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Re: 2008 Competition Preparation
wow.
wow.
2008 Competition Prep and Training
- Thread starter Tatyana
- Start date
Re: 2008 Competition Preparation
Nice Tatyana! so you run with the fresh air of the sea..
Tatyana said:Thanks
A little update, I have been getting my butt out of bed in the morning to do fasted cardio.
I forgot how much I love running
38 min, 271 kcals, 134 bpm average
A few pics from the sea-front
Nice Tatyana! so you run with the fresh air of the sea..
Tatyana
Elite Mentor
Re: 2008 Competition Preparation
I really didn't think that I would be lifting more now that I am on reduced calories, I was hoping to just keep lifting the same amount, but tonight I DID.
I added another 5 kg to T-bar rows, so I was training with 55 kg/121 lbs + the olympic bar
I did seated rows on the hammerstrength with 45 kg/99 lb/side and after wide grip pull ups, weighted dips (20 kg/44 lb) and skull crushers with 38-40 kg/ aroung 90 lbs, I still managed dead lifts with 100 kg/220 lbs
I really didn't think that I would be lifting more now that I am on reduced calories, I was hoping to just keep lifting the same amount, but tonight I DID.
I added another 5 kg to T-bar rows, so I was training with 55 kg/121 lbs + the olympic bar
I did seated rows on the hammerstrength with 45 kg/99 lb/side and after wide grip pull ups, weighted dips (20 kg/44 lb) and skull crushers with 38-40 kg/ aroung 90 lbs, I still managed dead lifts with 100 kg/220 lbs
Re: 2008 Competition Preparation
So pictures are absolutely amazing. They would get ME out of bed...lol
So pictures are absolutely amazing. They would get ME out of bed...lol
Scotsman
New member
Re: 2008 Competition Preparation
Great work. Your pics look awesome. The beach pics are great looks like a great place for a sunrise/sunset walk.
Cheers,
Scotsman
Tatyana said:I really didn't think that I would be lifting more now that I am on reduced calories, I was hoping to just keep lifting the same amount, but tonight I DID.
I added another 5 kg to T-bar rows, so I was training with 55 kg/121 lbs + the olympic bar
I did seated rows on the hammerstrength with 45 kg/99 lb/side and after wide grip pull ups, weighted dips (20 kg/44 lb) and skull crushers with 38-40 kg/ aroung 90 lbs, I still managed dead lifts with 100 kg/220 lbs
Great work. Your pics look awesome. The beach pics are great looks like a great place for a sunrise/sunset walk.
Cheers,
Scotsman
Bikini Mod
New member
Re: 2008 Competition Preparation
Running? Very catabolic lady... be carefull. You don't want to give up too much mass not to mention compromise your joints.
(What can I say, once a body's uterus has been stretched she thinks she is like everybody's mum!) <---- that's brit for MOM!
Running? Very catabolic lady... be carefull. You don't want to give up too much mass not to mention compromise your joints.
(What can I say, once a body's uterus has been stretched she thinks she is like everybody's mum!) <---- that's brit for MOM!
Tatyana
Elite Mentor
Re: 2008 Competition Preparation
Body - not lean enough
Head - wondering what in the hell was I thinking wanting to compete, thinking I am not ready blah blah blah, but I also know that if I don't do it, I will regret it.
I do get 'the nerves'.
I am going to see my coach in about a week.
Qualifiers can be really funny things, you can show up and be the only woman, one of two, or one of a group of 10.
bluey2u said:
Body - not lean enough
Head - wondering what in the hell was I thinking wanting to compete, thinking I am not ready blah blah blah, but I also know that if I don't do it, I will regret it.
I do get 'the nerves'.
I am going to see my coach in about a week.
Qualifiers can be really funny things, you can show up and be the only woman, one of two, or one of a group of 10.
Tatyana
Elite Mentor
Re: 2008 Competition Preparation
I think that the running is catabolic is a bit of a BBing myth, it does depend on the individual.
If you are an ectomorph type, I would avoid it.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2270108
J Physiol. 2000 October 1; 528(Pt 1): 3.
doi: 10.1111/j.1469-7793.2000.t01-1-00003.x. PMCID: PMC2270108
Copyright © The Physiological Society 2000
How to avoid running on empty
Michael J Rennie
Department of Anatomy and Physiology, University of Dundee, Dundee DD1 4HN, UK
Energy production by skeletal muscle shows a range of output which is unmatched by any other tissue. At rest, muscle oxygen consumption trickles along at about 2 ml kg−1 min−1 using mainly fatty acids and a little bit of carbohydrate, processed to lactate only. However, when the system is activated (for example in a 5000 m runner), working muscle oxygen consumption may be nearly 200-fold more.
If ATP were not resynthesized after its use by myosin ATPase a marathon runner would need over 20 kg to finish! Even this power output is not maximal: the ultimate rate of ATP utilization occurs during jumping and throwing events and it may be many times higher than during maximal aerobic work.
In mechanical engines a single type of fuel (gas, diesel oil, petrol, electricity) is used at all power outputs but in muscle a number of different types of fuel are used (e.g. creatine phosphate, glucose, glycogen, lactate, ketone bodies, free fatty acids and triglycerides) as appropriate to the task. Some fuels are stored in muscle and some are imported via the blood.
Some are catabolized to produce ATP without the involvement of oxygen and some are fully oxidized to CO2 and water. By and large the processes which have the highest power output rely on fuels stored in very small amounts (e.g. creatine phosphate) and those which have the highest capacity (e.g. ATP production from fatty acid oxidation) can sustain only moderate power outputs.
How all this is integrated and controlled remains a major mystery but recent rapid advances in the field are allowing us to perceive the outlines of some general control mechanisms. The linchpin appears to be a protein kinase which is activated by adenosine monophosphate (AMP).
AMP-activated protein kinase (AMPK) was discovered by Graham Hardie's group when working on the phosphorylation and inactivation of enzymes of lipid metabolism (Carling et al. 1987). It has now been recognized that AMPK phosphorylates enzymes in a wide range of other metabolic pathways which show acute and chronic adaptation to various forms of cellular stress including heat shock, contractile activity and nutrient deprivation.
Indeed, Hardie has christened the phosphorylation cascade involving AMPK ‘the cellular fuel gauge’, conceiving it as monitoring the energy status of the cell (Fig. 1). AMPK is allosterically activated by 5′-AMP which promotes its phosphorylation by an upstream kinase (AMPKK) and inhibits its dephosphorylation.
Because of the reaction of adenylate kinase (2ADP ATP + AMP) the change in AMP concentration as a result of the utilization of ATP is amplified, making the AMP concentration an acutely sensitive indicator of the rate of ATP utilization (Hardie & Carling, 1997).
The creatine kinase enzyme, which buffers sarcoplasmic ATP concentrations during contractile activity, is phosphorylated in muscle cells by AMPK, a change which is stimulated by creatine and low pH and inhibited by phosphocreatine (Ponticos et al. 1998) – all characteristics which would stimulate AMPK activity during muscular contraction.
Will Winder and his colleagues from Brigham Young University have been very active in demonstrating the possible involvement of AMPK in the regulation of muscle metabolism during exercise.
They showed that in electrically stimulated rat muscle and in running rats, AMPK was activated with appropriate catabolic effects such as activation of fatty acid oxidation (Rasmussen & Winder, 1997). The effect appeared to be dependent upon exercise intensity and to occur mainly in red, rather than white, muscle.
The catalogue of metabolic processes involving activation of 5′-AMP is now said to include increases in the concentration of glycogen, the glucose transporter GLUT4, hexokinase, and of mitochondrial enzymes in skeletal muscle (Holmes et al. 1999; Winder et al. 2000).
Figure 1
AMPK is activated by ATP-using processes via AMP, thus increasing ATP availability.
Until very recently, all of the available information has come from work in non-human tissues. It is therefore somewhat of a relief (as well as being a harbinger of a likely flood of new work) to see that the phenomenon also occurs in human muscle.
Two groups have independently obtained almost identical results showing this. Fujii and colleagues (Fujii et al. 2000) of the Joslin Diabetes Center, Harvard Medical School, and Wojtaszewski and co-workers from the Copenhagen Muscle Research Centre (this issue of The Journal of Physiology) showed, by analysing AMPK activity in biopsies from vastus lateralis muscle obtained before and immediately after bicycle exercise (at 70 % VO2,max for 20–60 min) that there was a substantial covalent activation of the α2-subunit of AMPK.
Exercise at a lower intensity for a longer period did not activate the enzyme although the stimulation was greater after 60 min of exercise than after 20 min (Wojtaszewski et al. 2000; Fujii et al. 2000). Both groups showed that the α1-subunit was never activated, but that the activation of the α2-subunit persisted for at least 30 min post-exercise.
These papers document the logical next step in transferring the investigation of AMPK into human physiology. I predict that this work will have an important heuristic effect. It should stimulate physiologists to investigate the role of AMPK in the control of many phenomena associated with muscle metabolism and contractile activity, including the relationship between fatty acid and glucose oxidation, the expression of particular genes associated with specific modes of contractile activity and the utilization of phosphocreatine during high intensity exercise.
However, one phenomenon which may not be associated (somewhat surprisingly) with AMP activation is the stimulation of glucose transport observed in rat skeletal muscle during electrically stimulated contraction (Derave et al. 2000). But there again, the definitive experiment has not been done – in human muscle!
BIKINIMOM said:Running? Very catabolic lady... be carefull. You don't want to give up too much mass not to mention compromise your joints.
(What can I say, once a body's uterus has been stretched she thinks she is like everybody's mum!) <---- that's brit for MOM!
I think that the running is catabolic is a bit of a BBing myth, it does depend on the individual.
If you are an ectomorph type, I would avoid it.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2270108
J Physiol. 2000 October 1; 528(Pt 1): 3.
doi: 10.1111/j.1469-7793.2000.t01-1-00003.x. PMCID: PMC2270108
Copyright © The Physiological Society 2000
How to avoid running on empty
Michael J Rennie
Department of Anatomy and Physiology, University of Dundee, Dundee DD1 4HN, UK
Energy production by skeletal muscle shows a range of output which is unmatched by any other tissue. At rest, muscle oxygen consumption trickles along at about 2 ml kg−1 min−1 using mainly fatty acids and a little bit of carbohydrate, processed to lactate only. However, when the system is activated (for example in a 5000 m runner), working muscle oxygen consumption may be nearly 200-fold more.
If ATP were not resynthesized after its use by myosin ATPase a marathon runner would need over 20 kg to finish! Even this power output is not maximal: the ultimate rate of ATP utilization occurs during jumping and throwing events and it may be many times higher than during maximal aerobic work.
In mechanical engines a single type of fuel (gas, diesel oil, petrol, electricity) is used at all power outputs but in muscle a number of different types of fuel are used (e.g. creatine phosphate, glucose, glycogen, lactate, ketone bodies, free fatty acids and triglycerides) as appropriate to the task. Some fuels are stored in muscle and some are imported via the blood.
Some are catabolized to produce ATP without the involvement of oxygen and some are fully oxidized to CO2 and water. By and large the processes which have the highest power output rely on fuels stored in very small amounts (e.g. creatine phosphate) and those which have the highest capacity (e.g. ATP production from fatty acid oxidation) can sustain only moderate power outputs.
How all this is integrated and controlled remains a major mystery but recent rapid advances in the field are allowing us to perceive the outlines of some general control mechanisms. The linchpin appears to be a protein kinase which is activated by adenosine monophosphate (AMP).
AMP-activated protein kinase (AMPK) was discovered by Graham Hardie's group when working on the phosphorylation and inactivation of enzymes of lipid metabolism (Carling et al. 1987). It has now been recognized that AMPK phosphorylates enzymes in a wide range of other metabolic pathways which show acute and chronic adaptation to various forms of cellular stress including heat shock, contractile activity and nutrient deprivation.
Indeed, Hardie has christened the phosphorylation cascade involving AMPK ‘the cellular fuel gauge’, conceiving it as monitoring the energy status of the cell (Fig. 1). AMPK is allosterically activated by 5′-AMP which promotes its phosphorylation by an upstream kinase (AMPKK) and inhibits its dephosphorylation.
Because of the reaction of adenylate kinase (2ADP ATP + AMP) the change in AMP concentration as a result of the utilization of ATP is amplified, making the AMP concentration an acutely sensitive indicator of the rate of ATP utilization (Hardie & Carling, 1997).
The creatine kinase enzyme, which buffers sarcoplasmic ATP concentrations during contractile activity, is phosphorylated in muscle cells by AMPK, a change which is stimulated by creatine and low pH and inhibited by phosphocreatine (Ponticos et al. 1998) – all characteristics which would stimulate AMPK activity during muscular contraction.
Will Winder and his colleagues from Brigham Young University have been very active in demonstrating the possible involvement of AMPK in the regulation of muscle metabolism during exercise.
They showed that in electrically stimulated rat muscle and in running rats, AMPK was activated with appropriate catabolic effects such as activation of fatty acid oxidation (Rasmussen & Winder, 1997). The effect appeared to be dependent upon exercise intensity and to occur mainly in red, rather than white, muscle.
The catalogue of metabolic processes involving activation of 5′-AMP is now said to include increases in the concentration of glycogen, the glucose transporter GLUT4, hexokinase, and of mitochondrial enzymes in skeletal muscle (Holmes et al. 1999; Winder et al. 2000).
Figure 1
AMPK is activated by ATP-using processes via AMP, thus increasing ATP availability.
Until very recently, all of the available information has come from work in non-human tissues. It is therefore somewhat of a relief (as well as being a harbinger of a likely flood of new work) to see that the phenomenon also occurs in human muscle.
Two groups have independently obtained almost identical results showing this. Fujii and colleagues (Fujii et al. 2000) of the Joslin Diabetes Center, Harvard Medical School, and Wojtaszewski and co-workers from the Copenhagen Muscle Research Centre (this issue of The Journal of Physiology) showed, by analysing AMPK activity in biopsies from vastus lateralis muscle obtained before and immediately after bicycle exercise (at 70 % VO2,max for 20–60 min) that there was a substantial covalent activation of the α2-subunit of AMPK.
Exercise at a lower intensity for a longer period did not activate the enzyme although the stimulation was greater after 60 min of exercise than after 20 min (Wojtaszewski et al. 2000; Fujii et al. 2000). Both groups showed that the α1-subunit was never activated, but that the activation of the α2-subunit persisted for at least 30 min post-exercise.
These papers document the logical next step in transferring the investigation of AMPK into human physiology. I predict that this work will have an important heuristic effect. It should stimulate physiologists to investigate the role of AMPK in the control of many phenomena associated with muscle metabolism and contractile activity, including the relationship between fatty acid and glucose oxidation, the expression of particular genes associated with specific modes of contractile activity and the utilization of phosphocreatine during high intensity exercise.
However, one phenomenon which may not be associated (somewhat surprisingly) with AMP activation is the stimulation of glucose transport observed in rat skeletal muscle during electrically stimulated contraction (Derave et al. 2000). But there again, the definitive experiment has not been done – in human muscle!
