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At what point does muscle mass overcome muscle strength to affect speed?

At what point does muscle mass overcome muscle strength to affect speed?


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I'm trying to think in terms of "how fast" someone can do something, like swing a bat or push a crate. Someone might have a lot of muscle mass, but that also increases how much mass an arm has to move which also increases the torque. Is there anything referable in biology that has found at least some estimate of where these two factors trade off?


Preserve your muscle mass

The saying goes there are two certainties in life: death and taxes. But men should also add loss of muscle mass to the list.

Age-related muscle loss, called sarcopenia, is a natural part of aging. After age 30, you begin to lose as much as 3% to 5% per decade. Most men will lose about 30% of their muscle mass during their lifetimes.

Less muscle means greater weakness and less mobility, both of which may increase your risk of falls and fractures. A 2015 report from the American Society for Bone and Mineral Research found that people with sarcopenia had 2.3 times the risk of having a low-trauma fracture from a fall, such as a broken hip, collarbone, leg, arm, or wrist.

But just because you lose muscle mass does not mean it is gone forever. "Older men can indeed increase muscle mass lost as a consequence of aging," says Dr. Thomas W. Storer, director of the exercise physiology and physical function lab at Harvard-affiliated Brigham and Women's Hospital. "It takes work, dedication, and a plan, but it is never too late to rebuild muscle and maintain it."


Author Summary

An individual's genetic profile can play a role in defining their natural skills and talents. The canine species presents an excellent system in which to find such associative genes. The purebred dog has a long history of selective breeding, which has produced specific breeds of extraordinary strength, intelligence, and speed. We have discovered a mutation in the canine myostatin gene, a negative regulator of muscle mass, which affects muscle composition, and hence racing speed, in whippets. Dogs that possess a single copy of this mutation are more muscled than normal and are among the fastest dogs in competitive racing events. However, dogs with two copies of the same mutation are grossly overmuscled, superficially resembling double-muscled cattle known to possess similar mutations. This result is the first to quantitatively link a mutation in the myostatin gene to athletic performance. Further, it emphasizes what is sure to be a growing area of research for performance-enhancing polymorphisms in competitive athletics. Future implications include screening for myostatin mutations among elite athletes. However, as little is known about the health issues and potential risks associated with being a myostatin-mutation carrier, research in this arena should proceed with extreme caution.

Citation: Mosher DS, Quignon P, Bustamante CD, Sutter NB, Mellersh CS, Parker HG, et al. (2007) A Mutation in the Myostatin Gene Increases Muscle Mass and Enhances Racing Performance in Heterozygote Dogs. PLoS Genet 3(5): e79. https://doi.org/10.1371/journal.pgen.0030079

Editor: Joseph S. Takahashi, Northwestern University, United States of America

Received: January 27, 2007 Accepted: April 4, 2007 Published: May 25, 2007

This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

Funding: EAO gratefully acknowledges support from the Intramural Program of the National Human Genome Research Institute. CSM acknowledges the Kennel Club Charitable Trust for financial support of canine genetics research at the Animal Health Trust. CDB acknowledges support from National Science Foundation grant number 0516310.

Competing interests: The authors have declared that no competing interests exist.

Abbreviations: indel, insertion/deletion MSTN,, myostatin


Low Muscle Tone

‘Low muscle tone’ is a condition of abnormally low muscle tone, the amount of tension or resistance to movement in a muscle. Low muscle tone occurs when the length of the resting muscle is slightly longer than typical. This means that the muscle fibers are not overlapping at an optimal level and there are fewer points where the fibers can attach and generate pull on the muscle. As a result, the person’s muscle needs to go through a greater range of motion and, as a result, more energy is used. On top of this, it often takes greater stimulation for the muscle to activate, which also increases the response time of the muscle and it directly influences the child’s performance abilities. The use of extra energy contributes to the decrease in the child’s endurance.

What are the common features of low muscle tone?

  • Decreased strength.
  • Increased flexibility and movement in joints.
  • Poor endurance.

Common difficulties often (but not always) experienced by those with low muscle tone:

  • Fatigues quickly.
  • Poor posture.
  • Increased flexibility, increasing susceptibility to injuries.
  • Poor persistence to gross motor tasks.
  • Lack appropriate body awareness feedback.
  • Avoids chewy foods.
  • Preference to engage in sedentary activities.

Management strategies that support the child with low muscle tone (at preschool, school and/or home):

  • Reward system.
  • Appropriate set up for school desk.
  • Encouragement.
  • Provide opportunities to succeed by simplifying activities.
  • Extra time to complete tasks.
  • Recognise and reinforce the child’s strengths.

Occupational Therapy approaches and activities that can support the child with low muscle tone and/or their carers include:

  • Gross motor activities: Increase participation in gross motor activities.
  • Motivation: Make activities achievable and appealing for the child.:
  • Fun/play: A child is more likely to persist with tasks if they are fun and play based.
  • Develop underlying skills: such as postural control, endurance and body awareness.
  • Play based activities to promote longer participation.
  • Graded activities so they gradually develop a child’s strength and endurance.
  • Hard muscle work exercises/games to build strength and endurance.

Speech Therapy approaches and activities that can support the child with low muscle tone and/or their carers include:

  • Muscle strength in the face: Activities to increase muscle strength in the face (e.g. drink yoghurt/thick-shakes through a straw, blowing up balloons).
  • Articulation: Improving articulation of specific speech sounds within words.
  • Oral awareness: Developing oral awareness (i.e. movement of the tongue in the mouth).
  • Alternative forms of communication: Teaching alternative ways of communicating through sign language or PECS (Picture Exchange Communication System) whilst muscle tone is improving.
  • Communication strategies: Working together with parents to devise goals and strategies to help develop areas of communication which the child is having difficulty with.
  • Daily activities: Providing families with strategies and advice that can be utilised at home within daily activities and routines to help develop communication skills.
  • Step by step goals: Making small step by step goals that are achievable and show the child’s progression within the skill areas.
  • Visual information: Incorporating extra visual information through the use of a more formalised gesture system, pictures and/or symbols to aid understanding and use of language where appropriate.
  • Positive reinforcement: Providing lots of positive reinforcement and encouragement throughout therapy to help build confidence and self esteem.
  • Liaising with educational staff (where appropriate) about the child’s communication skills and providing information and ideas that can be used in the educational setting to help the child access the curriculum.

Why should I seek therapy for my child with low muscle tone?

Diagnosis alone is NOT the solution. It simply opens the door to getting the help that is needed by arming all involved with the relevant information.

The ‘help’ still needs to be provided. The help that is provided (at least from a therapy perspective) will reflect:

  • First and foremost what medical intervention is needed.
  • What the parents/teachers/carers biggest concerns are for the child (i.e. what are the most significant functional challenges).
  • The specific areas that are problematic to the child (which will vary even within children with the same diagnosis).
  • The capacity of the child’s environments to meet the child’s needs.

If left untreated the child with low muscle tone may have difficulties with:

  • Learning to talk, speech intelligibility and clarity.
  • Managing a full school day due to poor strength and endurance.
  • Participating in sporting activities leading to an inactive lifestyle, increasing the risks of other health related issues such as obesity, diabetes, cardiovascular disease or similar conditions.
  • Self esteem and confidence when they realise their skills do not match their peers.
  • Bullying when others become more aware of a child’s difficulties.
  • Fine motor skills (e.g. writing, drawing and cutting) due to poor core stability, meaning they do not have a strong base to support the use of their arms and hands.
  • Completing self-care tasks (e.g. doing up shoelaces, buttons, zips, using cutlery).
  • Accessing the curriculum because they are unable to attend to tasks long enough to complete assessment criteria.
  • Anxiety and stress in a variety of situations leading to difficulty reaching their academic potential.
  • Academic performance: Developing literacy skills such as reading and writing and coping in the academic environment.
  • Academic assessment: Completing tests, exams and academic tasks in higher education.

More specific implications of not seeking treatment will be influenced by the common difficulties that are most influencing your individual child.

For more information see the relevant fact sheets under areas of concern or refer to the other relevant resources section below.

What does this diagnosis really mean for the child?

Diagnoses are used to label a specific set of symptoms that are being experienced by a child.

This label then helps to narrow down and specifically tailor what:

  • Other issues commonly occur simultaneously.
  • Medication might be appropriate.
  • Therapies might help the child (e.g. Medical, Occupational Therapy, Speech Therapy, Psychology).
  • Course of intervention (medical and/or allied health) might be and what outcome might be expected (prognosis).
  • Can be done to help the child.

A diagnosis helps the child and their carers (parents, teachers, health professionals, carers) to:

  • Access information about the relevant cluster of symptoms.
  • Communicate the salient features of the child’s challenges to all people involved in the child’s care.
  • Possibly interpret certain behaviours differently in light of the diagnosis.
  • Obtain information about what can be done to help the child.
  • Determine specifically where and how to help the child.
  • Access funding or services that might not otherwise be accessible.

Other useful resources

Kid Sense was one of the earliest providers to register for the NDIS and has helped hundreds of parents navigate their way through the funding regulations. We can help you prepare for your NDIS planning meeting and guide you through the application process.


How to Improve Leg Strength at Any Age

Combine everything we have learned so far with the fact that most people will lose a quarter of their muscle strength by the age of 70, and it’s not difficult to see why late-life disease is running rampant and ending lives way too early. Improving your activity level or going for casual walks isn’t enough to maintain leg strength, but those activities may serve as your starting point.

Use this cheat sheet as a guide to determine how you take action to pump up your legs starting today:

  • If your lifestyle is currently sedentary, start by getting up and moving as much as possible. If taking short walks throughout the day is all that you can do safely, then that’s your starting point. If you can do strength-building exercises during commercial breaks when watching television as well, then that’s even better. Think about seeing your doctor to determine what you can do safely, and then gradually build up to a more rigorous workout routine with time. We’ll tell you about some of the simplest and most effective leg-strengthening exercises below, so jump down for the list and start using them as much as possible.
  • If you’re moderately active but you don’t workout consistently, it’s time to take your workout routine to the next level. You don’t have to designate certain days “leg day,” but you should start adding some weight-bearing exercises that target your leg muscles into your routine. Look below for a list of leg exercises proven to strengthen and build muscle.
  • If you workout regularly or you’re an athlete, then you probably already have strong leg muscles. Make it a rule never to skip leg day, and maybe consider increasing the amount of time that you focus on your legs.

Research has shown that runners have strong leg muscles that can extend their lives by nearly two decades, and it’s likely that other athletes who regularly train their leg muscles have the same benefit. Perhaps you’re not an athlete or runner, but you can still participate in sports.

You’ll work the same muscles whether you’re playing basketball at the YMCA with the kids or on a professional court. Tennis, badminton, soccer and flag football will work as well. If you can’t run, start with power walking.

Swimmers also have strong legs, and exercising in the water applies virtually no impact on your body. This makes water aerobics and swimming laps another great starting point for those unable to move comfortably on dry land. Try walking laps across the shallow end of the pool while lunging and kicking your legs. Holding the edge of the pool, jump your feet from the bottom of the pool up onto the wall repeatedly. Many strength-building exercises that you can do on dry land are also possible in the water.

You can also do some simple leg-strengthening exercises from the comfort of your home. Take a peek at this list of the most common moves suitable for people of all ages:

    – Stand with your feet shoulder-width apart. Bend at the knees, pushing your glutes backwards as if trying to sit on the edge of a chair. You should hold your body weight in your heels. As you return to a standing position, squeeze your buns at the top of the movement. You can place your feet wider or closer together to work different leg muscles. – Standing with your feet slightly apart, take one foot out in front of your body so that you’re standing with your legs in an open-scissor pattern. Bend both knees, taking your back knee toward the ground and maintaining a 90-degree angle with the front leg. Hold for a moment before rising back to a standing position and pushing your front leg off the ground to return to your starting position. Rotate legs. You can also walk while lunging each leg. – These are also called glute bridges. Rest on your back with knees bent and feet flat on the floor. Place your hands slightly under your glutes on each side, and then push your hips up. Your feet should plant firmly into the floor as your hips and glutes move straight up. Keep your shoulders and neck on the ground. Lower back to starting position and repeat. Try to squeeze your glutes before lowering to the floor each time. – This is as simple as stepping up onto a raised platform. Rotate your lead leg with each step, squeezing your glutes a little as you pull your second leg up to the step. You can do this with an exercise step, the bottom step of a staircase, a bench or any other raised platform that is secure and at the right height to challenge you without presenting a safety concern. Start with low steps and work your way up to higher platforms with time.

With time, you can make these simple movements harder by adding jumps or holding weight. Simply increasing the number of repetitions in a set or the number of sets performed can challenge your legs with time as well. You may also want to learn some moves that combine your lower and upper body for maximum health benefits. For instance, try squatting and then raising your hands up over your head as you come back up to standing.

Simple calf raises while sitting on the couch or standing in line can help as well. Your calves are critical to longevity and cognitive health, but they also serve as the “second heart” and are critical to the health of your circulatory system.

Curious about the latest research on longevity?
Download your FREE 40-page eBook: The Science Longevity. 5 Proven Life-Lengthening Strategies


Prevalence of Bone Mass Loss

In 2010, it was estimated that more than 99 million adults aged 50 years and older had severely decreased bone density mass in the United States [43]. Based on the overall 10.3% prevalence of osteoporosis, it was estimated that in 2010, 10.2 million older adults (65 years and older) had osteoporosis in the United States. The overall prevalence of low bone mass was 43.9%, from which it was estimated that 43.4 million older adults had osteopenia, from mild to severe levels [43]. It is projected that by 2020, the number of adults over age 50 with low bone mass, including osteoporosis, will grow from approximately 54 million to 64.4 million. By 2030, that number will further increase to 71.2 million (a 29% increase from 2010) [44]. It is anticipated that the number of fractures will grow proportionally [44].


DISCUSSION

The muscle strength of the knee extensors improved after the 10 weeks of eccentric exercise in all training protocols however, we found a significant increase of

14% in the fascicle length of the vastus lateralis muscle only after the intervention with the high lengthening velocity. Therefore, our hypothesis has not been confirmed. These findings provide evidence that not every eccentric exercise loading causes an increase in fascicle length and that the lengthening velocity of the fascicles seems to be an important factor for longitudinal muscle growth. Furthermore, our results show that the fascicle kinetics of the vastus lateralis muscle during eccentric knee extension contractions is different to the elongation behavior expected from the knee joint angle motion. In the beginning of all contractions, the fascicles contract concentrically, despite a lengthening of the muscle-tendon unit (i.e. flexion in the knee joint), and the main lengthening of the fascicles occurs in the phase where the knee extension moment decreases. Furthermore, only in the last phase (i.e. lengthening of the fascicles while the knee joint moment decreased) did protocol 4 show a higher lengthening velocity of the muscle fascicles in comparison with the other protocols. The above fascicle behavior can be explained by the tendon compliance, which affects the fascicle kinetics in eccentric contractions. In conclusion, we can argue that muscle-tendon unit movement cannot predict fascicle kinetics during eccentric contractions in humans.

Although the underling mechanisms regarding the longitudinal growth of the muscle (i.e. increase of the number of sarcomeres in series) are not well known, it has been suggested that structural damage in the sarcomeres after eccentric muscle contractions is the major stimulus for the increase in fiber length (Lynn and Morgan, 1994 Proske and Morgan, 2001). Several studies report that eccentric muscle contractions with high lengthening velocity cause more severe muscle damage compared with eccentric contractions with low lengthening velocity (Chapman et al., 2008 Shepstone et al., 2005). Therefore, this type of loading (i.e. eccentric loading with high lengthening velocity) might be advantageous to induce longitudinal muscle growth and can partly explain our findings. Furthermore, we can argue that a high lengthening velocity of the fascicles might affect the interaction between titin and its interacting structures (i.e. Z-disc, M-line, I-band), affecting the titin-based stretch sensing and signaling in a lengthening-velocity-dependent manner. Accordingly, we found an increase of vastus lateralis fascicle length only in protocol 4. However, we did not find evidence for an intensity-dependent longitudinal muscle growth in relation to eccentric loading as stated in our hypothesis. In agreement with our results, Koh and Herzog (Koh and Herzog, 1998) found an increase of muscle mass in response to 12 weeks of eccentric exercise in rabbits. However, as they did not find an increase in the number of sarcomeres in series, as was the case in three out of four eccentric exercise protocols in the present study, it seems that not only the eccentric load per se but also the type of the fascicle kinetic affects longitudinal muscle growth.

Reports from the literature provide evidence that, during different kinds of sporting activity, the achieved maximal angular velocity at the knee joint is higher compared with the maximum angular velocity that we used in our experiment (i.e. 240 deg s −1 ). For running and sprinting the reported maximal knee flexion angular velocities during the stance phase ranged from 500 to 600 deg s −1 (Albracht and Arampatzis, 2013 Bezodis et al., 2008) and for counter movement and drop jumps from 280 to 540 deg s −1 (Bobbert et al., 1987a Bobbert et al., 1987b). However, these are peak values lasting only for some milliseconds. The average angular velocity for these activities ranged from 190 to 230 deg s −1 for running (Arampatzis et al., 1999 Arampatzis et al., 2000), 70 deg s −1 to 225 deg s −1 for jumping (Arampatzis et al., 2001) and achieved values of

320 deg s −1 for sprinting (Stafilidis and Arampatzis, 2007). In the present interventions, the training velocity was constant within the whole range of motion. Further, the participants in our experiments (i.e. protocols 2, 3 and 4) had to produce high forces (i.e. 100% MVC) during the whole eccentric contraction. Therefore, the maximal angular velocity used in our study can be considered as high with respect to the movement duration, magnitude of muscle loading and range of motion.

Fascicle length of vastus lateralis muscle in relation to knee joint angle. Mean values and s.e.m. of the fascicle length of the vastus lateralis muscle as a function of knee angle before (pre) and after (post) the exercise intervention protocols at rest (protocol 1, low load magnitude protocol protocol 2, high load magnitude protocol protocol 3, short muscle length protocol protocol 4, high lengthening velocity protocol control, control group). *Statistically significant (P<0.05) differences between pre and post values.

Fascicle length of vastus lateralis muscle in relation to knee joint angle. Mean values and s.e.m. of the fascicle length of the vastus lateralis muscle as a function of knee angle before (pre) and after (post) the exercise intervention protocols at rest (protocol 1, low load magnitude protocol protocol 2, high load magnitude protocol protocol 3, short muscle length protocol protocol 4, high lengthening velocity protocol control, control group). *Statistically significant (P<0.05) differences between pre and post values.

In the past few years, some studies (Blazevich et al., 2007 Duclay et al., 2009 Potier et al., 2009 Reeves et al., 2009) have reported longitudinal growth in human muscles from 7% to 34% in response to eccentric exercise. However, to our knowledge, there is only one study (Butterfield and Herzog, 2006) that investigated the fiber kinetics during eccentric contractions and this was on rabbit muscles. It was found that, in addition to the magnitude of the generated joint moment during the eccentric contraction, the lengthening of the muscle fiber and especially the lengthening during the deactivation of the muscle (i.e. decrease of joint moment) were the best predictors for the increase of the sarcomeres in series. In our training protocols 2, 3 and 4, the magnitude of the generated knee joint moment was equal (i.e. 100% MVC) and, therefore, cannot be the reason for the different findings regarding the fascicle length increase following protocol 4. Furthermore, the maximal strain magnitude of the vastus lateralis fascicle did not differ between the four protocols. However, in training protocol 4, the fascicle lengthening velocity of the vastus lateralis muscle in the phase where the knee joint moment decreased was significantly higher compared with that of the other three training protocols. In our experiments, we did not measure the electromyography (EMG) activity of knee extensors and therefore it could be argued that the decrease in knee extension moment in the last phase of motion (i.e. phase 3) is due to the force–length relationship curve (i.e. descending part) and not due to muscle deactivation. Fig. 6 shows the average normalized knee joint moment from 25 to 90 deg of knee joint angle for the maximal isometric contractions and for the isokinetic eccentric contraction we used in the protocols 2 (100% MVC, 90 deg s −1 , 75 deg range of movement) and 4 (100% MVC, 240 deg s −1 , 75 deg range of movement). It is clearly visible that in the protocol with the high angular velocity, the decrease in knee joint moment was higher than that expected due to the moment–angle relationship, indicating a deactivation of the knee extensor muscles at the end of movement in protocol 4. In contrast, in protocol 2, reduction of the knee joint moment was in line with that expected due to the moment–angle relationship (Fig. 6). The rapid lengthening of the muscle fibers in the descending part of the force–length relationship (i.e. long muscle fiber length) combined with a decrease in muscle force (i.e. deactivation of the muscle) may be an important trigger for muscle damage due to the instability of the sarcomeres and, thus, the homeostatic perturbation that facilitates longitudinal muscle growth (Butterfield and Herzog, 2005). Although we did not examine any biomarkers for muscle damage in our experiments and, therefore, there is no direct evidence regarding the amount of muscle damage between the investigated exercise protocols, we can argue that a high lengthening velocity of the fascicles combined with a decrease in muscle force is an important mechanical stimulus to trigger a homeostatic perturbation in muscles to induce longitudinal plastic changes.

Maximum resultant knee joint moment in relation to knee joint angle. Mean values and s.e.m. of the resultant knee joint moments as a function of the knee joint angle before (pre) and after (post) the exercise intervention protocols (protocol 1, low load magnitude protocol protocol 2, high load magnitude protocol protocol 3, short muscle length protocol protocol 4, high lengthening velocity protocol control, control group). *Statistically significant (P<0.05) differences between pre and post values.

Maximum resultant knee joint moment in relation to knee joint angle. Mean values and s.e.m. of the resultant knee joint moments as a function of the knee joint angle before (pre) and after (post) the exercise intervention protocols (protocol 1, low load magnitude protocol protocol 2, high load magnitude protocol protocol 3, short muscle length protocol protocol 4, high lengthening velocity protocol control, control group). *Statistically significant (P<0.05) differences between pre and post values.

Muscle strength was increased in all four interventions, providing evidence for the effectiveness of our training protocols. Furthermore, protocol 2 (i.e. 100% MVC, 90 deg s −1 ) showed a tendency for a higher increase in muscle strength compared with protocol 4 (i.e. 100% MVC, 240 deg s −1 ). These findings indicate a specificity of the lengthening velocity on the radial and longitudinal muscle growth. In protocol 2, we could not identify in phase 3 any decrease in knee joint moment due to the deactivation of the knee extensor muscles as in protocol 4 (Fig. 6), which might be a reason for the absence of longitudinal growth. Reeves et al. (Reeves et al., 2009) also report a specificity of the training stimulus for adding sarcomeres in series and in parallel by comparing conventional resistance training (i.e. concentric and eccentric contractions) to training with only eccentric contractions. However, Reeves et al. used, in both their interventions, a wide range of angular velocities (i.e. 50 to 200 deg s −1 ) and therefore it is not possible to differentiate the effect of angular velocity on the longitudinal growth.

Ratio of maximal resultant knee joint moment. Mean values and s.e.m. of the ratio (i.e. post to pre values) of maximal resultant knee joint moment in the different exercise protocols and the control group (protocol 1, low load magnitude protocol protocol 2, high load magnitude protocol protocol 3, short muscle length protocol protocol 4, high lengthening velocity protocol control, control group). *Statistically significant (P<0.05) difference to control group ‡ statistically significant (P<0.05) difference to protocol 1 § statistically significant (P<0.05) difference to protocol 3 ¶ tendency towards a statistically significant (P=0.055) difference to protocol 4.

Ratio of maximal resultant knee joint moment. Mean values and s.e.m. of the ratio (i.e. post to pre values) of maximal resultant knee joint moment in the different exercise protocols and the control group (protocol 1, low load magnitude protocol protocol 2, high load magnitude protocol protocol 3, short muscle length protocol protocol 4, high lengthening velocity protocol control, control group). *Statistically significant (P<0.05) difference to control group ‡ statistically significant (P<0.05) difference to protocol 1 § statistically significant (P<0.05) difference to protocol 3 ¶ tendency towards a statistically significant (P=0.055) difference to protocol 4.

We examined an additional functional parameter (i.e. moment–angle relationship), which is often used in the literature as an indicator for longitudinal muscle growth (Butterfield and Herzog, 2006 Proske and Morgan, 2001). The functional consequence of a longitudinal muscle adaptation is a shift of the maximum knee joint moment to longer muscle length (i.e. greater knee joint angle). However, in all investigated training protocols, we did not find a shift of the maximum knee joint moment. Even in the training protocol with the high lengthening velocity, where we measured an increase of

14% in the vastus lateralis fascicle length, the maximum knee joint moment was achieved at the same knee joint angle in the pre and post conditions. These findings show how difficult it is to assess morphological changes in the fascicles from functional parameters, as there can be more than one possible adaptational change in the muscle-tendon unit that affects the moment–angle relationship of the knee extensors after an exercise intervention. Because the tendon is in series with the muscle, the magnitude of fascicle shortening may be affected by the elongation of the tendon (Narici and Maganaris, 2006). Recent studies show that resistance training increases the stiffness of the tendon (Arampatzis et al., 2007 Arampatzis et al., 2010 Reeves et al., 2004). Therefore, from a theoretical point of view, a shift of the maximum knee joint moment to a greater knee angle by an increase in fascicle length of the vastus lateralis could be compensated by an exercise-induced increase of the quadriceps tendon stiffness (i.e. shift of the maximum joint moment to a lower knee joint angle).

Ratio of knee joint angle in which the maximum resultant knee moment was achieved. Mean values and standard errors of the ratio (i.e. post to pre values) of knee joint angle in which the maximum resultant knee joint moment was achieved in the different exercise protocols and the control group (protocol 1, low load magnitude protocol protocol 2, high load magnitude protocol protocol 3, short muscle length protocol protocol 4, high lengthening velocity protocol control, control group).

Ratio of knee joint angle in which the maximum resultant knee moment was achieved. Mean values and standard errors of the ratio (i.e. post to pre values) of knee joint angle in which the maximum resultant knee joint moment was achieved in the different exercise protocols and the control group (protocol 1, low load magnitude protocol protocol 2, high load magnitude protocol protocol 3, short muscle length protocol protocol 4, high lengthening velocity protocol control, control group).

Normalised knee joint moment over the range of movement. Mean values and s.e.m. of the average normalized knee joint moment from 25 to 90 deg of knee joint angle for the maximal isometric contractions (Isometric) and for the isokinetic eccentric contractions we used in the protocol 2 (high load magnitude protocol, top) and protocol 4 (high lengthening velocity protocol, below). The isometric values were measured at 30, 65 and 100 deg of the knee joint angle and then fitted with a second order polynomial to calculate the knee joint moment–angle relationship over the entire range of motion.

Normalised knee joint moment over the range of movement. Mean values and s.e.m. of the average normalized knee joint moment from 25 to 90 deg of knee joint angle for the maximal isometric contractions (Isometric) and for the isokinetic eccentric contractions we used in the protocol 2 (high load magnitude protocol, top) and protocol 4 (high lengthening velocity protocol, below). The isometric values were measured at 30, 65 and 100 deg of the knee joint angle and then fitted with a second order polynomial to calculate the knee joint moment–angle relationship over the entire range of motion.

In summary, we conclude that not every type of eccentric exercise loading causes an increase in fascicle length. The lengthening velocity of the fascicles during the eccentric loading, and particularly in the phase where the knee joint moment decreases (i.e. deactivation of the muscle), seems to be an important factor for longitudinal muscle growth.


Take a close look at the athletes competing in this year's Summer Olympic Games in London&mdashtheir musculature will tell you a lot about how they achieved their elite status. Endless hours of training and commitment to their sport played a big role in building the bodies that got them to the world's premier athletic competition. Take an even closer look&mdashthis one requires microscopy&mdashand you'll see something else, something embedded in the genetic blueprints of these young men and women that's just as important to their success.

In nearly all cases, these athletes have realized the full potential laid out by those genes. And that potential may be much greater to begin with than it was for the rest of us mortals. For instance, the genes in the cells that make up sprinter Tyson Gay's legs were encoded with special instructions to build up lots of fast-fiber muscles, giving his legs explosive power out of the starting blocks. In comparison, the maximum contraction velocity of marathoner Shalane Flanagan's leg muscles, as dictated by her genes, is much slower than Gay's yet optimized for the endurance required to run for hours at a time with little tiring. Such genetic fine-tuning also helps competitors in basketball, volleyball and synchronized swimming, although the impact might be much less because effective teamwork and officiating also influence success in those sports.

When the gun goes off for the 100-meter sprint, when swimmers Michael Phelps and Ian Thorpe hit the water, when Tom Daley leaps from his diving platform, we will be seeing the finest that the world's gene pool has to offer, even though scientists are still trying to figure out which genes those are. Unfortunately, history dictates that we may also see the finest in gene manipulation, as some athletes push for peak performance with the help of illegal substances that are becoming increasingly difficult to detect.

The skinny on muscles
The human body produces two types of skeletal muscle fibers&mdashslow-twitch (type 1) and fast-twitch (type 2). The fast-twitch fibers contract many times faster and with more force than the slow-twitch ones do, but they also fatigue more quickly. Each of these muscle types can be further broken down into subcategories, depending on contractile speed, force and fatigue resistance. Type 2B fast-twitch fibers, for example, have a faster contraction time than type 2A.

Muscles can be converted from one subcategory to another but cannot be converted from one type to another. This means that endurance training can give type 2B muscle some of the fatigue-resistant characteristics of type 2A muscle and that weight training can give type 2A muscle some of strength characteristics of type 2B muscle. Endurance training, however, will not convert type 2 muscle to type 1 nor will strength training convert slow-twitch muscle to fast. Endurance athletes have a greater proportion of slow-twitch fibers, whereas sprinters and jumpers have more of the fast-twitch variety.

Just as we can alter our muscle mix only to a certain degree, muscle growth is also carefully regulated in the body. One difference between muscle composition and size, however, is that the latter can more easily be manipulated. Insulinlike growth factor 1 (IGF-1) is both a gene and the protein it expresses that plays an important role during childhood growth and stimulates anabolic effects&mdashsuch as muscle building&mdashwhen those children become adults. IGF-1 controls muscle growth with help from the myostatin (MSTN) gene, which produces the myostatin protein.

More than a decade ago H. Lee Sweeney, a molecular physiologist at the University of Pennsylvania, led a team of researchers who used genetic manipulation to create the muscle-bound "Schwarzenegger mice". Mice injected with an extra copy of the IGF-1 gene added muscle and became as much as 30 percent stronger. Sweeney concluded that it is very likely that differences in a person's IGF-1 and MSTN protein levels determine his or her ability to put on muscle when exercising, although he admits this scenario has not been studied widely.

Slow-fiber muscle growth and endurance can likewise be controlled through gene manipulation. In August 2004 a team of researchers that included the Salk Institute for Biological Study's Ronald Evans reported that they altered a gene called PPAR-Delta to enhance its activity in mice, helping nurture fatigue-resistant slow-twitch muscles. These so-called "marathon mice" could run twice as far and for nearly twice as long as their unmodified counterparts.

This demonstrated ability to tinker with either fast- or slow-twitch muscle types begs the question: What would happen if one were to introduce genes for building both fast- and slow-twitch muscle in an athlete? "We've talked about doing it but have never done it," Sweeney says. "I assume you'd end up with a compromise that would be well suited to a sport like cycling, where you need a combination of endurance and power." Still, Sweeney adds, there has been little scientific reason (which translates into funding) to conduct such a study in mice, much less humans.

Gene manipulation will have its most significant impact in treating diseases and promoting health rather than enhancing athletic abilities, although sports will certainly benefit from this research. Scientists are already studying whether gene therapies can help people suffering from muscle diseases such as muscular dystrophy. "A lot has been learned about how we can make muscles stronger and bigger and contract with greater force," says Theodore Friedmann, a geneticist at the University of California, San Diego, and head of a gene-doping advisory panel for the World Anti-Doping Agency (WADA). Scientific studies have introduced IGF-1 protein to mouse tissue to prevent the normal muscle degradation during aging. "Somewhere down the road efforts could be made to accomplish the same in people," he adds. "Who would not stand in line for something like this?"

Gene therapy has already proved useful in studies unrelated to muscle treatment. In December 2011, for example, a team of British researchers reported in The New England Journal of Medicine that they were able to treat six patients with hemophilia B&mdasha disease in which blood cannot clot properly to control bleeding&mdashby using a virus to deliver a gene enabling them to produce more of the clotting agent, factor IX.

Hard targets
Despite experiments with IGF-1 and MSTN protein levels in mouse muscle, identifying which genes are directly responsible for athletic prowess is a complicated matter. "What we've learned over the past 10 years since the sequencing of the human genome is that there's a heck of a lot more complexity here than we first envisioned," says Stephen Roth, a University of Maryland associate professor of exercise physiology, aging and genetics. "Everybody wants to know what are the genes that are contributing to athletic performance broadly or muscular strength or aerobic capacity or something like that. We still don't have any hard targets solidly recognized by the scientific community for their contribution to athletic performance."

By 2004 scientists had discovered more than 90 genes or chromosomal locations they thought were most responsible for determining athletic performance. Today the tally has risen to 220 genes.

Even with this lack of certainty, some companies have already tried to exploit what has been learned so far to market genetic tests they claim can reveal a child's athletic predispositions. Such companies "are sort of cherry-picking some literature and saying, 'Oh, these four or five gene variations are going to tell you something,'" Roth explains. But the bottom line is the more studies we've done, the less certain we are that any of these genes are really strong contributors by themselves."

Atlas Sports Genetics, LLC, in Boulder, Colo., began selling a $149 test in December 2008 the company said could screen for variants of the gene ACTN3, which in elite athletes is associated with the presence of the protein alpha-actinin-3 that helps the body produce fast-twitch muscle fibers. Muscle in lab mice that lacks alpha-actinin-3 acts more like slow-twitch muscle fiber and uses energy more efficiently, a condition better suited to endurance than mass and power. "The difficulty is that more advanced studies have not found exactly how loss of alpha-actinin-3 affects muscle function in humans," Roth says.

ACE, another gene studied in relation to physical endurance, has rendered uncertain results. Researchers originally argued that people with one variant of ACE would be better at endurance sports and those with a different variant would be better suited to strength and power, but the findings have been inconclusive. So although ACE and ACTN3 are the most recognized genes when it comes to athletics, neither is clearly predictive of performance. The predominant idea 10 or 15 years ago that there might be two, three or four really strong contributing genes to a particular trait like muscular strength "is kind of falling apart," Roth says. "We've been realizing, and it's just been borne out over the past several years, that it's not on the order of 10 or 20 genes but rather hundreds of genes, each with really small variations and huge numbers of possible combinations of those many, many genes that can result in a predisposition for excellence.

"Nothing about the science changed," he adds. "We made a guess early on that turned out not to be right in most instances&mdashthat's science."

Gene doping
WADA turned to Friedmann for help after the 2000 Sydney Summer Olympics after rumors started flying that some of the athletes there had been genetically modified. Nothing was found, but the threat seemed real. Officials were well aware of a recent gene therapy trial at the University of Pennsylvania that had resulted in the death of a patient.

"In medicine, such risks are accepted by patients and by the profession that danger is being undertaken for purposes of healing and preventing pain and suffering," Friedmann says. "If those same tools when applied to a healthy young athlete were to go wrong, there would be far less ethical comfort for having done it. And one would not like to be in the middle of a society that blindly accepts throwing [erythropoietin (EPO)] genes into athletes so they can have improved endurance performance." EPO has been a favorite target for people interested in manipulating blood production in patients with cancer or chronic kidney disease. It has also been used and abused by professional cyclists and other athletes looking to improve their endurance.

Another scheme has been to inject an athlete's muscles with a gene that suppresses myostatin, a protein that inhibits muscle growth. With that, Sweeney says, "you're off and running as a gene doper. I don't know if anyone is doing it, but I think if someone with scientific training read the literature they might be able to figure out how to succeed at this point," even though testing of myostatin inhibitors injected directly into specific muscles has not progressed beyond animals.

Myostatin inhibitors as well as EPO and IGF-1 genes have been early candidates for gene-based doping, but they're not the only ones, Friedmann says. The vascular endothelial growth factor (VEGF) gene instructs the body to form signal proteins that help it increase blood flow by sprouting new blood vessels in muscle. These proteins have been used to treat macular degeneration and to restore the oxygen supply to tissues when blood circulation is inadequate. Other tempting genes could be those that affect pain perception, regulate glucose levels, influence skeletal muscle adaptation to exercise and aid respiration.

Games at the 2012 Olympics
Gene manipulation is a big wild card at this year's Olympics, Roth says. "People have been predicting for the past several Olympics that there will be gene doping at the next Olympics, but there's never been solid evidence." Gene therapy is often studied in a medical context, and it fails a lot of the time, he notes. "Even if a gene therapy is known to be solid in terms of treating a disease, when you throw it into the context of athletic performance, you're dealing with the unknown."

The presence of gene doping is hard to detect with certainty. Most of the tests that might succeed require tissue samples from athletes under suspicion. "We're talking about a muscle biopsy, and there aren't a lot of athletes who will be willing to give tissue samples when they're getting ready to compete," Roth says. Gene manipulation is not likely to show up in the blood stream, urine or saliva, so the relatively nonintrusive tests of those fluids are not likely to determine much.

In response, WADA has adopted a new testing approach called the Athlete Biological Passport (ABP), which will be used at the London Olympics. Several international sporting authorities such as the International Cycling Union have also begun to use it. The key to ABP's success is that, rather than looking ad hoc for a specific agent&mdashsuch as EPO&mdashthe program monitors an athlete's body over time for sudden changes, such as a jump up in red blood cell count.

Another way to detect the presence of gene doping is to recognize how the body responds to a foreign gene&mdashnotably, defense mechanisms it might deploy. "The effect of any drug or foreign gene will be complicated by an organism trying to prevent harm from that manipulation," Friedmann says&mdashrather than from intended changes induced by EPO, for example.

The Olympic games make clear that all athletes are not created equal, but that hard work and dedication can give an athlete at least an outside chance of victory even if competitors come from the deeper end of the gene pool. "Elite performance is necessarily a combination of genetically based talent and training that exploits those gifts," Roth says. "If you could equalize all environmental factors, then the person with some physical or mental edge would win the competition. Fortunately those environmental factors do come into play, which gives sport the uncertainty and magic that spectators crave."


Too Much Protein

So think twice when you consider sacrificing the carbohydrates for a protein-dominant diet, Butterfield says. Drastically cutting carbohydrates from your diet may force your body to fight back.

She says that's because a diet in which protein makes up more than 30% of your caloric intake causes a buildup of toxic ketones. So-called ketogenic diets can thrust your kidneys into overdrive in order to flush these ketones from your body. As your kidneys rid your body of these toxic ketones, you can lose a significant amount of water, which puts you at risk of dehydration, particularly if you exercise heavily.

That water loss often shows up on the scale as weight loss. But along with losing water, you lose muscle mass and bone calcium. The dehydration also strains your kidneys and puts stress on your heart.

And dehydration from a ketogenic diet can make you feel weak and dizzy, give you bad breath, or lead to other problems.


At what point does muscle mass overcome muscle strength to affect speed? - Biology

Article Reviewed:
Charge, S. B. P., and Rudnicki, M.A. (2004). Cellular and molecular regulation of muscle regeneration. Physiological Reviews, Volume 84, 209-238.

Introduction
Personal trainers and fitness professionals often spend countless hours reading articles and research on new training programs and exercise ideas for developing muscular fitness. However, largely because of its physiological complexity, few fitness professionals are as well informed in how muscles actually adapt and grow to the progressively increasing overload demands of exercise. In fact, skeletal muscle is the most adaptable tissue in the human body and muscle hypertrophy (increase in size) is a vastly researched topic, yet still considered a fertile area of research. This column will provide a brief update on some of the intriguing cellular changes that occur leading to muscle growth, referred to as the satellite cell theory of hypertrophy.

Trauma to the Muscle: Activating The Satellite Cells
When muscles undergo intense exercise, as from a resistance training bout, there is trauma to the muscle fibers that is referred to as muscle injury or damage in scientific investigations. This disruption to muscle cell organelles activates satellite cells, which are located on the outside of the muscle fibers between the basal lamina (basement membrane) and the plasma membrane (sarcolemma) of muscles fibers to proliferate to the injury site (Charge and Rudnicki 2004). In essence, a biological effort to repair or replace damaged muscle fibers begins with the satellite cells fusing together and to the muscles fibers, often leading to increases in muscle fiber cross-sectional area or hypertrophy. The satellite cells have only one nucleus and can replicate by dividing. As the satellite cells multiply, some remain as organelles on the muscle fiber where as the majority differentiate (the process cells undergo as they mature into normal cells) and fuse to muscle fibers to form new muscle protein stands (or myofibrils) and/or repair damaged fibers. Thus, the muscle cells’ myofibrils will increase in thickness and number. After fusion with the muscle fiber, some satellite cells serve as a source of new nuclei to supplement the growing muscle fiber. With these additional nuclei, the muscle fiber can synthesize more proteins and create more contractile myofilaments, known as actin and myosin, in skeletal muscle cells. It is interesting to note that high numbers of satellite cells are found associated within slow-twitch muscle fibers as compared to fast-twitch muscle fibers within the same muscle, as they are regularly going through cell maintenance repair from daily activities.

Growth factors
Growth factors are hormones or hormone-like compounds that stimulate satellite cells to produce the gains in the muscle fiber size. These growth factors have been shown to affect muscle growth by regulating satellite cell activity. Hepatocyte growth factor (HGF) is a key regulator of satellite cell activity. It has been shown to be the active factor in damaged muscle and may also be responsible for causing satellite cells to migrate to the damaged muscle area (Charge and Rudnicki 2004).
Fibroblast growth factor (FGF) is another important growth factor in muscle repair following exercise. The role of FGF may be in the revascularization (forming new blood capillaries) process during muscle regeneration (Charge and Rudnicki 2004).
A great deal of research has been focused on the role of insulin-like growth factor-I and –II (IGFs) in muscle growth. The IGFs play a primary role in regulating the amount of muscle mass growth, promoting changes occurring in the DNA for protein synthesis, and promoting muscle cell repair.
Insulin also stimulates muscle growth by enhancing protein synthesis and facilitating the entry of glucose into cells. The satellite cells use glucose as a fuel substrate, thus enabling their cell growth activities. And, glucose is also used for intramuscular energy needs.

Growth hormone is also highly recognized for its role in muscle growth. Resistance exercise stimulates the release of growth hormone from the anterior pituitary gland, with released levels being very dependent on exercise intensity. Growth hormone helps to trigger fat metabolism for energy use in the muscle growth process. As well, growth hormone stimulates the uptake and incorporation of amino acids into protein in skeletal muscle.
Lastly, testosterone also affects muscle hypertrophy. This hormone can stimulate growth hormone responses in the pituitary, which enhances cellular amino acid uptake and protein synthesis in skeletal muscle. In addition, testosterone can increase the presence of neurotransmitters at the fiber site, which can help to activate tissue growth. As a steroid hormone, testosterone can interact with nuclear receptors on the DNA, resulting in protein synthesis. Testosterone may also have some type of regulatory effect on satellite cells.

Muscle Growth: The ‘Bigger’ Picture
The previous discussion clearly shows that muscle growth is a complex molecular biology cell process involving the interplay of numerous cellular organelles and growth factors, occurring as a result of resistance exercise. However, for client education some important applications need to be summarized. Muscle growth occurs whenever the rate of muscle protein synthesis is greater than the rate of muscle protein breakdown. Both, the synthesis and breakdown of proteins are controlled by complimentary cellular mechanisms. Resistance exercise can profoundly stimulate muscle cell hypertrophy and the resultant gain in strength. However, the time course for this hypertrophy is relatively slow, generally taking several weeks or months to be apparent (Rasmussen and Phillips, 2003). Interestingly, a single bout of exercise stimulates protein synthesis within 2-4 hours after the workout which may remain elevated for up to 24 hours (Rasmussen and Phillips, 2003). Some specific factors that influence these adaptations are helpful to highlight to your clients.

All studies show that men and women respond to a resistance training stimulus very similarly. However, due to gender differences in body size, body composition and hormone levels, gender will have a varying effect on the extent of hypertrophy one may possibly attain. As well, greater changes in muscle mass will occur in individuals with more muscle mass at the start of a training program.

Aging also mediates cellular changes in muscle decreasing the actual muscle mass. This loss of muscle mass is referred to as sarcopenia. Happily, the detrimental effects of aging on muscle have been shown be restrained or even reversed with regular resistance exercise. Importantly, resistance exercise also improves the connective tissue harness surrounding muscle, thus being most beneficial for injury prevention and in physical rehabilitation therapy.

Heredity differentiates the percentage and amount of the two markedly different fiber types. In humans the cardiovascular-type fibers have at different times been called red, tonic, Type I, slow-twitch (ST), or slow-oxidative (SO) fibers. Contrariwise, the anaerobic-type fibers have been called the white, phasic, Type II, fast-twitch (FT), or fast-glycolytic (FG) fibers. A further subdivision of Type II fibers is the IIa (fast-oxidative-glycolytic) and IIb (fast-glycolytic) fibers. It is worthy of note to mention that the soleus, a muscle involved in standing posture and gait, generally contains 25% to 40% more Type I fibers, while the triceps has 10% to 30% more Type II fibers than the other arm muscles (Foss and Ketyian, 1998). The proportions and types of muscle fibers vary greatly between adults. It is suggested that the new, popular periodization models of exercise training, which include light, moderate and high intensity training phases, satisfactorily overload the different muscle fiber types of the body while also providing sufficient rest for protein synthesis to occur.

Muscle Hypertrophy Summary
Resistance training leads to trauma or injury of the cellular proteins in muscle. This prompts cell-signaling messages to activate satellite cells to begin a cascade of events leading to muscle repair and growth. Several growth factors are involved that regulate the mechanisms of change in protein number and size within the muscle. The adaptation of muscle to the overload stress of resistance exercise begins immediately after each exercise bout, but often takes weeks or months for it to physically manifest itself. The most adaptable tissue in the human body is skeletal muscle, and it is remarkably remodeled after continuous, and carefully designed, resistance exercise training programs.