EVIDENCE-BASED RESISTANCE TRAINING RECOMMENDATIONS
Really good review of the clinical studies involving strength training, below the summary and recommendations from the article.....
*All credit goes to the authors of the above linked article ofcourse.
Intensity
Persons should train until momentary muscular failure to actively recruit all of the available motor units and muscle fibres, as opposed to a pre-determined number of repetitions.
Load and Repetition Range
Persons should self-select a weight >80% 1RM and perform repetitions to failure. Evidence suggests this is optimal for maximising strength and muscular endurance gains, whilst helping to improve bone mineral density.
Resistance Type
Persons should select resistance type based on personal choice, although evidence appears to suggest that resistance machines might have a lower risk of injury than free-weights.There appears to be no difference in strength gains between using free-weights, machines or other resistance types.Free weights and sport specific movements show no enhancement in sporting performance or force throughout that movement.
Repetition Duration
Persons should maintain steady force production throughout a range of motion, and reduce external forces such as momentum; movements should be of a pace that maintains muscular tension, not ballistic or explosive in nature.Faster movements cause greater peaks in both muscular and ground reaction forces which likely transfer through joints and connective tissue, potentially causing injury.
Volume of Exercise, Frequency and Periodization
Persons can obtain appreciably the same strength gains by performing only a single set of each exercise 1 x / 2 x week, compared to higher volume workouts.Persons should train when they feel physically and mentally ready to do so. Both physical and mental fatigue have the potential to negatively affect a workout and/or muscular growth and development.No specific periodized routine is unequivocally supported within the literature.
Genetics
Persons should consider their somatotype and that their genetics will dictate their muscular growth and development. Previous success with a routine is not evidence that it is optimal, genetic differences might dictate interpersonal differences in volume and frequency.
Wednesday, 10 August 2011
Sunday, 7 August 2011
Brain control of fat metabolism
Brain insulin controls adipose tissue lipolysis and lipogenesis.
"Here, we show that insulin infused into the mediobasal hypothalamus (MBH) of Sprague-Dawley rats increases WAT lipogenic protein expression, inactivates hormone-sensitive lipase (Hsl), and suppresses lipolysis"
"Conversely, mice that lack the neuronal insulin receptor exhibit unrestrained lipolysis and decreased de novo lipogenesis in WAT. Thus, brain and, in particular, hypothalamic insulin action play a pivotal role in WAT functionality."
Hypothalamic control of lipid metabolism: focus on leptin, ghrelin and melanocortins.
"In mammals, neurons, particularly in the arcuate nucleus of the hypothalamus (ARC), are involved in the regulation of energy homeostasis. One regulatory pathway consists of neurons co-expressing neuropeptide Y (NPY) and agouti-related protein (AgRP), both potent stimulators of food intake, and an adjacent set of ARC neurons co-express proopiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART), which suppress food intake."
"The anorectic effect of these drugs requires the accumulation of malonyl-CoA in the hypothalamus, which may be sensed as a signal of nutrient abundance by critical neurons regulating food intake (‘malonyl-CoA hypothesis’) and decreased expression of orexigenic (AgRP and NPY) and elevated expression of anorexigenic (CART, POMC) neuropeptides in the ARC"
"Leptin induces opposite effects on two ARC neuronal subpopulations: it directly inhibits the orexigenic NPY/AgRP-containing neurons and it stimulates the electrical activity of anorexigenic POMC neurons"
"One of the factors required by leptin to exert its anorectic effect is hypothalamic AMPK"
"suppression of AMPK activity in the medial hypothalamus is necessary for leptin’s anorexic and weight loss effects and that lack of suppression causes leptin resistance"
"The most relevant receptors in terms of energy balance regulation are MC3R and MC4R. Receptor agonist delivery into the hypothalamus reduces food intake, body weight and fat mass"
"Anatomical studies have demonstrated that central WAT sympathetic outflow neurons express MC4R"
" Central melanocortins modulate the norepinephrine turnover, which is the principal initiator of lipolysis in mammals. Norepinephrine is released from the sympathetic nerves innervating WAT, and the central injection of a MC3/4R agonist increased the norepinephrine turnover in specific fat depots"
Overall this is a very good study and needs to read in its entirety.
Hyperphagia and increased fat accumulation in two models of chronic CNS glucagon-like peptide-1 loss of function.
More evidence for the power of GLP-1 in obesity.
"Collectively, these data provide the strongest evidence to date that CNS GLP-1 plays a physiologic role in the long-term regulation of energy balance. Moreover, they suggest that this role is distinct from that of circulating GLP-1 as a short-term satiation signal."
"Here, we show that insulin infused into the mediobasal hypothalamus (MBH) of Sprague-Dawley rats increases WAT lipogenic protein expression, inactivates hormone-sensitive lipase (Hsl), and suppresses lipolysis"
"Conversely, mice that lack the neuronal insulin receptor exhibit unrestrained lipolysis and decreased de novo lipogenesis in WAT. Thus, brain and, in particular, hypothalamic insulin action play a pivotal role in WAT functionality."
Hypothalamic control of lipid metabolism: focus on leptin, ghrelin and melanocortins.
"In mammals, neurons, particularly in the arcuate nucleus of the hypothalamus (ARC), are involved in the regulation of energy homeostasis. One regulatory pathway consists of neurons co-expressing neuropeptide Y (NPY) and agouti-related protein (AgRP), both potent stimulators of food intake, and an adjacent set of ARC neurons co-express proopiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART), which suppress food intake."
"The anorectic effect of these drugs requires the accumulation of malonyl-CoA in the hypothalamus, which may be sensed as a signal of nutrient abundance by critical neurons regulating food intake (‘malonyl-CoA hypothesis’) and decreased expression of orexigenic (AgRP and NPY) and elevated expression of anorexigenic (CART, POMC) neuropeptides in the ARC"
"Leptin induces opposite effects on two ARC neuronal subpopulations: it directly inhibits the orexigenic NPY/AgRP-containing neurons and it stimulates the electrical activity of anorexigenic POMC neurons"
"One of the factors required by leptin to exert its anorectic effect is hypothalamic AMPK"
"suppression of AMPK activity in the medial hypothalamus is necessary for leptin’s anorexic and weight loss effects and that lack of suppression causes leptin resistance"
"The most relevant receptors in terms of energy balance regulation are MC3R and MC4R. Receptor agonist delivery into the hypothalamus reduces food intake, body weight and fat mass"
"Anatomical studies have demonstrated that central WAT sympathetic outflow neurons express MC4R"
" Central melanocortins modulate the norepinephrine turnover, which is the principal initiator of lipolysis in mammals. Norepinephrine is released from the sympathetic nerves innervating WAT, and the central injection of a MC3/4R agonist increased the norepinephrine turnover in specific fat depots"
Overall this is a very good study and needs to read in its entirety.
Hyperphagia and increased fat accumulation in two models of chronic CNS glucagon-like peptide-1 loss of function.
More evidence for the power of GLP-1 in obesity.
"Collectively, these data provide the strongest evidence to date that CNS GLP-1 plays a physiologic role in the long-term regulation of energy balance. Moreover, they suggest that this role is distinct from that of circulating GLP-1 as a short-term satiation signal."
Saturday, 6 August 2011
Cross-talk between adipose and gastric leptins
Cross-talk between adipose and gastric leptins for the control of food intake and energy metabolism.
" In accordance with the lipostatic theory stated by Kennedy in 1953, leptin was originally discovered in white adipose tissue. Its expression by other tissues was later established."
"Among them, the gastric mucosa has been shown to secrete large amounts of leptin."
" However while adipose tissue secretes leptin in a slow constitutive endocrine way, the gastric mucosa releases leptin in a rapid regulated exocrine fashion into the gastric juice."
"Scrutiny into transport mechanisms revealed that a significant amount of the exocrine leptin crosses the intestinal wall by active transcytosis."
" Exocrine-secreted gastric leptin thus participates in a physiological axis independent in terms of time and regulation from that of adipose tissue to rapidly control food intake and nutrient absorption."
" In accordance with the lipostatic theory stated by Kennedy in 1953, leptin was originally discovered in white adipose tissue. Its expression by other tissues was later established."
"Among them, the gastric mucosa has been shown to secrete large amounts of leptin."
" However while adipose tissue secretes leptin in a slow constitutive endocrine way, the gastric mucosa releases leptin in a rapid regulated exocrine fashion into the gastric juice."
"Scrutiny into transport mechanisms revealed that a significant amount of the exocrine leptin crosses the intestinal wall by active transcytosis."
" Exocrine-secreted gastric leptin thus participates in a physiological axis independent in terms of time and regulation from that of adipose tissue to rapidly control food intake and nutrient absorption."
Insulin responsible for poor incretin response?
Insulin-dependent suppression of cholesterol 7α-hydroxlase is a possible link between glucose and cholesterol metabolisms.
cholesterol 7a-hydroxlase is the rate-limiting step for the synthesis of bile acids from cholesterol.
Is this why obese people have high cholesterol and poor postprandial bile acid/incretin responses?
Food for thought anyway.
cholesterol 7a-hydroxlase is the rate-limiting step for the synthesis of bile acids from cholesterol.
Is this why obese people have high cholesterol and poor postprandial bile acid/incretin responses?
Food for thought anyway.
Friday, 5 August 2011
Incretin's continued......
Role of incretins in the regulation of bone metabolism
"GIP has anabolic effects on bone mainly by stimulating osteoblastic bone formation through intermittent elevation of intracellular cAMP levels. On the other hand, GLP-1 is suggested to regulate bone resorption indirectly through the thyroid C cell."
Effects of GIP receptor antagonist for treatment of obesity
"GIP receptor antagonists possess favorable effects such as, decreased body adiposity or improvement of glucose intolerance through change of fat metabolism in high-fat diet induced or genetically induced obese experimental animals.
Loss of incretin effect is a specific, important, and early characteristic of type 2 diabetes.
Good review and free article.
Reversal of obesity and insulin resistance by a non-peptidic glucagon-like peptide-1 receptor agonist in diet-induced obese mice.
"Different from Boc5 treatment, caloric restriction did not affect adiposity significantly and circulating adipocytokines levels remained abnormal"
"These apparent differences imply that the regulatory role exerted by Boc5 (and hence, incretin mimetics in general) on lipid metabolism is independent of its inhibition on food intake."
Well well well, so much for the whole calorie restriction thing.
"Our results indicate that the basal glucose incorporation was significantly elevated in adipocytes isolated from obese mice while their response to insulin stimulation was severely impaired"
"the role of caloric restriction (pair-feeding) in modifying fat cell lipogenesis and lipolysis was minimal"
"GIP has anabolic effects on bone mainly by stimulating osteoblastic bone formation through intermittent elevation of intracellular cAMP levels. On the other hand, GLP-1 is suggested to regulate bone resorption indirectly through the thyroid C cell."
Effects of GIP receptor antagonist for treatment of obesity
"GIP receptor antagonists possess favorable effects such as, decreased body adiposity or improvement of glucose intolerance through change of fat metabolism in high-fat diet induced or genetically induced obese experimental animals.
Loss of incretin effect is a specific, important, and early characteristic of type 2 diabetes.
Good review and free article.
Reversal of obesity and insulin resistance by a non-peptidic glucagon-like peptide-1 receptor agonist in diet-induced obese mice.
"Different from Boc5 treatment, caloric restriction did not affect adiposity significantly and circulating adipocytokines levels remained abnormal"
"These apparent differences imply that the regulatory role exerted by Boc5 (and hence, incretin mimetics in general) on lipid metabolism is independent of its inhibition on food intake."
Well well well, so much for the whole calorie restriction thing.
"Our results indicate that the basal glucose incorporation was significantly elevated in adipocytes isolated from obese mice while their response to insulin stimulation was severely impaired"
"the role of caloric restriction (pair-feeding) in modifying fat cell lipogenesis and lipolysis was minimal"
Wednesday, 3 August 2011
Bile acid signalling, how important is it?
Bile-induced secretion of glucagon-like peptide-1: pathophysiological implications in type 2 diabetes?
"it has become clear that bile acids not only act as simple fat solubilizers, but additionally represent complex hormonal metabolic integrators."
"bile acids are ligands for the nuclear receptor FXR controlling transcription of genes involved in, for example, bile acid, cholesterol, and glucose metabolism"
"Bile acid activation of TGR5 results in increased intracellular cAMP levels, which in brown adipose tissue and muscle cells modulates energy expenditure by activating type 2 iodothyronine deiodinase, which in turn deiodinates thyroxine to the active thyroid hormone triiodothyronine"
"The reason for these limitations may be due to the fact that current GLP-1-based drugs exert their effects via elevated plasma levels of “GLP-1 receptor agonists”, and therefore, allegedly, may not elicit the local effects that endogenous secreted GLP-1 might have."
"Roux-en-Y gastric bypass (RYGB) surgery incurs remission of type 2 diabetes in the majority of patients (4), a “cure” of type 2 diabetes that has been linked to increased endogenous GLP-1 secretion"
"recent studies provide evidence for L cell expression of several G protein-coupled receptors (for example GPR120), which can be activated by long-chain fatty acids and, hence, result in GLP-1 secretion"
"Recently, the G protein-coupled receptor TGR5 was found in the enteroendocrine GLP-1-secreting cell line STC-1 (17) and in primary L cells from mice"
"These findings suggest that postprandial gall bladder contraction and increased flow of bile acids to the intestine potentiate nutrient-induced GLP-1 secretion from the L cells via TGR5 activation. "
"The newly described role of bile-induced TGR5 activation in L cell secretion combined with findings of reduced postprandial gall bladder emptying in type 2 diabetes (38, 39) [worsened by diabetic neuropathy typical for patients with long-standing disease (39)] suggests that reduced postprandial GLP-1 responses in patients with type 2 diabetes may, hypothetically, arise as a consequence of diabetic gall bladder dysmotility, which in turn might reduce postprandial bile flow to the intestine and, thereby, TGR5 activation in the L cells."
"Last, serum bile acids have been found to increase following RYGB (positively correlated with GLP-1 and negatively correlated with thyrotropic hormone) (33). As direct access of bile acids to L cell-rich parts of the small intestine is established following RYGB"
The Changes of Pro-opiomelanocortin Neurons in Type 2 Diabetes Mellitus Rats After Ileal Transposition: The Role of POMC Neurons.
"The Ileal transposition group demonstrated significantly improved plasma glucose homeostasis with increased glucagon-like peptide 1 secretion.
"associated with increased central neuronal activity with increased pro-opiomelanocortin and derivative gene expression in the hypothalamus and increased protein expression in the pituitary gland."
"More pro-opiomelanocortin neurons in the hypothalamus of diabetes rats were activated after ileal transposition. "
"it has become clear that bile acids not only act as simple fat solubilizers, but additionally represent complex hormonal metabolic integrators."
"bile acids are ligands for the nuclear receptor FXR controlling transcription of genes involved in, for example, bile acid, cholesterol, and glucose metabolism"
"Bile acid activation of TGR5 results in increased intracellular cAMP levels, which in brown adipose tissue and muscle cells modulates energy expenditure by activating type 2 iodothyronine deiodinase, which in turn deiodinates thyroxine to the active thyroid hormone triiodothyronine"
"The reason for these limitations may be due to the fact that current GLP-1-based drugs exert their effects via elevated plasma levels of “GLP-1 receptor agonists”, and therefore, allegedly, may not elicit the local effects that endogenous secreted GLP-1 might have."
"Roux-en-Y gastric bypass (RYGB) surgery incurs remission of type 2 diabetes in the majority of patients (4), a “cure” of type 2 diabetes that has been linked to increased endogenous GLP-1 secretion"
"recent studies provide evidence for L cell expression of several G protein-coupled receptors (for example GPR120), which can be activated by long-chain fatty acids and, hence, result in GLP-1 secretion"
"Recently, the G protein-coupled receptor TGR5 was found in the enteroendocrine GLP-1-secreting cell line STC-1 (17) and in primary L cells from mice"
"These findings suggest that postprandial gall bladder contraction and increased flow of bile acids to the intestine potentiate nutrient-induced GLP-1 secretion from the L cells via TGR5 activation. "
"The newly described role of bile-induced TGR5 activation in L cell secretion combined with findings of reduced postprandial gall bladder emptying in type 2 diabetes (38, 39) [worsened by diabetic neuropathy typical for patients with long-standing disease (39)] suggests that reduced postprandial GLP-1 responses in patients with type 2 diabetes may, hypothetically, arise as a consequence of diabetic gall bladder dysmotility, which in turn might reduce postprandial bile flow to the intestine and, thereby, TGR5 activation in the L cells."
"Last, serum bile acids have been found to increase following RYGB (positively correlated with GLP-1 and negatively correlated with thyrotropic hormone) (33). As direct access of bile acids to L cell-rich parts of the small intestine is established following RYGB"
The Changes of Pro-opiomelanocortin Neurons in Type 2 Diabetes Mellitus Rats After Ileal Transposition: The Role of POMC Neurons.
"The Ileal transposition group demonstrated significantly improved plasma glucose homeostasis with increased glucagon-like peptide 1 secretion.
"associated with increased central neuronal activity with increased pro-opiomelanocortin and derivative gene expression in the hypothalamus and increased protein expression in the pituitary gland."
"More pro-opiomelanocortin neurons in the hypothalamus of diabetes rats were activated after ileal transposition. "
Dairy pwns
Dairy attentuates oxidative and inflammatory stress in metabolic syndrome.
adequate-dairy decreased malondialdehyde and oxidized LDL at 7 d (35% and 11%, respectively; P < 0.01), with further decreases by 12 wk. Inflammatory markers were suppressed with intake of adequate-dairy, with decreases in tumor necrosis factor-α at 7 d and further reductions through 12 wk (35%; P < 0.05);
and a corresponding 55% increase in adiponectin at 12 wk (P < 0.01).
adequate-dairy significantly reduced waist circumference and trunk fat (P < 0.01 for both)
adequate-dairy decreased malondialdehyde and oxidized LDL at 7 d (35% and 11%, respectively; P < 0.01), with further decreases by 12 wk. Inflammatory markers were suppressed with intake of adequate-dairy, with decreases in tumor necrosis factor-α at 7 d and further reductions through 12 wk (35%; P < 0.05);
and a corresponding 55% increase in adiponectin at 12 wk (P < 0.01).
adequate-dairy significantly reduced waist circumference and trunk fat (P < 0.01 for both)
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