Friday, 23 March 2012

Muscluar Hypertrophy – What is it and How you do it

What is it?
Muscle hypertrophy is an increase in the size of the muscle cells. It differs from muscle hyperplasma, which is the formation of new muscle cells.

The two types of Hypertrophy are Myofibrillar& Sarcoplasmic.

Skeletal muscles are made up of myofibrils which are contractile proteins (basically the fibres that actually generate force) and sarcoplasm which include water, glycogen, minerals, connective tissues, etc.  

There lies a distinction between myofibrillar growth, the growth of the actual contractile fibres which leads to the greatest improvement in athletic performance and sarcoplasmic growth. Sarcoplasmic growth, meaning increases in storage of glycogen, water, etc. does not have a great deal of positive impact on overall performance but there is still physical growth.  This may also be referred as functional hypertrophy vs. non-functional hypertrophy.

How you do it

Myofibrillar and scaroplasmic hypertrophy are not purely individual. Meaning you can’t solely focus on one or the other. Yes certain training protocols may stimulate more myofibrillar growth than scarcoplasmic or vice versa but you don’t get one without the other. 

From now on the topic will be on muscular hypertrophy as a whole. Look at it from the point of view of the lower end of the recommendations being for a greater percentage of scaroplasmic growth and the top end for more myofibrillar growth.

The stimulus for muscle growth falls into three distinct (which overlap each other somewhat) categories: progressive tension overload, muscle damage and metabolic stress.

Each may play some sort of role instimulating the overall growth processes.  It has commonly referred to growth as being related to primarily tension (load on the bar) or fatigue (metabolic stress issues) but damage also appears to be involved.

Studies have suggested that hypertrophy can be stimulated at an optimum degree with a resistance ranging from 60% to 85% of your 1 repetition maximum load weight.  For most people that is the maximum weight use to perform about 5 to 8 repetitions (85%).

Studies that have looked at the volume (work amount) have found to be a higher amount of ‘sets’ have produced maximum training adaptations and stimulated maximal hypertrophy. In subjects that performed either, one, three or eight sets (at 85% of 1RM) showed that 8 sets was superior to 4 and 4 sets were superior to 1.

Meta-analysis reviews on total training volumes have found that a total volume of 30-60 per session (per muscle group) yielded the greatest results in stimulating hypertrophy and training performed twice per week.

Another important factor in training load is the rest time between sets.Rest times have a great impact on the metabolic stress part of the equation (progressive tension overload, muscle damage and metabolic stress).

 Research has shown that there is very little benefit from rest times longer than 2 or 3 minutes. Rest times ranging from 1 minute to 5 minutes have been reviewed and found that strength gains, training adaptations, neuromuscular/fibre recruitment, hormonal  and performance are not significantly better after 3 minutes of rest between sets.

Frequency is the last piece of the puzzle. Most people these days look at training any given muscle group more than once a week as over-training. Well again, research has begged to differ with untrained people gaining most benefits (growth, strength etc) from three times per week for each muscle group and trained individuals having a frequency of twice per week or once every 4-5 days. That also includes the previously mentioned training volumes and loads, which the research was based on for the frequency of training studies.

So summing it all up and what research has found, is by doing each muscle group with a rep range of 5-8 (load of 60% to 85% of 1RM) over 8 sets(which works out to be 40-64 repetitions in a session)with 2 to 3 minutes rest between sets and training each muscle two times per week will be optimum for stimulating muscular hypertrophy and ensure continual progression.

Just as a side note, typically the more highly trained the individual, the higher the work load is needed to stimulate hypertrophy at optimum levels. So beginners will be best suited to using the lower end of the recommendations.

Setting up a routine

So the basics of what stimulates muscular hypertrophy have been discussed and with all of it in mind, now it is up to setting up a routine.

Within the context of the article, doing a 3 day training split would be most suitable. The training split would be broken down into a Push day, Pull day and Legs for maximum and most optimum results, in my opinion. The Push day is made up of Chest, Shoulders and Triceps, the Pull day is Back and Biceps and the final day of Legs is self-explanatory.

Implementing the already outlined information on volume for the routine, it brings me to the point of the smaller/minor/secondary/accessory/assistance muscle groups and the amount of volume and frequency they should be trained. 

Deltoids, Biceps, Triceps, Abdominals (yes they are still made in the kitchen), Hamstrings and Calves are the secondary muscle groups I’m talking about. They are the muscle groups which offer assistance in the core movements of the primary muscle groups of Chest, Back and Quadriceps.

Considering all factors like injury prevention, indirect activation, physical and psychological burn out, training performance and progression the small muscle groups should be trained as frequently as the major muscle groups, but the volume should be less with slightly varying load ranges. Something in the realms of half to 2/3rds of the volume with certain movements being performed in the higher end of the optimal repetition range for hypertrophy.


As it always seems, someone will always take this out of context and not comprehend the article for what it is. This is not for everyone nor is it meant to be so please keep that in mind before you start picking it apart (which is perfectly fine).

This is purely talking about maximising muscular hypertrophy without any outside factors impacting on it. This article was written to de-bunk the typical myths with hypertrophy training etc. I’ve constructed it all from relevant, credible, practical and methodical scientific research and studies on human kinetics and physiology etc.

I’m not factoring in peoples time schedule, lifestyle, training abilities or inabilities, physiological functions, dietary intake and individual goals.They alone determine what amount and type of resistance/hypertrophy training is performed!

 Studies Referenced/Used 

Thursday, 22 March 2012

Gaining Muscle while Dropping Body Fat & Carbohydrate Cycling

Muscle growth/increasing LBM is done by stimulating the body with the appropriate stimulus. Increasing load on the muscle forces growth due the body needing to adapt to be able to handle the volume of work.

The next part of that is to ensure protein synthesis is greater than protein breakdown. Consuming adequate protein and resistance training stimulates protein synthesis.
FYI resistance training stimulates protein synthesis for 24 hours REGARDLESS of being in a FED or Fasted state.
Meaning nutrient timing is irrelevant unless you have multiple glycogen depleting sessions for the same group of muscles in the one day and have limited time to get nutrients in before the next session. Carbohydrates for replenishment of glycogen can be consumed over a 24hr period to achieve full levels. 

When a subject exercises, muscle glycogen declines and is slowly restored over the following 24 h if carbohydrate intake is normal. Not to mention Glycogen also starts to be replenished even without the presence of carbohydrates
Therefore, when two exercise sessions of 1 h is separated by 2 h, the second bout of exercise is undertaken with low muscle glycogen at its start, whereas muscle glycogen is restored before each exercise bout when the exercise is separated by 24 h.

Also carbohydrate type is irrelevant on either performance or replenishment.
Consuming adequate protein in time of CALORIE DEFICITS limits any LMB losses and ensuring the calorie deficit is not excessive LBM gains can be made
Protein synthesis is stimulated at a great rate with the ingestion of >1.5g/kg and REGARDLESS of frequency makes NO difference in the protein retention.

There are many different pathways/methods go into increasing LBM and decreasing BF, but on the basis it is being in a calorie deficit will induce BF decreases (due to the BF being the primary source of STORED ENERGY) and ensuring protein synthesis is greater than protein breakdown (via adequate protein and performing resistance training).

Now being in a calorie SURPLUS will allow for muscle gain at optimum/fast rates. Also the amount of BF will also play a part in how fast an increase in LBM can occur. 

An individual with a higher BF will have the ability to gain LBM at a fast rate due to of course a higher amount of STORED ENERGY.  That should seem quite common sense. For a leaner individual of course it is the harder/close to impossible to drop BF and increase LBM, and at that it is a SLOW rate. Mainly due to hormonal functions, but that is beyond the realms of this essay.

There are macronutirent and calorie cycling methods that can be used to maximize LBM gains while dieting and for the most part unless you are a competitive NATURAL bodybuilder and have hormonal imbalances there is no real need to even focus on that but for completeness I will go into some protocols for carbohydrate cycling.

Carbohydrate loading/cycling

The process of carbohydrate loading/cycling when dieting (dropping body fat while attempting to gain/maintain muscle or enhance exercise performance) has been the subject of many different protocols over the years.

The primary purpose of carbohydrate loading/cycling is to A) refill muscle glycogen and B) manipulate hormonal function (Thyroid,Leptin and Insulin).

PLEASE NOTE – Depending on the individual’s bodyfat levels, goal (desired body fat& overall composition), hormonal function, general day-to-day activity and training volume, carbohydrate cycling/loading may or may not be required/beneficial. Each case should be looked at on it’s own merits.

While long-term macronutrient, calorie intake and training stimulus determine body composition, it can be a little deep than that. Hormonal function and exercise performance also play a part in body composition, be it indirectly (stimulus load/volume ability – exercise performance) or directly (BMR and overall EE – hormonal function).

The two main carbohydrate loading/cycling protocols are the A) higher carbohydrate intake on training days (with lower fats and at maintenance calories or just above) and lower carbohydrate intake on non training days (with higher fats and in a calorie deficit) or B) 4 or 5 days of low carbohydrate intake followed be 3 or 2 of higher carbohydrate intake.

I could go quite in-depth on protocol’s pros and cons but IMO the only real thing that matters is what suits the individuals schedule and what ultimately allows for the best long term dietary adherence.

Martin Berkhan’s protocol (training days cycling) -

I normally suggest a 4 or 5-day of low carbohydrate intake (while in a calorie deficit) followed by 3 or 2 days of carbohydrate loading (eating at maintenance or slightly above 5-10%). So the net result at the end of the cycle is still a calorie deficit, all be it small. I also find that the easiest way to adhere to the calorie requirements for the long term and also allowing for some added flexibility during the more social parts of the week (the weekend).

Even thought muscle glycogen is restored and can be restored in 1 day (with the right carbohydrate intake), other mechanisms like hormonal function have more of a positive reaction for the length of time with increased carbohydrate consumption not simply total amount consumed.

Expanding on exercise performance point. The existing exercise performance data (all be it done on endurance cardiovascular exercise) is mixed. Studies have suggested that once adaptations to the utilization of fat for fuel (5 days), a shorter carbohydrate load (1 day) still may not be enough to improve exercise performance. For a more in-depth look, check out this article by Lyle McDonald -

So with that in mind, from a performance point of view, maybe a more regular and more moderate cycling period may be of some benefit.

The key point being the amount of carbohydrates to be consumed, the length of time with increased consumption, the amount being used during exercise and the amount we can store that ultimately lead manipulating intake to maximize muscle gain or at least maintaining muscle while dropping body fat.

Technical Shit

Carbohydrate amount does not equal the amount of glycogen. They have separate units of measure are not of equal quantities/units of measure. 5.5 grams of carbohydrates = 1 millimole (mmol) of glycogen.

Trained individuals have higher glycogen storage abilities both due to dietary carbohydrate intake and larger/active muscle tissues.  They (athletes) have glycogen levels at 110-130 mmol/kg.

Fat oxidization increases at rest and during aerobic exercise at muscle glycogen levels of 70 mmol/kg (or 12 grams carbohydrates/kg). Levels below 40 mmol/kg = 7 grams of carbohydrates/kg impairs exercise performance and increases the potential for protein to be used as fuel.

Glycogen super-compensation can increase levels to 175 mmol/kg if glycogen is depleted to a great amount (which is around 25-30 mmol/kg). Total exhaustion during exercise occurs when levels drop to 15-25 mmol/kg and the enzymes for super-compensation are also impaired at that level (below 25 mmol/kg).

At 70% 1RM, glycogen is depleted at approx. 1.3 mmol/kg/repetition. Basically for every 2 sets of 10 reps, you will use 5.5 grams of carbohydrates as fuel. Endurance athletes will use more during a training session compared to a weight lifter.

Thursday, 22 December 2011

40 Things You Should Know – The Science (part 11)

Point 49

Effect of caffeine ingestion after creatine supplementation on intermittent high-intensity sprint performance.


The aim of this study was to investigate the effects of acute caffeine ingestion on intermittent high-intensity sprint performance after 5 days of creatine loading. After completing a control trial (no ergogenic aids, CON), twelve physically active men were administered in a double-blind, randomized crossover protocol to receive CRE + PLA (0.3 g kg(-1) day(-1) of creatine for 5 days then followed by 6 mg kg(-1) of placebo) and CRE + CAF (0.3 g kg(-1) day(-1) of creatine for 5 days and followed by 6 mg kg(-1) of caffeine), after which they performed a repeated sprint test. Each test consisted of six 10-s intermittent high-intensity sprints on a cycling ergometer, with 60-s rest intervals between sprints. Mean power, peak power, rating of perceived exertion (RPE), and heart rates were measured during the test. Blood samples for lactate, glucose, and catecholamine concentrations were drawn at specified intervals. The mean and peak power observed in the CRE + CAF were significantly higher than those found in the CON during Sprints 1 and 3; and the CRE + CAF showed significantly higher mean and peak power than that in the CRE + PLA during Sprints 1 and 2. The mean and peak power during Sprint 3 in the CRE + PLA was significantly greater than that in the CON. Heart rates, plasma lactate, and glucose increased significantly with CRE + CAF during most sprints. No significant differences were observed in the RPE among the three trials. The present study determined that caffeine ingestion after creatine supplements augmented intermittent high-intensity sprint performance.

Caffeine is ergogenic after supplementation of oral creatinemonohydrate.



The purpose of this investigation was to assess the acute effects of caffeine ingestion on short-term, high-intensity exercise (ST) after a period of oral creatine supplementation and caffeine abstinence.


Fourteen trained male subjects performed treadmill running to volitional exhaustion (T(lim)) at an exercise intensity equivalent to 125% VO(2max). Three trials were performed, one before 6 d of creatine loading (0.3 g x kg x d(-1) baseline), and two further trials after the loading period. One hour before the postloading trials, caffeine (5 mg x kg(-1)) or placebo was orally ingested in a cross-over, double-blind fashion. Four measurements of rating of perceived exertion were taken, one every 30 s, during the first 120 s of the exercise. Blood samples were assayed for lactate, glucose, potassium, and catecholamines, immediately before and after exercise.


Body mass increased (P < 0.05) over the creatine supplementation period, and this increase was maintained for both caffeine and placebo trials. There was no increase in the maximal accumulated oxygen deficit between trials; however, total VO(2) was significantly increased in the caffeine trial in comparison with the placebo trial (13.35 +/- 3.89 L vs 11.67 +/- 3.61 L). In addition, caffeine T(lim) (222.1 +/- 48.9 s) was significantly greater (P < 0.05) than both baseline (200.8 +/- 33.4 s) and placebo (198.3 +/- 45.4 s) T(lim). RPE was also lower at 90 s in the caffeine treatment (13.8 +/- 1.8 RPE points) in comparison with baseline (14.6 +/- 1.9 RPE points).


As indicated by a greater T(lim), acute caffeine ingestion was found to be ergogenic after 6-d of creatine supplementation and caffeine abstinence.

Point 50

Fluid, electrolyte, and renal indices of hydration during 11 days of controlled caffeine consumption.


This investigation determined if 3 levels of controlled caffeine consumption affected fluid-electrolyte balance and renal function differently. Healthy males (mean +/- standard deviation; age, 21.6 +/- 3.3 y) consumed 3 mg caffeine . kg(-1) . d(-1). on days 1 to 6 (equilibration phase). On days 7 to 11 (treatment phase), subjects consumed either 0 mg (C0; placebo; n= 20), 3 mg (C3; n = 20), or 6 mg (C6; n = 19) caffeine . kg(-1) . d(-1) in capsules, with no other dietary caffeine intake. The following variables were unaffected (P > 0.05) by different caffeine doses on days 1, 3, 6, 9, and 11 and were within normal clinical ranges: body mass, urine osmolality, urine specific gravity, urine color, 24-h urine volume, 24-h Na+ and K+ excretion, 24-h creatinine, blood urea nitrogen, serum Na+ and K+, serum osmolality, hematocrit, and total plasma protein. Therefore, C0, C3, and C6 exhibited no evidence of hypohydration. These findings question the widely accepted notion that caffeine consumption acts chronically as a diuretic.

Rehydration with a caffeinated beverage during the nonexercise periods of 3 consecutive days of 2-a-day practices.


The purpose of this study was to assess the influence of rehydration with a caffeinated beverage during nonexercise periods on hydration status throughout consecutive practices in the heat. Ten (7 women, 3 men) partially heat- acclimated athletes (age 24 +/-1y, body fat 19.2 +/- 2 %, weight 68.4 +/- 4.0 kg, height 170 +/- 3 cm) completed 3 successive days of 2-a-day practices (2 h/practice, 4 h/d) in mild heat (WBGT = 23 C). The 2 trials (double-blind, random, cross-over design) included; 1) caffeine (CAF) rehydrated with Coca-Cola and 2) caffeine-free (CF) rehydrated with Caffeine-Free Coca-Cola. Urine and psychological measures were determined before and after each 2-h practice. A significant difference was found for urine color for the post-AM time point, F = 5.526, P = 0.031. No differences were found among other variables (P > 0.05). In summary, there is little evidence to suggest that the use of beverages containing caffeine during nonexercise might hinder hydration status.

Caffeine during exercise in the heat: thermoregulation and fluid-electrolyte balance.



To investigate the effects of caffeine ingestion on thermoregulation and fluid-electrolyte losses during prolonged exercise in the heat.


Seven endurance-trained ( .VO2max = 61 +/- 8 heat-acclimated cyclists pedaled for 120 min at 63% .VO2max in a hot-dry environment (36 degrees C; 29% humidity) on six occasions: 1) without rehydration (NF); 2) rehydrating 97% of sweat losses with water (WAT); 3) rehydrating the same volume with a 6% carbohydrate-electrolytes solution (CES); or combining these treatments with the ingestion of 6 mg (-1) body weight 45 min before exercise, that is, 4) C(AFF) + NF; 5) C(AFF) + WAT; and 6) C(AFF) + CES.


Without fluid replacement (NF and C(AFF) + NF), final rectal temperature (T(REC)) reached 39.4 +/- 0.1 degrees C, whereas it remained at 38.7 +/- 0.1 degrees C during WAT (CES and C(AFF)+ WAT; (P < 0.05). Caffeine did not alter heat production, forearm skin blood flow, or sweat rate. However, C(AFF) + CES tended to elevate T(REC) above CES alone (38.9 +/- 0.1 degrees C vs 38.6 +/- 0.1 degrees C; P = 0.07). Caffeine ingestion increased sweat losses of sodium, chloride, and potassium ( approximately 14%; P < 0.05) and enlarged urine flow (28%; P < 0.05).


Caffeine ingested alone or in combination with water or a sports drink was not thermogenic or impaired heat dissipation. However, C(AFF) + CES tended to have a higher T(REC) than CES alone. Caffeine increased urine flow and sweat electrolyte excretion, but these effects are not enough to affect dehydration or blood electrolyte levels when exercising for 120 min in a hot environment.