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  1. #1
    Busy Dude Dr.Dave1's Avatar
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    interesting studies w/ implications for vasodilaors

    Here are some interesting articles that I came across while looking at mechanisms to increase muscle hypertrophy. These findings are surprising but quite interesting. While obviously using venous occlusive method is not a supp it does relate to N.O. as it brings to question the benefit of increased blood flow associated w/ vasodilators (yes, I know there are other benefits) Obviously, the low-intensity training may be different than what most people here use but I thought the findings were intriguing. I’m not advocating exercising with tourniquets on your limbs . . . yet

    Title Resistance training with vascular occlusion: metabolic adaptations in human muscle.
    Source Medicine & Science in Sports & Exercise. 35(7):1203-8, 2003 Jul.

    Burgomaster KA. Moore DR. Schofield LM. Phillips SM. Sale DG. Gibala MJ.
    Two recent studies have reported increases in strength and whole muscle cross-sectional area after low-intensity resistance training (LIT) with vascular occlusion (OCC) that are greater than LIT alone (e.g., 22, 25). The OCC stress might be expected to induce metabolic alterations that are consistent with compromised oxygen delivery rather than an increase in strength per se, but this has not been studied. PURPOSE: We examined the effect of LIT and LIT+OCC on resting metabolites in m. biceps brachii and elbow flexor strength. METHODS: Eight men (19.5 +/- 0.4 yr) performed 8 wk of LIT at approximately 50% of one-repetition maximum (2 sessions per week; 3-6 sets, 8-10 repetitions, final set to failure); one arm trained with OCC and the other without (CON). :Biopsies obtained before and 72 h after the final training bout revealed that resting [glycogen] was higher (P <or= 0.05) in both arms after LIT (CON: 452 +/- 20 vs 325 +/- 28, OCC: 501 +/- 12 vs 332 +/- 28 mmol.kg-1 dry weight) and the increase was larger in the OCC arm (P <or= 0.05). Resting [ATP] was lower (P <or= 0.05) after LIT in both arms (CON: 20.5 +/- 0.5 vs 22.8 +/- 0.7, OCC: 18.2 +/- 0.6 vs 23.1 +/- 0.5 mmol.kg-1 dry weight), and the decrease was larger in the OCC arm (P <or= 0.05). Maximal isotonic and isokinetic elbow flexor strength increased (P <or= 0.05) after training to a similar extent in both arms. CONCLUSION: We conclude that [glycogen] was increased and [ATP] was decreased in resting human muscle, 72 h after an 8-wk LIT protocol. OCC potentiated the metabolic changes, perhaps by inducing an ischemic stimulus that enhanced muscle glucose transport and adenine nucleotide catabolism after LIT, but did not augment the increases in strength.
    -Occlusion method - For the OCC condition, an occlusion cuff (12-cm width) was placed around the upper-arm approximately 2 cm proximal to the biceps brachii, and pneumatically inflated to 100 mm Hg. A cuff pressure of 100 mm Hg was employed in order to restrict venous blood flow outflow and cause pooling of blood in capacitance vessels distal to the cuff, ultimately restricting arterial blood inflow (25). The cuff remained in place and inflated throughout the first set of three sets during each training session.


    Title Neuromuscular adaptations in human muscle following low intensity resistance training with vascular occlusion.
    Source European Journal of Applied Physiology. 92(4-5):399-406, 2004 Aug.
    Authors Moore DR. Burgomaster KA. Schofield LM. Gibala MJ. Sale DG. Phillips SM.


    Low-intensity (approximately 50% of a single repetition maximum-1 RM) resistance training combined with vascular occlusion results in increases in muscle strength and cross-sectional area [Takarada et al. (2002) Eur J Appl Physiol 86:308-331]. The mechanisms responsible for this hypertrophy and strength gain remain elusive and no study has assessed the contribution of neuromuscular adaptations to these strength gains. We examined the effect of low-intensity training (8 weeks of unilateral elbow flexion at 50% 1 RM) both with (OCC) and without vascular occlusion (CON) on neuromuscular changes in the elbow flexors of eight previously untrained men [19.5 (0.4) years]. Following training, maximal voluntary dynamic strength increased (P<0.05) in OCC (22%) and CON (23%); however, isometric maximal voluntary contraction (MVC) strength increased in OCC only (8.3%, P<0.05). Motor unit activation, assessed by interpolated twitch, was high (approximately 98%) in OCC and CON both pre- and post-training. Evoked resting twitch torque decreased 21% in OCC (P<0.05) but was not altered in CON. Training resulted in a reduction in the twitch:MVC ratio in OCC only (29%, P<0.01). Post-activation potentiation (PAP) significantly increased by 51% in OCC (P<0.05) and was not changed in CON. We conclude that low-intensity resistance training in combination with vascular occlusion produces an adequate stimulus for increasing muscle strength and causes changes in indices of neuromuscular function, such as depressed resting twitch torque and enhanced PAP.

    Title Skeletal muscle hypertrophy after chronic restriction of venous blood flow in rats.[erratum appears in Med Sci Sports Exerc. 2005 Oct;37(10):1824].
    Source Medicine & Science in Sports & Exercise. 37(7):1144-50, 2005 Jul.
    Authors Kawada S. Ishii N.

    PURPOSE: Some previous studies have shown that resistance exercise training with venous occlusion causes an enhanced hypertrophy in human muscles. To investigate the effects of blood flow on muscular size at either cellular or subcellular level, we developed an animal model in which several veins from hindlimb muscles of the rat are surgically crush-occluded. METHODS: Twenty-four male Wister rats were randomly assigned into either a group for sham operation (sham group) or a group for venous occlusion (experimental group; N = 12 for each group). Fourteen days after the operation, plantaris, soleus, gastrocnemius, extensor digitorum longus, and tibialis anterior muscles were dissected from hindlimbs and subjected to morphological and biochemical analyses. RESULTS: Fourteen days after the operation, the muscles expect for soleus showed similar increases in wet weight/body weight (by 7-12%) as compared with the sham-operated group (P < 0.05). Further analyses on the plantaris muscle showed increases in muscle dry weight/ body weight (by 10%) and the concentrations of myofibrillar protein (by 23%), glycogen (by 93%) and lactate (by 23%) after the operation (P < 0.05). Mean fiber cross-sectional area was larger by 34% in the experimental group than in the sham-operated group (P < 0.01). The content of HSP-72 increased, whereas that of myostatin protein decreased (P < 0.01). The expression of nitric oxide synthase-1 (NOS-1) mRNA increased (P < 0.01), whereas that of IGF-1 mRNA showed no significant change (P = 0.36). Although the muscle nitric oxide (NO) concentration tended to increase, but the change was not significant (P = 0.10). CONCLUSIONS: Changes in muscle blood flow may affect the muscular size through actions of HSP-72, myostatin, and NOS-1.
    Excerpt
    In
    - accordance with previous studies (4), myosin ATPase staining showed that the percentage of Type 1 fibers in the soleus muscle was much larger than in other hypertrophied muscles (data not shown). Therefore, the effects of venous occlusion may depend on the muscle-fiber composition.
    - The hypertrophy of the plantaris muscle was associated with an increased content of HSP-72. . . . HSP-72 is induced by such stressors as heat, ischemia, hypoxia, and free radicals, and acts as chaperone to prevent misfolding or aggregation of proteins
    - An increased expression of NOS-1 within muscle fibers may also play an important role in muscular hypertrophy, because several recent studies have shown that NO stimulates the muscle growth
    - The hypertrophy of the plantaris muscle was associated with the decrease in muscle myostatin content.
    - venous occlusion did not cause a significant increase in IGF-1 expression . . . results suggest that IGF-1 would not be always essential for muscle hypertrophy, if such factors as myostatin, HSP-72, and NOS-1 would change in favor of the muscular growth
    Disclaimer: While I have an M.D. the views I express are not to be taken as medical advice under any circumstances. Please check with your own doctor if you want medical advice as he/she has access to your info and can provide the most accurate advice.


    www.pubmed.gov . . . gotta love it
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  2. #2
    unscathed xven's Avatar
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    Bump for this, very interesting read.

    OCC potentiated the metabolic changes, perhaps by inducing an ischemic stimulus that enhanced muscle glucose transport and adenine nucleotide catabolism after LIT, but did not augment the increases in strength.
    We conclude that low-intensity resistance training in combination with vascular occlusion produces an adequate stimulus for increasing muscle strength
    A little conflicting, don't you think? Or am I just reading this wrong?
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  3. #3
    nom nom nom deserusan's Avatar
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    Here is something from Will Brink:

    Originally Posted by WillBrink
    Several recent studies done on NO2

    The basics:


    Posters 13,14,15, 18.
    _
    As you know, Arginine-alpha-ketoglutarate (AAKG) has been purported to increase nitric oxide synthesis and thereby enhance blood flow, oxygen delivery, and glucose uptake to muscle leadingto greater gains in strength and muscle mass during training. For this reason, nitric oxide stimulating supplements have become a popular supplement among resistance trained athletes. While there is some theoretical rationale as to the potential ergogenic value, the effects of AAKG supplementation during training has yet to be determined.
    _
    -> 1.
    _
    PURPOSE:
    _This study examined the effects of AAKG supplementation during training on body composition and training adaptations in experienced resistance trained men (30-50 yrs).
    _
    METHODS:
    Subjects took 4 grams of the supplements three times daily (12 g/d) for 8-weeks during standardized training. At 0, 4, and 8-weeks, subjects had DEXA body composition determined and performed 1RM bench press,
    _
    RESULTS:
    No significant differences were observed between groups in changes in body mass , fat free mass, fat mass , or percent body fat.
    Changes in bench press 1RM , sprint peak power , time to peak power , and rate to fatigue were significantly greater in the AAKG group while no differences were observed in average power_ or total work .
    No significant differences were observed in isokinetic leg extension peak torque, maxrepetition total work, time to peak torque, total work, work fatigue, or average power during the muscular endurance test or maximal oxygen uptake.
    _
    CONCLUSION: Results indicate that AAKG supplementation may augment 1RM strength and sprint power in response to training but does not appear to significantly effect body composition. (Sponsor: Medical Research Institute, San Francisco, CA)
    _
    -> 2.
    PURPOSE:_
    This study examined the effects of AAKG supplementation during training on markers of health status in experienced resistance trained men (30-50 yrs).
    _
    METHODS:
    Subjects took 4 grams of the supplements three times daily (12 g/d) for 8-weeks during standardized training. At 0, 4, and 8-weeks, subjects donated fasting blood samples and had resting heart rate and blood pressure determined.
    _
    RESULTS:
    No significant interactions were observed between groups in resting or maximal systolic blood pressure, diastolic blood pressure, mean arterial pressure, or rate pressure product responses.
    No clinically significant side effects or adverse events were reported in weekly follow-up assessments or during the maximal stress tests.
    _
    CONCLUSION: AAKG supplementation does not appear to significantly affect markers of catabolism or adversely affect general markers of health. (Sponsor: Medical Research Institute, San Francisco, CA)
    _

    -> 3.
    _
    PURPOSE:
    This study examined the effects of arginine alphaketoglutarate (AAKG) supplementation during training on QOL and perceptions about training, health, and libido in experienced resistance trained men (30-50 yrs).
    _
    METHODS:
    Subjects took 4 grams of the supplements three times daily (12 g/d) for 8-weeks during standardized training. At 0, 4, and 8-weeks, subjects completed the SF-36 quality of life questionnaire and a training, health, and libido questionnaire.
    _
    RESULTS:
    No significant interactions were observed between groups in the SF-36 subscales of bodily pain , general health , mental health , physical functioning , role emotional , social functioning , vitality , or role physical. Likewise, no significant differences were foundbetween groups in positive attitude toward training , ability to recover from training sessions ,body satisfaction in terms of muscularity and muscle hardness, sexual desire/libido , erectile function/quality , quality of sleep , or feeling of energy when waking up .
    _
    CONCLUSION:
    Though non-significant results are reported, a number of interesting trends were observed in response to AAKG supplementation that deserves additional study. (Sponsor: MedicalResearch Institute, San Francisco, CA)

    Additional info and other studies of interest found at:

    _
    http://www.sportsnutritionsociety.or...1-14-2004b.pdf
    "I just use my muscles as a conversation piece, like someone walking a cheetah down 42nd Street." - Arnold Schwarzenegger

    Heretic....
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  4. #4
    Registered User Phosphate bond's Avatar
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    Originally Posted by Dr.Dave1
    Here are some interesting articles that I came across while looking at mechanisms to increase muscle hypertrophy. These findings are surprising but quite interesting. While obviously using venous occlusive method is not a supp it does relate to N.O. as it brings to question the benefit of increased blood flow associated w/ vasodilators (yes, I know there are other benefits) Obviously, the low-intensity training may be different than what most people here use but I thought the findings were intriguing. I’m not advocating exercising with tourniquets on your limbs . . . yet

    Title Resistance training with vascular occlusion: metabolic adaptations in human muscle.
    Source Medicine & Science in Sports & Exercise. 35(7):1203-8, 2003 Jul.

    Burgomaster KA. Moore DR. Schofield LM. Phillips SM. Sale DG. Gibala MJ.
    Two recent studies have reported increases in strength and whole muscle cross-sectional area after low-intensity resistance training (LIT) with vascular occlusion (OCC) that are greater than LIT alone (e.g., 22, 25). The OCC stress might be expected to induce metabolic alterations that are consistent with compromised oxygen delivery rather than an increase in strength per se, but this has not been studied. PURPOSE: We examined the effect of LIT and LIT+OCC on resting metabolites in m. biceps brachii and elbow flexor strength. METHODS: Eight men (19.5 +/- 0.4 yr) performed 8 wk of LIT at approximately 50% of one-repetition maximum (2 sessions per week; 3-6 sets, 8-10 repetitions, final set to failure); one arm trained with OCC and the other without (CON). :Biopsies obtained before and 72 h after the final training bout revealed that resting [glycogen] was higher (P <or= 0.05) in both arms after LIT (CON: 452 +/- 20 vs 325 +/- 28, OCC: 501 +/- 12 vs 332 +/- 28 mmol.kg-1 dry weight) and the increase was larger in the OCC arm (P <or= 0.05). Resting [ATP] was lower (P <or= 0.05) after LIT in both arms (CON: 20.5 +/- 0.5 vs 22.8 +/- 0.7, OCC: 18.2 +/- 0.6 vs 23.1 +/- 0.5 mmol.kg-1 dry weight), and the decrease was larger in the OCC arm (P <or= 0.05). Maximal isotonic and isokinetic elbow flexor strength increased (P <or= 0.05) after training to a similar extent in both arms. CONCLUSION: We conclude that [glycogen] was increased and [ATP] was decreased in resting human muscle, 72 h after an 8-wk LIT protocol. OCC potentiated the metabolic changes, perhaps by inducing an ischemic stimulus that enhanced muscle glucose transport and adenine nucleotide catabolism after LIT, but did not augment the increases in strength.
    -Occlusion method - For the OCC condition, an occlusion cuff (12-cm width) was placed around the upper-arm approximately 2 cm proximal to the biceps brachii, and pneumatically inflated to 100 mm Hg. A cuff pressure of 100 mm Hg was employed in order to restrict venous blood flow outflow and cause pooling of blood in capacitance vessels distal to the cuff, ultimately restricting arterial blood inflow (25). The cuff remained in place and inflated throughout the first set of three sets during each training session.


    Title Neuromuscular adaptations in human muscle following low intensity resistance training with vascular occlusion.
    Source European Journal of Applied Physiology. 92(4-5):399-406, 2004 Aug.
    Authors Moore DR. Burgomaster KA. Schofield LM. Gibala MJ. Sale DG. Phillips SM.


    Low-intensity (approximately 50% of a single repetition maximum-1 RM) resistance training combined with vascular occlusion results in increases in muscle strength and cross-sectional area [Takarada et al. (2002) Eur J Appl Physiol 86:308-331]. The mechanisms responsible for this hypertrophy and strength gain remain elusive and no study has assessed the contribution of neuromuscular adaptations to these strength gains. We examined the effect of low-intensity training (8 weeks of unilateral elbow flexion at 50% 1 RM) both with (OCC) and without vascular occlusion (CON) on neuromuscular changes in the elbow flexors of eight previously untrained men [19.5 (0.4) years]. Following training, maximal voluntary dynamic strength increased (P<0.05) in OCC (22%) and CON (23%); however, isometric maximal voluntary contraction (MVC) strength increased in OCC only (8.3%, P<0.05). Motor unit activation, assessed by interpolated twitch, was high (approximately 98%) in OCC and CON both pre- and post-training. Evoked resting twitch torque decreased 21% in OCC (P<0.05) but was not altered in CON. Training resulted in a reduction in the twitch:MVC ratio in OCC only (29%, P<0.01). Post-activation potentiation (PAP) significantly increased by 51% in OCC (P<0.05) and was not changed in CON. We conclude that low-intensity resistance training in combination with vascular occlusion produces an adequate stimulus for increasing muscle strength and causes changes in indices of neuromuscular function, such as depressed resting twitch torque and enhanced PAP.

    Title Skeletal muscle hypertrophy after chronic restriction of venous blood flow in rats.[erratum appears in Med Sci Sports Exerc. 2005 Oct;37(10):1824].
    Source Medicine & Science in Sports & Exercise. 37(7):1144-50, 2005 Jul.
    Authors Kawada S. Ishii N.

    PURPOSE: Some previous studies have shown that resistance exercise training with venous occlusion causes an enhanced hypertrophy in human muscles. To investigate the effects of blood flow on muscular size at either cellular or subcellular level, we developed an animal model in which several veins from hindlimb muscles of the rat are surgically crush-occluded. METHODS: Twenty-four male Wister rats were randomly assigned into either a group for sham operation (sham group) or a group for venous occlusion (experimental group; N = 12 for each group). Fourteen days after the operation, plantaris, soleus, gastrocnemius, extensor digitorum longus, and tibialis anterior muscles were dissected from hindlimbs and subjected to morphological and biochemical analyses. RESULTS: Fourteen days after the operation, the muscles expect for soleus showed similar increases in wet weight/body weight (by 7-12%) as compared with the sham-operated group (P < 0.05). Further analyses on the plantaris muscle showed increases in muscle dry weight/ body weight (by 10%) and the concentrations of myofibrillar protein (by 23%), glycogen (by 93%) and lactate (by 23%) after the operation (P < 0.05). Mean fiber cross-sectional area was larger by 34% in the experimental group than in the sham-operated group (P < 0.01). The content of HSP-72 increased, whereas that of myostatin protein decreased (P < 0.01). The expression of nitric oxide synthase-1 (NOS-1) mRNA increased (P < 0.01), whereas that of IGF-1 mRNA showed no significant change (P = 0.36). Although the muscle nitric oxide (NO) concentration tended to increase, but the change was not significant (P = 0.10). CONCLUSIONS: Changes in muscle blood flow may affect the muscular size through actions of HSP-72, myostatin, and NOS-1.
    Excerpt
    In
    - accordance with previous studies (4), myosin ATPase staining showed that the percentage of Type 1 fibers in the soleus muscle was much larger than in other hypertrophied muscles (data not shown). Therefore, the effects of venous occlusion may depend on the muscle-fiber composition.
    - The hypertrophy of the plantaris muscle was associated with an increased content of HSP-72. . . . HSP-72 is induced by such stressors as heat, ischemia, hypoxia, and free radicals, and acts as chaperone to prevent misfolding or aggregation of proteins
    - An increased expression of NOS-1 within muscle fibers may also play an important role in muscular hypertrophy, because several recent studies have shown that NO stimulates the muscle growth
    - The hypertrophy of the plantaris muscle was associated with the decrease in muscle myostatin content.
    - venous occlusion did not cause a significant increase in IGF-1 expression . . . results suggest that IGF-1 would not be always essential for muscle hypertrophy, if such factors as myostatin, HSP-72, and NOS-1 would change in favor of the muscular growth

    Interesting info. If you think about it "anaerobic" metabolism (locally in the muscle) is what leads to adaptations when you train. Right?
    Last edited by Phosphate bond; 04-10-2006 at 05:19 AM.
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  5. #5
    C6H13NO2 pu12en12g's Avatar
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    Originally Posted by Dr.Dave1
    Here are some interesting articles that I came across while looking at mechanisms to increase muscle hypertrophy. These findings are surprising but quite interesting...
    Interesting re: the myostatin... related read:

    Nicotine Accelerates Angiogenesis and Wound Healing in Genetically Diabetic Mice

    .PDF Format

    We recently discovered that nicotine is a potent angiogenic
    agent both in vivo and in vitro.11 Nicotine stimulated
    migration, proliferation, and tube formation of endothelial
    cells in vitro, all of which are major steps of angiogenesis.
    18 The findings in the present study are consistent
    with our previous work and reports from other investigators
    showing that nicotine stimulates DNA synthesis and
    proliferation of endothelial cells in vitro.13,19 The mechanisms
    by which nicotine induces angiogenesis are likely
    multifactorial. Nicotine has been shown to directly alter
    the activity of endothelial nitric-oxide synthase and the
    release of prostacyclin in endothelial cells lines derived
    from dogs and humans.20–22 Furthermore, nicotine is
    known to induce changes in the release of growth factors
    such as of bFGF and TGF-1.23,24 Most recently, it was
    shown that nicotine and its major metabolite cotinine
    up-regulate the expression of vascular endothelial growth
    factor (VEGF) in endothelial cells.25 Changes in the expression
    of VEGF elicited by nicotine may help to explain
    the effects of this agent on atherosclerotic plaque neovascularization
    and tumor angiogenesis previously reported
    by our group.
    http://forum.bodybuilding.com/attach...7&d=1142676406
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    Occlusion-based training has been around for a while and seems to be effective for rehab purposes. Kaatsu training is based on these scientific findings and uses pressurized cuffs to restrict circulation to the limbs being exercised. Some believe that pump-based training ("blood pumping", etc.) leads to muscle growth through similar mechanisms due to the occlusion it causes. There is a fine line between occlusion to promote muscle growth and occlusion to cause necrosis, so until further research is available I wouldn't suggest using any homemade torniquets just yet...
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    Busy Dude Dr.Dave1's Avatar
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    Originally Posted by deserusan
    Here is something from Will Brink:
    Interesting AAKG research . . . I have tried AAKG and must say it did not do much for me . . . although I was not using 12g a day like those guys . . . that's a lotta AAKG

    Originally Posted by Phosphate bond
    Interesting info. If you think about it "anaerobic" metabolism (locally in the muscle) is what leads to adaptations when you train. Right?
    Good point . . . I was wondering if it worked with the hypothesis that you need to break down muscle to rebuild it . . . if your hypoxic you would probably break down more muscle thus leading to a larger response . . . or maybe not, just a thought (hopefully that makes sense I had too little sleep last night . . . it might be jibberish for all I know)

    Originally Posted by pu12en12g
    Interesting re: the myostatin... related read:

    Nicotine Accelerates Angiogenesis and Wound Healing in Genetically Diabetic Mice

    .PDF Format

    http://forum.bodybuilding.com/attach...7&d=1142676406
    That is pretty cool . . . .Aight guys, I'm hedin out to buy some cigs. . . j/k. I had not heard of that effect of nicotine before, interesting possibilities. . .

    Originally Posted by Jotun
    There is a fine line between occlusion to promote muscle growth and occlusion to cause necrosis, so until further research is available I wouldn't suggest using any homemade torniquets just yet...
    Nor would I
    Disclaimer: While I have an M.D. the views I express are not to be taken as medical advice under any circumstances. Please check with your own doctor if you want medical advice as he/she has access to your info and can provide the most accurate advice.


    www.pubmed.gov . . . gotta love it
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  8. #8
    Registered User Phosphate bond's Avatar
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    Originally Posted by Dr.Dave1

    Good point . . . I was wondering if it worked with the hypothesis that you need to break down muscle to rebuild it . . . if your hypoxic you would probably break down more muscle thus leading to a larger response . . . or maybe not, just a thought (hopefully that makes sense I had too little sleep last night . . . it might be jibberish for all I know)

    Sounds good to me. In general it seems that increasing ATP leads to health, but challenging the ATP system leads to adaptations.
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    Originally Posted by Dr.Dave1
    Good point . . . I was wondering if it worked with the hypothesis that you need to break down muscle to rebuild it . . . if your hypoxic you would probably break down more muscle thus leading to a larger response . . . or maybe not, just a thought (hopefully that makes sense I had too little sleep last night . . . it might be jibberish for all I know)
    Mild breakdown of muscle proteins stimulates the rebuilding process. There are 3 primary causes for muscle damage, mechanical, hormonal, and oxidative. Mechanical refers to the stess placed on muscles when the muscle contracts, leading to torn muscle fibers. Hormonal, catabolism must happen to generate energy ATP (Since ATP is the only source of energy that can drive muscle contraction) such as a rise in cortisol levels in the body to breakdown proteins to form ATP. Oxidative refers to free radical generation due to increased oxygen consumption during exercise.

    People assume anabolism and only anabolism is the way to go. Catabolism is needed, it works towards your body composition goals. For example, people drink carb filled gatorade drinks during their workouts, and this is probaly one of the most terrible things you can do body composition wise during your workout.

    Bodys response to carb filled drink:
    1) Insulin levels will rise
    2) Adrenaline & Glucagon levels in response will fall

    Body composition is compromised due to a concept called intermediary catabolism, which is essential for both muscle growth and fat loss. You need muscle breakdown for muscle growth.
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    Originally Posted by Phosphate bond
    Sounds good to me. In general it seems that increasing ATP leads to health, but challenging the ATP system leads to adaptations.
    Could you expand more on this? Challenging the ATP system for adaption? I myself wouldnt necessarily say challenging the ATP system leads to adaption, but that challenging the breakdown/buildup (anabolism vs. catabolism) leads to adaption (hypertrophy, strength)

    This adaption by the body is shown by the Overload Principle, that the body adapts by becoming stronger and more efficient when it is worked harder than it is normally accustomed to, muscle breakdown/buildup (anabolism and catabolism)

    There are 3 systems the body uses to make ATP
    -Cellular respiration
    -Glycolysis
    -Creatine Phosphate System

    I dont see how limiting one could lead to adaption, and if it did, how it would be beneficial. Cellular respiration is the most efficient of the 3 but the most slowest. This system is limited by your bodys V02max. When you surpass a certain point where your body cannot make sufficient amounts of ATP anymore from aerobic respiration (Cellular respiration), your body switches to the anaerobic (Glycolysis & Creatine Phosphate) systems. These produce ATP quickly but very ineffeciently. Again, I dont see how limiting one system produces any adaption in terms of beneficial adaption
    Last edited by Trans_Isomer; 04-11-2006 at 05:55 PM.
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    Originally Posted by Trans_Isomer
    There are 3 systems the body uses to make ATP
    -Cellular respiration
    -Glycolysis
    -Creatine Phosphate System

    I dont see how limiting one could lead to adaption, and if it did, how it would be beneficial. Cellular respiration is the most efficient of the 3 but the most slowest. This system is limited by your bodys V02max. When you surpass a certain point where your body cannot make sufficient amounts of ATP anymore from aerobic respiration (Cellular respiration), your body switches to the anaerobic (Glycolysis & Creatine Phosphate) systems. These produce ATP quickly but very ineffeciently. Again, I dont see how limiting one system produces any adaption in terms of beneficial adaption
    You don't want to limit ATP production at all. You want it to be the highest it can be!

    The whole point of lifting weights is that it challenges your bodies ability to keep supply up with the demand. Muscle contractions take ATP. The heavier weights you lift the greater the "challenge" there is.

    The muscles sense for example there is not enough oxygen....so there is stimulation of angiogenesis, etc. The new blood vessel growth brings in more oxygen over time to help things out. That's just one type of adaptation.
    Last edited by Phosphate bond; 04-11-2006 at 06:42 PM.
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    Originally Posted by Phosphate bond
    You don't want to limit ATP production at all. You want it to be the highest it can be!

    The whole point of lifting weights is that it challenges your bodies ability to keep supply up with the demand. Muscle contractions take ATP. The heavier weights you lift the greater the "challenge" there is.

    The muscles sense for example there is not enough oxygen....so there is stimulation of angiogenesis, etc.
    Yes, that is what I was saying with my post, you had stated above that challenging the ATP system lead to adaptions, and I was checking to see if you meant these were beneficial adaptions, or that challenging the ATP system lead to any adaptions at all
    Last edited by Trans_Isomer; 04-11-2006 at 06:48 PM.
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    Originally Posted by Trans_Isomer
    Yes, that is what I was saying with my post, you had stated above that challenging the ATP system lead to adaptions, and I was checking to see if you meant these were beneficial adaptions

    I guess its easy for that to get misunderstood since this thread revolves around a tourniquet. I was thinking of how to apply that observation more to real life.

    If you walked around with a tourniquent all the time (permanently challenging the ATP system) It would be a different story.

    The beauty of working out is that the stress is intermittent (which lets the situation recover)
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    Originally Posted by Phosphate bond
    I guess its easy for that to get misunderstood since this thread revolves around a tourniquet. I was thinking of how to apply that observation more to real life.

    If you walked around with a tourniquent all the time (permanently challenging the ATP system) It would be a different story.

    The beauty of working out is that the stress is intermittent (which lets the situation recover)
    Ahh, ok.

    Just misunderstood what your specifically meant
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    Small study but interesting results. I'm going to assume that we are all familiar with the role PGs play in promoting protein synthesis (aka theory behind X-factor and such). Here is a tie in to that with the tourniquet study I mentioned above.

    J Appl Physiol. 2005 Jul;99(1):45-52. Epub 2005 Mar 3.
    Contribution of prostaglandins to the dilation that follows isometric forearm contraction in human subjects: effects of aspirin and hyperoxia.
    Win TS, Marshall JM.

    In 11 healthy volunteers, we evaluated, in a double-blind crossover study, whether the vasodilation that follows isometric contraction is mediated by prostaglandins (PGs) and/or is O2 dependent. Subjects performed isometric handgrip for 2 min at 60% maximal voluntary contraction (MVC), after pretreatment with placebo or aspirin (600 mg orally), when breathing air or 40% O2. Forearm blood flow was measured in the dominant forearm by venous occlusion plethysmography. Arterial blood pressure was also recorded, allowing calculation of forearm vascular conductance (FVC; forearm blood flow/arterial blood pressure). During air breathing, aspirin significantly reduced the increase in FVC that followed contraction at 60% MVC: from a baseline of 0.09 +/- 0.011 [mean +/- SE, conductance units (CU)], the peak value was reduced from 0.24 +/- 0.03 to 0.14 +/- 0.01 CU. Breathing 40% O2 similarly reduced the increase in FVC relative to that evoked when breathing air; the peak value was 0.24 +/- 0.03 vs. 0.15 +/- 0.02 CU. However, after aspirin, breathing 40% O2 had no further effect on the contraction-evoked increase in FVC (the peak value was 0.15 +/- 0.02 vs. 0.16 +/- 0.02 CU). Thus the present study indicates that prostaglandins make a substantial contribution to the peak of the vasodilation that follows isometric contraction of forearm muscles at 60% MVC. Given that hyperoxia similarly reduced the vasodilation and attenuated the effect of aspirin, we propose that the stimulus for prostaglandin synthesis and release is hypoxia of the endothelium
    Taking this into account, the above "tourniquet" method would induce hypoxia leading to an increased release of PGs, which would then lead to increases in protein synthesis.
    Just to make it clear I am not suggesting everyone goes around with tourniquets on their arms. I do not want to see a post on here that someone's arm fell off b/c they read lifitng with a tourniquet would increase their gains. This is more informational at the moment
    Disclaimer: While I have an M.D. the views I express are not to be taken as medical advice under any circumstances. Please check with your own doctor if you want medical advice as he/she has access to your info and can provide the most accurate advice.


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    Also be careful of blood clots when occluding blood flow

    No one needs a blood clot to form, break off and fly to their brain right after a tough set...
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    Originally Posted by Valveman
    No one needs a blood clot to form, break off and fly to their brain right after a tough set...
    Again to clarify I am not advocating that method of training . . . I am more interested in the mechanisms behind the results. PGs release due to hypoxia and other czs) seem to be a possibility.
    Disclaimer: While I have an M.D. the views I express are not to be taken as medical advice under any circumstances. Please check with your own doctor if you want medical advice as he/she has access to your info and can provide the most accurate advice.


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    new study

    J Appl Physiol. 2007 Jun 14
    Blood Flow Restriction during Low-Intensity Resistance Exercise Increases S6K1 Phosphorylation and Muscle Protein Synthesis.
    Fujita S, Abe T, Drummond MJ, Cadenas JG, Dreyer HC, Sato Y, Volpi E, Rasmussen BB.

    Low-intensity resistance exercise training combined with blood flow restriction (REFR) increases muscle size and strength as much as conventional resistance exercise with high-loads. However, the cellular mechanism(s) underlying the hypertrophy and strength gains induced by REFR are unknown. We have recently shown that the mTOR signaling pathway is involved in the increase in muscle protein synthesis after an acute bout of high-intensity resistance exercise in humans. Therefore, we hypothesized that an acute bout of REFR would enhance mTOR signaling and stimulate muscle protein synthesis (MPS). We measured MPS and phosphorylation status of mTOR-associated signaling proteins in 6 young male subjects. Subjects were studied once during blood flow restriction (REFR, bilateral leg extension exercise at 20% of 1-RM while a pressure cuff was placed on the proximal end of both thighs and inflated at 200mmHg) and a second time using the same exercise protocol but without the pressure cuff (CTRL). MPS in the vastus lateralis muscle was measured by using stable isotope techniques and the phosphorylation status of signaling proteins were determined by immunoblotting. Blood lactate, cortisol, and growth hormone were higher following REFR as compared to CTRL (P<0.05). S6K1 phosphorylation, a downstream target of mTOR, increased concurrently with a decreased eEF2 phosphorylation and a 46% increase in MPS following REFR (P<0.05). MPS and S6K1 phosphorylation were unchanged in the CTRL group post-exercise. We conclude that the activation of the mTOR signaling pathway appears to be an important cellular mechanism which may help explain the enhanced muscle protein synthesis during REFR. Key words: mTOR , ischemia, hypertrophy, protein metabolism, post-exercise recovery.


    again . . . not saying we should al go out and cut off the blood flow while we work out, just putting the info out there.
    Disclaimer: While I have an M.D. the views I express are not to be taken as medical advice under any circumstances. Please check with your own doctor if you want medical advice as he/she has access to your info and can provide the most accurate advice.


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    Originally Posted by Dr.Dave1 View Post
    new study




    again . . . not saying we should al go out and cut off the blood flow while we work out, just putting the info out there.

    excellent find - as usual!

    A further excellent example for the incredible capability of the body to adapt to dissociating energy demands and -production are patients with claudicatio intermittens: due to arterial occlusion, the blood supply to muscle tissue is substantially impaired, but it is exactely this impariment that - in combination with training - leads to extreme adaptations not only on a local metabolic and cellular levels but also on angiogenesis. There is a huge potential for the creation of new vessels and the opening of dormant vessels due to training under local hypoxia and isch?mia, so the msucle tissue becomes revascularized. the same mecahnisms are active in people with normal circulation but under strenous and prolonged anaerobic exercise.
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    http://www.t-nation.com/findArticle....7-073-training

    This article had some interesting ideas that might be applicable to this discussion. Basically I'm thinking that you could incorporate some isometrics to achieve low-level vascular occlusion.
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    Originally Posted by Dr.Dave1 View Post
    new study




    again . . . not saying we should al go out and cut off the blood flow while we work out, just putting the info out there.
    Originally Posted by Dr.P View Post
    excellent find - as usual!

    A further excellent example for the incredible capability of the body to adapt to dissociating energy demands and -production are patients with claudicatio intermittens: due to arterial occlusion, the blood supply to muscle tissue is substantially impaired, but it is exactely this impariment that - in combination with training - leads to extreme adaptations not only on a local metabolic and cellular levels but also on angiogenesis. There is a huge potential for the creation of new vessels and the opening of dormant vessels due to training under local hypoxia and isch?mia, so the msucle tissue becomes revascularized. the same mecahnisms are active in people with normal circulation but under strenous and prolonged anaerobic exercise.
    awesome thread, i had never seen it before this! will read more thoroughly after dinner.

    so basically when I get an awesome pump going and remove my outer shirt when it gets too tight I'm robbing myself of gains?
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    new study
    Med Sci Sports Exerc. 2007 Oct;39(10):1708-13. Links
    Effects of exercise load and blood-flow restriction on skeletal muscle function.Cook SB, Clark BC, Ploutz-Snyder LL.
    Musculoskeletal Research Laboratory, Department of Exercise Science, Syracuse University, Syracuse, NY.

    Resistance training at low loads with blood flow restriction (BFR) (also known as Kaatsu) has been shown to stimulate increases in muscle size and strength. It is unclear how occlusion pressure, exercise intensity, and occlusion duration interact, or which combination of these factors results in the most potent muscle stimulus. PURPOSE:: To determine the effect of eight BFR protocols on muscle fatigue (decrement in maximal voluntary contraction (MVC) after the performance of exercise), and to compare the decrement in MVC with the currently recommended resistance exercise intensity (~80% MVC). METHODS:: During five test sessions, 21 subjects (14 males and 7 females, 27.7 +/- 4.9 yr) completed nine protocols, each consisting of three sets of knee extensions (KE) to failure. One protocol was high-load (HL) exercise (80% MVC) with no BFR, and the other eight were BFR at varying levels of contraction intensity (20 or 40% MVC), occlusion pressure (partial (~160 mm Hg) or complete (~300 mm Hg)), and occlusion duration (off during the rest between sets or continuously applied). To evaluate each protocol, MVC were performed before and after exercise, and the decrement in force was calculated. RESULTS:: Three sets of KE at 20% MVC with continuous partial occlusion (20%ConPar) resulted in a greater decrement in MVC compared with HL (31 vs 19%, P = 0.001). None of the other BFR protocols were different from the HL protocol, nor were they different from 20%ConPar (P > 0.05). CONCLUSION:: All BFR protocols elicited at least as much fatigue as HL, even though lower loads were used. The 20%ConPar protocol was the only one that elicited significantly more fatigue than HL. Future research should evaluate protocol training effectiveness and overall safety of BFR exercise.

    PMID: 17909396 [PubMed - in process]
    Another study showing the possible benefits of limiting blood flow.
    Notice the safety disclaimer at the end . . . safety still has to be evaluated, in other words I don't recommend that you try it
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    new study using lower pressure vasoocclusion

    1: J Sci Med Sport. 2007 Dec 14 [Epub ahead of print] Links
    Effect of resistance exercise training combined with relatively low vascular occlusion.Sumide T, Sakuraba K, Sawaki K, Ohmura H, Tamura Y.


    Previous studies have demonstrated that a low-intensity resistance exercise, combined with vascular occlusion, results in a marked increase in muscular size and strength. We investigated the optimal pressure for reduction of muscle blood flow with resistance exercise to increase the muscular strength and endurance. Twenty-one subjects were randomly divided into four groups by the different application of vascular occlusion pressure at the proximal of thigh: without any pressure (0-pressure group), with a pressure of 50mmHg (50-pressure group), with a pressure of 150mmHg (150-pressure group), and with a pressure of 250mmHg (250-pressure group). The isokinetic muscle strength at angular velocities of 60 and 180 degrees /s, total muscle work, and the cross-sectional knee extensor muscle area were assessed before and after exercise. Exercise was performed three times a week over an 8-week period at an intensity of approximately 20% of one-repetition maximum for straight leg raising and hip joint adduction and maximum force for abduction training. A significant increase in strength at 180 degrees /s was noted after exercise in all subjects who exercised under vascular occlusion. Total muscle work increased significantly in the 50- and 150-pressure groups (P<0.05, P<0.01, respectively). There was no significant increase in cross-sectional knee extensor muscle area in any groups. In conclusion, resistance exercise with relatively low vascular occlusion pressure is potentially useful to increase muscle strength and endurance without discomfort.

    PMID: 18083635 [PubMed - as supplied by publisher]
    So, low pressure vascular occlusion looks to have benefits for strength gains although cross sectional area was not significantly increased
    Disclaimer: While I have an M.D. the views I express are not to be taken as medical advice under any circumstances. Please check with your own doctor if you want medical advice as he/she has access to your info and can provide the most accurate advice.


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    1: Med Sci Sports Exerc. 2008 Jan 11 [Epub ahead of print]
    Cross-Transfer Effects of Resistance Training with Blood Flow Restriction.
    Madarame H, Neya M, Ochi E, Nakazato K, Sato Y, Ishii N.


    PURPOSE:: This study investigated whether muscle hypertrophy-promoting effects are cross-transferred in resistance training with blood flow restriction, which has been shown to evoke strong endocrine activation. METHODS:: Fifteen untrained men were randomly assigned into the occlusive training group (OCC, N = 8) and the normal training group (NOR, N = 7). Both groups performed the same unilateral arm exercise (arm curl) at 50% of one-repetition maximum (1RM) without occlusion (three sets, 10 repetitions). Either the dominant or nondominant arm was randomly chosen to be trained (OCC-T, NOR-T) or to serve as a control (OCC-C, NOR-C). After the arm exercise, OCC performed leg exercise with blood flow restriction (30% of 1RM, three sets, 15-30 repetitions), whereas NOR performed the same leg exercise without occlusion. The training session was performed twice a week for 10 wk. In a separate set of experiments, acute changes in blood hormone concentrations were measured after the same leg exercises with (N = 5) and without (N = 5) occlusion. RESULTS:: Cross-sectional area (CSA) and isometric torque of elbow flexor muscles increased significantly in OCC-T, whereas no significant changes were observed in OCC-C, NOR-T, and NOR-C. CSA and isometric torque of thigh muscles increased significantly in OCC, whereas no significant changes were observed in NOR. Noradrenaline concentration showed a significantly larger increase after leg exercise with occlusion than after exercises without occlusion, though growth hormone and testosterone concentrations did not show significant differences between these two types of exercises. CONCLUSION:: The results indicate that low-intensity resistance training increases muscular size and strength when combined with resistance exercise with blood flow restriction for other muscle groups. It was suggested that any circulating factor(s) was involved in this remote effect of exercise on muscular size.

    PMID: 18202577 [PubMed - as supplied by publisher]
    I thought this study was very interesting in that it showed using vaso-occlusive training in one muscle group not only resulted in increased gains in that muscle group but also increased gains in other muscle groups trained near that time. My original assumption was that the gains associated with vaso-occlusive training were due to the harsh environment secondary to restricting/blocking blood flow to the muscle. It appears that while this may still be true, the stimulus provided by vaso-occlusive training results in the release of other systemic mediators resulting in a pro-anabolic state for other muscle groups
    Disclaimer: While I have an M.D. the views I express are not to be taken as medical advice under any circumstances. Please check with your own doctor if you want medical advice as he/she has access to your info and can provide the most accurate advice.


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  26. #26
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    Vasoocclusion can greatly enhance the effects of low-intensity training, but it cannot further enhance the effects of high-intensity resistance exercise:




    Int J Sports Med. 2008 Jan 22 [Epub ahead of print]
    Effects of Strength Training and Vascular Occlusion.
    Laurentino G, Ugrinowitsch C, Aihara AY, Fernandes AR, Parcell AC, Ricard M, Tricoli V.
    Department of Physical Education, Paulista University, Sao Paulo, Brazil.

    The purpose of our study was to determine if vascular occlusion produced an additive effect on muscle hypertrophy and strength performance with high strength training loads. Sixteen physically active men were divided into two groups: high-intensity (HI = 6 RM) and moderate-intensity training (MI = 12 RM). An occlusion cuff was attached to the proximal end of the right thigh, so that blood flow was reduced during the exercise. The left leg served as a control, thus was trained without vascular occlusion. Knee extension 1 RM and quadriceps cross-sectional area (MRI) were evaluated pre- and post-8 weeks of training. We only found a main time effect for both strength gains and quadriceps hypertrophy (p < 0.001). Therefore, we conclude that vascular occlusion in combination with high-intensity strength training does not augment muscle strength or hypertrophy when compared to high-intensity strength training alone.
    Last edited by Dr.P; 01-29-2008 at 03:33 PM.
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    Would overexpression of nitric oxide synthase be a viable method to induce vascular occlusion?
    Yes, there is indeed a deeper component to it all.
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    Originally Posted by wanderlei View Post
    Would overexpression of nitric oxide synthase be a viable method to induce vascular occlusion?

    wouldn't eNOS upregulation/overexpression lead to markedly increased NO levels with the consequence of largely dilated vessels?
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    Originally Posted by :P View Post
    wouldn't eNOS upregulation/overexpression lead to markedly increased NO levels with the consequence of largely dilated vessels?
    I would definintely say so
    Disclaimer: While I have an M.D. the views I express are not to be taken as medical advice under any circumstances. Please check with your own doctor if you want medical advice as he/she has access to your info and can provide the most accurate advice.


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    Originally Posted by :P View Post
    wouldn't eNOS upregulation/overexpression lead to markedly increased NO levels with the consequence of largely dilated vessels?
    Yes, but taken to a far enough state it may induce vascular occlusion. There's an excess of blood flow to the muscles and the increased volume eventually induces vascular occlusion and blood just pools in the muscle.
    Yes, there is indeed a deeper component to it all.
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