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Issue: #10October 2010
Dear Exercise Physiologists,

Thank you for being part of our community. ASEP is the specific voice for (historically under-represented) Exercise Physiologists. Please use this Newsletter as a link to ASEP resources from scientific journals to professional papers, to employment and related opportunities. And be sure to click on "More On Us" at the left for the ASEP-Newsletter's parent web site.
Yours in health, 
-Lonnie Lowery and Jonathan Mike, ASEP-Newsletter Editors 
 Editor's Corner


A Member of How Many Professional Groups?


Of how many professional organizations are you a member? I was counting the other day. I am a member of five - at times. For financial and simply temporal reasons, I tend to rotate a couple of them, depending on whether I'm actively participating in a meeting that year. I simply have to make choices at times. I bet many readers are similar, having para-involvement in somewhat different groups / disciplines.

Sometimes I miss getting the newsletter from a particular group when I find membership impossible that year. Some years I get locked out of online job search offerings or networking opportunities or journals or databases of information. It's just something I've come to accept. Do any of you know what I mean?

I'm not sure if you've noticed, but ASEP is extremely open in its offerings. You don't get locked out. All one needs to do to get this free newsletter is subscribe online via a little box. All she or he needs to do to read the Journal of Exercise Physiology (JEP) is to surf on over to that part of Need job postings? There are a few at any given time on and in this ASEP-Newsletter. Have a serious, burning question? Often either I or Co-Editor Jonathan Mike or Tommy Boone himself will reply to your email.

I'm proud of these aspects of ASEP, and it's why I do my best to stay involved - including working on this Newsletter monthly. ASEP is not huge; it's not able to guarantee you licensure or necessarily solve your employment (or research) concerns. But there are people in this group who are darn sure going to try, whether it's by offering a home base for your collective voice as Exercise Physiologists or providing a code of ethics for our profession or hosting a national meeting such as next year's in Albuquerque, New Mexico.

Please consider your regular membership in ASEP - or even your time as a conference attendee - as a donation to keep ASEP running strong. Few groups I have experienced are as selfless, as concerned and determined, or as free and open as the American Society of Exercise Physiologists.


Lonnie Lowery, PhD,
ASEP-Newsletter Editor 
Ask the EP 
Q:   What are the physiological mechanisms and causes behind Metabolic Acidosis? What are the differences between the terms Lactic Acid and Lactate? How is lactate involved with specific energy systems and how is lactate production and removal regulated? 


A:      Lactic acid is the chemical name of 2- hydroxypropanoic acid and is a 3 carbon carboxylic acid. When the proton has been removed from the carboxylytic functional group, the molecule is called Lactate. The remaining negative charge can be balanced by a cation, such as sodium or potassium, which can form sodium or potassium lactate. For Lactic Acid, 50% of it metabolite is in the form of Lactic Acid, and 50% of its form is Lactate, for example when pH is 3.67. This represents a very acidic environment given the normal pH range of 6.1- 7.05. Therefore, the proportion of unbound Lactate varies from 99.06- 99.38, therefore, trace amount of Lactic Acid occur inside the body, and thus this terms "Lactic Acid", and "Lactic Acidosis" should not be used. The reader is referred the review by Robergs and Colleagues (2004) for a further in depth discussion.


Understanding this fundamental difference between Lactic Acid and Lactate are essential to understanding of what the true markers of acidosis actually are. Considering for more than 60 years, the idea/belief that Lactic Acid causes acidosis and that Lactate is a negative aspect of exercise physiology and high intensity exercise involving a high rate of ATP turnover is just not true.


Lactate Production


Lactate production is incredibly important during skeletal muscle contraction, during intense contractions, and involving a high rate of ATP turnover. In addition, it is a rapid and valuable resource for the muscle cytosol to maintain NAD+ supply, as well as buffer the release of protons during Glycolysis. It is produced by the LDH reaction:


Pyruvate + NADH + H+ < > Lactate + NAD+


*Pyruvate conversion to Lactate is termed the "mass action effect"


Essentially, since pyruvate is in the acid salt form, means no H+ (hydrogen ion) is released on the carboxylytic acid groups during lactate production, therefore, the protons that are released from Glycolysis DO NOT come from the production of metabolic acids. Therefore, Lactate is not detrimental but instead of producing a proton, lactate production CONSUMES a proton, and termed "metabolic proton buffering", thereby retarding acidosis.


For example, accumulation of muscle and blood lactate after exercise, lactate can be oxidized back to pyruvate for gluconeogenic conversion to glucose in the liver or converted to pyruvate in the muscle and other tissues for further catabolism within the mitochondria for ATP production.


During intense exercise sessions, there is a substantial increase in the rate of substrate flux through glycolysis simply because the stimulation of glycogenolysis (i.e. increased Pi, increased AMP, increased CA++) and glycolysis are so high. Depending on the distribution and/or proportion of fast twitch and slow twitch muscle fibers and motor units, the ability for converting pyruvate to acetyl CoA and in conjunction of the glycerol-3- phosphate shuttle to run at similar rates, all depend on the mitochondrial mass of working skeletal muscle. Highly trained endurance individuals have a greater affinity of the contracting muscle to use Mitochondrial Respiration to supply most of the ATP production to regenerate most of NAD+. Nonetheless, there are many circumstances (high intensity resistance training or interval training) where the rate of ATP demand exceeds the ability of muscle fibers to maintain ATP demand from mitochondrial respiration. Therefore, in these specific situations, contracting muscle must depend on the LDH reaction to regenerate NAD+. Hence, the increased Lactate production (not caused by lack of 02 or being the cause of acidosis) represents the increased reliance on the glycolytic and phosphagen  energy systems to regenerate ATP for muscle contraction. Thus, the production of lactate coincides with the release of a proton (H+) and decrease in pH. It is the decrease in cellular and blood pH with high rates of lactate production that has a detrimental effect to enzymes of energy metabolism and muscle contraction.


 In addition, because of the increased rate of these pathways,  it also involves the CrP (creatine phosphate reaction/shuttle). Since the CrP reaction involves free protons, acidosis effects restoration of CrP stores. Hence, the greater the acidosis, the longer the recovery period. Muscle CrP recovery reveals a dual exponential curve having a fast and slow component. This fast component is complete within 2 minutes and represents 80-90% of complete CrP recovery.


Interestingly, if muscle did not produce or could not produce lactate, and as soon as exercise intensity increased, there would be no means to rely on addition ATP from glycolysis, and no reactions would take place in the cytosol to regenerate NAD+ from NADH, and thus this "redox potential" would decrease the rate of the glyeraldehyde-3-phosphate dehydrogenase reaction and completely shut down the glycolytic energy pathway.


So, what are the causes of metabolic acidosis in skeletal muscle? Acidosis develops when the rate of H+ production exceeds the rate of H+ removal/buffering.



H+ Production                          H+ Removal/buffering

            Glycolytic Flux                          CrP Hydrolysis

            ATP Hydrolysis                         Mitochondria Transport

            Fast Twitch motor units              Protein/amino acids


                                                            Inorganic Phosphate

                                                            Sarcolemmal Transport


Lactate Production (on the removal side) is beneficial for:


-          Regenerating NAD+

-          Consuming Protons

-          Facilitating proton efflux from cells






Robergs, R.A., Ghiasvand, F., & Parker, D. (2004). Biochemistry of exercise-induced metabolic acidosis. American Journal of Physiology: Regulatory, Integrative and Comparative Physiology. 287: R502-R516.

Jonathan Mike, MS, CSCS, USAW, NSCA-CPT, Doctoral Student, Assistant Editor 
Advertisements & Announcements

Opportunities Related to Exercise Physiology

Community Announcement: Iron has issued a call for brief submissions from EP students or professionals interested in getting their first involvement in legitimate Internet / pod casting settings. Opinions on professional issues or micro reviews and recent research are welcomed. Students' audio submissions (see National Public Radio (NPR]) and / or the Iron web site for examples) will be editor-reviewed by ASEP-Newsletter Editors Dr. Lonnie Lowery and Jonathan Mike. The submissions should be 300-500 word essays read aloud and recorded with Windows Sound Recorder or similar software and sent via email to Iron is not ASEP-affiliated.

 National Meeting 2011!

The American Society of Exercise Physiologists is pleased to announce the 2011 National Meeting on September, 22nd, 23rd and 24th in Albuquerque, NM. This will be the fourth time the national meeting has been held here in Albuquerque. This exciting 3-day event will be held at the Radison Hotel and Water Park, New Mexico Sports and Wellness, and The University of New Mexico, and partly hosted by the Exercise Science Program, Department of Health, Exercise, and Sports Science of the University of New Mexico.


Our 2011 Conference Theme:  Empowering The Undergraduate and Graduate Students of Exercise Physiology.


This conference is about expanding and further developing the education, training, and professional practice for our undergraduates and graduates. In addition, it will advance those who have or will be furthering their professional mark to become a board certified exercise physiologists (EPC).


Special highlights of the 2011 conference include:


  • Undergraduate and Graduate Research and Poster Presentations
  • Helping students to develop their individual businesses and business ideas after graduation
  • Networking opportunities with Physicians, Dieticians, and Sports Nutritionists, and Physical Therapists
  • Many hands-on sessions to enhance skills in clinical exercise physiology, sports physiology and tons more including Resistance Training Variety, Measuring V02 Max and Ventilation Threshold, 12- lead EKG, and Body Composition Assessment


Follow the links below to learn more about this conference.  See you in Albuquerque in 2011!




Exercise Physiology Research Scientist opening in the Division of Space Life Sciences at the NASA Johnson Space Center:

NOTE: ASEP Board of Directors with approval of The Center for Exercise Physiology-online developed the "EPC Petition Guidelines" for doctorate exercise physiologists to become Board Certified.

Thank you for perusing our opinions, facts and opportunities in this edition of the ASEP-Newsletter.

Lonnie Lowery
American Society of Exercise Physiologists

All contents are copyright 1997-2007 American Society of Exercise Physiologists.

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American Society of Exercise Physiologists | Dept. of Exercise Physiology | College of St. Scholastica | 1200 Kenwood Avenue | Duluth | MN | 55811