Post by John A. Casler on Jul 14, 2009 11:31:16 GMT -8
This is from Jamie Carruthers as posted to SuperTraining
To visit SUPERTRAINING FORUM
health.groups.yahoo.com/group/Supertraining/?yguid=44276758
Strength and Conditioning Journal:Volume 31(3)June 2009pp 77-84
The Use of Occlusion Training to Produce Muscle Hypertrophy
Loenneke, Jeremy Paul BS; Pujol, Thomas Joseph EdD, CSCS
Metabolic by-product accumulation seems to be the primary mechanism behind the benefits seen with occlusion training. Whole blood lactate (10,34), plasma lactate (9,28,34,38), and muscle cell lactate (15,14) accumulation due to the blood flow restriction results in increased GH. This is significant because GH has shown to be stimulated by an acidic intramuscular environment (38). Evidence indicates that a low pH stimulates sympathetic nerve activity through a chemoreceptive reflex mediated by intramuscular metaboreceptors and group III and IV afferent fibers (41). Consequently, the same pathway has recently been shown to play an important role in the regulation of hypophyseal secretion of GH (11,41). One study showed an increase in GH approximately 290 times greater than baseline measurements (35). This increase in GH levels is higher than what is typically seen with regular resistance training (18,17). Heat shock protein 72 (HSP 72), nitric oxide synthase-1 (NOS-1), and myostatin seem to also contribute to the increase in muscle cross-sectional area (CSA) (3,14,21,20,25,31,40). Kawada and Ishii (15) found that 2 weeks of chronic occlusion in rats caused a fiber-type shift from slow to fast. They attributed this to the additional recruitment of large motor units and their associated type II fibers at the expense of rapid fatigue in slow oxidative fibers during blood flow restriction.
HSP 72 levels have been shown to be increased in response to occlusion training (14). HSP 72 is induced by such stressors as heat, ischemia, hypoxia, and free radicals. HSP 72 acts as a chaperone to prevent misfolding or aggregation of proteins. An increase in HSP 72 content has been shown to attenuate atrophy so that it may play a role in occlusion-induced muscle hypertrophy (25). Increased expression of NOS-1 has also been shown to stimulate muscle growth through increased satellite cell activation (3,40). Myostatin is a negative regulator of muscle, and mutations of this gene result in overgrowth of musculature in mice, cattle, and humans (21,20,31). Myostatin gene expression is significantly decreased in response to occlusion training (14).
Fujita et al. (9) have shown that low-intensity resistance training increases ribosomal S6 kinase 1 (S6K1) phosphorylation and muscle protein synthesis. They suggest that enhanced mammalian target of rapamycin (mTOR) signaling may be another important cellular mechanism that may in part explain the hypertrophy induced by low-intensity occlusion training. S6K1 is involved in the regulation of messenger RNA (mRNA) translation initiation and seems to be a critical regulator of exercise-induced muscle protein synthesis and training-induced hypertrophy (4,29). Signaling to S6K1 also inhibits eukaryotic translation elongation factor 2 (eEF2) kinase, which reduces eEF2 phosphorylation and thus promotes translation elongation (42).
A follow-up study showed that REDD1 (regulated in development and DNA damage responses 1), which is normally expressed in states of hypoxia, is not increased in response to occlusion training even though hypoxia-inducible factor-1 alpha (HIF-1á) is elevated. A reduced REDD1 mRNA expression may prove to be important because a reduction in REDD1 would relieve inhibition on mTOR, promoting a stimulation of mTOR signaling, mRNA translation, and muscle cell growth (7). Possible explanations for the increase in HIF-1á without the increase in REDD1 might be that there is another unknown factor that influences the transcription of REDD1, so although HIF-1á may upregulate REDD1, another factor that is increased to a greater extent by exercise may result in downregulation of HIF-1á, resulting in a net decrease in REDD1. There might also be a factor that inhibits or stimulates HIF-1á effects on REDD1 expression, so even though HIF-1á expression is higher, its activity is not. Also, occlusion training itself may increase HIF-1á but then reperfusion after exercise may inhibit its action.
iEMG activity was significantly higher in the occluded group compared with control, and this elevated activation level of the muscle at a low level of force generation may be related to a hypoxic intramuscular environment, in which motor units of more glycolytic fibers are to be activated to keep the same level of force generation. The authors concluded that an extremely light resistance exercise combined with occlusion greatly stimulates the secretion of GH through regional accumulation of metabolites without considerable tissue damage (35).
==========================
Journal of PHYSIOLOGICAL ANTHROPOLOGY
Vol. 25 (2006) , No. 5 pp.339-344
Time under Tension and Blood Lactate Response during Four Different Resistance Training Methods
Paulo Gentil1), Elke Oliveira1) and Martim Bottaro2)
Abstract:
Mechanical stimuli have often been suggested to be the major determinant of resistance training adaptations; however, some studies suggested that metabolic changes also play an important role in the gains of muscle size and strength. Several resistance training methods (RTM) have been employed with the purpose of manipulating mechanical and metabolic stimuli; however, information about their physiological effects are scarce. The objective of this study was to compare the time under tension (TUT) and blood lactate responses among four different RTM reported in the literature. The four RTM were performed in a knee extension machine at 10 repetition maximum (RM) load by 12 recreationally trained young men. The RTM tested were: 10RM, super-slow (SL-subjects performed one 60-second repetition with 30 seconds for eccentric and 30 seconds for concentric phase), functional isometrics (FI-in each repetition, a five-second maximal isometric contraction was executed with the knees fully extended) and adapted vascular occlusion (VO-subjects performed a 20-second maximal isometric contraction with the knees fully extended and immediately proceeded to normal isoinertial lifts). According to the results, all RTM produced significant increases in blood lactate levels.
However, blood lactate responses during FI (4.48±1.57 mM) and VO (4.23±1.66 mM) methods were higher than the SL method (3.41±1.14 mM). The TUT for SL (60 s), FI (56.33±6.46 s), and VO (53.08±4.76 s) methods were higher than TUT for 10RM (42.08±3.18 s). Additionally, TUT for the SL method was higher than TUT during the VO method. Therefore, the SL method may not be recommended if one wants to provide a high metabolic stimulus. The FI method appeared to be especially effective in promoting both type of stimuli.
================
Dr Shield wrote:
The hypothesis that is actually being tested in these studies (Jones and
Rutherford, 1987; Takarada et al., 2000a; Takarada et al., 2000b) is that the metabolic stress induced by resistance training is a stimulus for hypertrophy.
Metabolic stress takes the form of substrate depletion (eg. creatine phosphate
breakdown) and the consequent build up of metabolites such as creatine, Pi, ADP, AMP, H+, lactate or something else! The exact stimulant is not identified any more clearly than this and it is probably naive to consider whether any one of these products acts
alone as a stimulus. (Lactic acid gets blamed for almost everything in exercise
science despite a distinct lack of evidence). Clearly, there is a lot more going on at the cellular level than acidosis! For example, it has been hypothesised that the occlusion of blood flow in a contracting muscle and the resulting hypoxia stimulates free radical production (Takarada et al., 2000b). In addition to causing tissue damage, there are good reasons to believe that free radicals may have a role in the regulation of muscle growth (see Takarada et al., 2000b for the references).
The most convincing evidence that metabolic stress acts as a powerful stimulant
for hypertrophy comes from Takarada et al., (2000b) (as pointed out previously by Gus Karageorgos). In this study a fairly conventional moderate-resistance
training program (employing ~80% 1 RM) for the elbow flexors was compared to a
light-resistance program (employing ~50% 1 RM) with partial vascular occlusion, a light-resistance program (employing ~50% 1 RM) without vascular occlusion and no training (control group). The vascular occlusion (applied via a blood pressure cuff)
ensured that metabolites produced during exercise were not removed from the
muscle, thus maximising metabolic stress.
After 16 weeks training the changes in muscle CSA for biceps brachii and
brachialis were significantly greater for the
80% 1 RM group and 50%-with-occlusion group than the 50% without occlusion
group. No significant differences were
found between the 80% 1 RM group and 50%-with-occlusion group but the trend was
for the 50% with-occlusion group
to exhibit greater hypertrophy, particularly in the brachialis. Interestingly,
the triceps of the occlusion group increased
in size by approximately 13-14% without being trained.
The major limitation of the study is that vascular occlusion may have had its
anabolic effects directly via increasing the
metabolite load or indirectly by raising the level of recruitment necessary to
lift the light loads. However, the former
possibility remains plausible when one considers other findings (Takarada et
al., 2000a and 2000c). Firstly, growth
hormone (GH) release has been observed to increase 290 fold over rest levels
when extremely light (~20% 1 RM)
resistance training is combined with vascular occlusion. Exercise alone resulted
in negligible changes in GH (Takarada
et al., 2000a). Secondly, a study of young subjects demonstrated that the disuse
atrophy caused by bed rest was prevented
by occasional vascular occlusion in the absence of exercise (Takarada et al.,
2000c). Presumably both effects were
mediated by GH's action on IGF-1 which has potent anabolic and anti-catabolic
effects.
It might also pay to consider some observations regarding creatine that could
arguably unify the creatine's ergogenic
effects with the metabolic stress hypothesis. Firstly, creatine induces
significant hypertrophy in unexercised embryonic
chick muscle (Ingwall, 1976). Secondly, creatine appears to stimulate protein
synthesis by increasing MRF4 and myogenin
expression in adult humans undergoing resistance training (Hespel et al., 2001).
Finally creatine is a metabolite produced
during high intensity exercise such as resistance training. One might therefore
hypothesise that creatine accumulation acts
to stimulate hypertrophy after resistance training and that supplementary
creatine magnifies this effect.
Regarding some of the valid critiques offered by list members.
1.. It is true that most of the work so far has been carried out on the
relatively untrained elderly. Work is clearly needed
on younger and more highly trained groups. However, in the aforementioned study
the effect of light resistance training
without occlusion was almost zero so it can not be said that the 50% load was
sufficient in the absence of vascular occlusion.
2.. Powerlifters and weightlifters may trigger hypertrophy almost solely via
tension mediated mechanisms while programs
employed by bodybuilders may trigger hypertrophy via a combination of tension
and metabolic stress mechanisms. The recent
research shows that those who employ lighter loads (<50% 1 RM) may still
stimulate muscle growth via maximising the
metabolic stress of the workout - even if the tension levels alone are
insufficient.
To visit SUPERTRAINING FORUM
health.groups.yahoo.com/group/Supertraining/?yguid=44276758
Strength and Conditioning Journal:Volume 31(3)June 2009pp 77-84
The Use of Occlusion Training to Produce Muscle Hypertrophy
Loenneke, Jeremy Paul BS; Pujol, Thomas Joseph EdD, CSCS
Metabolic by-product accumulation seems to be the primary mechanism behind the benefits seen with occlusion training. Whole blood lactate (10,34), plasma lactate (9,28,34,38), and muscle cell lactate (15,14) accumulation due to the blood flow restriction results in increased GH. This is significant because GH has shown to be stimulated by an acidic intramuscular environment (38). Evidence indicates that a low pH stimulates sympathetic nerve activity through a chemoreceptive reflex mediated by intramuscular metaboreceptors and group III and IV afferent fibers (41). Consequently, the same pathway has recently been shown to play an important role in the regulation of hypophyseal secretion of GH (11,41). One study showed an increase in GH approximately 290 times greater than baseline measurements (35). This increase in GH levels is higher than what is typically seen with regular resistance training (18,17). Heat shock protein 72 (HSP 72), nitric oxide synthase-1 (NOS-1), and myostatin seem to also contribute to the increase in muscle cross-sectional area (CSA) (3,14,21,20,25,31,40). Kawada and Ishii (15) found that 2 weeks of chronic occlusion in rats caused a fiber-type shift from slow to fast. They attributed this to the additional recruitment of large motor units and their associated type II fibers at the expense of rapid fatigue in slow oxidative fibers during blood flow restriction.
HSP 72 levels have been shown to be increased in response to occlusion training (14). HSP 72 is induced by such stressors as heat, ischemia, hypoxia, and free radicals. HSP 72 acts as a chaperone to prevent misfolding or aggregation of proteins. An increase in HSP 72 content has been shown to attenuate atrophy so that it may play a role in occlusion-induced muscle hypertrophy (25). Increased expression of NOS-1 has also been shown to stimulate muscle growth through increased satellite cell activation (3,40). Myostatin is a negative regulator of muscle, and mutations of this gene result in overgrowth of musculature in mice, cattle, and humans (21,20,31). Myostatin gene expression is significantly decreased in response to occlusion training (14).
Fujita et al. (9) have shown that low-intensity resistance training increases ribosomal S6 kinase 1 (S6K1) phosphorylation and muscle protein synthesis. They suggest that enhanced mammalian target of rapamycin (mTOR) signaling may be another important cellular mechanism that may in part explain the hypertrophy induced by low-intensity occlusion training. S6K1 is involved in the regulation of messenger RNA (mRNA) translation initiation and seems to be a critical regulator of exercise-induced muscle protein synthesis and training-induced hypertrophy (4,29). Signaling to S6K1 also inhibits eukaryotic translation elongation factor 2 (eEF2) kinase, which reduces eEF2 phosphorylation and thus promotes translation elongation (42).
A follow-up study showed that REDD1 (regulated in development and DNA damage responses 1), which is normally expressed in states of hypoxia, is not increased in response to occlusion training even though hypoxia-inducible factor-1 alpha (HIF-1á) is elevated. A reduced REDD1 mRNA expression may prove to be important because a reduction in REDD1 would relieve inhibition on mTOR, promoting a stimulation of mTOR signaling, mRNA translation, and muscle cell growth (7). Possible explanations for the increase in HIF-1á without the increase in REDD1 might be that there is another unknown factor that influences the transcription of REDD1, so although HIF-1á may upregulate REDD1, another factor that is increased to a greater extent by exercise may result in downregulation of HIF-1á, resulting in a net decrease in REDD1. There might also be a factor that inhibits or stimulates HIF-1á effects on REDD1 expression, so even though HIF-1á expression is higher, its activity is not. Also, occlusion training itself may increase HIF-1á but then reperfusion after exercise may inhibit its action.
iEMG activity was significantly higher in the occluded group compared with control, and this elevated activation level of the muscle at a low level of force generation may be related to a hypoxic intramuscular environment, in which motor units of more glycolytic fibers are to be activated to keep the same level of force generation. The authors concluded that an extremely light resistance exercise combined with occlusion greatly stimulates the secretion of GH through regional accumulation of metabolites without considerable tissue damage (35).
==========================
Journal of PHYSIOLOGICAL ANTHROPOLOGY
Vol. 25 (2006) , No. 5 pp.339-344
Time under Tension and Blood Lactate Response during Four Different Resistance Training Methods
Paulo Gentil1), Elke Oliveira1) and Martim Bottaro2)
Abstract:
Mechanical stimuli have often been suggested to be the major determinant of resistance training adaptations; however, some studies suggested that metabolic changes also play an important role in the gains of muscle size and strength. Several resistance training methods (RTM) have been employed with the purpose of manipulating mechanical and metabolic stimuli; however, information about their physiological effects are scarce. The objective of this study was to compare the time under tension (TUT) and blood lactate responses among four different RTM reported in the literature. The four RTM were performed in a knee extension machine at 10 repetition maximum (RM) load by 12 recreationally trained young men. The RTM tested were: 10RM, super-slow (SL-subjects performed one 60-second repetition with 30 seconds for eccentric and 30 seconds for concentric phase), functional isometrics (FI-in each repetition, a five-second maximal isometric contraction was executed with the knees fully extended) and adapted vascular occlusion (VO-subjects performed a 20-second maximal isometric contraction with the knees fully extended and immediately proceeded to normal isoinertial lifts). According to the results, all RTM produced significant increases in blood lactate levels.
However, blood lactate responses during FI (4.48±1.57 mM) and VO (4.23±1.66 mM) methods were higher than the SL method (3.41±1.14 mM). The TUT for SL (60 s), FI (56.33±6.46 s), and VO (53.08±4.76 s) methods were higher than TUT for 10RM (42.08±3.18 s). Additionally, TUT for the SL method was higher than TUT during the VO method. Therefore, the SL method may not be recommended if one wants to provide a high metabolic stimulus. The FI method appeared to be especially effective in promoting both type of stimuli.
================
Dr Shield wrote:
The hypothesis that is actually being tested in these studies (Jones and
Rutherford, 1987; Takarada et al., 2000a; Takarada et al., 2000b) is that the metabolic stress induced by resistance training is a stimulus for hypertrophy.
Metabolic stress takes the form of substrate depletion (eg. creatine phosphate
breakdown) and the consequent build up of metabolites such as creatine, Pi, ADP, AMP, H+, lactate or something else! The exact stimulant is not identified any more clearly than this and it is probably naive to consider whether any one of these products acts
alone as a stimulus. (Lactic acid gets blamed for almost everything in exercise
science despite a distinct lack of evidence). Clearly, there is a lot more going on at the cellular level than acidosis! For example, it has been hypothesised that the occlusion of blood flow in a contracting muscle and the resulting hypoxia stimulates free radical production (Takarada et al., 2000b). In addition to causing tissue damage, there are good reasons to believe that free radicals may have a role in the regulation of muscle growth (see Takarada et al., 2000b for the references).
The most convincing evidence that metabolic stress acts as a powerful stimulant
for hypertrophy comes from Takarada et al., (2000b) (as pointed out previously by Gus Karageorgos). In this study a fairly conventional moderate-resistance
training program (employing ~80% 1 RM) for the elbow flexors was compared to a
light-resistance program (employing ~50% 1 RM) with partial vascular occlusion, a light-resistance program (employing ~50% 1 RM) without vascular occlusion and no training (control group). The vascular occlusion (applied via a blood pressure cuff)
ensured that metabolites produced during exercise were not removed from the
muscle, thus maximising metabolic stress.
After 16 weeks training the changes in muscle CSA for biceps brachii and
brachialis were significantly greater for the
80% 1 RM group and 50%-with-occlusion group than the 50% without occlusion
group. No significant differences were
found between the 80% 1 RM group and 50%-with-occlusion group but the trend was
for the 50% with-occlusion group
to exhibit greater hypertrophy, particularly in the brachialis. Interestingly,
the triceps of the occlusion group increased
in size by approximately 13-14% without being trained.
The major limitation of the study is that vascular occlusion may have had its
anabolic effects directly via increasing the
metabolite load or indirectly by raising the level of recruitment necessary to
lift the light loads. However, the former
possibility remains plausible when one considers other findings (Takarada et
al., 2000a and 2000c). Firstly, growth
hormone (GH) release has been observed to increase 290 fold over rest levels
when extremely light (~20% 1 RM)
resistance training is combined with vascular occlusion. Exercise alone resulted
in negligible changes in GH (Takarada
et al., 2000a). Secondly, a study of young subjects demonstrated that the disuse
atrophy caused by bed rest was prevented
by occasional vascular occlusion in the absence of exercise (Takarada et al.,
2000c). Presumably both effects were
mediated by GH's action on IGF-1 which has potent anabolic and anti-catabolic
effects.
It might also pay to consider some observations regarding creatine that could
arguably unify the creatine's ergogenic
effects with the metabolic stress hypothesis. Firstly, creatine induces
significant hypertrophy in unexercised embryonic
chick muscle (Ingwall, 1976). Secondly, creatine appears to stimulate protein
synthesis by increasing MRF4 and myogenin
expression in adult humans undergoing resistance training (Hespel et al., 2001).
Finally creatine is a metabolite produced
during high intensity exercise such as resistance training. One might therefore
hypothesise that creatine accumulation acts
to stimulate hypertrophy after resistance training and that supplementary
creatine magnifies this effect.
Regarding some of the valid critiques offered by list members.
1.. It is true that most of the work so far has been carried out on the
relatively untrained elderly. Work is clearly needed
on younger and more highly trained groups. However, in the aforementioned study
the effect of light resistance training
without occlusion was almost zero so it can not be said that the 50% load was
sufficient in the absence of vascular occlusion.
2.. Powerlifters and weightlifters may trigger hypertrophy almost solely via
tension mediated mechanisms while programs
employed by bodybuilders may trigger hypertrophy via a combination of tension
and metabolic stress mechanisms. The recent
research shows that those who employ lighter loads (<50% 1 RM) may still
stimulate muscle growth via maximising the
metabolic stress of the workout - even if the tension levels alone are
insufficient.