[/quote]
Om man ska gå upp i vikt och bygga muskler så ska man äta ofta, men inte så mycket. En bodybuilder äter 6-8 gånger per dag och dom äter inte så mycket varje gång.[/quote]
De va typ så jag menade, äta mer mat och ofta men en bodybuilder äter ju ofta men mycket när dom bulkar, men dom äter ofta vi deff med men dom tar bort kalorier från dieten.
Tycker de är rätt kul att ni väldigt duktig på och dra alla över en kam...
Angående dieter och hur olika tränande personer äter så är väl DEA den med mest rätt.
Det finns flera olika sätt tränande individer äter på, de beror på vilka mål personen har, hur dom har möjlighet och äta, hur stora dom är, osv osv.
För och rätta er lite, om du vill bygga muskler eller massa överhuvud taget då äter du mycket överlag. Du blir INTE starkare eller större bara för att du sprider ut dina 3000 kcal över 8 måltider istället för 3.
Man kan förklara de enkelt så att kcal=energi. Kroppen gör av med en viss mängd energi per dag. Så länge du får i dig mer energi än vad kroppen "kan" bränna så går du upp i vikt. De som spelar roll vilken sorts vikt du lägger på dig det beror på vart din energi kommer ifrån.
Även det med att byggare som går på diet inför t.ex. en tävling drar ner på kcal är inte helt sant. Det finns flera personer som inte drar ner på kcal, men där emot ökar sitt energi behov, och på så vis gör så att kroppen har en högre energiförbrukning än den får i sig. Då minskar man i vikt.
En fråga till er andra nu då. Mr.O, vad tyckte ni om årets tävling? Va den som förväntat? Blev resultatet så som ni trodde osv. Diskutera!
Snabba svar mrandersson. Ska gå ner i vikt nu 7kg (till att börja med). Vill få en mer rippad kropp, har musklerna och fettet. Tränar måndag, tisdag, torsdag, fredag. Sen ska jag börja med att köra powerwalk 2ggr i veckan. (Som med tiden övergår i joggning osv.)
Hur ska jag träna och äta?
Mr. O gick inte som jag trott. Höll stenhårt på Kai ! Dock är topp 3 exakt dom jag trott. Hoppades stoinhaurt på kai, tycker han har överlägset bäst rygg och ben. Det han fallerade på var ju dock hur hans "bål" ser ut, inte lika symmetrisk och fin som de andras ( gener ).
Phil har dock snyggast muskelinfästning osv och ser överlag bäst ut, så han var väl värdig vinnare. KAI VAR DOCK STÖRRE. :##:#:#: Nästa år!
Axel skrev:Mr. O gick inte som jag trott. Höll stenhårt på Kai ! Dock är topp 3 exakt dom jag trott. Hoppades stoinhaurt på kai, tycker han har överlägset bäst rygg och ben. Det han fallerade på var ju dock hur hans "bål" ser ut, inte lika symmetrisk och fin som de andras ( gener ).
Phil har dock snyggast muskelinfästning osv och ser överlag bäst ut, så han var väl värdig vinnare. KAI VAR DOCK STÖRRE. :##:#:#: Nästa år!
Tycker sådanna tävlingar är skit, dom trycker in steroider och olja i kroppen för att se större ut. Domarna dömer även efter genetik så det gäller att ha tur, men självklart också hård träning och kost.
Tycker tävlingar som strongman etc är roligare för då handlar det verkligen om styrka och det är vell egentligen det muskler är till för?
Men när det kommer till Mr. O så tycker jag att det var bra gjort av phil, han såg riktigt bra ut.
Ska dock bli intressan att få se micke hancic på scen nästa år i Mr. O
Axel skrev:Mr. O gick inte som jag trott. Höll stenhårt på Kai ! Dock är topp 3 exakt dom jag trott. Hoppades stoinhaurt på kai, tycker han har överlägset bäst rygg och ben. Det han fallerade på var ju dock hur hans "bål" ser ut, inte lika symmetrisk och fin som de andras ( gener ).
Phil har dock snyggast muskelinfästning osv och ser överlag bäst ut, så han var väl värdig vinnare. KAI VAR DOCK STÖRRE. :##:#:#: Nästa år!
Phils symmetri är galen! Såg även hårdare ut än Kai om jag ska va ärlig! Även Cutler var ju en riktig besvikelse tyvärr, trodde han skulle prestera bättre.. Men Phil förtjäna första platsen!
Blir de ett bra år för Kai kan de dock bli annorlunda nästa tävling
DEA!! skrev:Snabba svar mrandersson. Ska gå ner i vikt nu 7kg (till att börja med). Vill få en mer rippad kropp, har musklerna och fettet. Tränar måndag, tisdag, torsdag, fredag. Sen ska jag börja med att köra powerwalk 2ggr i veckan. (Som med tiden övergår i joggning osv.)
Hur ska jag träna och äta?
'
Hur ligger du till med vikten nu? Ökar du eller ligger du ungefär på samma vikt vecka in och vecka ut?
Axel skrev:Mr. O gick inte som jag trott. Höll stenhårt på Kai ! Dock är topp 3 exakt dom jag trott. Hoppades stoinhaurt på kai, tycker han har överlägset bäst rygg och ben. Det han fallerade på var ju dock hur hans "bål" ser ut, inte lika symmetrisk och fin som de andras ( gener ).
Phil har dock snyggast muskelinfästning osv och ser överlag bäst ut, så han var väl värdig vinnare. KAI VAR DOCK STÖRRE. :##:#:#: Nästa år!
Phils symmetri är galen! Såg även hårdare ut än Kai om jag ska va ärlig! Även Cutler var ju en riktig besvikelse tyvärr, trodde han skulle prestera bättre.. Men Phil förtjäna första platsen!
Blir de ett bra år för Kai kan de dock bli annorlunda nästa tävling
DEA!! skrev:Snabba svar mrandersson. Ska gå ner i vikt nu 7kg (till att börja med). Vill få en mer rippad kropp, har musklerna och fettet. Tränar måndag, tisdag, torsdag, fredag. Sen ska jag börja med att köra powerwalk 2ggr i veckan. (Som med tiden övergår i joggning osv.)
Hur ska jag träna och äta?
'
Hur ligger du till med vikten nu? Ökar du eller ligger du ungefär på samma vikt vecka in och vecka ut?
Förmodligen vätska eller lite hur mycket kolhydrater du laddat med.
Mitt tips är, ät som vanligt ev. dra ner lite på kolhydraterna. 40-50g mindre/dag. Sedan lägga in 20 min lågintensiv cardio innan gympassen.
När du sedan märker att vikten börjar stå stilla igen då lägger du till 20 lågintensiv cardio efter gympassen.
När du gjort detta borde du gått ner mellan 4-6kg. Om du vill ner de sista kilona då så kan du ev. dra ner ytligare på kolhydraterna 40-50g till. ELLER så kan du köra 20 min lågintensiv cardio innan gymmet och 20 min högintensiv efter.
Som låg intensiv cardio tänker jag en lugnare powerwalk, eller lite cykling. T.ex. till gymmet eller så.
Medans högintensivt tänker jag mer kettelballs, löpning, muskelups osv.
Men börja med och dra ner LITE på kolhydraterna, och lägga in cardio innan gymmet.
Håll sedan koll på progressionen varje dag, försök väga dig samma tidpunkt också. Rekommenderar på morgonen efter dagens första toabesök
Något du inte förstår eller undrar över skriv bara!
Antar också att de är en självklarhet att du ska undvika alkohol, sötsaker osv. under denna perioden. (Så gott de går...!)
Räkna med att de tar 6-8 veckor ungefär!
Märker du att du minskar snabbt eller mycket i styrka under perioden då äter du lite mer kolhydrater. Du ska se till och förlora så lite muskelmassa och styrka som möjligt.
Hellre att de tar 2 veckor längre tid och du har mer muskelmassa kvar efteråt, än tvärtom. Enligt mig då!
DEA!! skrev:Okej hur ska man träna? Alltså rep osv?
Du tränar på som vanligt, (antar att du tar ut dig på alla pass). Annars så ökar du intensiteten lite. Inte för mycket dock, du vill inte bränna för mycket. Det är den extra cardion som ska få dig och minska, och det sakta! 0,3-0,5kg i veckan skulle jag säga är en bra riktpunkt!
Men, vad jag hört om detta som ni diskuterar, så ska cardio EFTER passet vara rätt dåligt då man är i en sån metabolisk fas. Alltså så kommer man börja förbränna muskler typ?
Gyllene reglen är ju att inte träna intensiv styrka mer än 1.5h i sträck utan vila och kost, då man förbränner musklerna.
Men att köra cardio före är skitbra, uppvärmning + förbränning!
Personligen hade jag nog dock lagt cardio på en annan dag eller också på morgonar ( inte för att jag har tid till det )
Som du kan läsa så säger jag dock att han ska börja med cardio innan, sedan efter när resultaten minskar. Jag säger även, lågintensiv cardio, t.ex. en lugn powerwalk. Dock så är cykling bättre än löpning.
Säger även att han ska lyssna på kroppen och se hur de känns med styrkan också. Det är ju inte heller så att om du tränar 89 minuter så mår kroppen bra. Men kör du 91 minuter så bryts den ner.
Du lyssnar på kroppen och ser hur de känns helt enkelt.
Högintensiv cardio innan gymmet är enligt mig idiotiskt. Du förbränner dina energireserver i kroppen och kroppen blir "trött" redan innan du börjar lyfta. Vilken kan resultera i att du är väldigt olika stark varje pass. Även skaderisken ökar något markant.
Lite mer om de jag skriver kan ni läsa i spoilern.
[spoiler]Concurrent Strength and Endurance Training: From Molecules to Man. Medicine & Science in Sports & Exercise.
Concurrent Strength and Endurance Training: From Molecules to Man. Medicine & Science in Sports & Exercise. 38(11):1965-1970, November 2006.
Adaptations to exercise are highly dependent on the specific type of training performed (4,20,26,35). Endurance training, which represents one extreme of physical activity, generally encompasses exercise durations of several minutes up to several hours at various exercise intensities, increasing the capacity to sustain repetitive high-intensity, low-resistance exercise such as cycling, running, and swimming. This increased ability to perform is mainly accomplished through an increase in maximal oxygen uptake (VO2max) and an increased ability of skeletal muscle to generate energy via oxidative metabolism without improvements in muscle strength (4,20). Strength training, which represents the other extreme of physical activity, encompasses short-duration activity at high or maximal exercise intensities, increases the capacity to perform high-intensity, high-resistance exercise of a single or relatively few repetitions such as Olympic weightlifting, powerlifting, and throwing events in track and field. Improved strength-related performance is accomplished through neuromuscular learning and increased fiber-recruitment synchronicity, muscle cell hypertrophy, and, possibly, hyperplasia without changes in VO2max or in the capacity to generate ATP via oxidative metabolism (26,27,31). Given such contrasting modes of exercise, and the fact that a large number of sports activities such as sprint running (middle distance), rugby, football, swimming, and the decathlon (among many others) seem to require combinations of both components of strength and endurance training for peak performance, a hypothetical model of a strength-endurance continuum (SEC) can be defined to illustrate the range of strength, endurance, and metabolic combinations that training should stress for improved performance. As a consequence, training for many of these sports will likely encounter some logistical problems and some possible biological limitations during the course of performance development.
The strength-endurance continuum (SEC) is depicted in the context of sports performance and its relation to duration and energy metabolism. From a muscle-energy and training-specificity standpoint, exercise activities of several seconds up to 1 min generally use immediate sources of energy such as ATP, creatine phosphate, and glycolysis and require maximal power and strength. Exercise durations of several minutes in length generally use glycolysis, glucose oxidation, and some fatty-acid oxidation that require near-maximal or maximal O2 uptake with varying degrees of strength. Long-term exercise from approximately 20-30 min up to several hours in duration use primarily aerobic glycolysis and fatty-acid oxidation at submaximal work rates as close to VO2max as possible, and seem to require a small amount of strength. Although training for sports at the ends of the SEC seems relatively straightforward, a more complicated scenario emerges when designing training programs for those sports requiring combinations of strength and endurance and a mixture of fuel-generating sources.
In view of the divergent adaptations induced by strength- and endurance-training regimes and the potential limitations observed when both forms of exercise are performed simultaneously, the main goal of the present review is to briefly describe, based on the existing evidence, whether simultaneously training for strength and endurance results in enhanced or diminished performances that occur when either type of training is performed alone. A second goal is to outline potential physiological, biochemical, and molecular mechanisms associated with the responses of skeletal muscle to different forms of exercise that may contribute to the interference of strength development during concurrent training.
The goal of the initial study describing the phenomenon of concurrent training was to determine how individuals would adapt to a combination of strenuous heavy-resistance strength and high-intensity endurance training compared with the adaptations produced by either the same strength- or endurance-training regimes separately. This study was published by Robert C. Hickson in 1980 (19) and (intellectually) originated during his postdoctoral studies with Dr. John Holloszy after a running program had been added to his ongoing strength-training regime (Robert C. Hickson, personal communication, 1997).
The following considerations were taken into account in the experimental design: a) both types of training would involve the same muscle groups; b) the response to the endurance and strength programs would not overlap, that is, there would be no increase in strength with endurance training and there would be no increase in VO2max with strength training; and c) the magnitude of change in the criteria variables (VO2max and strength) would be large enough to detect any divergent responses by the groups. There were three exercise groups: a strength group (S) that exercised 30 min·d-1, 5 d·wk-1 for 10 wk; an endurance group (E) that exercised 40 min·d-1, 6 d·wk-1 for 10 wk; and a S & E group that performed the same daily exercise regimens as the S group and the E groups combined. For the strength-training programs, all exercises were performed with as much weight as possible. As strength increased, additional weight was continually adjusted throughout training to maintain maximal resistance for the required repetitions. Similarly, for the endurance-training programs, as the subjects' power output increased during training, the cycling work rate also was increased as needed to approach VO2max. The running program consisted of continuous running as fast as possible for 30 min·d-1 during the first week, 35 min·d-1 during the second week, and 40 min·d-1 thereafter. In the present study, VO2max was used as the major criterion variable to establish an endurance-training effect. VO2max, when measured during cycling or treadmill running and expressed in absolute (L·min-1) or relative terms (mL·kg-1·min-1), increased to the same extent (20-25%) in the E group and in the S & E group. VO2max increased slightly (4%) in the S group during cycling; otherwise, strength training did not result in any other significant changes in VO2max when expressed in either absolute or relative values. As expected, endurance training did not significantly increase strength. Strength training produced increases in strength such that on a weekly basis it was possible to note significant improvement in the parallel squat throughout the 10-wk training program. In contrast, heavy resistance training combined with a program of endurance training produced significant improvement in strength during the first 6-7 wk, followed by a leveling-off period, and then, surprisingly, strength decreased during the last 2 wk of the training program. These results provide the first evidence suggesting that at the upper limits of strength development, endurance training inhibits or interferes with further increases in strength. These results also suggest that there is little relationship between the acquisition of strength and the rate of increase in aerobic power.
Additional studies have confirmed the finding that concurrent training interferes with the development of strength. For example, Dudley and Djamil (13) studied the combination of high-intensity interval cycling endurance training and high-velocity isokinetic strength training. In this study, cycling VO2max increased to the same extent (~18%) in both the E and S & E groups when measured several times over the 7-wk period, but strength improvements were different between S and S & E groups. The S group had increases in maximal torque at 0.00-4.19 rad·s-1, whereas the S & E group had a significant improvement only at 0.00, 0.24, and 1.68 rad·s-1, suggesting that, in this case, the interference in strength development occurred at high but not low velocity rates of force production. Further evidence demonstrating the interference of strength development by concurrent training was provided by Kraemer et al. (22), who found that combining strength and endurance training affected strength training-induced increases in fiber cross-sectional areas. Such observation suggests that the interference of strength development can also occur at the cellular level. In addition, these authors also found that concurrent training compromised strength development only when both modes of exercise engaged the same muscle group, again suggesting a local effect rather than a systemic one.
Other investigations have reported no inhibition of strength development by concurrent strength and endurance training. For example, Sale et al. (32) trained two groups, one leg in one group completed a strength program and the other leg a strength endurance program. In the second group, one leg was endurance trained and the other endurance and strength trained. Endurance training consisted of five 3-min bouts of cycling at work rates requiring 90-100% VO2max, whereas strength training consisted of six sets of 15-22 repetitions on the leg press at maximal resistance for a total of 22 wk. All types of training produced similar responses, including increased strength, VO2max, and vastus lateralis muscle citrate synthase activity. In view of the similarity of responses to these regimens, it is understandable that no inhibition of strength was observed by the combination of training, because the training regimes seem to have been more synergistic rather than antagonistic.
After these initial studies, a number of other investigations either favored or disagreed with the interference of strength development during concurrent training. Many such discrepancies among studies of concurrent training stem from a number of logistical issues. Based on the evidence provided so far, the interference effect seems to hold true in specific situations. Some of the different results were postulated to be related to dependent-variable selection (outcome measures), modality of training programs, characteristics of the subjects (age, sex, training status), and duration of the study (24). Moreover, such differences make comparisons across the different studies difficult, which complicates the understanding of the adaptations to concurrent training.
Over the years, several mechanisms have been proposed as limiting factors for optimal skeletal muscle adaptation, and have been identified as "responsible" for or contributing to the inhibition of strength development during concurrent training. These include neural components, fuel substrate availability, fiber-type transformation, overtraining, and alterations in protein synthesis (24).
Neural component. TOP
Dudley and Djamil (13) and Chromiak and Mulvaney (8) have discussed the possibility that neural factors and motor unit recruitment may have a significant role in restricting strength development with strength and endurance training. However, no specific factors have yet been isolated to strongly support this mechanism, with the exception of a study by Hakkinen et al. (15), in which the effects of concurrent training on rates of force development were postulated to have been a consequence of neural and muscle components, because this type of training attenuated the development of explosive strength by limiting rapid voluntary neural activation.
Successive bouts of either strength or endurance exercise may produce chronically low muscle-glycogen levels, which could retard or impair subsequent performances. Repeated endurance training on consecutive days can reduce resting muscle glycogen levels in muscle (9), and glycogen depletion has been shown to occur after resistance exercise (35). A possible implication of low glycogen levels on concurrent training-induced muscle adaptation is highlighted by the findings of Creer et al. (10), who recently reported that low muscle-glycogen levels impaired the intracellular signaling responses to an acute bout of resistance exercise. Therefore, carrying out a training program that entitles daily or even twice-daily sessions may impair the responses to, and recovery from, exercise and/or performance during the execution of subsequent training sessions, thereby reducing the magnitude of the strength-training adaptations.
Changes in muscle-fiber composition, particularly as a function of isomyosin alterations, have been considered previously as a possible mechanism of endurance training-associated inhibition of strength development (8,14). Skeletal muscle hypertrophy after strength training occurs to a greater extent in fast-twitch than in slow-twitch fibers (16,34). Intense endurance training has been observed to reduce the maximal shortening speed of type II or fast-twitch fibers and to change skeletal muscle-fiber population as measured by changes in myosin ATPase (25,33), which suggests that a reduction in the relative number of type II fibers by endurance training could play a major role in limiting strength development during concurrent training.
Overtraining. TOP
Two previous reviews (8,14) of concurrent strength and endurance training have considered the term "overtraining" to account for the inability to attain optimal strength gains when strength and endurance training are performed. Overtraining remains a rather poorly defined term despite recent efforts by exercise physiologists to identify its origins. Overtraining is an imbalance between training and recovery (23). In general, it is characterized by a decline in performance or by a lack of improvement. In the first strength- and endurance-training study, strength declined in the 9th and 10th weeks of concurrent training (19). Because the subjects were training 80 min·d-1, an argument could be made that the marked impairment of strength development by the S & E groups was the result of the development of residual fatigue. Yet, this may not have been the case. Endurance work per week performed on the bicycle ergometer increased at approximately the same rate in the E and S & E groups, particularly during the 9th and 10th weeks of training, at a time when strength gains in the S & E group were dramatically decreasing. Thus, the S & E effects on strength development seem to be selective for the strength-training response. Furthermore, the studies of Dudley and Djamil (13) and Hickson (19) as well as other concurrent training studies encompassed somewhat different endurance- and strength-training protocols (intensity, duration, frequency, type of training), including the sequence of days when either one or both types of training were performed. Based on these differences, it is difficult to uniquely identify the factor(s) leading to the inhibition of strength by overtraining during both types of training.
Protein turnover.
Acute endurance exercise bouts have generally been found to reduce total protein-synthesis rates of mixed skeletal muscles during the exercise. This depression is transient and can lead to a temporary decrease in protein synthesis within several hours after exercise (5,12,29). Overlapping endurance exercise bouts with resistance exercise may result in impaired adaptive responses in protein synthesis and, therefore, a decrease in strength-related performance, in part, due to the suboptimal or lack of increase in muscle-fiber cross-sectional areas (22). When performed several times a week, such combination training may be sufficient to disrupt the protein-synthesis mechanisms involved with the normal adaptation to the individual bouts of strength exercise, thus altering the long-term adaptations to training and resulting in impaired muscle-dependent strength gains. Another possibility, although hypothetical, is that the adaptive protein synthesis resulting from either form of exercise may create some sort of cellular incompatibility in which the muscle cell needs to decide whether to grow or manage the synthesis of its metabolic machinery.
We are now at a stage in which technologies from fields such as biochemistry and molecular biology can allow exercise scientists to explore the biology of exercise-induced skeletal muscle adaptation in more mechanistic terms. Studies on protein phosphorylation of intracellular signaling molecules have begun to reveal specific cellular regulatory processes induced by different forms of exercise. For example, acute resistance exercise, which, over time, can result in muscle hypertrophy, induces the activation of a growth-associated signaling network. Experiments in humans and rodents demonstrated that a single bout of resistance exercise results in an increased activity of the phosphoinositide-3-dependent kinase (PI3k) (18), protein kinase B (PKB) (28), the mammalian target of Rapamycin (mTOR) (3), and the ribosomal protein S6 kinase 1 (S6k1) (1,21,28). Activation of such a signaling network by acute resistance exercise modulates muscle-protein synthesis both in animals and humans (18,11). Activation of PI3-k leads to an increase in PKB and mTOR activity and subsequent inhibition (phosphorylation) of the cap-binding protein 4E-BP1 (3,18), which, in turn, inhibits cap-dependent mRNA translation and, hence, protein synthesis via sequestration of the eukaryotic initiation factor 4E (eIF4E). An increase in eIF4E activity will result in increased muscle-protein synthesis rates. Endurance exercise, on the other hand, is associated with signaling mechanisms related to metabolic adaptations, such as the activation of the AMP-activated protein kinase (AMPK) signaling. One of AMPK's main functions is to monitor the energy status of the cell; therefore, the processes regulated by AMPK seem to be related to the maintenance of energy homeostasis (17,37). AMPK activity is modulated mainly by changes in the levels of energy phosphates and by a decrease in the energy charge of the muscle cell, that is, an increase in ADP/ATP ratio. Such fluctuations in metabolic regulation as it occurs during exercise (38,39) can also cause changes in gene expression and substrate content via AMPK signaling (17,37).
Interestingly, recent studies have shown antagonistic activities between the anabolic signaling mechanisms induced by the PI3k/mTOR/PKB/S6k1/4E-BP1 network and the energy-modulating signaling by AMPK. More precisely, activation of AMPK signaling by a pharmacologic agonist reduces skeletal muscle-protein synthesis by inhibiting mTOR signaling, presumably via activation of the tuberous sclerosis complex (TSC). Bolster et al. (2) have found that an injection of the AMPK analog AICAR (5-aminoimidazole-4-carboxamide 1-beta-d-ribonucleoside) had no effect on a1 AMPK activity, but it did increase a2 AMPK activity by ~50%. AMPK activation by AICAR treatment was correlated with a 45% decrease in protein synthesis and was associated with a decreased activation of the PKB/mTOR/S6K1 pathway. This was also associated with a reduced inhibition of the eIF4E-binding protein (4E-BP1) and a reduction in eIF4E associated with eIF4G. As previously mentioned, one potent stimulus for the increase in AMPK activity is an increase in ADP/ATP ratio; this mechanism may help explain previous observations by Bylund -Fellenius et al. (7), who demonstrated that contractile activity resulted in an increase in ADP/ATP ratio, which, in turn, was correlated with a fall in muscle-protein synthesis rates. These findings indicate that the decrease in protein synthesis commonly seen during contractile activity could be mediated in part by an increase AMPK activity and a concomitant decrease in the anabolic response downstream of mTOR signaling. Indeed, Thomson and Gordon (36) have recently made the interesting observation in aged animals that muscle mass was negatively correlated with AMPK activity, once again implicating this kinase in the negative modulation of skeletal muscle mass.
Another potential mechanism for the inhibition of protein synthesis during muscular activity may be at the elongation step (6). In a recent study, Rose et al. (30) detected a rapid increase in eukaryotic elongation factor 2 (eEF2) phosphorylation during cycling exercise. In this study, subjects exercised at approximately 67% VO2max, and muscle biopsies were obtained at rest and after 1, 10, 30, 60, and 90 min of exercise. Exercise caused a rapid (within 1 min) increase (five- to sevenfold) in eEF2 phosphorylation that persisted during the entire exercise period. Surprisingly, a rather small decrease in eEF2 kinase (eEF2k) activity was detected, suggesting that even with a minor decrease in eEF2k activity, the remaining activated kinase may have been sufficient to inhibit and, therefore, phosphorylate eEF2, causing a decrease in protein synthesis. The mechanisms by which eEF2k activation by exercise seems to occur in a calcium-dependent fashion, because eEF2k from exercised muscle was potently activated by calcium-dependent calmodulin (Ca2+CaM) in vitro. This suggests that the higher eEF2 phosphorylation in working skeletal muscle may be mediated by an allosteric activation of eEF2 kinase by Ca2+CaM.
Although hypothetical, it is reasonable to assume that activation of AMPK and inhibition of the eEF2 by endurance exercise and/or too-frequent exercise sessions will impinge on the responses to resistance exercise by affecting training-induced increases in adaptive protein synthesis, because activation/inhibition of these signaling proteins independently or collectively can alter the induction of an anabolic response. The obvious consequence of such antagonism will be a negative impact on long-term strength-training adaptations, perhaps by ameliorating the hypertrophic response. Therefore, this may be one mechanism responsible for the observed detrimental effects of concurrent strength and endurance training on strength development (Fig. 3).
A working model of the intracellular signaling networks mediating exercise-induced skeletal muscle adaptations. Resistance exercise is capable of inducing an increase in the activity of a network comprising PI3k/PKB/mTOR/S6K1/S6/4E-BP1 signaling to modulate protein-synthesis rates and muscle growth. Endurance exercise is associated with signaling involved in metabolic homeostasis, comprising AMPK signaling, among others. Activation of AMPK by endurance exercise or contractile activity may inhibit mTOR signaling via TSC and suppress resistance exercise-induced muscle-protein synthesis. In addition, calcium fluxes resulting from prolonged contractile activity may inhibit protein synthesis in a Ca2+M-dependent manner by inhibiting peptide-chain elongation via activation of eEF2k and a subsequent increase in eEF2 phosphorylation. AMPK may also inhibit protein synthesis by activating eEF2k.
In summary, when strength and endurance training are performed simultaneously, a potential interference in strength development may occur. Such interference may be caused by alterations in the adaptive protein synthesis changes induced by endurance exercise or by too-frequent training sessions, in addition to several other unknown factors. Novel technologies are allowing us to understand the molecular mechanisms involved in exercise-induced skeletal muscle adaptations (e.g., genome-wide gene-expression analysis). This knowledge is not only improving the way we implement training programs for sports and rehabilitation, it is also important for the correct design of future studies in exercise training and skeletal muscle adaptation, particularly those involving the investigation of mechanisms of signal transduction and gene expression.
[/spoiler]
Som du kan läsa så säger jag dock att han ska börja med cardio innan, sedan efter när resultaten minskar. Jag säger även, lågintensiv cardio, t.ex. en lugn powerwalk. Dock så är cykling bättre än löpning.
Säger även att han ska lyssna på kroppen och se hur de känns med styrkan också. Det är ju inte heller så att om du tränar 89 minuter så mår kroppen bra. Men kör du 91 minuter så bryts den ner.
Du lyssnar på kroppen och ser hur de känns helt enkelt.
Högintensiv cardio innan gymmet är enligt mig idiotiskt. Du förbränner dina energireserver i kroppen och kroppen blir "trött" redan innan du börjar lyfta. Vilken kan resultera i att du är väldigt olika stark varje pass. Även skaderisken ökar något markant.
Lite mer om de jag skriver kan ni läsa i spoilern.
[spoiler]Concurrent Strength and Endurance Training: From Molecules to Man. Medicine & Science in Sports & Exercise.
Concurrent Strength and Endurance Training: From Molecules to Man. Medicine & Science in Sports & Exercise. 38(11):1965-1970, November 2006.
Adaptations to exercise are highly dependent on the specific type of training performed (4,20,26,35). Endurance training, which represents one extreme of physical activity, generally encompasses exercise durations of several minutes up to several hours at various exercise intensities, increasing the capacity to sustain repetitive high-intensity, low-resistance exercise such as cycling, running, and swimming. This increased ability to perform is mainly accomplished through an increase in maximal oxygen uptake (VO2max) and an increased ability of skeletal muscle to generate energy via oxidative metabolism without improvements in muscle strength (4,20). Strength training, which represents the other extreme of physical activity, encompasses short-duration activity at high or maximal exercise intensities, increases the capacity to perform high-intensity, high-resistance exercise of a single or relatively few repetitions such as Olympic weightlifting, powerlifting, and throwing events in track and field. Improved strength-related performance is accomplished through neuromuscular learning and increased fiber-recruitment synchronicity, muscle cell hypertrophy, and, possibly, hyperplasia without changes in VO2max or in the capacity to generate ATP via oxidative metabolism (26,27,31). Given such contrasting modes of exercise, and the fact that a large number of sports activities such as sprint running (middle distance), rugby, football, swimming, and the decathlon (among many others) seem to require combinations of both components of strength and endurance training for peak performance, a hypothetical model of a strength-endurance continuum (SEC) can be defined to illustrate the range of strength, endurance, and metabolic combinations that training should stress for improved performance. As a consequence, training for many of these sports will likely encounter some logistical problems and some possible biological limitations during the course of performance development.
The strength-endurance continuum (SEC) is depicted in the context of sports performance and its relation to duration and energy metabolism. From a muscle-energy and training-specificity standpoint, exercise activities of several seconds up to 1 min generally use immediate sources of energy such as ATP, creatine phosphate, and glycolysis and require maximal power and strength. Exercise durations of several minutes in length generally use glycolysis, glucose oxidation, and some fatty-acid oxidation that require near-maximal or maximal O2 uptake with varying degrees of strength. Long-term exercise from approximately 20-30 min up to several hours in duration use primarily aerobic glycolysis and fatty-acid oxidation at submaximal work rates as close to VO2max as possible, and seem to require a small amount of strength. Although training for sports at the ends of the SEC seems relatively straightforward, a more complicated scenario emerges when designing training programs for those sports requiring combinations of strength and endurance and a mixture of fuel-generating sources.
In view of the divergent adaptations induced by strength- and endurance-training regimes and the potential limitations observed when both forms of exercise are performed simultaneously, the main goal of the present review is to briefly describe, based on the existing evidence, whether simultaneously training for strength and endurance results in enhanced or diminished performances that occur when either type of training is performed alone. A second goal is to outline potential physiological, biochemical, and molecular mechanisms associated with the responses of skeletal muscle to different forms of exercise that may contribute to the interference of strength development during concurrent training.
The goal of the initial study describing the phenomenon of concurrent training was to determine how individuals would adapt to a combination of strenuous heavy-resistance strength and high-intensity endurance training compared with the adaptations produced by either the same strength- or endurance-training regimes separately. This study was published by Robert C. Hickson in 1980 (19) and (intellectually) originated during his postdoctoral studies with Dr. John Holloszy after a running program had been added to his ongoing strength-training regime (Robert C. Hickson, personal communication, 1997).
The following considerations were taken into account in the experimental design: a) both types of training would involve the same muscle groups; b) the response to the endurance and strength programs would not overlap, that is, there would be no increase in strength with endurance training and there would be no increase in VO2max with strength training; and c) the magnitude of change in the criteria variables (VO2max and strength) would be large enough to detect any divergent responses by the groups. There were three exercise groups: a strength group (S) that exercised 30 min·d-1, 5 d·wk-1 for 10 wk; an endurance group (E) that exercised 40 min·d-1, 6 d·wk-1 for 10 wk; and a S & E group that performed the same daily exercise regimens as the S group and the E groups combined. For the strength-training programs, all exercises were performed with as much weight as possible. As strength increased, additional weight was continually adjusted throughout training to maintain maximal resistance for the required repetitions. Similarly, for the endurance-training programs, as the subjects' power output increased during training, the cycling work rate also was increased as needed to approach VO2max. The running program consisted of continuous running as fast as possible for 30 min·d-1 during the first week, 35 min·d-1 during the second week, and 40 min·d-1 thereafter. In the present study, VO2max was used as the major criterion variable to establish an endurance-training effect. VO2max, when measured during cycling or treadmill running and expressed in absolute (L·min-1) or relative terms (mL·kg-1·min-1), increased to the same extent (20-25%) in the E group and in the S & E group. VO2max increased slightly (4%) in the S group during cycling; otherwise, strength training did not result in any other significant changes in VO2max when expressed in either absolute or relative values. As expected, endurance training did not significantly increase strength. Strength training produced increases in strength such that on a weekly basis it was possible to note significant improvement in the parallel squat throughout the 10-wk training program. In contrast, heavy resistance training combined with a program of endurance training produced significant improvement in strength during the first 6-7 wk, followed by a leveling-off period, and then, surprisingly, strength decreased during the last 2 wk of the training program. These results provide the first evidence suggesting that at the upper limits of strength development, endurance training inhibits or interferes with further increases in strength. These results also suggest that there is little relationship between the acquisition of strength and the rate of increase in aerobic power.
Additional studies have confirmed the finding that concurrent training interferes with the development of strength. For example, Dudley and Djamil (13) studied the combination of high-intensity interval cycling endurance training and high-velocity isokinetic strength training. In this study, cycling VO2max increased to the same extent (~18%) in both the E and S & E groups when measured several times over the 7-wk period, but strength improvements were different between S and S & E groups. The S group had increases in maximal torque at 0.00-4.19 rad·s-1, whereas the S & E group had a significant improvement only at 0.00, 0.24, and 1.68 rad·s-1, suggesting that, in this case, the interference in strength development occurred at high but not low velocity rates of force production. Further evidence demonstrating the interference of strength development by concurrent training was provided by Kraemer et al. (22), who found that combining strength and endurance training affected strength training-induced increases in fiber cross-sectional areas. Such observation suggests that the interference of strength development can also occur at the cellular level. In addition, these authors also found that concurrent training compromised strength development only when both modes of exercise engaged the same muscle group, again suggesting a local effect rather than a systemic one.
Other investigations have reported no inhibition of strength development by concurrent strength and endurance training. For example, Sale et al. (32) trained two groups, one leg in one group completed a strength program and the other leg a strength endurance program. In the second group, one leg was endurance trained and the other endurance and strength trained. Endurance training consisted of five 3-min bouts of cycling at work rates requiring 90-100% VO2max, whereas strength training consisted of six sets of 15-22 repetitions on the leg press at maximal resistance for a total of 22 wk. All types of training produced similar responses, including increased strength, VO2max, and vastus lateralis muscle citrate synthase activity. In view of the similarity of responses to these regimens, it is understandable that no inhibition of strength was observed by the combination of training, because the training regimes seem to have been more synergistic rather than antagonistic.
After these initial studies, a number of other investigations either favored or disagreed with the interference of strength development during concurrent training. Many such discrepancies among studies of concurrent training stem from a number of logistical issues. Based on the evidence provided so far, the interference effect seems to hold true in specific situations. Some of the different results were postulated to be related to dependent-variable selection (outcome measures), modality of training programs, characteristics of the subjects (age, sex, training status), and duration of the study (24). Moreover, such differences make comparisons across the different studies difficult, which complicates the understanding of the adaptations to concurrent training.
Over the years, several mechanisms have been proposed as limiting factors for optimal skeletal muscle adaptation, and have been identified as "responsible" for or contributing to the inhibition of strength development during concurrent training. These include neural components, fuel substrate availability, fiber-type transformation, overtraining, and alterations in protein synthesis (24).
Neural component. TOP
Dudley and Djamil (13) and Chromiak and Mulvaney (8) have discussed the possibility that neural factors and motor unit recruitment may have a significant role in restricting strength development with strength and endurance training. However, no specific factors have yet been isolated to strongly support this mechanism, with the exception of a study by Hakkinen et al. (15), in which the effects of concurrent training on rates of force development were postulated to have been a consequence of neural and muscle components, because this type of training attenuated the development of explosive strength by limiting rapid voluntary neural activation.
Successive bouts of either strength or endurance exercise may produce chronically low muscle-glycogen levels, which could retard or impair subsequent performances. Repeated endurance training on consecutive days can reduce resting muscle glycogen levels in muscle (9), and glycogen depletion has been shown to occur after resistance exercise (35). A possible implication of low glycogen levels on concurrent training-induced muscle adaptation is highlighted by the findings of Creer et al. (10), who recently reported that low muscle-glycogen levels impaired the intracellular signaling responses to an acute bout of resistance exercise. Therefore, carrying out a training program that entitles daily or even twice-daily sessions may impair the responses to, and recovery from, exercise and/or performance during the execution of subsequent training sessions, thereby reducing the magnitude of the strength-training adaptations.
Changes in muscle-fiber composition, particularly as a function of isomyosin alterations, have been considered previously as a possible mechanism of endurance training-associated inhibition of strength development (8,14). Skeletal muscle hypertrophy after strength training occurs to a greater extent in fast-twitch than in slow-twitch fibers (16,34). Intense endurance training has been observed to reduce the maximal shortening speed of type II or fast-twitch fibers and to change skeletal muscle-fiber population as measured by changes in myosin ATPase (25,33), which suggests that a reduction in the relative number of type II fibers by endurance training could play a major role in limiting strength development during concurrent training.
Overtraining. TOP
Two previous reviews (8,14) of concurrent strength and endurance training have considered the term "overtraining" to account for the inability to attain optimal strength gains when strength and endurance training are performed. Overtraining remains a rather poorly defined term despite recent efforts by exercise physiologists to identify its origins. Overtraining is an imbalance between training and recovery (23). In general, it is characterized by a decline in performance or by a lack of improvement. In the first strength- and endurance-training study, strength declined in the 9th and 10th weeks of concurrent training (19). Because the subjects were training 80 min·d-1, an argument could be made that the marked impairment of strength development by the S & E groups was the result of the development of residual fatigue. Yet, this may not have been the case. Endurance work per week performed on the bicycle ergometer increased at approximately the same rate in the E and S & E groups, particularly during the 9th and 10th weeks of training, at a time when strength gains in the S & E group were dramatically decreasing. Thus, the S & E effects on strength development seem to be selective for the strength-training response. Furthermore, the studies of Dudley and Djamil (13) and Hickson (19) as well as other concurrent training studies encompassed somewhat different endurance- and strength-training protocols (intensity, duration, frequency, type of training), including the sequence of days when either one or both types of training were performed. Based on these differences, it is difficult to uniquely identify the factor(s) leading to the inhibition of strength by overtraining during both types of training.
Protein turnover.
Acute endurance exercise bouts have generally been found to reduce total protein-synthesis rates of mixed skeletal muscles during the exercise. This depression is transient and can lead to a temporary decrease in protein synthesis within several hours after exercise (5,12,29). Overlapping endurance exercise bouts with resistance exercise may result in impaired adaptive responses in protein synthesis and, therefore, a decrease in strength-related performance, in part, due to the suboptimal or lack of increase in muscle-fiber cross-sectional areas (22). When performed several times a week, such combination training may be sufficient to disrupt the protein-synthesis mechanisms involved with the normal adaptation to the individual bouts of strength exercise, thus altering the long-term adaptations to training and resulting in impaired muscle-dependent strength gains. Another possibility, although hypothetical, is that the adaptive protein synthesis resulting from either form of exercise may create some sort of cellular incompatibility in which the muscle cell needs to decide whether to grow or manage the synthesis of its metabolic machinery.
We are now at a stage in which technologies from fields such as biochemistry and molecular biology can allow exercise scientists to explore the biology of exercise-induced skeletal muscle adaptation in more mechanistic terms. Studies on protein phosphorylation of intracellular signaling molecules have begun to reveal specific cellular regulatory processes induced by different forms of exercise. For example, acute resistance exercise, which, over time, can result in muscle hypertrophy, induces the activation of a growth-associated signaling network. Experiments in humans and rodents demonstrated that a single bout of resistance exercise results in an increased activity of the phosphoinositide-3-dependent kinase (PI3k) (18), protein kinase B (PKB) (28), the mammalian target of Rapamycin (mTOR) (3), and the ribosomal protein S6 kinase 1 (S6k1) (1,21,28). Activation of such a signaling network by acute resistance exercise modulates muscle-protein synthesis both in animals and humans (18,11). Activation of PI3-k leads to an increase in PKB and mTOR activity and subsequent inhibition (phosphorylation) of the cap-binding protein 4E-BP1 (3,18), which, in turn, inhibits cap-dependent mRNA translation and, hence, protein synthesis via sequestration of the eukaryotic initiation factor 4E (eIF4E). An increase in eIF4E activity will result in increased muscle-protein synthesis rates. Endurance exercise, on the other hand, is associated with signaling mechanisms related to metabolic adaptations, such as the activation of the AMP-activated protein kinase (AMPK) signaling. One of AMPK's main functions is to monitor the energy status of the cell; therefore, the processes regulated by AMPK seem to be related to the maintenance of energy homeostasis (17,37). AMPK activity is modulated mainly by changes in the levels of energy phosphates and by a decrease in the energy charge of the muscle cell, that is, an increase in ADP/ATP ratio. Such fluctuations in metabolic regulation as it occurs during exercise (38,39) can also cause changes in gene expression and substrate content via AMPK signaling (17,37).
Interestingly, recent studies have shown antagonistic activities between the anabolic signaling mechanisms induced by the PI3k/mTOR/PKB/S6k1/4E-BP1 network and the energy-modulating signaling by AMPK. More precisely, activation of AMPK signaling by a pharmacologic agonist reduces skeletal muscle-protein synthesis by inhibiting mTOR signaling, presumably via activation of the tuberous sclerosis complex (TSC). Bolster et al. (2) have found that an injection of the AMPK analog AICAR (5-aminoimidazole-4-carboxamide 1-beta-d-ribonucleoside) had no effect on a1 AMPK activity, but it did increase a2 AMPK activity by ~50%. AMPK activation by AICAR treatment was correlated with a 45% decrease in protein synthesis and was associated with a decreased activation of the PKB/mTOR/S6K1 pathway. This was also associated with a reduced inhibition of the eIF4E-binding protein (4E-BP1) and a reduction in eIF4E associated with eIF4G. As previously mentioned, one potent stimulus for the increase in AMPK activity is an increase in ADP/ATP ratio; this mechanism may help explain previous observations by Bylund -Fellenius et al. (7), who demonstrated that contractile activity resulted in an increase in ADP/ATP ratio, which, in turn, was correlated with a fall in muscle-protein synthesis rates. These findings indicate that the decrease in protein synthesis commonly seen during contractile activity could be mediated in part by an increase AMPK activity and a concomitant decrease in the anabolic response downstream of mTOR signaling. Indeed, Thomson and Gordon (36) have recently made the interesting observation in aged animals that muscle mass was negatively correlated with AMPK activity, once again implicating this kinase in the negative modulation of skeletal muscle mass.
Another potential mechanism for the inhibition of protein synthesis during muscular activity may be at the elongation step (6). In a recent study, Rose et al. (30) detected a rapid increase in eukaryotic elongation factor 2 (eEF2) phosphorylation during cycling exercise. In this study, subjects exercised at approximately 67% VO2max, and muscle biopsies were obtained at rest and after 1, 10, 30, 60, and 90 min of exercise. Exercise caused a rapid (within 1 min) increase (five- to sevenfold) in eEF2 phosphorylation that persisted during the entire exercise period. Surprisingly, a rather small decrease in eEF2 kinase (eEF2k) activity was detected, suggesting that even with a minor decrease in eEF2k activity, the remaining activated kinase may have been sufficient to inhibit and, therefore, phosphorylate eEF2, causing a decrease in protein synthesis. The mechanisms by which eEF2k activation by exercise seems to occur in a calcium-dependent fashion, because eEF2k from exercised muscle was potently activated by calcium-dependent calmodulin (Ca2+CaM) in vitro. This suggests that the higher eEF2 phosphorylation in working skeletal muscle may be mediated by an allosteric activation of eEF2 kinase by Ca2+CaM.
Although hypothetical, it is reasonable to assume that activation of AMPK and inhibition of the eEF2 by endurance exercise and/or too-frequent exercise sessions will impinge on the responses to resistance exercise by affecting training-induced increases in adaptive protein synthesis, because activation/inhibition of these signaling proteins independently or collectively can alter the induction of an anabolic response. The obvious consequence of such antagonism will be a negative impact on long-term strength-training adaptations, perhaps by ameliorating the hypertrophic response. Therefore, this may be one mechanism responsible for the observed detrimental effects of concurrent strength and endurance training on strength development (Fig. 3).
A working model of the intracellular signaling networks mediating exercise-induced skeletal muscle adaptations. Resistance exercise is capable of inducing an increase in the activity of a network comprising PI3k/PKB/mTOR/S6K1/S6/4E-BP1 signaling to modulate protein-synthesis rates and muscle growth. Endurance exercise is associated with signaling involved in metabolic homeostasis, comprising AMPK signaling, among others. Activation of AMPK by endurance exercise or contractile activity may inhibit mTOR signaling via TSC and suppress resistance exercise-induced muscle-protein synthesis. In addition, calcium fluxes resulting from prolonged contractile activity may inhibit protein synthesis in a Ca2+M-dependent manner by inhibiting peptide-chain elongation via activation of eEF2k and a subsequent increase in eEF2 phosphorylation. AMPK may also inhibit protein synthesis by activating eEF2k.
In summary, when strength and endurance training are performed simultaneously, a potential interference in strength development may occur. Such interference may be caused by alterations in the adaptive protein synthesis changes induced by endurance exercise or by too-frequent training sessions, in addition to several other unknown factors. Novel technologies are allowing us to understand the molecular mechanisms involved in exercise-induced skeletal muscle adaptations (e.g., genome-wide gene-expression analysis). This knowledge is not only improving the way we implement training programs for sports and rehabilitation, it is also important for the correct design of future studies in exercise training and skeletal muscle adaptation, particularly those involving the investigation of mechanisms of signal transduction and gene expression.
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Axel skrev:Ja du ha rså rättså. läste inte så noga .
Uppdatera resultat efter hand Dea!
sen tycker jag det är lite taskigt med formbilder här, vem tar första steget?
Hoppas verkligen på att vi får höra hur de går DEA!
Skulle kunna slänga upp en om jag för tillfället inte vore sjuk, har vart sjuk i 4veckor, rasat 10kg. Vet fortfarande inte vad som är felet. Ligger inne, men permission för tillfället. Lagom kul.... Finns inte så mycket muskler kvar känns de som. Haha....
DEA!! skrev:Tänkte faktiskt göra det
Dum fråga. . Men blir alltid sugen på mjölk och flingor på kvällarna... kcal? Ovärt? Kellogs K
Ska ju inte skada egentligen. Dock så kan du ju försöka avstå. Säg 250 kcal per tallrik. Beroende på vilken mjölk o hur stor tallrik de är. För antar att du syftar på Special K?
Som sagt, försök undvika de. Men hellre de än en påse godis eller chips! Är ju relativt nyttigt ändå.
Axel skrev:kellogs har en jävla massa onödiga kalorier. 133 kcal per 30g, vilket är sjukt jämfört med hur pass minimalt mätt man blir av det.
Stek lite bacon krispigt som fan och blanda ner det i keso, namnamnam!
Jämfört med vad? En banan, en påse chips, en godispåse? Allting är relativt!
Läs om vad jag skrev så förstår du vad jag menar
Fö. så har jag just nu "ofrivillig" fasta. Lagom kul.. Eller jag får dricka klara vätskor.
Som jag sa tidigare är ju sjuk, och imorgon ska jag sövas och göra en lång gastroskopi..
Kul och tvingas fasta när man gått ner 10kg....
Axel skrev:kellogs har en jävla massa onödiga kalorier. 133 kcal per 30g, vilket är sjukt jämfört med hur pass minimalt mätt man blir av det.
Stek lite bacon krispigt som fan och blanda ner det i keso, namnamnam!
Jämfört med vad? En banan, en påse chips, en godispåse? Allting är relativt!
Läs om vad jag skrev så förstår du vad jag menar
Fö. så har jag just nu "ofrivillig" fasta. Lagom kul.. Eller jag får dricka klara vätskor.
Som jag sa tidigare är ju sjuk, och imorgon ska jag sövas och göra en lång gastroskopi..
Kul och tvingas fasta när man gått ner 10kg....
Jämfört med annat me lika mkt kcal! Fett o protein mättar ju mycket mer än vad kolhydrater gör ( högre blodsocker sänker mättnadskänslan)
Fyfan va drygt, hoppas dom hittar felet iaf. inge kul.
En fråga angående kosten till deffen.
Frukost: proteindrink
Frukost jobbet (kl.9) lättkvarg 500g.
Lunch vanlig matlåda
Proteindrink efter gymmet
Lättkvarg 500g på kvällen
DEA!! skrev:Så träligt! Du kanske får synliga abs iaf
En fråga angående kosten till deffen.
Frukost: proteindrink
Frukost jobbet (kl.9) lättkvarg 500g.
Lunch vanlig matlåda
Proteindrink efter gymmet
Lättkvarg 500g på kvällen
Vet inet hur pass bra dethär stämmer, men du ska ligga på ca 200kcal underskott per dag vad jag lyckats läsa mig till ( funkade bra som fan på mig när jag försökte, tröttnade efter ett tag men de får du int göra )
DEA!! skrev:3573kcal ska jag ha om jag ligger i sängen hela dagen. Hur ser det ut då?
Vanlig mat, inte jättemycket dock. .
Mät o räkna va de blir, finns en hemsida som svenska livsmedelverket har(tror jag) där man ser all energiinnehåll på olika livsmedel.
Tkr det låter rätt lite de du äter, själv äter ja kvällsmat( en pära o en rejäl köttbit osallad ) utöver de du skrivit. Sen är man ju fet med så..
DEA!! skrev:3573kcal ska jag ha om jag ligger i sängen hela dagen. Hur ser det ut då?
Vanlig mat, inte jättemycket dock. .
Vill du gå ner i vikt så ska du äta cirka 200-500g mindre kalorier än vad du föbränner, tänk på att äta ofta men mindre
Min kost ser ut ungefär så här just nu:
Fruost: havregrynsgröt, 3 ägg, banan
Mellanmål: banan/alt. något mer som jag köper i skolan
Lunch: skolmat, äter så jag blir riktigt mätt
Mellanmål havregrynsgröt/yoghurt med havregryn , banan
Träning: bcaa under träning och vassle protein efter
Middag: det jag får hemma, försöker att äta minst 150g pasta/potatis och 100g kött men brukar oftast bli mycket mer.
Kvällsmat: Havregrynsgröt/yoghurt med havregryn, banan
Bulkar just nu och tycker att den kosten funkar för mej, eftersom jag bor hemma och går i skolan så är det svårt att planera sin mat efter varje måltid så försöker äta så mycket som möjligt av det som bjuds på :)Du kan köra något liknande fast äta mindre givetvis http://www.kalorier.se/ här kan du se hur mycket kalorier det är i maten och försök att passa ihop det med din dag tänk på att mjölk och sånt man kanske dricker till maten ska räknas med
DEA, inte räkna kcal! Då går du emot hela meningen med dieten! Du ska inte räkna kcal, utan äta som vanligt. Sedan öka träningen, och efter ett tag. ev. dra ner kcal!
Lyssna på kroppen och räkna inte kcal!
Fö. synliga abs är inte ens något jag vill ha så..
Dom hittade inte heller felet idag... nu väntar vi på provsvaren!
jag får inte träningsvärk längre, på överkroppen,f asten jag tränar hur hårt som helst, och tillslut orkar jag knappt lyfta 10 kg med armarna längre. Varför får jag itne träningsverk?
MrAndersson skrev:DEA, inte räkna kcal! Då går du emot hela meningen med dieten! Du ska inte räkna kcal, utan äta som vanligt. Sedan öka träningen, och efter ett tag. ev. dra ner kcal!
Lyssna på kroppen och räkna inte kcal!
Fö. synliga abs är inte ens något jag vill ha så..
Dom hittade inte heller felet idag... nu väntar vi på provsvaren!
Asddfgf4 skrev:jag får inte träningsvärk längre, på överkroppen,f asten jag tränar hur hårt som helst, och tillslut orkar jag knappt lyfta 10 kg med armarna längre. Varför får jag itne träningsverk?
För att du har tränat tillräckligt regelbundet så dina muskelfästen inte är för klena för belastningen du utsatt dom för. Dock hoppas jag att du känner dig "utmattad" dagen efter, eller iallafall på morgonen? Man känner ju att man använt kroppen.
Tjena! Jag tänkte börja deffa nu efter sommaren så att sex packet blir synligare Dock så finns det ett problem. Jag vaknar och äter frukost vid 8. Då är jag så pass hungrig att 3 mackor räcker inte till. Det blir oftast två äggmackor och en skål yoghurt med musli eller i den stilen för att jag ska bli mätt. Skolan börjar 8.40 och lunchen är så tidig som 10:45. Då är jag inte särskilt hungrig och tvingar mest i mig maten. Mot eftermiddagen 13-14, blir jag riktigt hungrig, och då blir det ofta att när jag kommer hem 16 drar i mig alltför mycket mellanmål vilket gör att jag inte äter tillräckligt med middag då jag redan är mätt. Hur tycker ni att jag ska balansera ut mina måltider osv? funderar på att ha med mig lite protein pulver att blanda i skolan när jag blir hungrig..
hur ska man träna? Alltså rep osv?
