diabetes y ejercicio, 2012

NEWSACSM’S CERTIFIED

Tips forTraining ClientsWho Play Golf

PAGE 3

Exercise ImmunologyPAGE 4

DiabetesMedications:Guidelinesfor ExerciseSafety PAGE 6 Resistance

Training andDiabetes PAGE 9

HeartSounds

page 10

J U L Y — S E P T E M B E R , 2 0 1 2 • V O L U M E 2 2 : I S S U E 3

Exercise andBariatric SurgeryPAGE 11

2 ACSM’S CERTIFIED NEWS • JULY–SEPTEMBER 2012 • VOLUME 22: ISSUE 3

ACSM’S CERTIFIED NEWSApril–June 2012 • Volume 22, Issue 2

In this IssueTips for training clients who play golf ................... 3Exercise Immunology................................................... 4Diabetes Medications:

Guidelines for Exercise Safety................................ 6Coaching News........................................................... 8Resistance Training and Diabetes ............................. 9Part 3: Heart Sounds...................................................10Exercise and Bariatric Surgery....................................11

Co-EditorsPeter Magyari, Ph.D.

Peter Ronai, M.S., FACSM

Committee on Certificationand Registry Boards Chair

Deborah Riebe, Ph.D., FACSM

CCRB Publications Subcommittee ChairPaul Sorace, M.S.

ACSM National Center Certified News StaffNational Director of Certification

and Registry ProgramsRichard Cotton

Assistant Director of CertificationTraci Sue Rush

Publications ManagerDavid Brewer

Editorial ServicesLori Tish

Angela Chastain

Editorial BoardChris Berger, Ph.D., CSCS

Clinton Brawner, M.S., FACSMJames Churilla, Ph.D., MPH, FACSM

Ted Dreisinger, Ph.D., FACSMAvery Faigenbaum, Ed.D., FACSM

Riggs Klika, Ph.D., FACSMTom LaFontaine, Ed.D., FACSM

Thomas Mahady, M.S.Paul Sorace, M.S.Maria Urso, Ph.D.David Verrill, M.S.

Stella Volpe, Ph.D., FACSMJan Wallace, Ph.D.

For More Certification Resources Contact theACSM Certification Resource Center:

1-800-486-5643

Information for SubscribersCorrespondence Regarding Editorial Content

Should be Addressed to:Certification & Registry Department

E-mail: [email protected].: (317) 637-9200, ext. 115

For back issues and author guidelines visit:http://certification.acsm.org/certified-news

Change of Address or Membership Inquiries:Membership and Chapter Services

Tel.: (317) 637-9200, ext. 139 or ext. 136.

ACSM’s Certified News (ISSN# 1056-9677) is publishedquarterly by the American College of Sports MedicineCommittee on Certification and Registry Boards (CCRB). Allissues are published electronically and in print. The articlespublished in ACSM’s Certified News have been carefullyreviewed, but have not been submitted for consideration as, andtherefore are not, official pronouncements, policies,statements, or opinions of ACSM. Information published inACSM’s Certified News is not necessarily the position of theAmerican College of Sports Medicine or the Committee onCertification and Registry Boards. The purpose of thispublication is to provide continuing education materials to thecertified exercise and health professional and to inform theseindividuals about activities of ACSM and their profession.Information presented here is not intended to be informationsupplemental to the ACSM’s Guidelines for Exercise Testing andPrescription or the established positions of ACSM. ACSM’sCertified News is copyrighted by the American College ofSports Medicine. No portion(s) of the work(s) may bereproduced without written consent from the Publisher.Permission to reproduce copies of articles for noncommercialuse may be obtained from the Certification Department.

ACSM National Center401 West Michigan St., Indianapolis, IN 46202-3233.

Tel.: (317) 637-9200 • Fax: (317) 634-7817© 2012 American College of Sports Medicine.

ISSN # 1056-9677

INTRODUCINGTHE EXERCISE IS MEDICINE®

(EIM) CREDENTIAL

By Richard T. Cotton, National Director of Certification,American College of Sports Medicine

NEW CREDENTIAL BRIDGES GAP BETWEEN FITNESS PROS ANDPHYSICIANS ENCOURAGING PHYSICAL ACTIVITY TO PATIENTS

There is no bigger decision in managing a certification program than deciding to create a new cre-dential. I use “credential” quite intentionally, because not every credential needs to be a certification.In fact, in the case of the new Exercise is Medicine® (EIM) Credential, offering a new certification wasnot the answer because three out of the five core ACSM certifications (HFS, CES, RCEP) address theknowledge and skills related to working with special populations, and our personal trainer and groupexercise instructor certifications somewhat address special populations, as well. However, in orderto meet the level of proficiency the EIM Credential Committee felt was appropriate for referral byphysicians, a credential demonstrating specialized knowledge which can enhance any certification wasthe solution.

Our team headed into this adventure with a number of objectives:• Create a credential that will provide physicians with the confidence that the fitness

professional being referred has ability to safely and effectively address the needs ofthe referring physician’s patients

• Minimize the barriers to entry to earning this credential and at the same time avoidduplicating knowledge and skills already addressed by current ACSM certifications

• Address the need for the enhancement of knowledge and skills in the areas of work-ing within the health care system as well as supporting sustainable behavior change

• Grow the number of EIM credentialed fitness professionals as rapidly as possibleThe planning meeting to address these objectives was probably one of the most productive and

creative meetings of my entire career. We started by nixing the idea of creating another certification.We knew we had most of the knowledge and skills covered in three of the five ACSM certifications,yet we still wanted the holders of those certifications to be able to earn the EIM credential badge tobe able to share with physicians and support the promotion of these important services. Out of thisneed came the three levels of credential.

I don’t want to get too much into the details of the levels for all of that can be found at: http://certification.acsm.org/exercise-is-medicine-credential. The three levels correspond to both theincreasing scope of practice reflected for the most part in the ACSM Certified PersonalTrainer/Certified Group Exercise Instructor certification (Level One) to the ACSM Certified HealthFitness Specialist certification with a bachelor’s degree (Level Two) to the ACSM Registered ClinicalExercise Physiologist certification with a master’s degree (Level Three). The ACSM Clinical ExerciseSpecialist can either qualify for the Level Two or Level Three credential, depending on education andexperience.

The required education program is intended to enhance the knowledge and skill of those withoutbachelor’s degrees in exercise science. The education is provided as follows:

• Working with special populations (60%)• Working within the health care system (20%)• Supporting sustainable behavior change (20%)

The exam is composed of 50 questions with the percentage of the questions consistent with theabove.

We are quite proud of the work that we have done and feel confident that this new credential canmeet the needs of healthcare providers as well as enhance our profession to better integrate withthe healthcare system.

Golf (continued on page 15)

ACSM’S CERTIFIED NEWS • JULY–SEPTEMBER 2012 • VOLUME 22: ISSUE 3 3

Given that more than 25 million Americans play golf, a numberprojected by the World Golf Foundation to increase to 55 million by2020,6 there is a good chance that many of a personal trainer’s typi-cal clientele will include those who play golf — whether to compete atan elite, amateur or professional level, or simply for the enjoyment ofthe game. Such clients can generally benefit from a fitness programthat includes:

• A musculoskeletal screening• Suggestions for pre-round dynamic warm-up routines• Suitable exercise regimens

The above three elements will ensure that your client has moreefficient ball-striking in terms of distance, direction and trajectory,and, at the same time, reduced scope for injury.Musculoskeletal screening: Screen for neck rotation 80° in either

direction; undesirable excessive cervical or thoracic flexion; pelvicrotation (belt buckle turns 45°) along with disassociation from tho-racic rotation; trail shoulder external rotation; lead arm horizontaladduction (should be 130° for males, 155° for females); grip strengthand wrist flexibility (specifically radial and ulnar deviation). Othertests could include those for hamstrings tightness, calf flexibility, pelvictilt, leg extension and balance.Dynamic warmup: A good dynamic warm-up might include pulse-

raiser exercises which at the same time work the abductor/adductormuscles of the thigh, the quadriceps and hamstrings, the lateral flex-ors of the spine and shoulder flexor/extensor muscles.4,5,12

Exercises: A combination of exercises for improving overall and corestrength; flexibility of the spine and upper limb; neuromuscular speedand positional awareness (including plyometrics and uneven surface pro-prioception workouts); cardiovascular fitness for the endurancerequired to walk 18 holes often carrying a golf bag; balance; and agili-ty.1,2,7,11 A new trend is to include exercises which mimic the core move-ment patterns of crawling, rolling over and running.

The personal trainer also can benefit from a basic knowledge ofwhat aspects of the golf swing deliver better distance, direction andtrajectory; as well as an understanding of the regions of, and maincauses of pain or injury, either caused or exacerbated by golf.

The ‘modern’ golf swing which most golfers today aspire to makeemphasizes a large shoulder turn against a restricted hip turn(termed X-factor), along with a speedy trail-side lateral trunk flexionduring the downswing (termed ‘crunch factor’), and both these fac-tors require greater joint stability/mobility respectively, while alsoresulting in greater chance for injury.6

An efficient golf swing produces power and the resulting clubspeed from a combination of:

• Sequential summation of forces - proximal parts lead-ing the distal ones (that is, legs and hips start thedownswing, followed by trunk followed by shoulders,arms and wrists and finally the club)

• Stretch-shortening cycle (muscles which are stretchedduring the backswing — X-factor — or more impor-

tantly during early downswing X-factor stretch — con-tract more forcefully at impact) and

• Use of ground-reaction forces created by forcefulpushing off of the trail foot.8

A correct sequence of the downswing — proximal to distal — notonly helps to generate greater swing speed, but also delivers the golfclub from the correct direction to produce straight ball-flight.Conversely, an incorrect downswing sequence is one in which theupper-body starts the downswing out-of-sequence. Such a downswingis typically termed an ‘over-the-top’ (OTT) one, and usually resultsfrom a backswing with excessive flexion of lead side trunk and thuslead knee; excessive thoracic plus hip rotation; internal rotation oftrail shoulder; excessive pronation of trail forearm and early exten-sion of trail wrist. [More efficient and safer backswing joint positionswhich reduce the scope for the OTT downswing and thus for injury,are neutral wrists, semi supine trail forearm, minimal trail elbow flex-ion, external trail shoulder rotation together with backswing lateralflexion of the trail side trunk].9,10

Injury in the golf swing is mostly microtrauma, caused by poormechanics among the less skilled and occasional golfers; and byoveuse in the more elite ones.6 Poor-mechanics injury is almostalways the result of the over-the-top downswing, which forces greaterthan normal torques and loads on the spine, the lead knee, as well ason both elbows and the lead wrist.

The most common areas of injury3 are said to be wrist/hand 37%,low back 24%, shoulder 10%, elbow 7 and knee 7% for professionalgolfers. For amateur golfers they are low back 35%, elbow 33%,wrist/hand 20% shoulder 12% and knee 9%. Most of these injuriesare of the lead side of the body. Avoidance of the OTT downswingcould reduce the scope for all these injuries.

A well-balanced fitness plus nutrition and hydration package basedon a better basic understanding of golf swing mechanics and injurymechanisms can be an asset to any personal trainer and can addgreatly to his/her repertoire of client services.

The following websites offer golf-specific fitness information:• www.TitlestPerformanceInstitute.com • www.backtogolf.com • www.fitgolf.com • www.chekinstitute.com• www.back9fitness.com • www.golfhelp.com

About the AuthorKiran Kanwar, B.S., has been a golf instructor formore than 23 years and has worked with every skill-level of golfer. Based on over 17 years of research,she has developed The Minimalist Golf Swing whichplaces all the major golf-swing joints of the body inpositions from which they are designed to performoptimally, which increases swing efficiency anddecreases scope for injury. (www.yourgolfguru.com and www.kirankanwargolf.wordpress.com)

WELLNESS ARTICLE

TIPS FOR TRAINING CLIENTSWHO PLAY GOLF By Kiran Kanwar, B.S.


A crippled immune system can impair a training athlete, leaving thebody vulnerable to infection and disease, and subsequently can inhib-it exercise training and performance. Furthermore, changes inimmune functioning can have detrimental effects on physiological sys-tems other than the immune system, including the nervous and meta-bolic systems. In general, the immune response is divided into theinnate immune response (cellular and molecular components thatdefend against infection in a non-specific manner, e.g., macrophagesand neutrophils) and the adaptive immune response (specific cellularand molecular components that defend the body uniquely for eachspecific antigen, e.g., T-cells and B-cells). Both innate and adaptiveresponses are affected by exercise,32 but, how much of an effect doesexercise have, and how should these desired responses govern exer-cise prescription? The focus of this article is dedicated to answeringthese questions.

INNATE IMMUNE SYSTEM AND EXERCISE

The innate immune response is the first line of defense againstpathogens if they pass surface barriers of the body (e.g., mucous, hair,skin). Unlike the adaptive immune response, this system does notadapt to repeated exposures from the same pathogen. Nonetheless,the innate immune system is able to eliminate most invaders with acombination of leukocytes (white blood cells derived from multipo-tent hematopoietic stem cells) and inflammatory mediators (cell-derived messenger molecules that propagate inflammation). Innateimmunity relies heavily on four immune cells (neutrophils,macrophages, dendrites, and natural killer cells), with each respond-ing in a unique manner to exercise. Neutrophils constitute 50% to60% of all circulating leukocytes and typically are the first to respondto immune stimuli including exercise.22 Immediately following a singleaerobic exercise session, circulating neutrophils rapidly increase innumber.22 This initial increase is followed by another delayed rise sev-eral hours later. Both increases are dependent on the intensity andduration of the exercise session. However, the increased number ofneutrophils is not necessarily indicative of a heightened immuneresponse. Rather, following moderate to vigorous aerobic exercise(65 to 85%

.VO2max), mobilized neutrophils are less responsive to

bacterial stimuli for several hours post exercise, showing that theirfunction is blunted.25 In contrast to these results to acute exercise,chronic exercise training appears to leave concentrations of neu-trophils unaffected or reduced, while retaining function.8 Neutrophilresponse to exercise indicates that while intense acute exercise canleave the body vulnerable to infection, chronic training may have abeneficial anti-inflammatory effect. Essentially, exercise training couldcause a more tightly regulated release and sequestering of neu-trophils, helping the body control disease and infection.

A single aerobic exercise session (65% to 85% .VO2max) results in

temporal increases in circulating monocytes approximately 2-h postexercise.19 If muscle damage is involved macrophages in the muscle tis-

sue rise approximately 24-h post exercise.29 Macrophages are mono-cytes that have left circulation into surrounding tissue and differenti-ated into phagoctyic immune cells. The increase in circulating mono-cytes likely is linked to cortisol release from the endothelium duringexercise. Circulating monocytes typically have two predominant phe-notypes, based off of surface receptors (Cluster of Differentiationreceptors), CD14+/CD16+ (pro-inflammatory) and CD14+/CD16-

(homeostatic). Monocytes recruited to circulation within the first 24-h post exercise are primarily of CD14+/CD16+ phenotype while thesecond wave of monocytes (beyond 24-h post exercise) is composedmainly of CD14+/CD16- phenotype. Though there is substantial evi-dence regarding circulating monocytes post exercise, relatively little isknown concerning differentiated tissue macrophages.32 Nonetheless,animal studies have examined the influence of acute moderate aero-bic exercise on tissue macrophages and found some functions such asphagocytosis and reactive oxygen and nitrogen metabolism areenhanced by exercise.20,21,33 Conversely, macrophage MajorHistocompatibility Complex II (MHC II) expression and antigen pre-senting capacity are reduced with a single aerobic exercise session ofnear exhaustive exercise (70%-90%

.VO2max for up to 4 h).2,3 MHC

II are a group of proteins that help macrophages present specific anti-gens to T-helper cells of the adaptive immune system. In contrast tothe conflicting results of single acute exercise session investigations,chronic exercise training appears to consistently blunt the monocyticresponse to exercise. In multiple cross-sectional and longitudinal stud-ies, trained individuals exhibited a smaller monocytic response tolipopolysaccharide (LPS) than their untrained counterparts.7,14,15,28 LPSis a component of gram-negative bacteria, and elicits a reputableimmune response in mammals. The typical monocytic response toLPS was reduced with exercise training. Additionally, some animalstudies show that macrophage infiltration is reduced with exercisetraining. Once more, the effects of acute exercise on macrophageslike neutrophils could leave the body susceptible to infection for up toseveral days following recovery. Yet, the potential reductions inmacrophage infiltration observed with exercise training are seen asbeneficial in situations of chronic inflammation (i.e., cancer, obesity,cardiovascular disease, type 2 diabetes).32

Unlike macrophages and neutrophils, the role of dendritic cells hasbeen vastly under investigated despite the possible large role theyplay in the innate and adaptive immune response to exercise.Dendritic cells are named after their resemblance of neuronal den-drites, and serve largely as mediators between the innate and adap-tive immune response. Currently, only two studies have investigateddendritic cell responses to exercise, and both found that a single exer-cise session of moderate aerobic exercise (60%-85%

.VO2max)

increased circulating levels.5,9 Aside from these results, little else isknown about the dendritic cell response or function following acuteexercise. Only two animal studies have investigated exercise trainingand effects on dendritic cells.4,12 Liao et al.12 found an increase in circu-lating dendritic cells in exercise trained rats. Chiang et al.4 found thatMHC II expression and Interleukin 12 (IL-12) production were signifi-

HEALTH & FITNESS FEATURE

EXERCISE IMMUNOLOGYBy Benjamin T. Gordon, M.S., CES, CSCS

Exercise Immunology (continued on page 13)

cantly increased in dendritic cells. MHC II and IL-12 are heavilyinvolved in the development of T-cells and the adaptive immuneresponse. These investigations support a potentially large dendriticcell role in exercise recovery. Exercise training possibly aids in dendrit-ic function, but additional clinical trials are needed before conclusivestatements are made.

Circulating natural killer (NK) cells, much like other innate leuko-cytes, are rapidly increased in response to exercise. Following a singlesession of aerobic exercise (65%-95%

.VO2max for up to 4 h) a 50%-

100% increase in circulating NK cells10 has been reported. As is thecase with monocytes, the NK cell exercise response is phenotype spe-cific. NK cells can be grouped by their relative expression of CD56,a membrane adhesion molecule. CD56bright and CD56dim are thetwo common phenotypes of NK cell, and it appears CD56bright NKcells are less responsive to acute exercise than CD56dim. This couldindicate that NK cells have a reduced ability to defend againstpathogens following acute exercise, because CD56dim NK cells areless cytotoxic. In addition, with prolonged exercise, circulating NKcells decrease, which is likely a result of tissue infiltration.10

Nonetheless, the health implications following acute exercise-mediat-ed changes in NK cells are unknown, and the effects of exercise train-ing on NK cell functioning are complex. Fairey et al. completed a 15-week clinical trial and found increased NK cytotoxicity.6 Other clinicaltrials including a 12-month trial by Campbell et al. found no exercisetraining effect.1 Inter-study differences such as subject variability maycontribute as confounding factors. However, more decisive evidenceregarding NK cell functioning in response to exercise training is need-ed before conclusions are made.

THE ADAPTIVE IMMUNE SYSTEMAND EXERCISE

Adaptive immunity is the second division of the immune systemand uniquely responds to individual pathogens. The adaptive immunesystem almost always is activated by the presentation of an antigen(any foreign object that provokes the immune system to create anti-bodies), typically by a member of the innate immune system T helpercells (CD4+). T-cells are lymphocytes like NK cells and neutrophils,but all T-cells are distinguished by T-cell Receptors (TCR). CD4+ cellsare not the only T-cells in the immune system. There are several sub-divisions of T-cells including, Regulatory T-cells (Tregs), cytotoxic T-cells (CD8+), memory T-cells, and Natural Killer T-cells (NKT).However unlike CD4+ cells, other T-cells do not initiate the adaptiveimmune response. Furthermore, CD4+ cells are subdivided into type1(Th1) and type 2 (Th2) phenotypes. CD4+ cells and have no specif-ic mechanism for defending against pathogens, but may help otherimmune cells do so. CD4+ cell phenotype is determined by what acti-vates them and what pathways are followed after activation. Th1 cellsare activated by the presence of intracellular pathogens such as bac-teria or viruses. This activation usually is caused by CD4+ cell detec-tion of infected macrophages.32 In turn, Th2 cells are activated by thepresence of extracellular pathogens and toxins, which typically resultsin B-cell production of antibodies. Along with their adaptive immunesystem counterparts, B-cells another lymphocyte, make up the major-ity of the system and function in immune surveillance. These circulat-ing cells do not fully proliferate without CD4+ cells releasing soluble

mediators including cytokines (e.g., IL-4, IL-5, IL-6, and IL-13), whichdifferentiate the B-cells into plasma cells or memory cells. Plasma cellsrelease large amounts of specific antibody (Immunoglobulin, (Ig)) thathelp mark pathogens in the immune phagocytic destruction process.

A single exercise session substantially changes function of the adap-tive immune response.32 Typically, with moderate to vigorous exercise(60%-85%

.VO2max), T- and B-cells show a biphasic response with a

rapid increase in circulation followed by a dip below baseline values afew hours post-exercise. The decrease of T- and B-cells is dependenton how intense and how long the exercise is, meaning with increasesin intensity and duration there are larger decreases below base-line.13,26 Epinephrine interaction appears to cause much of the mobi-lization of these cells into circulation via direct and indirect mecha-nisms. Lymphocytes naturally express a high percentage of adrener-gic receptors causing them to react to the release of epinephrine.With exercise, both the activity and density of these receptors areincreased.27 CD4+ cells have the lowest expression of adrenergicreceptors with the CD8+ expressing the highest. The decrease fol-lowing initial mobilization of T-cells likely is due to an exaggerateddecrease in Th1 cells, whereas exercise seems to have little or noeffect on Th2 cells. Most likely the decrease in Th1 cells is a result ofredistribution of cells and not apoptosis. Similar to acute exercisestudies involving the innate immune system, the decrease in T-cellnumber may be indicative of immune suppression during exerciserecovery. However, T-cell function also must be analyzed.

Without proper functioning T-cells, which can happen with intenseacute exercise, the body is susceptible to all types of intracellularinvaders. This may explain why intense training and competition (e.g.,near maximal effort) leaves athletes temporarily more susceptible toupper respiratory tract infections (URTI).17 However, analysis of T-cellactivity following exercise is extremely difficult. In addition, T-cell func-tioning is measured only in vitro from blood samples obtained duringrecovery. The cell composition of blood samples taken before andafter exercise is often dramatically different making analysis more dif-ficult because the ratios of immune cells are not consistent betweenthe two measurements. Nonetheless, T- and B-cell function appearsusceptible to increases of greater that 15% per week in training load(duration, intensity, and frequency)31 of exercise training. T-cell prolif-erative responses and decreases in stimulated B-cell Ig synthesis havebeen reported with increases in intensity of exercise training.11,30

Further investigations are needed to clarify and fully understand theimpact of exercise training upon T-cell functioning.

B-cells, when properly stimulated by CD4+ cells, can differentiateinto plasma cells or memory cells. Following differentiation, plasma B-cells generally are localized in lymphoid and mucosal tissue with theirmain role being the secretion of Ig (antibody). The effects of exerciseon plasma cells have been measured through Ig mucosal concentra-tions in vivo and serum Ig creation following in vitro stimulation.Mucosal Ig concentrations allow for an estimation of plasma cellrelease of Ig, while serum Ig synthesis allows for the analysis of theplasma cells to create Ig outside of the body. Mucosal Ig concentra-tions following a single session of exercise and exercise trainingremain unchanged.18,23 However, Ig production following in vitro stim-ulation increases in response to both a single exercise session andexercise training,26 showing that B-cell functioning is potentially posi-tively influenced by exercise.30


6ACSM’S CERTIFIED NEWS • JULY–SEPTEMBER 2012 • VOLUME 22: ISSUE 3

DIABETES MEDICATIONS:GUIDELINES FOR EXERCISE SAFETY

WELLNESS ARTICLE

Diabetes mellitus is a chronic disease that is quicklybecoming an epidemic. Based on current data, 25.8 millionAmerican children and adults (or 8.3% of the United Statespopulation) have diabetes. Another 79 million Americanshave pre-diabetes.5 U.S. data released in 2010 predict that1 in 3 American adults could have diabetes by 2050 if cur-rent trends continue.6 Diabetes is the seventh leading causeof death in the United States, and individuals with diabetesare two to four times more likely to develop cardiovascu-lar disease than those without diabetes.5 Despite thesealarming statistics, there is a great deal that people can doto prevent diabetes and that those with the disease can doto avoid complications and stay healthy.

Type 1 diabetes is a disease of absolute insulin deficien-cy characterized by beta cell failure; it affects 5% to 10% ofindividuals with diabetes. Type 2 diabetes involves relativeinsulin deficiency and is characterized by some combinationof three main metabolic problems: 1) decreased beta cellfunction with reduced insulin production, 2) insulin resist-ance in the peripheral tissues, and 3) increased hepatic glu-cose production. Of the people with diabetes, 90% to 95%have type 2.1,7

Diabetes treatment components include healthy eating,regular physical activity, medication (if needed), blood glu-cose monitoring, and education on diabetes self-manage-ment.1,4 Medication options for diabetes treatment continueto expand and include oral medications, insulin, and otherinjectable preparations. Some of these medications maycause hypoglycemia (low blood glucose), particularly whencombined with increased activity. The remainder of thisarticle explores the various types of diabetes medicationsand implications for exercise/fitness professionals to helpensure a safe exercise experience for their clients.

ORAL DIABETES MEDICATIONS

Oral diabetes medications may be used to control bloodsugar in persons with type 2 diabetes. The oral medicationsare divided into six classes based on how they work toaffect blood glucose levels. These may or may not increasethe risk for hypoglycemia during exercise (Table 1).

INSULIN

Insulin is always used in the treatment of type 1 dia-betes, and sometimes in the treatment of type 2 diabetes.All types of insulin can cause hypoglycemia. The peakinsulin time is when an individual is at greatest risk forhypoglycemia. It is suggested that exercise be avoided dur-

By Mary Lobb Oyos, RN, MS, BC-ADM, CDE, and Sherry Barkley, Ph.D., CES, RCEP

Table 1: Oral Diabetes Medications1,4

CLASS HOW THEY WORK NAMES – Generic & (Brand)Name

RISK OFHYPOGLYCEMIA

Sulfonylurea Stimulate pancreas tomake more insulin,both right after a mealand for several hourslater

- Glimepiride (Amaryl)- Glipizide (Glucotrol, Glucotrol XL)- Glyburide (Diabeta,Micronase, Glynase)

Yes

Meglitinides Stimulate pancreas torelease more insulinright after a meal

- Nateglinide (Starlix)- Repaglinide (Prandin)

Yes

Biguanides Decrease amount ofglucose released fromliver

- Metformin,metformin XR

Not likely, but possible

Alpha-GlucosidaseInhibitors

Slow carbohydratedigestion

- Acarbose (Precose)- Miglitol (Glyset)

Yes, if used withsulfonylurea or insulin

Thiazolidinediones(TZDs)

Increase insulinsensitivity in muscleand fat tissue

- Pioglitazone (Actos)- Rosiglitasone(Avandia)

No

Dipeptidyl peptidase-4(DPP-4) inhibitors

Enhance insulinsecretion & decreaseamount of glucosereleased from liverafter a meal

- Linagliptin(Tradjenta)- Saxagliptin (Onglyza)- Sitagliptin (Januvia)

No

Note: Several of these medications are available in combination preparations.

Table 2: Insulin Types and Actions4

TYPE NAMEGeneric & (Brand)Name

ONSET PEAK DURATION

Rapid-acting Aspart (NovoLog)Glulisine (Apidra)Lispro (Humalog)

5-15 minutes 30-90 minutes <5 hours

Short-acting Regular 30-60 minutes 2-3 hours 5-8 hours

Intermediate-acting

NPH 2-4 hours 4-10 hours 10-16 hours

Long-acting Detemir (Levemir)Glargine (Lantus)

2-4 hours None 24 hours

Note: Several pre-mixed insulin combinations also are available.

Table 3: Carbohydrate Options for Treatmentof Hypoglycemia4

TREATMENT AMOUNT (15 grams carbohydrate)

Fruit juice ½ cup

Milk (skim preferred) 1 cup

Regular soda pop ½ cup (4 oz.)

Glucose tablets 3-4 (depends on brand)

Glucose gel Check package information for amount equalto 15 grams

Note: High fat foods/drinks slow gastric emptying and carbohydrate absorption and thereforetake longer to raise blood glucose levels.

Diabetes Medications (continued on page 14)

ing peak insulin action. See Table 2 for a summary of insulin types andduration of action.

NON-INSULIN INJECTABLE MEDICATIONS

There are other injectable diabetes medications that are notinsulin, but affect glucose control in other ways. These include exe-natide (Byetta & Bydureon), liraglutide (Victoza) and pramlintide(Symlin). These medications do not cause hypoglycemia by them-selves, but can do so if combined with other medications that maylead to low glucoses.4

HYPOGLYCEMIA SYMPTOMSAND TREATMENT

Anyone with diabetes who is taking insulin or an oral medicationthat can cause hypoglycemia should be aware of hypoglycemia symp-toms and have rapid-acting glucose available at all times, particularlyduring exercise. Hypoglycemia is defined as a glucose <70 mg/dl.4

Symptoms of hypoglycemia include:• Sweating • Shaking• Dizziness • Headache• Confusion/irritability • Personality change• Hunger • Weakness• Vision changes • Seizures or loss of

consciousness

If hypoglycemia is suspected, check blood glucose. If blood glucoseis below 70 mg/dl, treat the low blood sugar using the Rule of 15.Take 15 grams of carbohydrate, wait 15 minutes, then re-treat with15 grams of carbohydrate if symptoms have not improved (Table 3).In individuals with either type 1 or type 2 diabetes, exercise is notrecommended for blood glucose below 100 mg/dl until a carbohy-drate has been consumed, the glucose level has been rechecked, andhas increased to a safe level.2

Hypoglycemia prevention is key to a safe exercise experience forthe person with diabetes. Some tips for avoiding hypoglycemiainclude:

• Administer insulin injections in a part of the body thatwill not be used actively for exercise. The abdomen isoften a good site. Injecting into the subcutaneous tis-sue near a muscle that is being used during activitymay cause hypoglycemia. The increased blood flow tothe area causes more rapid insulin absorption withpossible resultant hypoglycemia.4,7

• Always check the blood glucose level before, during,and after exercise, at least until the effects of a specif-ic type and duration of activity are monitored for sev-eral exercise sessions.2,3

• Watch for delayed post-exercise hypoglycemia inpeople who take insulin. Because metabolism remainsincreased for several hours after exercise, peoplemay experience lows several hours after exercise,especially during the night. Advise people to checkglucose at bedtime and take a snack of 15-30 gramscarbohydrate plus protein if the glucose is <100mg/dl. A glucose check at 1–2:00 a.m. also is advis-able following a day of significantly increased activity.4

• Individuals who take a diabetes medication that cancause hypoglycemia should plan for increased activityby either increasing carbohydrate intake or decreas-ing insulin intake. These guidelines are a helpful start-ing point for additional carbohydrate prior to exer-cise. All extra food should be eaten before exerciseand is in addition to the regular meal plan (Table 4).

SUMMARY

Regular physical activity is an essential tool in glycemic control andoverall health for everyone with diabetes. Exercise professionals whoare prepared to provide advice and assist with hypoglycemia treat-ment can help to ensure that persons with diabetes have a safe andbeneficial exercise experience.

About the AuthorsMary Lobb Oyos RN, MS, BC-ADM, CDE, is diabetesprogram manager at avera McKennan Hospital andUniversity Health Center, Sioux Falls, SD.

Sherry Barkley, Ph.D., CES, RCEP, is an assistantprofessor and chair of the HPER Department atAugustana College, Sioux Falls, SD. She has manyyears of experience with exercise prescription forpersons with heart disease, diabetes, and otherclinical conditions. Sherry is past-president ofNACSM and current member of the CCRBPublications Subcommittee.

Suggested Resources• MedlinePlus.gov Drugs and Supplements:

http://www.nlm.nih.gov/medlineplus/druginformation.html

• X-Plain Patient Education Videos Available from MedlinePlus.gov:http://www.nlm.nih.gov/medlineplus/tutorials/diabetesintroduc-tion/htm/_yes_0_no_0.htm


Table 4: Recommended Pre-Exercise Carbohydrate IntakeBased on Blood Glucose Levels

GLUCOSEPRE-EXERCISE

INTENSITY AND DURATIONOF EXERCISE

EXTRA FOOD NEEDED

Less than 100 mg/dl Low(< 30 minutes)

Moderate(30-60 minutes)

Strenuous(>1 hour)

15 gms carbohydrate

30 gms carbohydrate

60 gms carbohydrate

101-170 mg/dl Low

Moderate

Strenuous

No extra food needed

15 gms carbohydrate

30 gms carbohydrat

171-300 mg/dl Low

Moderate

Strenuous



15 gms carbohydrate

Over 300 mg/dl **Don’t begin exercise until blood sugar is under better control.

THIS COLUMN CONTINUES THE NEW FORMAT FOR OUR COACHING

NEWS COLUMN. WE ARE EXPLORING A VARIETY OF CLIENT SCENAR-

IOS, ONE SCENARIO FOR EACH COLUMN. I DESCRIBE A FEW TIPS FROM

MY SCIENCE-BASED COACHING TOOLBOX TO HELP YOU HELP YOUR

CLIENTS ENGAGE FULLY IN A FIT LIFESTYLE THAT ALLOWS THEM TO

THRIVE, WHATEVER THRIVING MEANS IN THEIR LIVES.

Today we explore how to work with a client who is not engagedin following evidence-based or scientif ic guidelines, including pre-ventive tests, and is not seeking out reputable sources on theWeb and beyond. Instead, s/he hunts down information and rec-ommendations from non-reputable sources, while not listening toyour well-informed advice.

It goes without saying that those reading this article honor andrespect the scientific method, are skeptical of recommendations thatlack a scientific foundation, and stay within the bounds of evidence-based guidelines that are worthy of publication in a peer-reviewedjournal or textbook. The construct of evidence-based medicine hasbeen around for about 20 years and is a relatively new, but essentialparadigm in exercise program design and implementation.1 We aretaught to refrain from making recommendations that are not firmlyrooted in well-designed research studies, the more the better.

However, our clients may not be like us. They may not trust orrespect science-based recommendations. Perhaps they think of them-selves as right-brain types who didn’t enjoy science courses in theireducation, and value intuition and creativity more than the scientificmethod. Maybe they are frustrated with the limitations of the scien-tific method, which generates recommendations based upon aver-ages and bell curves that don’t seem relevant to their personal cir-cumstances. They may be more interested in what complementaryand alternative practitioners have to say because these practitionerstreat people who have been failed by conventional medicine.

Some are justifiably concerned about how medical guidelineschange dramatically over time.

Lively debates have emerged recently among scientists and in themedia about the pros/cons of mammograms, PSA tests for prostatecancer, and the value of annual physicals. Not long ago high carb/lowfat diets were the universal recommendation for heart health; this isno longer valid as the evidence for low carb/moderate healthful fatdiets is now compelling. The landmark June 2012 JAMA paper onweight loss maintenance by Ludwig et al., has overturned the science-based wisdom that a “calorie is a calorie” when it comes to energyexpenditure.2 It turns out that high carb diets lead to an average of300 fewer calories expended daily than low carb diets, a critical issuefor weight loss maintenance. No wonder our clients may havebecome cynical about evidence-based guidelines.

So how do we bridge the gap between our science-based wisdomand guidelines and our clients who don’t trust our science-basedguidelines and resist our recommendations?

1. APPRECIATE WITHOUT JUDGMENTThe only way a helping professional can

defuse resistance is to get fully onto yourclients’ side of the fence. Get down fromyour expert pedestal and honor your clients’biological drive for autonomy, to choose theirown path. Inquire openly and without even the tiniest whiff of judg-ment or expectation about how they make decisions on what to doto protect and improve their personal health. What is their approachto investigating options, whose advice do they trust most, how dothey weigh up their options and decide? What do they think aboutevidence-based medical guidelines? Perhaps they will share painful sto-ries about how they or close others have experienced difficulties withrecommendations of reputable health care providers. Validate andshow respect for their perspectives with authentic sincerity, howeveruncomfortable that might be.

2. COACH DON’T PREACHOnce your clients trust that you appreciate and

respect their viewpoints, bringing down the wallsof resistance, you have created an opening to facil-itate their finding a new and improved decision-making process. Move into a collaborative coaching conversationwhere you encourage clients to generate new ideas on how best tomake health decisions, and get permission to offer your ideas and wis-dom. While it’s tough for our expert minds to give up control of hav-ing the right answers, it is human nature for your clients to value whatthey discover more than what has been imposed. Allowing yourclients to discover a better path for themselves will, in fact, dramati-cally increase your impact and your clients’ success. And the bonus isthat they will be more likely to be interested in your best advice.

About the AuthorMargaret Moore (Coach Meg), M.B.A., is thefounder & CEO of Wellcoaches Corporation, astrategic partner of the ACSM, widely recognizedas setting a gold standard for professionalcoaches in healthcare and wellness. She is co-director of the Institute of Coaching, at McLeanHospital, an affiliate of Harvard Medical School and co-directs theannual Coaching in Leadership & Healthcare Conference offered byHarvard Medical School. She co-authored the ACSM-endorsedLippincott, Williams & Wilkins Coaching Psychology Manual, the firstcoaching textbook in healthcare and the Harvard Health Book publishedby Harlequin: Organize Your Mind, Organize Your Life.

References1. Donald A. Evidence-Based Medicine: Key Concepts. MedGenMed 4(2),

2002 [formerly published in Medscape Psychiatry & Mental HealtheJournal 7(2), 2002].

2. Ebbeling CB, Swain JF, Feldman HA, et al. Effects of DietaryComposition on Energy Expenditure in Weight Loss Maintenance.JAMA. 2012;307(24):2627-34.

COACHING NEWS


By Margaret Moore (Coach Meg), M.B.A.

HEALTH & FITNESS COLUMN

RESISTANCE TRAINING AND DIABETES

By Wayne L. Westcott, Ph.D.

Age-related muscle loss is associated with a variety of physiologicalproblems including metabolic decline,21 fat gain,20 and diabetes.8

Studies show muscle mass reductions of 3% to 8% each decade afterage 30,8 and 5% to 10% each decade after age 50,15 averagingapproximately one pound of muscle tissue every year following thefifth decade of life.16 According to an excellent research review byFlack et al.,8 decreased muscle mass directly influences the risk ofdeveloping glucose intolerance and diabetes because muscle tissue isthe primary site of glucose deposit and utilization.

Muscle Gain

Numerous studies have shown that gains in lean weight resultingfrom resistance training are associated with greater glucose tolerancein adults with type 2 diabetes,6 older adults with type 2 diabetes,4

men with type 2 diabetes,2 and women with type 2 diabetes.7

According to Phillips and Winett,17 resistance exercise is associatedwith improved glucose and insulin homeostasis due to increases inlean body mass and muscle cross-sectional area. Flack et al.8 alsofound that increased lean body mass was associated with improvedinsulin sensitivity and glucose tolerance.

Fat Loss

The primary result of resistance training is muscle gain, whichappears to have a positive impact on factors related to diabetes risk.However, a secondary outcome of resistance exercise is fat loss,which also may be advantageous with respect to diabetes risk.8

Although the duration of activity time in standard resistance exercisesessions is relatively low compared to standard aerobic exercise ses-sions, the training intensity is relatively high. A standard circuitstrength training workout (typically 10 to 15 exercises arranged sothat participants perform one set of an exercise then move quickly toan exercise for a different muscle group with minimal non-activitytime) uses approximately 6.7 to 8.5 calories per minute, or up to 170calories for a 20-minute exercise session.10 However, post-trainingmuscle tissue remodeling processes appear to be responsible forincreasing resting energy expenditure by 5% to 9% for 72 hours fol-lowing the strength workout.9,11 Using an average 7% increase inresting energy expenditure and a resting energy expenditure of1,600 calories/day, this would represent about 110 additional calo-ries used on a daily basis for people who perform at least two resist-ance training sessions/week.

Consequently, the cumulative calorie-burning benefit of regularresistance exercise could total about 4,800 calories/month (8 trainingsessions x 170 calories/session + 31 days x 110 calories/day = 4,770calories). The increased resting energy expenditure may be largelyresponsible for the approximately 4-pound reduction in fat weight

reported following 10 to 12 weeks of regular strength training.3, 22

More specifically, resistance exercise has been shown to decreaseintra-abdominal fat in older men and women12 and in people with dia-betes.13 This is important because research has revealed an associa-tion between abdominal fat and insulin resistance.5, 14 Based on their2010 meta-analysis of related studies, Strasser et al.19 concluded that“resistance training reduces total body fat mass and visceral adiposetissue independently from dietary restriction.” Based on their 2011review of related research, Flack et al.8 concluded that “resistancetraining alone may reduce abdominal and visceral fat, which is knownto increase with advancing age and influence insulin resistance.”

Resistance Training Recommendations

The American College of Sports Medicine (ACSM) guidelines forresistance exercise provide a sound basis for strength training that isappropriate for most people who are capable of performing muscu-lar activity.1 The general recommendations call for doing 8 to 10exercises per session, performing 2 to 4 sets of exercise for eachmuscle group, using a resistance that permits 8 to 12 repetitions,emphasizing complete movement range and controlled movementspeed, and training 2 or 3 non-consecutive days a week (1 page 172).This could be accomplished by performing two to four sets of a sin-gle exercise for a given muscle group (e.g., three sets of bench press-es for the pectoralis major muscles), or by performing one set of twoto four exercises for the same muscle group (e.g., one set each ofbench presses, incline presses, and dumbbell flies for the pectoralismajor muscles). The resistance training guidelines for older adults aresimilar, but recommend beginning with a resistance that permits 10to 15 repetitions at a lower effort level (1 page 172). With respect toglycemic control, Strasser et al.19 report that improvements haveresulted from a range of training volumes (4 to 9 exercise sets permuscle group per week) and training intensities (50% to 85% of max-imum resistance).

The American Diabetes Association (ADA) supports resistance exer-cise for people with type 2 diabetes, and recommends a training proto-col consistent with the ACSM guidelines. The ADA encourages resist-ance training for all the major muscle groups, progressing to three setsof 8 to 10 repetitions, performed at high intensity, three times a week.18

Upon examining the strength training research and recommendations,Flack et al.8 have proposed a progressive program of resistance exercisefor older diabetic and pre-diabetic individuals. They suggest beginningwith low intensity and low volume workouts (one set of 10 to 12 repe-titions performed two days a week), with gradual increases in the train-ing variables (intensity, volume, and frequency). All of these suggestedresistance training protocols appear to be appropriate for people withdiabetes, and, therefore, may be recommended for the prevention andmanagement of type 2 diabetes.19

Resistance Training (continued on page 14)


The first two heart sound articles, in this series of three,reviewed the anatomical positions to listen to the different valvesof the heart, correct use of the stethoscope and the rationale forcommon heart sounds. To recap briefly, systole (S1) “lub” and dias-tole (S2) “dub” are the typical healthy heart sounds. Less commonsounds that should be considered include (S3), caused by rapid ven-tricular filling and (S4), the onset of atrial contraction. The thirdheart sound may be an innocent normal variant in younger popu-lations and in pregnancy; however, as with a fourth heart sound itmay be associated with cardiac pathologies and would need furtherevaluation.

This third article in the heart sound series will describe the soundsassociated with the more common valvular diseases that producemurmurs. Murmurs are longer duration sounds that are attributed toturbulent blood flow. The two common valvular abnormalities arestenosis and regurgitation. Stenosis is reflective of a partially obstruc-tive valve that causes blood to be ejected through a smaller orificethan normal. Regurgitation is reflective of a valve that allows bloodto flow in a “retrograde” or opposite direction. Identifying the mur-murs associated with the possible presence of stenosis or regurgita-tion is based on determining where to best listen on the chest wall(previously described) and the ability to determine when they occurin the cardiac cycle.

Aortic Stenosis

Blood is being ejected through a smaller than normal opening inthe aortic valve, which creates a higher than normal pressure in theleft ventricle (LV). This creates a “nozzle” effect during systole. Thesound is greatest immediately following S1 and decreases to S2(decrescendo murmur). The turbulent blood flow against the aorticwalls is responsible for causing the vibration and loud murmur(Figure).

Aortic Regurgitation

The murmur is heard during diastole (between S2 and S1). The mur-mur is caused by turbulent blood flow traveling retrograde from theaorta through the aortic valve into the blood in the left ventricle. Thismurmur has been described as a “blowing” high pitch sound, but typical-ly not as loud as aortic stenosis due to a lesser pressure difference.

Mitral Stenosis

There is an increased challenge in blood flow from the left atrium(LA) to LV due to stenosis of the mitral valve. Typically, this is a lowerpitch sound in diastole because of a decreased pressure in the LA,

which usually doesn’t exceed 35mmHg. Because there is very littleblood in the LV at the onset of LA contraction, a vibration sound maynot occur until the LV is partially full. The increased amount of bloodin the LV will stretch the LV, which allows a vibration sound to be pro-duced when blood is ejected into the LV. Therefore, mitral stenosismay not be heard until 2/3 of the way through diastole. Becausemitral stenosis produces lower pitch sounds, using the bell side of thestethoscope may be helpful to hear this abnormality.

Mitral Regurgitation

Blood flow will travel retrograde through the mitral valve duringsystole, and will be heard as a “blowing” swishing sound in the LA.However, the LA is very deep in the chest wall and difficult to hear,and, therefore, it is best to identify this sound through the LV, at theapex of the heart. The murmur sound is produced by turbulent bloodbeing pushed back through the mitral valve into the blood in the LAor against the atrial wall. This sound is very similar to aortic regurgi-tation; however it occurs during systole versus diastole, making it veryimportant to recognize where the sound is heard in the cardiac cycle.

Personal Note

Becoming proficient at recognizing different heart sounds in yourClinical Exercise Physiology (CEP) academic training can be challeng-ing. Hopefully, the concepts of detecting heart sounds are being intro-

CLINICAL COLUMN

PART 3:

HEART SOUNDSBy Paul Visich, Ph.D., MPH

Adapted from: ttp://en.wikipedia.org/wiki/File:Phonocardiograms_from_normal_and_abnor-mal_heart_sounds.png

Figure: Phonocardiograms from normal andabnormal heart sounds

Heart Sounds (continued on page 15)



BACKGROUND

Bariatric surgery is becoming more and more prevalent as the num-ber of obese and morbidly obese adults increases. Currently, 35.5% ofadult men and 35.8% of adult women are considered obese (have abody mass index (BMI) greater than or equal to 30.0 kg/m2).5 Whensurgical treatment of obesity is contemplated, obesity and clinicallysevere obesity need to be differentiated. Clinically severe obesity (ormorbid obesity) is defined by the American Society for Metabolic andBariatric Surgery (ASMBS) as a disease of excess energy stores in theform of fat, correlating with a BMI of 40 kg/m2 or greater or with being100 pounds over ideal weight.3 The physical, emotional, and financialburden of obesity is now being recognized.3 Well-documented conse-quences of obesity include cardiac and pulmonary problems, metabolicdisease, endocrine disorders, digestive problems, orthopedic issues, andan increased rate of developing some cancers. However, the most alarm-ing consequence is the direct increase in mortality due to an increase inweight. In a 12-year follow-up study of approximately 750,000 men andwomen, mortality rates for those who were 50% over their averageweight were twice as high as those who were an average weight.7

Surgical treatment for obesity has become medically necessary forthe morbidly obese as being the only proven method of long-termweight control.3 Surgical treatment is not a form of cosmetic surgery buta tool to help reduce a person’s weight and improve or eliminate theassociated co-morbidities. There are several different types of bariatricsurgery, all decreasing the size of the stomach pouch, with or withoutsome sort of malabsorption. The changed anatomy from surgery makeslife-long vitamin treatment necessary for bariatric patients. The mostpopular procedure is the gastric bypass, with laparoscopic adjustable gas-tric banding as the second most popular procedure.4 More detailedinformation about the specific surgeries can be found through ASMBS(www.asmbs.org).

Candidates for bariatric surgery include patients who have a BMIover 40 kg/ms2 and have a decreased quality of life due to obesity.Less obese patients who have BMI between 35 and 40 kg/m2 maybe considered for surgery if they have high risk co-morbid conditionsrelated to their obesity. All patients must clearly understand the pro-cedure and life-changes that are necessary and must undergo psycho-logical evaluation of readiness for surgery. They must prove they havetried and failed at other weight loss attempts. They also usually gothrough some form of supervised weight loss with the bariatric team,which includes the surgeon, registered dietician, exercise physiologist,and behavioral coach, for a period of between 2 and 6 months priorto being cleared for surgery.3

As exercise professionals, we have to understand the bariatric patientand how exercise intervention can not only help with weight loss andweight maintenance, but also help improve the quality of life for thesepatients. We also must be compassionate and understanding, not judg-

mental, towards these individuals. A 2009 study of exercise science stu-dents showed that the students endorsed attitudes that “fat people” arelazy, physically unattractive, buy too much junk food, and could loseweight if they really wanted to.9 This perception must change if an exer-cise professional is to be successful at working with bariatric patients. Asmore bariatric centers are employing exercise physiologists as part ofthe multidisciplinary teams, and more clients that have undergonebariatric surgery present at fitness centers, we need to understand howto best manage these patients and help them on the path to improvedfitness.

THE PRE-OPERATIVE BARIATRIC PATIENT

Working with a bariatric patient pre-operatively can be a challengingtask. These patients usually have tried and failed at many weight lossattempts, including diet and exercise, and, therefore, may have a verynegative view of the efficacy of an exercise program. They also presentwith a myriad of co-morbidities that need to be addressed by the exer-cise physiologist. These include, but are not limited to, orthopedic prob-lems, metabolic diseases, pulmonary disease such as asthma or COPD,cardiac conditions and risk factors, and sleep apnea. Common barriersto exercise for the pre-operative patient include lack of motivation, painwith exercise, feeling uncomfortable while exercising, and severe decon-ditioning. The goal for the exercise intervention is to establish a consis-tent habit (3-5 times per week) of performing some sort of very lowintensity physical activity (35%-40% of heart rate reserve or VO2reserve). Patients should be encouraged to engage in at least 10 minutesof continuous aerobic exercise in the pre-operative phase, with a goal ofachieving 30 minutes of aerobic exercise per session. Weight bearingexercise such as treadmill walking is preferred if tolerated, but due to thephysical limitations of morbidly obese patients, nonweight bearing exer-cise may be the best option.

POST-OPERATIVE EXERCISE PRESCRIPTION

The exercise prescription for the post-operative bariatric patient isconsistent with the recommendations for obesity by the AmericanCollege of Sports Medicine’s (ACSM) Guidelines for Exercise Testingand Prescription, eighth edition. Increasing caloric expenditure and fatloss, as well as managing co-morbid conditions, is the main goal of exer-cise for these patients.

CardiorespiratoryThe primary mode for cardiorespiratory exercise for these patients

should be aerobic activity that involves large muscle groups, with walk-ing being the most common mode utilized. Usually weight bearing exer-cise is tolerated to some degree by most patients after a modest weightloss, but nonweight bearing options should be considered. The goal

CLINICAL FEATURE

EXERCISE ANDBARIATRIC SURGERY

By Kelly Drew, M.S., ACSM RCEP

Bariatric Surgery (continued on page 12)


should be a frequency of 5-6 days per week of moderately intense(40%-60% heart rate reserve or VO2 reserve) cardiorespiratory activ-ity, with fat loss being a primary goal. Duration is emphasized over inten-sity, with a minimum goal of 150 minutes per week and a long termobjective of achieving 300 minutes per week.2 A typical progression ispresented in Table 1.

ResistanceIt has been observed that during a significant weight loss, fat-free

mass is lost,5 which can be detrimental for long term success of weightmaintenance by bariatric patients. Exercise, especially resistance training,can help preserve fat-free mass after bariatric surgery. Bariatric patientsalso show a higher incidence of bone mineral deficiency post-surgerydue to the malabsorptive nature of certain bariatric procedures, specif-ically Roux-en-Y gastric bypass,8 and resistance training is recommendedto reduce the risk of developing osteoporosis.

Resistance training should not be started until clearance from the sur-geon is obtained, which can be anywhere from 6 weeks to 6 monthspost bariatric surgery. After clearance, higher repetition exercise is usu-ally better tolerated. A typical progression is provided in Table 2.

FlexibilityFlexibility training increases or maintains joint range of motion, which

can alleviate aches and pains associated with obesity.2 Stretching exercis-es should be incorporated after a brief warm-up or after an exercise ses-sion when muscles are warm. The recommendation by ACSM’sGuidelines for Exercise Testing and Prescription, eighth edition, is2-4 days per week and holding each stretch for at least 15 seconds.2

Special ConsiderationsExercise professionals should pay special attention to exercises that

require balance (e.g., unsupported lunges, squats) in the first year aftersurgery due to a changing center of mass associated with rapid weightloss. Many patients are not able to get on the floor to do resistanceexercises due to body habitus or musculoskeletal issues associated withobesity, so care and tact must be taken by the exercise professional toensure the patient is doing a safe routine that they are comfortable com-pleting. Other considerations should include ensuring the equipment

used has a sufficient weight limit to accommodate larger patients, andthat exercise machines have larger seats. If bariatric chairs are not avail-able, make sure you offer chairs with no arms. If you are doing exerciseon the floor, make sure to use a thicker and wider mat to make sure thepatient is more comfortable.

NUTRITIONAL CONSIDERATIONS

A brief overview of the diet a bariatric patient follows will be dis-cussed, with understanding that as exercise professionals we should notoffer dietary advice to bariatric patients due to the specific nature of thepost-operative diet. We do, however, need to be aware of what thepatient is experiencing so we can tailor an exercise program to fit with-in their nutritional status.

The diet progression post-surgery is as follows: clear liquids, full liquids,soft/puree diet, then very small portions of protein-focused meals.1 Thelength of time and contents of this diet can be found within the ASMBSguidelines. This restrictive caloric intake should be considered by theexercise professional in terms of energy levels and exercise timing. Thepatient should exercise after a meal or snack. Due to the limited caloriesconsumed, reasonable expectations as far as muscle gains should beacknowledged. Another exercise consideration should be the hydrationstatus of the individual. Because the stomach pouch is much smaller aftersurgery, staying hydrated can be difficult for the patient.1 This is of con-cern if they are participating in an exercise program. Having the patienttake small sips of water during an exercise session can help prevent dehy-dration. We need to encourage the patient to stay hydrated, and discon-tinue exercise if severe dehydration is present.

SUMMARY

Working with bariatric patients is both a rewarding and challengingundertaking. It is our responsibility as exercise professionals to under-stand the bariatric patient, both physically and emotionally, so we canhelp them achieve a healthy lifestyle. Remember the surgery is only atool; the lifestyle changes made are the best predictors of success!

About the AuthorKelly Drew, M.S., ACSM RCEP, is a clinical exercisephysiologist with Community Bariatric Surgeons atCommunity Health Network in Indianapolis, IN.Kelly is currently a member of ACSM RCEP PracticeBoard.

References1. Allis L, Blankenship J, Buffington C, Furtado M, Parrott J. ASMBS

Allied Health Nutritional Guidelines for the Surgical Weight LossPatient. Surgery for Obesity and Related Diseases 4. 2008:S73-S108.

2. American College of Sports Medicine. ACSM’s Guidelines forExercise Testing and Prescription, 8th ed. Thompson WR, GordonNF, Pescatello LS, editors. Baltimore (MD): Lippincott Williams &Wilkins; 2009.

3. American Society for Metabolic and Bariatric Surgery. Rationale forthe Surgical Treatment of Morbid Obesity [Internet]. Updated Nov23, 2005. [cited 2012 Jun 18]. Available from:http://asmbs.org/rationale-for-surgical-treatment/.

Bariatric Surgery (continued on page 15)

Table 1: Cardiorespiratory Exercise ProgressionTime PostSurgery

Frequency Duration

0-2 weeks Several times per day as tolerated

2-4 weeks 5-6 days per week 20-30 minutes in 10 minute increments

4-6 weeks 5-6 days per week 30-40 minutes

6+ weeks 5-6 days per week 40-60 minutes

Table 2: Resistance Exercise ProgressionResistanceTraining

Repetitions Frequency Muscle Groups

0-4 weeks 1 set of 20 2-3 days per week 8-10

4-8 weeks 2 sets of 15 2-3 days per week 8-10

8+ weeks 3 sets of 12-15 2-3 days per week 8-10

Bariatric Surgery (continued from page 11)

Exercise Immunology (continued on page 14)


Exercise for Immune Health

While some general aspects of the immune response to exerciseare known, more discoveries need to be made regarding specificevents following exercise. Mechanisms for leukocytosis (elevated con-centrations of neutrophils and monocytes, NK cells, dendritic cells, T-cells, and B-cells), which occurs directly following a single exercise ses-sion and reasoning for decreased concentrations of leukocytes follow-ing leukocytosis 24 h after exercise needs elucidation. This depressioncould be a result of leukocytes leaving circulation to differentiate insurrounding tissue, and not actual apoptosis (cell death). Regardlessof the mechanism, following acute exercise the body appears vulner-able to infection because of depression in leukocyte cell number andfunction. However, if the immune system is allowed complete recov-ery following each exercise session, there are no long term detrimen-tal effects of exercise training upon the system. Moreover, with mod-erate intensity (moderate is relative to the individual and the rangefor this value can vary with characteristics of the individual) exercisetraining beneficial anti-inflammatory effects and improvements inimmunosurveillance are achieved.16

Regular exercise and physical activity will, in most cases, positivelyinfluence immune function.16,31 While exercise training does influencethe immune system, other lifestyle behaviors, such as proper sleepand nutrition, also are influential and must be considered. In addition,overtraining can devastate the immune system. When starting anexercise program, moderate intensity and low exercise volumeshould be the foundation for the exercise prescription.31

Furthermore, using the same training mode for long durations oftencan cause decreased levels of circulating immune cells leading todecreased immune surveillance, so varying exercise modes is recom-mended.24 Between-athlete variability makes it difficult to predict howhard any individual athlete can train before immune function is com-promised. However, the more physically fit an individual is the morelikely they will be able to endure high exercise volume and high inten-sity (near maximal effort) workouts. Regardless of fitness level, thereshould be a heightened awareness during times of increased risk (e.g.,high intensity training, competition, and recovery periods immediate-ly following competition) with an emphasis on good hygiene, rest, andrecovery. If trainers and coaches actively monitor these criteria, thelikelihood of having a healthy immune system is enhanced.

About the AuthorBenjamin T. Gordon, M.S., CES, CSCS, is currentlypursuing a Ph.D. in applied physiology from theUniversity of South Carolina.

References1. Campbell PT, Wener MH, Sorensen B, Wood B, Chen-Levy Z, Potter JD,

McTiernan A, and Ulrich CM. Effect of exercise on in vitro immunefunction: a 12-month randomized, controlled trial among post-menopausal women. J Appl Physiol 104: 1648-1655, 2008.

2. Ceddia MA, Voss EW, Jr., and Woods JA. Intracellular mechanismsresponsible for exercise-induced suppression of macrophage antigenpresentation. J Appl Physiol 88: 804-810, 2000.

3. Ceddia MA, and Woods JA. Exercise suppresses macrophage antigenpresentation. J Appl Physiol 87: 2253-2258, 1999.

Exercise Immunology (continued from page 5)

4. Chiang LM, Chen YJ, Chiang J, Lai LY, Chen YY, and Liao HF.Modulation of dendritic cells by endurance training. Int J Sports Med28: 798-803, 2007.

5. Edwards AJ, Bacon TH, Elms CA, Verardi R, Felder M, and Knight SC.Changes in the populations of lymphoid cells in human peripheralblood following physical exercise. Clin Exp Immunol 58: 420-427,1984.

6. Fairey AS, Courneya KS, Field CJ, Bell GJ, Jones LW, and Mackey JR.Randomized controlled trial of exercise and blood immune function inpostmenopausal breast cancer survivors. J Appl Physiol 98: 1534-1540,2005.

7. Flynn MG, McFarlin BK, Phillips MD, Stewart LK, and Timmerman KL.Toll-like receptor 4 and CD14 mRNA expression are lower in resistiveexercise-trained elderly women. J Appl Physiol 95: 1833-1842, 2003.

8. Gleeson M, and Bishop NC. The T cell and NK cell immune responseto exercise. Ann Transplant 10: 43-48, 2005.

9. Ho CS, Lopez JA, Vuckovic S, Pyke CM, Hockey RL, and Hart DN.Surgical and physical stress increases circulating blood dendritic cellcounts independently of monocyte counts. Blood 98: 140-145, 2001.

10. Kappel M, Tvede N, Galbo H, Haahr PM, Kjaer M, Linstow M, KlarlundK, and Pedersen BK. Evidence that the effect of physical exercise on NKcell activity is mediated by epinephrine. J Appl Physiol 70: 2530-2534,1991.

11. Lancaster GI, Halson SL, Khan Q, Drysdale P, Wallace F, Jeukendrup AE,Drayson MT, and Gleeson M. Effects of acute exhaustive exercise andchronic exercise training on type 1 and type 2 T lymphocytes. ExercImmunol Rev 10: 91-106, 2004.

12. Liao HF, Chiang LM, Yen CC, Chen YY, Zhuang RR, Lai LY, Chiang J,and Chen YJ. Effect of a periodized exercise training and active recov-ery program on antitumor activity and development of dendritic cells. JSports Med Phys Fitness 46: 307-314, 2006.

13. McCarthy DA, and Dale MM. The leucocytosis of exercise. A reviewand model. Sports Med 6: 333-363, 1988.

14. McFarlin BK, Flynn MG, Campbell WW, Craig BA, Robinson JP,Stewart LK, Timmerman KL, and Coen PM. Physical activity status, butnot age, influences inflammatory biomarkers and toll-like receptor 4. JGerontol A Biol Sci Med Sci 61: 388-393, 2006.

15. McFarlin BK, Flynn MG, Campbell WW, Stewart LK, and Timmerman KL.TLR4 is lower in resistance-trained older women and related to inflam-matory cytokines. Med Sci Sports Exerc 36: 1876-1883, 2004.

16. Nieman DC. Special feature for the Olympics: effects of exercise on theimmune system: exercise effects on systemic immunity. Immunol Cell Biol78: 496-501, 2000.

17. Nieman DC, Johanssen LM, Lee JW, and Arabatzis K. Infectious episodesin runners before and after the Los Angeles Marathon. J Sports MedPhys Fitness 30: 316-328, 1990.

18. Nieman DC, Tan SA, Lee JW, and Berk LS. Complement andimmunoglobulin levels in athletes and sedentary controls. Int J SportsMed 10: 124-128, 1989.

19. Okutsu M, Suzuki K, Ishijima T, Peake J, and Higuchi M. The effects ofacute exercise-induced cortisol on CCR2 expression on human mono-cytes. Brain Behav Immun 22: 1066-1071, 2008.

20. Ortega E, Forner MA, and Barriga C. Exercise-induced stimulation ofmurine macrophage chemotaxis: role of corticosterone and prolactinas mediators. J Physiol 498 ( Pt 3): 729-734, 1997.

21. Ortega E, Rodriguez MJ, Barriga C, and Forner MA. Corticosterone,prolactin and thyroid hormones as hormonal mediators of the stimulat-ed phagocytic capacity of peritoneal macrophages after high-intensityexercise. Int J Sports Med 17: 149-155, 1996.

22. Peake JM. Exercise-induced alterations in neutrophil degranulationand respiratory burst activity: possible mechanisms of action. ExercImmunol Rev 8: 49-100, 2002.

23. Potteiger JA, Chan MA, Haff GG, Mathew S, Schroeder CA, HaubMD, Chirathaworn C, Tibbetts SA, McDonald J, Omoike O, andBenedict SH. Training status influences T-cell responses in women fol-lowing acute resistance exercise. J Strength Cond Res 15: 185-191,2001.

24. Pyne DB, Gleeson M, McDonald WA, Clancy RL, Perry C, Jr., andFricker PA. Training strategies to maintain immunocompetence in ath-letes. Int J Sports Med 21 Suppl 1: S51-60, 2000.


About the AuthorWayne L. Westcott, Ph.D., teaches exercise scienceand conducts fitness research at Quincy College inQuincy, MA.

References1. American College of Sports Medicine. ACSM’s Guidelines for

Exercise Testing and Prescription. 8th ed. Philadelphia (PA): Lippincott,Williams& Wilkins; 2010.

2. Baldi JC, Snowling N. Resistance training improves glycemic controlin obese type 2 diabetic men. Int. J. Sports Med. 2003; 24(6): 419-423.

3. Campbell WW, Crim MC, Young VR, Evans UJ. Increased energyrequirements and changes in body composition with resistance train-ing in older adults. Am. J. Clin. Nutr. 1994; 60: 167-175.

4. Castaneda C, Layne JE, Munez-Orians L, et al. A randomized con-trolled trial of resistance exercise training to improve glycemic con-trol in older adults with type 2 diabetes. Diabetes Care. 2002; 25:2335-2341.

5. Coon PJ, Rogus EM, Drinkwater D, et al. Role of body fat distributionin the decline in insulin sensitivity and glucose tolerance with age.J. Clin. Endocrinol. Metab. 1992; 75: 1125-1132.

6. Dunstan DW, Vulikh E, Owen N, et al. Community center-basedresistance training for the maintenance of glycemic control inadults with type 2 diabetes. Diabetes Care. 2006; 29(12): 2586-2591.

7. Fenicchia LM, Kanaley JA, Azevedo JL, et al. Influence of resistanceexercise training on glucose control in women with type 2 diabetes.Metabolism. 2004; 53(3): 284-289.

8. Flack KD, Davy KP, Huber MAW, et al. Aging, resistance training,and diabetes prevention. J. Aging Res. 2011; 2011:127315.

9. Hackney KJ, Engels HJ, Gretebeck RJ. Resting energy expenditure anddelayed-onset muscle soreness after full-body resistance trainingwith an eccentric concentration. J. Strength Cond. Res. 2008; 22:1602-1609.

10. Haltom RW, Kraemer RR, Sloan RA, et al. Circuit weight training andits effects on excess post-exercise oxygen consumption. Med. Sci.Sports Exerc. 1999; 31: 1613-1618.

11. Heden T, Lox C, Rose, P, et al. One-set resistance training elevates ener-gy expenditure for 72 hours similar to three sets. Eur. J. AppliedPhysiol. 2011; 111:477-484.

12. Hunter GR, Bryan DR, Wetzstein CJ, et al. Resistance training andintra-abdominal adipose tissue in older men and women. Med. Sci.Sports Exerc. 2002; 34: 1025-1028.

13. Ibanez J, Izquierdo M, Arguelles I, et al. Twice weekly progressiveresistance training decreases abdominal fat and improves insulin sen-sitivity in older men with type 2 diabetes. Diabetes Care. 2005; 28:662-667.

14. Kohrt WM, Kirwan JP, Staten MA, et al. Insulin resistance in aging isrelated to abdominal obesity. Diabetes. 1993; 42: 273-281.

15. Marcel TJ. Sarcopenia: causes, consequences, and preventions. J.Gerontol. A. Biol. Sci. Med. Sci. 2003; 58: M911-916.

16. Nelson ME, Fiatarone M. Morganti C, et al. Effects of high-intensitystrength training on multiple risk factors for osteoporotic fractures.JAMA. 1994; 272: 1909-1914.

17. Phillips SM, Winett RA. Uncomplicated resistance training andhealth-related outcomes: evidence for a public health mandate. Curr.Sports Med. Rep. 2010; 9: 208-213.

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19. Strasser B, Siebert U, Schobersberger W. Resistance training in thetreatment of metabolic syndrome. Sports Med. 2010; 40: 397-415.

20. Strasser B, Schobersberger W, Evidence of resistance training as atreatment therapy in obesity. J. Obes. 2011; 2011:482564.

21. Westcott, WL. Effects of strength training on resting energy expen-diture. ACSM Cert. News. 2010; 20: 10-11.

22. Westcott WL, Winett RA, Annesi JJ, et al. Prescribing physical activi-ty: applying the ACSM protocols for exercise type, intensity, and dura-tion across 3 training frequencies. Phys. Sportsmed. 2009; 2: 51-58.

Resistance Training (continued from page 9)

Exercise Immunology (continued from page 13)

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27. Shephard RJ. Adhesion molecules, catecholamines and leucocyte redis-tribution during and following exercise. Sports Med 33: 261-284,2003.

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29. Tidball JG. Inflammatory processes in muscle injury and repair. Am JPhysiol Regul Integr Comp Physiol 288: R345-353, 2005.

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33. Woods JA, Davis JM, Mayer EP, Ghaffar A, and Pate RR. Effects ofexercise on macrophage activation for antitumor cytotoxicity. J ApplPhysiol 76: 2177-2185, 1994.

Diabetes Medications (continued from page 7)

References 1. American Association of Clinical Endocrinologists. Medical guide-

lines for clinical practice for developing a diabetes mellitus comprehen-sive care plan. Endocrine Practice 2011;17(Supp 2):1-53.

2. American Diabetes Association. Exercise and Type 2 Diabetes: TheAmerican College of Sports Medicine and the American DiabetesAssociation: joint position statement. Diabetes Care 2010;33(12):e147-e167.

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4. The Art and Science of Diabetes Self-Management Education DeskReference, 2nd ed. Chicago, IL: American Association of DiabetesEducators, 2011.

5. Centers for Disease Control and Prevention. National diabetes factsheet: national estimates and general information on diabetes and pre-diabetes in the United States, 2011. Atlanta, GA: U.S. Department ofHealth and Human Services, Centers for Disease Control andPrevention, 2011.

6. Centers for Disease Control and Prevention. Press Release. Older,more diverse population and longer lifespans contribute to increase.Atlanta, GA: U.S. Department of Health and Human Services, Centersfor Disease Control and Prevention, October 22, 2010.

7. Medical Management of Type 1 Diabetes, 5th ed. Alexandria VA:American Diabetes Association, 2008.


duced into your didactic training. Integrating your didactic experi-ence with your clinical rotations is critical in developing proficiency atrecognizing heart sounds. An important tip in learning heart soundsis to listen to the heart sounds of someone with a known heart valveabnormality or other heart condition. While doing so, try to identifyand describe the sounds that you are hearing, the location of wherethey are best heard and when they occur in the cardiac cycle.Hospital (Phase 1) settings as well as diagnostic exercise settingsallow the learner opportunities to listen to normal heart sounds,heart sounds associated with cardiac disease and heart sounds thatmay change in relationship to exercise. Making these correlations isthe key in developing a clear understanding of the disease processand its impact on the individual.

Becoming knowledgeable about and proficient in the assessmentof heart sounds enables the clinician to identify significant findings,communicate findings to the health care team, and create appropri-ate exercise treatment plans that best contribute to the improve-ment of the health of the patient. This process demonstrates to mem-

bers of the health care team the valuable contribution that the CEPcan make toward patient recovery and helps to further develop arespect of the role of the CEP in a variety of clinical settings.

AUTHOR’S NOTE: The author would like to thank Joyce O’ConnorM.S., RN, NP-C, for reviewing and providing comments to improvethe quality of this article.

About the AuthorPaul Visich, Ph.D., MPH, is the current chair andprofessor of the Exercise and Sports PerformanceDepartment at the University of New England inBiddeford, Maine. Paul served as a team editor ofthe textbook, Clinical Exercise Physiology, publishedby Human Kinetics. Paul served as a member of thePractice Board for ACSM’s Registered ClinicalExercise Physiologist (RCEP) credential, thechairperson of the ACSM Professional Education Committee, and amember of ACSM’s Committee on Certification and Registry Boards(CCRB).

Golf (continued from page 3)

References1. Doan B K, Newton R U, Young H K, Kraemer W J. Effects of physical

conditioning on intercollegiate golfer performance. Journal ofStrength and Conditioning Research, 2006, 20(1), 62–72

2. Fletcher I M, Hartwell M. Effect of an 8-week combined weights andplyometrics training program on golf driving performance. Journalof Strength and Conditioning Research, 2004, 18(1), 59–62.

3. Foster L. Dr. Divot’s Guide to Golf Injuries: A handbook for golfinjury prevention and treatment. 2004

4. Fradkin A J, Sherman C A, Finch C F. Improving golf performancewith a warm up conditioning programme. Br J Sports Med2004;38:762–765.

5. Gergley J C. Latent effect of passive static stretching on driverclubhead speed, distance, accuracy, and consistent ball contact inyoung male competitive golfers. J Strength Cond Res. 2010Dec;24(12):3326-33.

6. Gluck G., Bendo JA., Spivak JM., The lumbar spine and low back painin golf: a literature review of swing biomechanics and injuryprevention. The Spine Journal 8:778-788, 2008.

7. Hetu F E, Christie C A, Faigenbaum A D. Effects of conditioning onphysical fitness and club head speed in mature golfers. Percept MotSkills. 1998 Jun;86(3 Pt 1):811-5.

8. Hume P A, Keogh J, Reid D.The Role of Biomechanics in maximizingdistance and accuracy of golf shots. Sports Med 2005; 35 (5): 429-449

9. Kanwar K. Applying simple and acute kinematic alterations to elicitchange in golf club speed and angle of approach. Proceedings ofThe World Scientific Congress of Golf 2012. Abstract.

10. Kanwar K., Chowgule RV. One move to better ball flight. Scienceand Golf II, Proceedings of The Second World Scientific Congressof Golf: 97-102. 1994

11. Lephart S M, Smoliga J M, Myers J B, Sell T C, Tsai Y-S. An eight-weekgolf-specific exercise program improves physical characteristics,swing mechanics, and golf performance in recreational golfers.Journal of Strength and Conditioning Research, 2007, 21(3), 860-869

12. Moran K A, McGrath T, Marshall B M, Wallace E S. Dynamicstretching and golf swing performance. Int J Sports Med. 2009Feb;30(2):113-8. Epub 2009 Jan 28.

Bariatric Surgery (continued from page 12)

4. Buchwald H, Consensus Conference Statement; Bariatric surgeryfor morbid obesity: Health implications for patients, health profes-sionals, and third-party payers. Surgery for Obesity and RelatedDiseases 1. 2008:71-381

5. Chaston T, Dixon J, O’Brien P, Changes in fat-free mass during sig-nificant weight loss: a systematic review. International Journal ofObesity (London). 2007; 31(5):743-50.

6. Flegal K, Carrol M, Kit B, Ogden C. Prevalence of Obesity andTrends in the Distribution of Body Mass Index Among US Adults,1999-2010. JAMA. 2012;307(5):491-97.

7. Lew EA, Garfinkel L. Variations in mortality by weight among750,000 men and women. Journal of Chronic Disease.1979;31:563-7.6

8. Ming S, Gornichec R, Therapeutic Treatment Options forOsteoporosis in the Surgical Weight Loss Population. BariatricTimes. 2011;8(4): 8-10

9. Puhl R, Heuer C. The Stigma of Obesity: A Review and Update.Obesity. 2009;17:941-64.

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ACSM’s Continuing Education Self-Tests Now Online!

As ACSM strengthened its certification program, we knewthat continuing education would be paramount. Healthand fitness professionals need to keep up with the latest

in their field, and we have provided two outstanding resources.Starting decades ago with ACSM’s Certified News, then addingACSM’s Health & Fitness Journal®, we have been providingcutting edge articles and CECs to thousands of eagerparticipants around the world. We are extremely excited toannounce that we will now be offering the convenience ofgaining instant credits through our new online learning platform.This will make all of your re-certification efforts easy and fast!

Bene%ts include:• Online access 24/7 to ACSM CEC tests and credits• Instant payment and email notification online (No more waiting4 to 6 weeks for credits through the mail)

• Immediate credit certificates issued online with passing grade• Past issues of eligible CEC Self-Tests available online

Instructions:To take the CEC quiz(zes) for instant results and a printablecertificate that you can immediately use for your certification(s),please do the following: • Go to www.onlinelearning-acsm.org• Select the self-test(s) you would like to take from the optionsavailable on the site and pay the processing fee.*

• Read the designated feature issue carefully.• Take the online test• Print your certificate(s) for your files

*If accessing a self-test from ACSM’s Health & Fitness Journal® you will need anaccess code that can be found printed in each issue of the journal. A subscriptionto the journal is required.

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