Friday 18 October 2013

Strength Training for Runners




Research has shown that strength training is effective for providing muscular and neural adaptations that can prevent injuries, correct imbalances, and improve running economy in runners (Kawamoto 2010).  As well as increased muscular strength, neural adaptations include improved rate of force development (how fast the muscle can generate force), improved stretch-shortening cycle capability (use of free energy generated from the elastic properties of the tendons), and motor unit recruitment and synchronization. All of these benefits combined can help runners to sustain attacks, climb hills better, and finish stronger in races (Yamamoto et al 2008).
The importance of increasing force production can be demonstrated with Newtons 2nd law of motion
F = m*a
F = (force)
m = (mass)
a = (acceleration)

The ability of a runner to accelerate their mass (body weight) is directly dependent on the capability of the muscles to generate force. Since acceleration is derived from velocity, a more relevant equation for sports performance is the power equation:

P = F*v
P = (Power)
F = (Force)
v = (velocity)

Power production, which is the product of force and velocity is one of the most important factors for determining success in both brief and endurance events, average power output is most often the main difference between winning and losing. Thus the ability to increase force production which has a major influence on power capacity and can be the key ingredient for improving athletic capability (Stone et al 2010).
Increases in strength  are accompanied by increases in running economy, basically this means that the runner is now using less energy over the same distance travelled in comparison to somebody with poorer running economy (poor economy results in more energy expended). 5-7% improvements in running economy are commonly reported in the literature following participation in a strength training program (Stone et al 2010).

Strength Training Program Design

Traditional maximum strength training protocols are recommended for middle to long- distance runners, involving lifting heavy weights (> 85% of 1 repetition maximum) for low reps (1-5) with long interest rest periods (3-5 mins). The aim of max strength training is to increase the weight to power ratio and maximize force production which will result in faster and more powerful muscle contractions that enhance power production (Kawamoto 2010).
As a result of increased max strength, less effort is required for each stride. Time to peak force in each stride is also decreased, this is very important as it allows for a longer relaxation time during each stride (Storen et al 2007). It is during this relaxation time that the delivery of Oxygen and Energy, and the removal of waste products takes place in the muscles.
It is recommended that bilateral exercises (e.g. Squat, Deadlift etc) be programmed in order to recruit the higher threshold motor units and type 2 fast twitch muscle fibres, and also unilateral exercises (e.g. Lunge, Step-Up etc) in order to eliminate any imbalances (Storen et al 2007).  
Runners should also perform upper body strength exercises in order to improve posture and optimize gas exchange in the lungs. It is recommended to perform at least two pulling exercises (e.g Pull-Up, Bent Over Row) for every pushing exercise (e.g. Bench Press).

Injury Prevention

Running injuries are common and studies show that upwards of 50% of runners get injured every year (Fields et al 2010), furthermore it has been shown that training errors such as excessive distance and sudden changes to training routines are responsible for 60-70% of all running injuries (Nielsen et al 2012). Typical running gait favours certain muscle groups leading to the development of muscular imbalances, typically runners’ hamstrings become dominant resulting in the gluteals becoming weak and inhibited, this is known as gluteal amnesia. Corrective exercises should be prescribed to promote normal muscle function. Muscle weakness, particularly hip muscle weakness (hip flexors and abductors) has been identified as one of  the leading causes of lower extremity injuries.
The three most common running related musculoskeletal injuries are medial tibial stress syndrome (shin splints), plantar fasciitis, and Achilles tendinopathy. All three are overuse injuries and can be prevented with simple corrective exercises which should be performed alongside your regular strength program in order to be proactive rather than reactive when it comes to injuries.
In order to minimise your injury risk it is recommended to follow the ‘10% rule’, this states that you should avoid increasing your weekly running volume by more than 10% in any given week (Johnston et al 2003).
Core training plays a pivotal role not only in improving running economy but also in reducing injury risk. Runners need to focus on stability when running, thus it is the role of the core to limit any unwanted movement. You should think of the core as anti-movement muscles and not as flexors as is commonly seen in most gyms with people performing sit ups. The strength of your core is evident especially during the latter stages of races when poor posture can lead to decreased performance and wasted energy (Holland 2007).


There you have just a brief snippet of the benefits of strength training for runners. Get in touch and attend my Strength Training for Runners classes and lets put all the research into practice and improve your athletic ability. 

Tuesday 9 July 2013

Resistance Circuit Training: The Benefits

What is Circuit Training?

Essentially, circuit training is just interval strength training. A strength exercise is performed for reps or time, a rest interval is then given before the performer moves onto the next exercise. It is the primary mode of training for developing strength endurance, raising work capacity, and changing body composition1. It is a very effective method for training teams or large groups because everybody can train at the same time. Circuit training can also be used to target specific parts of the body (such as legs, core, upper body), or can be used as a total body workout. The circuits can be tailored to satisfy every fitness level through modification and progression of the selected exercises.




Health & Performance Benefits

Scientific research on the benefits of circuit training have focused on four main areas relating to health & performance. These are:

·         Improvements in oxygen consumption (VO2max)
·         Improved body composition (body fat %)
·         Transformations of physiological health markers (cholesterol, vascular function, blood sugar)
·         Strength Improvements

Oxygen Consumption (VO2max) is the maximum amount of oxygen that can be delivered to the working muscles during exercise. It is an important marker for heart function and endurance exercise capacity, and provides an indication of the efficiency of the aerobic system to supply energy. The best effects of circuit training for improving VO2max are seen when implementing a circuit of 3 sets of 8-10 exercises 3 times per week2, displaying improvements in VO2max in excess of 18% in previously untrained adults and 12% in trained college aged athletes.

Body Composition is positively affected in terms of total body mass, lean body mass and body fat percentage (%). These beneficial changes have been shown to occur across a wide range of intensities3 (ranging from 40-75% of 1 repetition maximum) with the largest improvements witnessed when the work:rest ratios are between 1:1 and 2:1 and the rest interval is less than 1 minute. A combination of aerobic and strength exercises in the same circuit has also shown reductions in skinfold measurements, waist:hip measurements, and waist circumference in both men and women4.

Physiological Health Markers such as blood glucose, cholesterol (both HDL and LDL), and vascular function (blood flow, blood pressure) are improved after both acute and chronic bouts of circuit training. Significant increases in HDL cholesterol can be seen within 1 hour of a circuit training session, similarly decreases in LDL cholesterol occur as a result of repeated training bouts. Increases in the rate of blood glucose disposal indicate that circuit training may be the ideal method of training for Type 2 diabetics and people with Impaired Glucose Tolerance (Pre-Diabetes)5. Positive benefits in both resting and exercising blood pressure are also widely reported with increased blood flow during exercise and reduced resting blood pressure attributed to circuit training.

Strength Improvements depend on the training status of the participant and the intensity of the exercise (% 1 repetition maximum). Untrained individuals (both male and female) using loads of less than 60% 1RM for 1 circuit 3 times per week for 10 weeks showed increases in strength ranging from 15-42%6,7. When using circuit training for training athletes it is advisable to increase the training intensity in order to elicit the desired strength adaptations, thus loads in excess of 75% 1 RM is recommended for this population.

Circuit Training Target Population

Circuit Training is the ideal mode of training for the general population, especially those looking to improve body composition and overall general health. Athletes can use this method of training to improve VO2max, and improvements in Lactate tolerance also occur. Well trained athletes may be better served utilizing traditional strength training methods if improvements in strength are of primary importance. The work:rest ratio can be manipulated to provide a progressive overload for continued improvement. Overall, circuit training provides a great total body workout and the flexibility of exercise selection ensures that no two workouts need be the same, thus providing both mental and physical variety to the workouts.

  1. Gambetta, V. (2007) Athletic Development: The Art & Science of Functional Sports Conditioning, Champaign: Human Kinetics.
  2. Alcaraz, P.E., Sanches-Lorente, J., and Blazevich, A.J. (2008) 'Physical performance and cardiovascular responses to an acute bout of heavy resistance circuit training versus traditional strength training', J Strength Cond Res, 22, 667-671.
  3. Hass, C.J., Garzarella, L., DeHoyos, D., and Pollock, M.L. (2000) 'Single versus multiple sets in long term recreational weightlifters', Med Sci Sports Exerc, 32, 235-242.
  4. Maiorana, A., O'Driscoll, G., Dembo, L., Goodman, C., Taylor, R., and Green, D. (2001) 'Exercise training, vascular function, and functional capacity in middle-aged subjects', Med Sci Sports Exerc, 33, 2022-2028.
  5. Dunstan, D.W., Puddey, I.B., Beilin, L.J., Burke, V., Morton, A.R., and Stanton, K.G. (1998) 'Effects of a short-term circuit weight training program on glycaemic control in NIDDM', Diabetes Res Clin Pract, 40, 53-61.
  6. Haber, M.P., Fry, A.C., Rubin, M.R., Smith, J.C., and Weiss, L.W. (2004) 'Skeletal muscle and hormonal adaptation to circuit weight training in untrained men', Scand J Med Sci Sports, 14, 176-185.
  7. Marx, J.O., Ratamess, N.A., Nindl, B.C., Gotschalk, L.A., Volek, J.S., Dohi, K., Bush, J.A., Gomez, A.L., Matezzi, S.A., Fleck, S.J., Hakkinen, K., Newton R.U., and Kraemer, W.J. (2001) 'Low-volume circuit versus high-volume periodized resistance training in women', Med Sci Sports Exerc, 33, 635-643.




Thursday 16 May 2013

Creatine Supplementation : brief review



I've been meaning to getting around to writing this review since reading an article on independent.ie on march 31st. The piece was written by former Ireland rugby international Neil Francis which I can only describe as downright lies and scaremongering. The article can be accessed here http://www.independent.ie/sport/rugby/rugbys-obsession-with-bulk-threatening-lives-of-young-men-29165230.html , I encourage you to read it first before you read my review.

The review below is based on facts from the scientific research literature and will outline both the positive and negative consequences of creatine supplementation in an objective manner. I encourage you to come to your own conclusions based on the research, and don't hesitate to get in touch if you've any questions.

What is Creatine?

Creatine is a naturally occurring compound that is produced primarily by the liver and to a lesser extent by the pancreas and kidneys. Its main role in the body is to store high energy phosphate groups (creatine phosphate -PCr) which provide a rapid but short-duration (7-10 secs) energy supply for high intensity activities. It can also be obtained through dietary sources, with meat, fish, and eggs providing the best sources. This review will focus on the effects of creatine supplementation, specifically creatine monohydrate.

The Role of Creatine in Sports Performance

Creatine phosphate (PCr) provides a rapid supply of energy for high-intensity activities. It provides the main source of energy for events lasting up to 7-10 seconds, beyond which the intensity is not able to be maintained due to the rapid depletion of the bodys stores. Depletion of PCr is the primary reason for fatigue in short duration events like the 100m sprint, reductions of 35%-57% of resting levels can be seen after just 6 seconds of max effort sprinting. Thus, it can be reasoned that if the intramuscular PCr stores can be increased then this could prolong the ability to sustain high-intensity activities.





Performance Benefits


Creatine supplementation has been proven to increase the duration of single high-intensity sprints, and also has a positive effect on repeated sprint ability with the benefits coming from an improved ability to regenerate PCr between high-intensity bouts. Benefits are also seen in weight training performance, 2 to 3-fold increases (25kg) in strength have been observed in trained athletes when compared to a placebo (6kg), the main effects are attributed to reduced fatigue and enhanced postworkout recovery. Creatine supplementation can improve the quality of each training session resulting in enhanced long-term performance.

How Much?

Traditional protocols have advocated an initial loading phase of 20 grams or 0.3g/kg per day spread out over 4 x 5 gram doses for the first 5 days, followed by a maintenance dose of 2-3 gram per day afterwards.The initial loading phase is thought to facilitate faster saturation of muscle creatine content, however much of this loading dose will be excreted once the muscles are fully saturated. If no loading dose is taken then creatine content levels will just take a longer time to reach saturation point (30 days vs 5 days) with the recommended dose of 3 grams per day. Consumption of creatine with carbohydrate can increase the amount uptaken by the muscles. Muscle creatine levels will remain elevated so long as a maintenance dose of 2 grams per day is maintained, once supplementation is stopped muscle creatine levels will return to baseline after approximately 4 weeks.

Safety and Side Effects

Besides minor gastrointestinal distress associated with the loading phase and increases in body mass due to additional water being drawn into the cells, there are no clinically significant side affects due to creatine supplementation. There have been anecdotal reports of muscle cramps during creatine supplementation phases, however this has not been documented in any controlled scientific studies.

Conclusion

The International Society of Sports Nutrition have stated that creatine monohydrate is the most effective ergogenic aid available for athletes for increasing high-intensity exercise capacity and strength gains during training. Based on the available scientific research, creatine has been shown to be completely safe and there is no reason for any athlete not to take it. 

So there you have it folks, all of the above are facts. If anybody would like to see the references then give me a shout. Your kidneys and heart will not explode as a result of creatine despite what Neil Francis says. His article has so many untruths in it, some of my favorites are below :


"Everyone has an idea, however vague, about what creatine is, so there is little point going into an analysis of its constituent components or perceived benefits"

"I feel that the substance is a very poor supplement to take to try and improve performance (legally) in rugby"

"17 year old boys should be able to motor for 170 minutes before they tire"

"Creatine was the perfect supplement if you were a bodybuilder - of course a bodybuilder could choose any course of steroids he wanted".

"If you have an underlying liver or kidney problem you should not take creatine"

"If you are taking antibiotics for infection or acne your life is in danger if you mix the two"

"Who is to say creatine use/abuse is not to blame for at least one of those deaths per year"









Monday 11 March 2013

Caffeine as an Ergogenic Aid for Sports Performance and Weight Loss

Caffeine is the most commonly used drug in the world with about 90% of people worldwide consuming it in regular everyday items such as tea, coffee, chocolate, energy drinks, and other foods. The effect of caffeine for reducing fatigue and increasing alertness has been recognised for centuries. In fact, it was only removed from the WADA (World Anti Doping Agency) banned substance list in 2004, and is currently on the monitored substance list. Although widely considered to provide energy enhancing benefits, caffeine provides no nutritional value, and its effects are mediated through its stimulant effect on the central nervous system (CNS) which are similar to, yet weaker than, those associated with amphetamines.



Performance Benefits

There is evidence supporting the benefits of caffeine across a range of sports, from endurance events lasting several hours like marathon or triathlon, to high intensity intermittent sports such as soccer and rugby, and sustained high intensity events from 1-60 minutes in duration like middle-distance running. 
Caffeine has been shown to produce a small but worthwhile effect on endurance performance. It has been reported to alter the functioning of receptors in the brain that regulate fatigue, influence ratings of perceived exertion (how hard the exercise feels), and lowers pain perception, all of which can improve performance. 
  • In endurance events, caffeine has been shown to increase work (power) output and time to exhaustion. Caffeine mobilizes free fatty acids from the bodys adipose (fat) or intramuscular fat stores. This results in a greater use of fat for energy which slows the depletion of glycogen (carbs are broken down to glycogen in the body) and delays fatigue. As with all research on sports nutrition the improvements vary depending on the testing protocol used and benefits ranging from 0.7%-17% have been reported with improvements in the range of 4%-6% most common.
  • During high-intensity exercise, the primary benefit of caffeine is evident in enhanced speed, strength and power production. Enhanced neuromuscular functioning has been reported by several researchers, resulting in greater muscular force production and decreased reaction time. 
  • Caffeine also has benefits for cognitive tasks, improved short-term memory, motor learning, and an ability to sustain concentration have been reported.

How Much and When?

Research has shown that the beneficial effects of caffeine occurs when caffeine is consumed in anhydrous (tablet) form rather than in coffee or other food sources.  So how much caffeine is too much, and when should you take it?
  • Caffeine has been shown to be most effective at relatively low doses with 2-3 mg/kg deemed optimal (e.g a 70kg person should consume 140-210 mg of caffeine for optimal results).There is no further dose-response benefit when consumed at higher doses.
  • When taken in tablet form, caffeine reaches peak levels in the bloodstream after 20-75 minutes. It has been shown to improve performance for up to 6 hours after ingestion, and the majority of research recommends ingestion 60 minutes prior to performance for optimal absorption.

Weight Loss

As has been already noted, caffeine helps to increase endurance performance by mobilizing fatty acids which can then be burned as fuel. The best effect for fat metabolism is seen when exercising at low intensities and with relatively low doses of caffeine (2-3 mg/kg). When using caffeine to aid weight loss, it is important not to eat anything beforehand as this will cause the hormone insulin to be released and carbohydrate metabolism will begin. So the best time for fat loss will be in the morning, after an overnight fast, and with caffeine supplementation. But remember, the best way to increase fat oxidation is through regular exercise training, fat burning sessions can have a place in your training schedule but try to mix up your training by incorporating different intensities for the best response.

Adverse Effects

A common misconception is that caffeine induces dehydration during exercise.This is not supported by the literature, and several studies have failed to show any changes in sweat rate or fluid loss as a result of caffeine consumption. Several side effects are associated with caffeine consumption including gastrointestinal discomfort, increased anxiety, insomnia, heart palpitations, and tremors. It is also important to remember that caffeine is a drug and is physically addicting, discontinuation can cause some withdrawal symptoms. Typically, intakes greater than 9 mg/kg increases the risks of side effects.

Conclusion

So to conclude, caffeine has a performance enhancing effect across a broad range of sports independent of the duration. 2-3 mg/kg consumed in tablet form is optimal, taken approximately 60 minutes before you exercise.It can aid in weight loss provided it is taken under the right conditions. Finally,in order to limit your chances of side effects, keep your intake levels below 9 mg/kg.


Friday 1 March 2013

The Effect of Alcohol on Sports Performance and Recovery



Consumption of alcohol has been a time-honoured tradition for celebrating sporting performance. Alcohol is the most commonly consumed drug amongst the athletic population, with traditional field sports players of soccer, rugby, cricket, hurling, and gaelic football  found to have the highest percentage of consumption. Most players are aware of the negative effects of alcohol on performance on the night before an event. Alcohol is a depressant which affects the central nervous system and alters brain function. The results of which includes impairment of many mechanisms necessary for successful athletic performance like reaction time, hand-eye coordination, and balance. What is less understood however is how alcohol affects athletic recovery in both the short and long-term.



The Effect of a Hangover on Sporting Performance
It’s not uncommon for recreational athletes or ‘weekend warriors’ to have a few drinks (or a lot of drink J) on the night before a game. Irish researchers performed fitness assessments on rugby players and then asked the players to consume a regular amount of alcohol for a typical night out, and report for  re-assessment 16 hours later. They found that a hangover inhibited aerobic performance by 11.4% on average. The mechanisms behind the performance impairments are dehydration, acid-base disturbances, and alterations in glucose metabolism via insulin action. Heart function was also affected during the hangover phase and could be seen with an increased heart rate and blood pressure.
Short-Term Effects on Athlete Recovery
·         During a typical match lasting 80-90 minutes it is not uncommon to lose 2-5% of body weight through dehydration and depletion of muscle and liver glycogen (carbohydrates are broken down to glycogen in the body and stored in the liver and muscles to be used as fuel). Adequate rehydration and refuelling is essential after a game in order to speed up recovery for the next game or event, timing is important and a high protein and carbohydrate meal is recommended within 2 hours of the final whistle. Replacing fluid losses is also a priority and a good rule to follow is to replace 1.5 times the amount of fluid lost through sweat, so if you sweat 1 litre, then drink 1.5 litres. Simply weighing yourself before and after exercise will give you a good indication of how much sweat is lost, as 1kg of weight loss equates to about 1 litre of sweat.
·         However, rather than following these guidelines, what commonly occurs is that this important time period is spent drinking and this has a negative effect on recovery. A commonly held misconception is that beer is effective at replacing fluid losses. Beer, and other alcoholic beverages of about 4% alcohol volume have a diuretic effect on the kidneys and promote urine loss resulting in further dehydration. What is recommended is that in the immediate aftermath to consume some water, and then try to stick to some mid strength beers, or spirits served in large glasses with a non-alcoholic mixture before hitting the stronger stuff if you must.
·         Research has shown that those who consume alcohol on a regular basis are more likely to get injured than non-drinkers. Those who drink 1 night a week had an injury rate of 54.8%, whereas the non-drinkers injury rate was 23.5%. Collision injuries are common in team sports resulting in a temporary loss of function. Alcohol can impair optimal recovery, and if full recovery is not achieved then further injury is likely. The underlying mechanisms affected are inhibited immune system function, and inability to limit blood flow to the injury site that can result in an oedema or build up of fluid causing swelling.

Long Term Effects
·         Alcohol is high in calories, providing 7 kcal per gram which is more than carbohydrates and protein (4 kcal per gram) but less than fat (9 kcal per gram). However not all calories are created equal and alcohol is considered and ‘empty calorie’ as it does not provide glucose or nutrient benefits. A common misconception is that the carbohydrates in beer are responsible for the weight gain or beer belly associated with long-term consumption, this is not true, it is the alcohol in beer that is to blame.
·         When available, the body uses alcohol as its preferred fuel source. So when you have your high-fat takeaway at the end of the night, the fat in this food is stored in the stomach, hips, and thigh area as opposed to being used as fuel.

How to Survive a Night Out
So how can you enjoy a night out without severely negatively impacting performance or recovery? Well here’s a few tips on how to enjoy alcohol responsibly.
·         Eating before drinking can speed up the recovery process by providing your muscles with carbohydrate and protein rich foods (chicken, steak, fish, with veg or a sandwich with lean meat are good choices).
·         Try to pace yourself, if you are dehydrated you will drink much faster so aim to start with a non-alcoholic drink first to quench your thirst and replace fluid losses before having a couple of mid-strength drinks.
·         Try to avoid ‘rounds’ as this encourages drinking at a faster pace, also try to keep busy while drinking. Playing pool or darts are better options than sitting and drinking.
·         Always try to have a glass of water before you go to bed, this is a good way to prevent a hangover and get the rehydration process under way.

Sunday 24 February 2013

Exercise and Type 2 Diabetes



The world is in the midst of a global diabetes epidemic. Its occurrence, particularly type 2 diabetes, continues to rise unrelentingly in most developed and developing nations (Simpson et al 2003). Current estimates of the global prevalence of type 2 diabetes calculate that approximately 250 million people are affected, and this number is expected to rise to some 380 million people by the year 2025 (Praet and Van Loon 2007). Diabetes is currently the 9th leading cause of death worldwide (WHO 2012), and current epidemiological patterns show that the incidence of diabetes is progressively increasing in young and middle-aged people (Ehrman et al 2003). Death rates for young people with diabetes are staggeringly high in comparison to healthy individuals, with observations that in excess of 15% of people that develop diabetes before 30 years of age will die before they reach 40. The economic and social cost of this disease is huge, diabetes is associated with many severe clinical complications which result in disability and reduced life expectancy, placing an enormous burden on the economy in terms of healthcare costs and reduced productivity in the workplace (Simpson et al 2003). In Ireland alone, the cost of treating this disease accounts for 10% of the entire health budget totaling €1.4 billion per annum (Nolan et al 2006). Physical inactivity is one of the most important modifiable risk factors for primary prevention of type 2 diabetes. Exercise has long been considered to play a key role in the treatment and prevention of diabetes alongside diet and medication, however high-quality research on the importance of physical activity and exercise in this area was lacking until recently (Sigal et al 2006).  The focus of this article will be on the pathophysiology of the disease, the mechanisms through which exercise acts as a therapy, the role of exercise and in particular current recommendations in relation to the frequency, intensity, time, and type of exercise, as well as future recommendations to help combat this disease.


Figure 1. Increases in the prevalence of diabetes from 1995-2010 (Simpson et al 2003)
Pathophysiology
The pathophysiology of Type 2 Diabetes Mellitus (T2DM) is complex and controlled by many factors, including both genetic and environmental components that affect β-cell function and tissue insulin sensitivity (Frontera et al 2006). T2DM is characterized by defects in both insulin action and insulin secretion, which leads to a gradual increase in plasma glucose levels over time (Ehrman et al 2003). The role of insulin is to transport glucose into the cell. Insulin is a peptide hormone that is secreted by the β-cells in the islets of langerhans in the pancreas. Each time we eat, insulin is released into the bloodstream to induce the liver, muscles, and adipose tissue to remove glucose from the blood for metabolism or storage (Widmaier et al 2008). In a normal fed state there is an increase in blood glucose coming from the gut, insulin binds with its receptor which is embedded in the plasma membrane of the cell. Once insulin is bound to its receptor, it initiates the signaling pathway that causes the vesicles containing GLUT-4 to translocate to the plasma membrane and allow glucose to enter the cell.
In an insulin resistant state, where insulin action is not working properly, there is still the same or even an increased production of insulin from the pancreas in response to an increase in blood glucose but there is no translocation of the internal vesicle containing GLUT-4 to the plasma membrane, thus glucose cannot enter the cell (Frontera et al 2006). However, there is less glycogen synthesis because of the decreased uptake of glucose into the liver. Since insulin is not working effectively, the liver still maintains gluconeogenesis, thus there is already plenty of glucose in the blood but the liver is releasing even more causing hyperglycaemia (McArdle et al 2010). In a hyperglycaemic state glucose can attach to different proteins and glycosylate them. This glycosylation affects the proteins function and ability to work properly. De Novo lipogenesis still occurs because the effect of insulin to act on the cell is reduced, resulting in the uptake of fatty acids into the muscle causing a build-up of intra-myocellular lipid stores (Williams and Pickup 2004).
β-cell dysfunction can occur up to 10 years before hyperglycaemia takes place, this alteration is evident with a reduced insulin response to glucose (Scheen 2003). In the early stages of impaired β-cell function there is a reduced insulin response to glucose, causing increased postprandial hyperglycaemia. As the dysfunction progresses to its later stages, prolonged hyperglycaemia triggers insulin secretion to be sustained for a longer time, this has been hypothesized to overwork the β-cell and impair its function (Leahy 1996). A progression from IGT to T2DM occurs due to a combination of insulin resistance and β-cell dysfunction, increased β-cell insulin secretion can’t maintain its high rates in response to glucose and T2DM develops (Ehrman et al 2003). By the time the disease is diagnosed, β-cell function will typically already be reduced by approximately 50%, and a progressive linear decrease of β-cell insulin secretion capacity over subsequent years can explain the deterioration of blood glucose control (Bilous and Donnelly 2010, Scheen 2003).
There are a number of environmental and genetic risk factors that may contribute to the development on T2DM. Some of these are non-modifiable risk factors such as ethnic origin, age, and family history. However, there are several modifiable risk factors associated with lifestyle choices that can lead to the development of T2DM, namely, obesity, physical inactivity, and diet. In the majority of western populations, more than 60% of new cases of T2DM are occurring in obese patients (Watkins et al 2004). Obesity is achieved through overfeeding of modern calorie dense food, coupled with a sedentary lifestyle, resulting in prolonged positive net energy balance (Scheen 2003). While obesity has been recognized as an important determinant of insulin sensitivity, the distribution of body fat appears to be the decisive factor. The greatest risk of diabetes is associated with central obesity in which fat is deposited intra-abdominally (Williams and Pickup 2004). Excess fat in the visceral region releases greater amounts of non-esterified fatty acids (NEFAs) through lipolysis which increases gluconeogenesis in the liver and reduces glucose uptake at the muscular and hepatic sites (Scheen 2003). Long term positive energy balance not only increases fat stores in the adipose tissue but also results in an increase in intramuscular triglyceride storage. In addition, lipids can accumulate in other tissues and affect their normal function, hepatic steatosis is regular in obese subjects, and non-alcoholic fatty liver disease is now linked with insulin resistance (Ravussin and Smith 2002). The severity of insulin resistance in the tissues is related to the degree of intramuscular triglyceride deposits, and interestingly increased fatty deposits in the pancreatic islets has been reported as a contributing factor in β-cell dysfunction (Unger 2002).
Exercise as a Therapy
Skeletal muscle is the primary site for the disposal of glucose in the body. As discussed already, in the insulin resistant state this function is impaired. However, exercise, or more specifically, muscle contraction, has an insulin-like effect. Even though individuals with T2DM are resistant to insulin, they are not resistant to the effect that exercise has on glucose utilization (Sigal and Kenny 2004). Muscle contraction activates AKT independent of insulin, and invokes the translocation of the GLUT-4 receptor to the sarcolemma and t-tubules allowing glucose transport to take place (Henriksen 2002). The signal for translocation of GLUT-4 during exercise is different from the insulin mediated function, and does not require phosphorylation of the insulin receptor (Rockl et al 2008). A single bout of exercise can have a significant glucose lowering effect in individuals with T2DM, as well as lowering plasma insulin concentrations during the activity. There is one main difference between the insulin effect and exercise effect. Insulin has a half time in circulation of approximately 7 minutes, so as soon as it is produced, the body must utilize it. Once it is withdrawn, glucose uptake is suppressed. Exercise has a different effect, it has been shown that a single bout of exercise can have a residual effect on glucose uptake for up to 72 hours (Sigal and Kenny 2004).
Exercise increases energy expenditure, skeletal muscle is the largest organ in the body, much bigger than the liver and adipose tissue. The larger the amount of muscle mass engaged in exercise, the more glucose that will be taken up and metabolized. This helps to restore energy balance, and takes pressure off the β-cells to produce insulin because the amount of circulating glucose is decreased, thus reducing insulin resistance (Sigal and Kenny 2004). Post-exercise, the muscle and liver are more sensitive to insulin, glucose continues to be taken up into the muscle and stored as glycogen and glucose taken up by the liver is nonoxidatively metabolized (Hamilton et al 1996). Regular exercise causes a number of physical adaptations within the muscle that enables more efficient utilization of substrates for the generation of ATP. Increased GLUT-4 protein expression occurs alongside increased mitochondrial function, this helps to facilitate increased glucose uptake into the muscle cell. The highest levels of GLUT-4 are normally found in oxidative slow twitch muscle fibres. Interestingly, individuals with T2DM have a distinct phenotype with a decreased amount of such fibres and reduced concentration of GLUT-4 (Rockl et al 2008).  Exercise training stimulates protein synthesis which develops lean body mass, this lean tissue burns more calories at rest than adipose tissue and helps to increase the basal metabolic rate. Training also facilitates a shift in substrate utilization, the increased mitochondrial and enzymatic activity enhances the muscles ability to extract and oxidize glucose and NEFAs from the blood, as well as increase the utilization of intramuscular triglycerides (Sigal and Kenny 2004). Moderate exercise can increase fat oxidation approximately 10 fold due to increased fatty acid mobilization and energy expenditure. Increased adipocyte catecholamine sensitivity is the proposed reason for the enhanced capability to mobilize NEFAs and reduce intramuscular triglyceride stores (Sigal and Kenny 2004).

Figure 2. Diagram representing different signaling pathways for GLUT-4 translocation to facilitate glucose transport in response to insulin and exercise (Rockl et al 2008).
Role of Exercise in Prevention of T2DM
There is a substantial body of evidence in the diabetes research literature that supports the value of exercise in the prevention of T2DM (Sigal et al 2006, Simpson et al 2003, Hansen et al 2010, Praet and Van Loon 2007). Exercise has proven to be equally as effective in preventing the progression from IGT to T2DM when compared to a combination of diet and exercise, and its beneficial effect on glycaemic control is modulated independent of weight loss (Sigal et al 2004). Current clinical recommendations declare that performing moderate intensity exercise on at least 3 days of the week for a minimum of 30 minutes per session can result in significant health benefits for patients with IFG and T2DM (Sigal et al 2006). The benefits of exercise can be greatly enhanced depending on the frequency, intensity, type, and time spent exercising.
Frequency
Following an acute bout of exercise, insulin sensitivity is enhanced for up to 72 hours. Research indicates that regular exercise has a cumulative effect on improving glycaemic control, with each successive bout of exercise further enhancing the positive responsive adaptations (Praet and Van Loon 2007). The minimum recommendations for exercise frequency is 3 days per week, with no more than 2 consecutive days between exercise bouts according to the American Diabetes Association guidelines (American Diabetes Association 2007). Greater exercise frequency as part of a long term lifestyle intervention has been shown to improve body composition in obese individuals by facilitating greater adipose tissue mass loss by creating an energy deficit, however, it has also been shown that the long term benefits of exercise on glycaemic control may be lost within 6-14 days if exercise is discontinued (Hittel et al 2005).
Intensity
Recommendations for continuous endurance training intensity varies between 40%-85% of VO2max depending on what stage the patient is at in the lifestyle intervention (Hansen et al 2010). After exercising at intensities outlined above we get an increase in PGC-1α, this is considered as a master regulator for metabolism and increases the capability of the muscle to utilize glucose and fat (Canto and Auwerx 2009). For obese individuals, lower intensity exercise is recommended in the early stages of the intervention to assist in greater compliance to the training program. Low intensity continuous endurance-type training has shown to be as effective as high intensity continuous endurance-type training in improving glycaemic control provided that the exercise bouts are of sufficient duration (Hansen et al 2010).
Muscle glycogen plays a more important role in substrate metabolism as exercise intensity is increased. High intensity exercise depletes muscle glycogen stores to a greater degree and subsequent post-exercise glycogen synthesis is linked with improvements in glucose tolerance and insulin sensitivity (Praet and Van Loon 2007).  In theory, when the acute glucoregulatory effects of exercise are considered, high intensity exercise should be more effective than low intensity. However when both intensities have been compared, similar results were found in terms of loss of total-body adipose tissue and enhanced glycaemic control (Schjerve et al 2008). The total amount of energy expended during the exercise bout appears to be the most important factor for inducing changes in glucose homeostasis, thus low intensity exercise should be performed for longer durations than high intensity exercise (Praet and Van Loon 2007). 


Type
Current guidelines recommend the addition of resistance training alongside endurance-type regimens. The addition of resistance training results in enhanced glycaemic control for sufferers of T2DM (Hansen et al 2010). Resistance training increases energy expenditure and produces sizable gains in muscle mass, thus improving whole-body blood glucose disposal capacity (Praet and Van Loon 2007).  Resistance training improves bone density, balance, functional strength, and increases the resting basal metabolic rate which can improve long-term weight management and facilitate a more active and healthier lifestyle. Research has shown significant improvements in insulin sensitivity when resistance and endurance training is combined (77% increase) in comparison to endurance training alone (20% increase) after 16 weeks (Sigal et al 2007). One of the main factors for increased incidence of diabetes in older age is the loss of muscle mass, age-related sarcopenia can be attenuated with resistance training, thus improving the metabolic profile of older adults at risk of developing the disease (Hansen et al 2010).  The ACSM recommends 2-3 resistance training sessions per week, with 8-10 exercises that recruit the major muscle groups. 1 set of 10-15 repetitions is advised for beginners, with the aim of progressing to 3 sets of 8-10 repetitions over time (Sigal et al 2004). Although one set may be sufficient to promote strength gains, research has shown that 3 sets are optimal for producing the metabolic benefits for T2DM (Hansen et al 2010). 
Time
Currently, there is a lack of information in the scientific literature that provides guidelines on the optimal volume/duration for acute bouts of exercise (Praet and Van Loon 2007).  Rather, the intensity of exercise appears to have a greater importance. A study by Sriwijitkamol and colleagues (2007) found a greater decrease in blood plasma glucose levels in patients with T2DM after cycling for 40 minutes at 70% VO2max, when compared to a group that exercised at 50% VO2max. Recommendations currently focus on the energy cost of each exercise bout with energy expenditure in the region of 400-500 kcal deemed optimal regardless of the duration of the session (Praet and Van Loon 2007). 
Lifelong participation in exercise is recommended to manage and prevent T2DM. Adherence to extended exercise programs have resulted in significant improvements in glycaemic control and considerable reductions in fat mass in obesity patients with T2DM (Hansen et al 2010).  These improvements result in enhanced quality of life and life expectancy, as well as reductions in healthcare costs.
The Future Role of Exercise
Several recent studies have examined the effects of high-intensity intermittent training (HIIT) in T2DM patients. The results from these studies have so far been positive, Tjonna et al (2008) found significant increases in insulin sensitivity after a 16 week HIIT intervention in patients with IGT when compared to a continuous exercise intensity group. It has been discovered that the HIIT provides a much greater upregulation of PGC-1α, induces faster physiological adaptations in skeletal muscle, and improvements in body composition (Hansen et al 2010). This modality of training seems to provide greater benefits over traditional methods and is an area that warrants additional research in addition to future studies to provide a better understanding of the underlying mechanisms that promote the upregulation of GLUT-4 and insulin signaling features as a result of exercise. Muscle is now viewed as an endocrine hormone, not only is its contractility affecting energy expenditure during exercise but it is also releasing myokines which interact with other tissues in the body such as the liver and adipose (Pedersen 2009). Knowledge and understanding of these mechanisms can help clinicians and sports & exercise scientists to develop optimal exercise routines to enhance insulin action in patients with IGT and T2DM.
In order to combat this disease, there is a need to design strategies to address lifestyle choices on a large scale (Simpson et al 2003). A community-wide approach is recommended with special emphasis targeted at high risk groups such as pre-diabetic individuals. Education about appropriate lifestyle choices should be implemented at an early age and a structured program on lifestyle, exercise, and nutrition should form a compulsory part of the school curriculum (Simpson et al 2003). Putting these measures in place can help combat this largely preventable disease, improve quality of life, and reduce the economic burden associated with its treatment.





Tuesday 17 January 2012

Following on from my blog post on Beta-Alanine, this time i'm looking at current methods that are being used to determine an athletes readiness to train. On reviewing this subject I came across lots of methods that are used, but i've narrowed it down to what appears to be the most reliable and commonly used methods. Once again any feedback is appreciated whether good or bad.

Readiness to Train



Introduction



It is essential that fatigue is managed effectively by both the sports scientist and the athlete in order to optimize training adaptations and subsequent performance. Since performance and training will be compromised during periods of fatigue, it is crucial to determine an athlete’s readiness to train prior to starting a workout. At present there are no tools which can 100% tell you whether an athlete is ready to train, but a combination of subjective and objective variables can provide the best guide. Following a brief review of the current literature, outlined below are some of the current practical recommendations that can be applied, and I have also summarized some laboratory based tests that might only be available to elite athletes.



Fatigue Management



I came across what seems to be an endless list of tests and assessments that can be administered to athletes. My focus however will be on a small number of methods which seem to be deemed the most reliable, and will briefly touch on some of the other approaches currently used. Four main markers have been proposed to quantify training load, these are Biochemical, Psychological, Physiological, and Hormonal. Though there may be no optimal marker to differentiate between normal fatigue and over-training, a combination of the above markers, including performance tests and measures of mood will provide useful information to the coach and athlete.



1.      Profile of Mood States (POMS)

There is a general agreement that observing mood state changes is considered one of the most sensitive methods of monitoring training to avoid overtraining syndrome. The POMS is a questionnaire that is usually completed pre-workout by the athlete. POMS contains 65 questions, however a shortened POMS questionnaire has also been developed that is more practical and less time consuming. The athlete rates themselves against the following 6 questions:

  • I slept well last night
  • I am looking forward to today's workout
  • I am optimistic about my future performance
  • I feel vigorous and energetic
  • My appetite is great
  • I have little muscle soreness

And they rate each statement on the following range:

  • 1 - Strongly disagree
  • 2 - Disagree
  • 3 - Neutral
  • 4 - Agree
  • 5 - Strongly agree

If they score 20 or above then it is deemed that they are recovered enough to continue with the training program. Any score below 20 will require further investigation, and rest or scaling back of the training load could be necessary.

2.      Training Load

It is very important that the sports scientist is able to quantify the training load, high training loads are often associated with signs of overreaching, which may lead to the development of overtraining syndrome. Several approaches have been proposed to quantify training load, thus ensuring that adequate recovery strategies can be applied at appropriate times. First is the observational approach, this involves analysis of real time measurements such as the type and duration of a training session. Modern technology such as GPS can also help to quantify total distance covered as well as the speeds at which the athlete is running at. Here is a link to sports GPS manufacturer GPSPORTS http://gpsports.com/gpsnew/home.php   The second is a physiological approach, this requires monitoring and analysis of variables such as heart rate and lactate concentration during training. Measurement of lactate can provide an indication of training load but variations in muscle glycogen can affect lactate concentration, so conditions would require standardization for repeatable measures. Thirdly, a useful yet simple method of assessing training load is to have the athlete complete a daily training log and record subjective ratings such as session RPE, fatigue, stress, and muscle soreness.     

3.      Performance Tests

A decrease in muscular power and deteriorating neuromuscular function are found in athletes who are in an overreached state or are suffering from overtraining syndrome. Recent studies suggest that low-frequency neuromuscular fatigue is an important measure to quantify in elite level athletes, and measurement of functional stretch-shortening cycle activities, such as a countermovement jump (CMJ) may be capable of this. Tests have been carried out from a single CMJ to 5 consecutive CMJ’s with measurements such as flight time and height jumped being used to analyse performance. These tests can be carried out with the use of a portable jump mat which provides real time feedback to the coach and athlete, an example of which can be seen from this link http://biometricsmotion.intoto.nu/produkten.php?ms_id=214&Instrumenten/Sprongkracht/ProJump_springmat&taal_ID=GB  

A common problem encountered when taking these measurements was a lack of baseline measures. Other performance tests commonly used were a 10 step bound for distance test, this test is used as a measure of explosive strength capacity.

4.      Body Mass and Hydration

It is important to weigh the athlete both pre and post-workout, for every kg that the athlete loses during training this equates to 1 litre of fluid losses. When replacing these fluid losses it is important that the athlete consumes 1.5 times what was lost. So if the athlete loses 1 litre of sweat then they should consume 1.5 litres of water. It can be useful to add sodium to the mix as this will force the kidneys to retain the water and ensure that it doesn’t get excreted. Athletes can tolerate water losses of up to 2-3% of bodyweight before performance will be affected, however it is important that they do not commence training in an already dehydrated state. Simple tests such as checking the colour of the athletes urine against a urine colour chart such as the one below, will give an accurate indication of the athletes hydration status.


5.      Blood/Saliva Screening

For a long time the plasma cortisol/testosterone ratio was considered to be a good indicator of the overreached state. Cortisol and testosterone can be measured in the saliva, which provides the possibility for regular, non-invasive monitoring of hormonal status in response to training. This ratio decreases in relation to the intensity and duration of training, but current literature questions its accuracy in its use of diagnosis for overreaching and overtraining.

Conclusion

As athletes endeavour to improve performance, they will predictably experience varying levels of fatigue, which will require effective management by both the sports scientist and the athlete. Although there are currently no tools available that can be 100% accurate in diagnosing overtraining, there are several methods, both objective and subjective, that can indicate changes in training related stress. With an effective method for the management and monitoring of fatigue, athletes should be able to optimize training adaptations which should enhance performance.