view is that the capacity for mitochondrial energy production, and thus endurance capacity, is set by the mitochondria volume. However, increasing the mitochondrial inner membrane surface comprises an alternative mechanism for increasing the energy production capacity. In the present study, we show that mitochondrial inner membranes in leg muscles of endurance‐trained athletes have an increased ratio of surface per mitochondrial volume. We show a positive correlation between this ratio and whole body oxygen uptake and muscle fibre mitochondrial content. The results obtained in the present study help us to understand modulation of mitochondrial function, as well as how mitochondria can increase their oxidative capacity with increased demand.

Mechanical Muscle Function and Lean Body Mass During Supervised Strength Training and Testosterone Therapy in Aging Men with Low-Normal Testosterone Levels

To examine the effect of strength training and testosterone therapy on mechanical muscle function and lean body mass (LBM) in aging men with low‐normal testosterone levels in a randomized, double‐blind, placebo‐controlled 24‐week study.

Carbohydrate restricted recovery from long term endurance exercise does not affect gene responses involved in mitochondrial biogenesis in highly trained athletes

The aim was to determine if the metabolic adaptations, particularly PGC‐1α and downstream metabolic genes were affected by restricting CHO following an endurance exercise bout in trained endurance athletes. A second aim was to compare baseline expression level of these genes to untrained. Elite endurance athletes (VO2max 66 ± 2 mL·kg−1·min−1, n = 15) completed 4 h cycling at ~56% VO2max. During the first 4 h recovery subjects were provided with either CHO or only H2O and thereafter both groups received CHO. Muscle biopsies were collected before, after, and 4 and 24 h after exercise. Also, resting biopsies were collected from untrained subjects (n = 8). Exercise decreased glycogen by 67.7 ± 4.0% (from 699 ± 26.1 to 239 ± 29.5 mmol·kg−1·dw−1) with no difference between groups. Whereas 4 h of recovery with CHO partly replenished glycogen, the H2O group remained at post exercise level; nevertheless, the gene expression was not different between groups. Glycogen and most gene expression levels returned to baseline by 24 h in both CHO and H2O. Baseline mRNA expression of NRF‐1, COX‐IV, GLUT4 and PPAR‐α gene targets were higher in trained compared to untrained. Additionally, the proportion of type I muscle fibers positively correlated with baseline mRNA for PGC‐1α, TFAM, NRF‐1, COX‐IV, PPAR‐α, and GLUT4 for both trained and untrained. CHO restriction during recovery from glycogen depleting exercise does not improve the mRNA response of markers of mitochondrial biogenesis. Further, baseline gene expression of key metabolic pathways is higher in trained than untrained.

Repeated high-intensity exercise modulates Ca(2+) sensitivity of human skeletal muscle fibers

The effects of short‐term high‐intensity exercise on single fiber contractile function in humans are unknown. Therefore, the purposes of this study were: (a) to access the acute effects of repeated high‐intensity exercise on human single muscle fiber contractile function; and (b) to examine whether contractile function was affected by alterations in the redox balance. Eleven elite cross‐country skiers performed four maximal bouts of 1300 m treadmill skiing with 45 min recovery. Contractile function of chemically skinned single fibers from triceps brachii was examined before the first and following the fourth sprint with respect to Ca2+ sensitivity and maximal Ca2+‐activated force. To investigate the oxidative effects of exercise on single fiber contractile function, a subset of fibers was incubated with dithiothreitol (DTT) before analysis. Ca2+ sensitivity was enhanced by exercise in both MHC I (17%, P < 0.05) and MHC II (15%, P < 0.05) fibers. This potentiation was not present after incubation of fibers with DTT. Specific force of both MHC I and MHC II fibers was unaffected by exercise. In conclusion, repeated high‐intensity exercise increased Ca2+ sensitivity in both MHC I and MHC II fibers. This effect was not observed in a reducing environment indicative of an exercise‐induced oxidation of the human contractile apparatus.

Transient impairments in single muscle fibre contractile function after prolonged cycling in elite endurance athletes

Prolonged muscle activity impairs whole‐muscle performance and function. However, little is known about the effects of prolonged muscle activity on the contractile function of human single muscle fibres. The purpose of this study was to investigate the effects of prolonged exercise and subsequent recovery on the contractile function of single muscle fibres obtained from elite athletes.

Local depletion of glycogen with supra-maximal exercise in human skeletal muscle fibres

Glycogen is stored in local spatially distinct compartments within skeletal muscle fibres and is the main energy source during supramaximal exercise. Using quantitative electron microscopy, we show that supramaximal exercise induces a differential depletion of glycogen from these compartments and also demonstrate how this varies with fibre types. Repeated exercise alters this compartmentalized glycogen depletion. The results obtained in the present study help us understand the muscle metabolic dynamics of whole body repeated supramaximal exercise, and suggest that the muscle has a compartmentalized local adaptation to repeated exercise, which affects glycogen depletion.

No superior adaptations to carbohydrate periodization in elite endurance athletes

Purpose The present study investigated the effects of periodic carbohydrate (CHO) restriction on endurance performance and metabolic markers in elite endurance athletes. Methods Twenty-six male elite endurance athletes (maximal oxygen consumption (V˙O2max), 65.0 mL O2·kg−1·min−1) completed 4 wk of regular endurance training while being matched and randomized into two groups training with (low) or without (high) CHO manipulation 3 d·wk−1. The CHO manipulation days consisted of a 1-h high-intensity bike session in the morning, recovery for 7 h while consuming isocaloric diets containing either high CHO (414 ± 2.4 g) or low CHO (79.5 ± 1.0 g), and a 2-h moderate bike session in the afternoon with or without CHO. V˙O2max, maximal fat oxidation, and power output during a 30-min time trial (TT) were determined before and after the training period. The TT was undertaken after 90 min of intermittent exercise with CHO provision before the training period and both CHO and placebo after the training period. Muscle biopsies were analyzed for glycogen, citrate synthase (CS) and &bgr;-hydroxyacyl-coenzyme A dehydrogenase (HAD) activity, carnitine palmitoyltransferase (CPT1b), and phosphorylated acetyl-CoA carboxylase (pACC). Results The training effects were similar in both groups for all parameters. On average, V˙O2max and power output during the 30-min TT increased by 5% ± 1% (P < 0.05) and TT performance was similar after CHO and placebo during the preload phase. Training promoted overall increases in glycogen content (18% ± 5%), CS activity (11% ± 5%), and pACC (38% ± 19%; P < 0.05) with no differences between groups. HAD activity and CPT1b protein content remained unchanged. Conclusions Superimposing periodic CHO restriction to 4 wk of regular endurance training had no superior effects on performance and muscle adaptations in elite endurance athletes.

Reliability of maximal mitochondrial oxidative phosphorylation in permeabilized fibers from the vastus lateralis employing high‐resolution respirometry

The purpose was to assess the impact of various factors on methodological errors associated with measurement of maximal oxidative phosphorylation (OXPHOS) in human skeletal muscle determined by high‐resolution respirometry in saponin‐permeabilized fibers. Biopsies were collected from 25 men to assess differences in OXPHOS between two muscle bundles and to assess the correlation between OXPHOS and the wet weight of the muscle bundle. Biopsies from left and right thighs of another five subjects were collected on two occasions to compare limbs and time‐points. A single muscle specimen was used to assess effects of the anesthetic carbocaine and the influence of technician. The difference in OXPHOS between two fiber‐bundles from the same biopsy exhibited a standard error of measurement (SEM) of 10.5 pmol · s−1 · mg−1 and a coefficient of variation (CV) of 15.2%. The differences between left and right thighs and between two different time‐points had SEMs of 9.4 and 15.2 pmol · s−1 · mg−1 and CVs of 23.9% and 33.1%, respectively. The average (±SD) values obtained by two technicians monitoring different bundles of fibers from the same biopsy were 31.3 ± 7.1 and 26.3 ± 8.1 pmol · s−1 · mg−1. The time that elapsed after collection of the biopsy (up to a least 5 h in preservation medium), wet weight of the bundle (from 0.5 to 4.5 mg) and presence of an anesthetic did not influence OXPHOS. The major source of variation in OXPHOS measurements is the sample preparation. The thigh involved, time‐point of collection, size of fiber bundles, and time that elapsed after biopsy had minor or no effect.

Changes in metabolism but not myocellular signaling by training with CHO‐restriction in endurance athletes

Carbohydrate (CHO) restricted training has been shown to increase the acute training response, whereas less is known about the acute effects after repeated CHO restricted training. On two occasions, the acute responses to CHO restriction were examined in endurance athletes. Study 1 examined cellular signaling and metabolic responses after seven training‐days including CHO manipulation (n = 16). The protocol consisted of 1 h high‐intensity cycling, followed by 7 h recovery, and 2 h of moderate‐intensity exercise (120SS). Athletes were randomly assigned to low (LCHO: 80 g) or high (HCHO: 415 g) CHO during recovery and the 120SS. Study 2 examined unaccustomed exposure to the same training protocol (n = 12). In Study 1, muscle biopsies were obtained at rest and 1 h after 120SS, and blood samples drawn during the 120SS. In Study 2, substrate oxidation and plasma glucagon were determined. In Study 1, plasma insulin and proinsulin C‐peptide were higher during the 120SS in HCHO compared to LCHO (insulin: 0 min: +37%; 60 min: +135%; 120 min: +357%, P = 0.05; proinsulin C‐peptide: 0 min: +32%; 60 min: +52%; 120 min: +79%, P = 0.02), whereas plasma cholesterol was higher in LCHO (+15–17%, P = 0.03). Myocellular signaling did not differ between groups. p‐AMPK and p‐ACC were increased after 120SS (+35%, P = 0.03; +59%, P = 0.0004, respectively), with no alterations in p‐p38, p‐53, or p‐CREB. In Study 2, glucagon and fat oxidation were higher in LCHO compared to HCHO during the 120SS (+26–40%, P = 0.03; +44‐76%, P = 0.01 respectively). In conclusion, the clear respiratory and hematological effects of CHO restricted training were not translated into superior myocellular signaling after accustomization to CHO restriction.