Thursday, February 15, 2018

Alpha Fuel XT Review

Alpha Fuel XT is the testosterone boosting agent made by the “brand” Science Alpha. If you’re reading this review, then you probably...

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Wednesday, February 14, 2018

What is Biceps Tendonitis and What Can You Do to Avoid It?

You’ve probably heard the term biceps tendonitis as gym members highlight an ache or pain at the front of their shoulder. But what is biceps tendonitis and what can be done to avoid it?

What is Biceps Tendonitis (aka: Tendinitis) and what can you do?

Tendonitis, tendinosis, and tendinopathy are frequently used terms that mean different things. These terms, in fact, are often used incorrectly and require some clarification. An –itis, –osis, or –opathy all indicate that something has gone array, which has led to too much pressure, tension, and stress accumulating in one part of the soft tissue in the body. An –opathy, such as tendinopathy, refers to a classification of tendon diseases, such as tendonitis and tendinopathy. Used to describe inflamed tissue, -itis happens because of acute trauma or stress. Inflammation is the body’s natural response mechanism and usually shouldn’t be interfered with as it is due to micro-tears from the tissue being overloaded. –Osis differs from -itis because there is no inflammation and it’s associated with chronic or long-term tissue stress. Tendinosis, for example, implies that the chronic stress has led to degeneration at the cellular level (Armstrong & Hubbard, 2016). When this happens, the tissue begins to degrade. Tendinosis is diagnosed by a clinician through palpation and resisted muscle testing. If you suspect you have tendinosis, consult with your physician. However, self-intervention can often help when it comes to tendonitis. Therefore, the rest of this article will focus on tendonitis.

More about Tendonitis

Tendonitis is in the category of overuse syndromes and usually plays an active role in conditions such as cumulative trauma disorder, repetitive strain injury, repetitive stress injury, and occupational overuse. The majority of overuse syndromes involve inflammatory responses, which are provoked by repetitive movements, stress, or sustained tension/exertion of a muscle group or tendon. Armstrong and Hubbard (2016) stated that tendonitis usually comes secondary to repetitive microtrauma that often produces fatigue and inflammation. Tendonitis represents infiltration of the tendon or fibrous sheath with inflammatory cells and mediators (Singaraju et al., 2008). As mentioned above, if acute, this is not associated with cellular degeneration. However, if the stress is not removed, then the inflammation will lead to a tissue breakdown overtime and the degenerative process begins (i.e., tendinosis).

Tendonitis can occur in many different tendons located throughout the body. However, Almekinders (1998) listed the following as the most common diagnosis and locations of tendonitis:

  • Rotator cuff—supraspinatus tendon insertion
  • Lateral epicondylitis—common wrist extensor tendon origin (tennis elbow)
  • de Quervain disease and trigger finger—sheath/pulley of abductor pollicis longus and long finger flexors
  • Hamstring tendonitis—hamstring tendon origin
  • Quadriceps tendonitis—quadriceps tendon origin
  • Patellar tendonitis—patellar tendon origin (jumper’s knee)
  • Achilles tendonitis—sheath, midsubstance, or calcaneal insertion
  • Posterior tibial tendonitis—midsubstance, posterior tibia.

Surprisingly, one area that did not make Almekinders’ 1998 list, but is on the rise as a popular site for tendonitis is biceps tendonitis. Biceps tendonitis has been explained as an inflammatory process of the long head of the biceps tendon and is a common cause of shoulder pain due to its position (Ahrens & Boileau, 2007). The authors continued that one of the reasons it is so susceptible to injury is because it is exposed on the anterior shoulder as it passes through the humeral bicipital ground and inserts onto the superior aspect of the labrum of the glenohumeral joint. Thus, the tendon often sustains acute damage by being impinged in the subacromial space. Such an insult, over time, can easily lead to or at least contribute to biceps tendonitis. Also, biceps tendonitis is often associated with rotator cuff disease as a component of impingement syndrome (Singaraju et al., 2008).

Due to the position, it is easy to see how overhead activities, such as hitting a tennis ball, throwing a baseball time-and-time again, and swimming can irritate the tissue initiating the inflammatory process. However, a four-year study of rowing athletes also revealed an increased prevalence in biceps tendinitis (Hadala & Barrios, 2007). Such injuries may occur during rowing because the arm is moved into excessive abduction and external rotation, possibly causing direct injury to the biceps tendon. Therefore, biceps tendinitis may also show up in the left shoulder of a right-handed batter and the left shoulder of a right-handed golfer. Furthermore, the injury is not only sustained in competitive athletes but also becomes prevalent in the average gym-goer with the inability to properly extend the thoracic spine and demonstrate adequate length in the pectorals or latissimus dorsi.

Functional Shoulder Position

It is often clear to see how overhead athletes, whom subsequently performs explosive overhead movements over-and-over, may be subjected to a shoulder condition such as biceps tendonitis. However, anyone who can’t freely move their arms overhead yet forces the arms overhead, is also at increased risk of the condition. To fully understand how the biceps tendon becomes injured, it’s important to have a foundational understanding of the anatomy of the shoulder. The biceps has two heads that originate near the shoulder and merge into a common tendon to insert on the radius. Thus, the biceps have a functional role at the shoulder, and elbow–including supination and flexion. The short head of the biceps inserts external to the shoulder joint and is rarely involved in shoulder impingement and the subsequent inflammation that may lead to biceps tendonitis. However, the long head of the biceps passes through the bicipital groove of the upper arm, then turns approximately 90 degrees crossing the humeral head to attach to the upper edge of the glenoid labrum and supraglenoid tubercle. Therefore, the long head of the biceps tendon takes a peculiar route and has a unique stabilization and movement function of the entire arm.

Optimal movement of the humerus, scapula, and clavicle is necessary to keep the muscles and tendons of the upper arm safe. One way of detecting optimal movement is by investigating scapulohumeral rhythm. Scapulohumeral rhythm consists of integrated movements of the glenohumeral (GH), scapulothoracic, acromioclavicular, and sternoclavicular joints, which should occur sequentially. Such coordinated movement serves three purposes:

  1. Allows for greater overall range of motion.
  2. Maintains optimal contact between the humeral head and glenoid fossa (scapula).
  3. Assists with maintaining optimal length-tension relationships for ideal stabilization, force production, and force reduction (Norkin & Levangie, 1992).

The rhythm and coordinated movement of the shoulder should follow the sequence below:

  1. 0-90 degrees of movement begins with the scapula setting against the ribs to provide initial stability as the humerus abducts to 30 degrees.
  2. 30-90 degrees entails another 30 degrees of movement from the humerus while the scapula upwardly rotates to 30 degrees. The upward rotation results from the clavicle elevating at the sternoclavicular and acromioclavicular joints.
  3. 90-180 degrees involves 60 degrees of additional movement from the humerus and 30 more degrees of upward scapular The scapula rotation is associated with 5 degrees of elevation at the sternoclavicular joint and 25 degrees of rotation at the acromioclavicular joint (Inman & Saunders, 1996).

This information suggests that the key to both prevention and treatment is to restore mechanics of the entire shoulder girdle.

Shoulder Assessments

The NASM Essentials of Corrective Exercise cites Bongers (2001), Urwin, Symmons, and Allison (1998), and van der Heijden (1999) stating that “shoulder pain occurs in up to 21% of the general population with 40% persisting for at least one year.” This suggests that shoulder pain, once it occurs, is very hard to treat. Thus, prevention is key. Identifying potential shoulder impairments, which may lead to shoulder injuries, such as biceps tendonitis, is quick and easy. The first step is to begin with a total body movement pattern like the overhead squat. An overhead squat is a great assessment tool because from the very beginning one can notice if the client is having a tough time getting their arms overhead. The arms should be fully flexed to 180 degrees (arms in line with the torso) for a set of three to four squats. If the arms fall forward, any amount, it indicates that additional testing is warranted.

If the arms fall forward, the next step is to attempt to isolate certain movements at the shoulder, which will provide information as to what is the most problematic in the dysfunctional shoulder. These additional test will include isolated shoulder flexion, horizontal abduction, and glenohumeral external and internal rotation at 90 degrees of abduction.

Shoulder Flexion

Begin the next series of tests with the clients back against a sturdy wall. The wall will provide the fitness professional with a better reference to help determine a more precise cause. During shoulder flexion, the client’s feet, hips, shoulders, and head should begin against the wall. Have the client lock out their elbows and slowly reach as far as they can overhead to touch the wall. If the clients low back arches then it indicates that the latissimus dorsi may be the primary cause of the dysfunction. 

Horizontal Abduction

With the client still against the wall and elbows locked out, have them reach their arms out wide all the way back to the wall. If the arms can’t reach the wall, it indicates the pectorals may be short. However, the most common compensation is elevation of the shoulder or shrugging. If this happens, it indicates that a short upper trapezius and perhaps scalenes are interfering with optimal shoulder mechanics. 

GH External Rotation

Again, against the wall have the client abduct the arms to 90 degrees. Then, externally rotate the arm, so the hand and forearm begin to move toward the wall. If the client can’t reach the wall, it indicates short internal rotators. 

GH Internal Rotation

Again, against the wall and with arms abducted to 90 degrees, have the client attempt to bring the hand and forearm down toward the wall, internally rotating the GH joint. If the client can’t move about 70 degrees (as determined by simple observation) without dropping the arm or tipping the scapula forward, it indicates a problematic posterior capsule.

Two of the most common compensations observed is the inability to move the arms into full shoulder flexion and a lack of internal glenohumeral rotation. If these are noticed, regardless if there is shoulder pain yet, a CEx program should be implemented as part of movement prep.

CEx for Decreased Shoulder Flexion and Glenohumeral Internal Rotation


  1. Latissimus dorsi: Get into a side-lying position with the foam roller positioned toward the bottom of the shoulder blade. Slowly roll all way up to the armpit and the back of the shoulder joint. 
  2. Posterior capsule: Position a massage ball just behind the shoulder joint, on the rear deltoid. 
  3. Thoracic spine: In a supine position, slowly roll the length of the thoracic spine. Perform shoulder flexion motions to encourage thoracic extension.

Lengthen – Static Stretching

  1. Latissumus dorsi: Take to the first point of tension and hold for 30-45 seconds. 
  2. Sleeper Stretch: Side-lying with the arm abducted to 90 degrees and shoulders stacked, slowly internally rotate arm with opposite hand and hold for 30-45 seconds. 
  3. Thoracic Extension: In a supine position with a foam roller positioned mid-thoracic spine and hands supporting the head, slowly lean back to the first point of tension. DO NOT let bottom ribs flare up as this indicates the lumbar spine is beginning to extend. 


  1. Stability Ball Cobra: Perform 10-12 reps with slow tempo. 
  2. Ball Combo II: Perform 10-12 reps with a slow complete movement that is: a) row; b) external rotation; c) press (shown below); d) pull down; e) eccentric internal rotation; and f) eccentric press.
  3. GH IR: Perform 10-12 reps with a slow tempo, supine w/tubing and 90 degrees of abduction to reduce pec major and latissimus dorsi assistance.  


  1. Bear Crawl: Maintain shoulder blade stabilized against ribs cage—perform 20 walks forward.  
  2. Wide-grip Row: Perform 15-20 reps with a slow tempo and light resistance. 




Ahrens, P. M., & Boileau, P. (2007). The long head of biceps and associated tendinopathy. Journal of Bone & Joint Surgery, 89(8), 1001-1009.

Almekinders, L. C. (1998). Tendinitis and other chronic tendinopathies. Journal of American Academy of Orthopaedic Surgeons, 6(3), 157-164.

Armstrong, A. D., & Hubbard, M. C. (Eds.). (2016). Essentials of musculoskeletal care (5th ed.). Rosemont, IL: American Academy of Orthopaedic Surgeons.

Bongers, R. M. (2001). The cost of shoulder pain at work. BMJ, 322(7278), 64-65.

Clark, M. A., Lucett, S. C., & Sutton, B. G. (Eds.). (2014). NASM’s essentials of corrective exercise training. Burlington, MA: Jones & Barlett Learning.

Hadala, M., & Barrios, C. (2007). Sports injuries in an America’s Cup yachting crew: A 4-year epidemiological study covering the 2007 challenge. Journal of Sports Science, 27(7), 711-717.

Inman, V. T., & Saunders, S. J. (1996). Observations on the function of the shoulder joint. Clinical Orthopedics, 330, 3-12.

Norkin, C. C., & Levangie, P. K. (1992). The shoulder complex. In Joint Structure and Function: A comprehensive analysis (2nd ed., pp. 240-261). Philadelphia: PA: FA Davis.

Singaraju, V. M., Kang, R. W., Yanke, A. B., McNickle, A. G., Lewis, P. B., Wang, V. M., … Cole, B. J. (2008). Biceps tendinitis in chronic rotator cuff tears: A histologic perspective. Journal of Shoulder & Elbow Surgery, 17(6), 898-904.

Urwin, M., Symmons, D., & Allison, T. (1998). Estimating the burden of musculoskeletal disorders in the community: The comparative prevalence of symptoms at different anatomical sites, and the relation to social deprivation. Ann Rheum Di, 57(11), 649-655.

van der Heijden, G. (1999). Shoulder disorders: A state of the art review. Baillieres Best Pract Res Clin Rheumatol, 13(2), 287-309.

More on the shoulder:

Shoulder Pain Prevention

Shoulder Function: Enhancing Scapular Stabilization

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Tuesday, February 13, 2018

Research in Review: Does a caring fitness staff play a role in member motivation and retention?

Simple friendly staff interactions might just be the motivation members need to keep exercising and coming back to your fitness center.

Journal Article:

Brown, T.C., Volberding, J., Baghurst, T., & Sellers, J. (2017). Comparing current fitness center members’ perceptions of the motivational climate with non-members. Global Health Promotion, 24(1), 5-13.

Purpose of the Study:

The purpose of this study was to explore the perceptions and motivations behind non-gym user’s reasons of not going. To do this, researchers formulated two questions:

  1. What was the perceived motivational climate of the campus fitness staff:
    1. Task-involving climate—emphasis on self-improvement, cooperation, and individual effort
    2. Ego-involving climate—social comparisons occur, peers compete for attention, and individuals feel embarrassed when they make a mistake
    3. Caring climate—a setting where individuals feel safe, supported, and valued
  2. Was there a difference in perception for users versus non-users of the facility?

Study Participants:

657 faculty and staff of a large university were invited (via email) to participate in an online survey. The survey was specific to the use of the campus fitness facility. This was chosen because it was in a convenient location and free to the staff. One potential flaw, admittedly by the authors, is that participants may have been members of other fitness facilities.

Procedure or Methods:

The survey included three separate versions to ensure that the questions matched the patterns of usage (i.e. never used, former users, or current users). Subjects that had never used were asked to base their perceptions on what they had heard about the on-campus fitness facility.

There were two scales used to fully capture study subjects perceptions: Caring Climate Scale (CCS) and Specific Behaviors of Staff (SBS) questionnaire. The CCS contained 13 questions and assessed the extent to which individuals perceived they would feel welcomed and be treated with kindness and respect at the fitness facility. The questions were ranked on a sliding scale from 0 (did not have an impact) to 10 (had a significant impact) on importance.

The SBS questionnaire contained 17 questions and was used to determine what actual behaviors staff engaged to create a task-involving and caring climate. The questions were ranked on a sliding from 0 (entirely ego-involving—defined above) to 10 (entirely task-involving—defined above).


Difference between types of users:

  • All participants (current users, former users, and never users) preferred a setting that was more caring
  • All participants (current users, former users, and never users) preferred to exercise in settings that were more task involving than neutral or ego involving
  • Current users were more likely to perceive a caring climate where staff engaged in task-involving and caring behaviors compared to those who no longer (or never) used the facility

Perceptions of the climate:

  • Positive perceptions:
    • Most commonly reported by current users (47%)
    • The comments from subjects centered on feelings of being welcomed and invited as well as specific behaviors that staff engaged to help members focus on their fitness goals
    • Current users voiced an appreciation for staff interaction. They enjoyed staff that greeted them, said hello, knew their names, smiled, and helped out when necessary
  • Negative perceptions:
    • Most commonly reported by former users (24%) and never users (21%). Some current users (10%) also reported negative perceptions
    • Some users distinguished between feeling harassed and feeling welcomed by staff who engaged in positive interaction
      • One current user stated “I’m not going to the gym to make friends; it’s my meditative time—it would bother me if people were all chatty, chatty while I’m trying to work out. All I want is basic friendliness as the front desk”.
    • Many never users comments reflected experiences that occurred during their first visit to the facility
      • One commented “I have walked in before and went to the front desk and asked questions regarding the facility, but they were short and not really interested in me”.
      • Another commented “I perceive it as a youth oriented facility, run by youthful people at which older or overweight people will not fit in”.
    • Positive and negative perceptions simultaneously:
      • A few participants made comments that were both positive and negative
        • One stated “The instructors of the fit classes were always friendly and helpful, but most of the rest of the employees seemed to be just putting in their time”.


The authors of this study suggest that it can assist fitness and recreation center managers in determining best ways to train staff in order to increase usage of the facilities, address retention of members, and maximize potential for positive exercise experiences.

Take away for NASM-CPTs:

Increasing member retention is an important aspect of running a successful health club. This study suggests that the responsibility of member retention falls on everyone’s shoulders. Members want to exercise in an environment where they feel supported, motivated, and welcomed. This begins with the front desk staff. Employees should do their best to always smile, say hello, and use the members name when appropriate. Providing assistance to members that need it is acceptable, but it should not be in an attempt to “sell” them on personal training or anything else—at least not initially. Spending time with the member, answering questions and offering genuine support, will help to build a potential foundation for personal trainers.

An additional factor that should be noted is that potential members, whether they join the health club or not, will form their opinions off of the first visit. Therefore, it’s important to always be kind and courteous. Chances are that the person you pass in the entrance is forming an opinion of the entire company based on whether or not you choose to interact with them.

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The Value of VO2 – Health Measure or Performance Marker?

The Nordic combined, a combination of cross-country skiing and jumping was one of the original five sports at the first-ever Winter Olympics held in France in 1924. To this day, endurance sports like the biathlon, cross country skiing and the Nordic combined continue as bastions of the quadrennial event and, in fact, the six most decorated Winter Olympians of all time are all aerobic athletes who participated in these grueling endurance races. But, considering how the Winter Olympics are generally held at higher elevations where oxygen pressures are lower than at lower elevations, it does raise questions over how these environments impact VO2 and subsequently their aerobic training and performance, and whether these high-elevation athletes are any different from their summer counterparts who generally live and train at lower-elevations?

To understand these questions and more, we need to first dig a little deeper into the science and value of measuring oxygen consumption or VO2. This article will examine some physiology, application and the value of measuring VO2 given how this parameter is often considered synonymous with athletic performance.

Absolute versus Relative VO2 (1-3)

Oxygen utilization holds great relevance in understanding human metabolism. The amount of oxygen consumed (at the cellular level) reflects energy utilization and the amount of work performed by the body. Of interest is maximal oxygen consumption or VO2max, which is also referred to as peak VO2. In its simplest form, VO2 is the difference between oxygen inspired and oxygen expired in a unit of time (e.g., one minute), and VO2max would be the greatest quantity the body is able to consume. Two measures are frequently used in science; absolute VO2 and relative VO2. As the word denote, absolute VO2 reflects the total (absolute) amount of oxygen consumed by a body, regardless of size, age or gender whereas relative VO2 indicates that score corrected to some reference, which happens to be a unit of mass or one kilogram (1 kg.). The units of measurement are all metric:

  • Absolute VO2 = Liters per min (L/min)
  • Relative VO2 = milliliters per minute per kilogram (a unit of mass) which is rewritten as milliliters per kilogram per minute or mL/kg/min (1,000 mL = 1.0 L). For example, if Peter weighs 220 lbs. (100 kg) and has a VO2max of 4.0 L/min, his relative VO2max would be 40 mL/kg/min (refer to Table 1-1 below).

Both absolute and relative VO2 provide valuable information. Considering the role of oxygen in metabolism (i.e., to burn fuels) quantifying the total amount of oxygen consumed provides an estimate of calories expended. While not exact, scientists use an average of five (5) calories for every liter of oxygen consumed. Therefore, if Mary was running on a treadmill and consuming 2.0 L/min, she would be expending 10 kcal per minute or 200 kcal over a 20-minute period. Unfortunately, absolute VO2 scores cannot be used to compare individuals against each other or against norms (i.e., occupational requirements) given the many differences that exist, especially in body weight (a heavier person burns more oxygen at rest). Consequently, absolute VO2 scores are converted to relative scores for purposes of comparison. For example, is Peter who weighs 200 lbs. (100 kg) with a VO2max of 4.0 L/min more fit than Jane who weighs 125 lbs. (56.8 kg) with a VO2max of 2.5 L/min (Table 1-1)?

Table 1-1: Calculating relative VO2 scores

Peter Jane
Weight 220 lbs. (100 kg) 125 Lbs. (56.8 kg)
Absolute VO2max 4.0 L/min 2.5 L/min
Relative VO2max 40 mL/kg/min * 44 mL/kg/min *

* 2.5 L/min = 2,500 mL / min ÷ 56.8 kg = 44 mL/kg/min

VO2max Value and Performance

VO2 is either measured directly using gas analysis (i.e., analyzers that sample gas volumes and concentrations) or estimated indirectly from work performed (e.g., treadmill speed/grade) or from sub-maximal heart rate responses. Regardless of the assessment technique, VO2max has long been considered a predictor of maximal exercise performance (i.e., higher VO2max scores imply greater athletic performances). As illustrated in Figure 1-1, this is not true. The VO2-work slope demonstrates a somewhat linear relationship with incremental work (A-B) until a sub-maximal threshold point is reached (B) after which VO2 levels off, but additional intensities of work can be performed (B-C), albeit it for brief periods (i.e., contributions from the anaerobic energy pathways). This plateau is believed to either represent a maximal capacity for mitochondrial oxidative capacity or an inability to further supply oxygen to the mitochondria through the blood (4).

Figure 1-1: Relationship between VO2 and work intensity

Additionally, a peak VO2 or VO2max is a one-time best shot (i.e., incrementally staged lab test) and does not represent a sustainable intensity, which is what all endurance sports require. This fact has generated a shift in mindset to measuring markers called respiratory compensation point (RCP) or onset of blood lactate accumulation (OBLA) as predictors of sustainable performance rather than VO2max. These markers represent the highest intensity that one can sustain over time and are often referred to as lactate threshold (LT), which is incorrect (1). Lactate threshold represents the intensity of exercise at which the amount of blood lactate begins to rise disproportionally above normal resting values and it generally occurs early at moderate-to-vigorous intensities of exercise (3). Furthermore, VO2 is influenced by a myriad of other intra- and interpersonal factors that include (5):

  • Age – gradual decline in scores after late teens / early twenties, although many world class athletes only peak in the late twenties to early thirties.
  • Gender – men have more hemoglobin to carry oxygen and a greater quantity of muscles cells for mitochondrial oxidation.
  • Genetics – perhaps the most influential.
  • Conditioning level (VO2max scores generally increase with training).
  • Altitude and temperature – discussed in subsequent section.
  • Inter-personal physiological variances – ventilatory muscles, muscle fiber types, oxidative enzyme levels, etc.
  • Economy of movement – experienced runners run more efficiently than novice runners, running requires more muscle action than cycling (i.e., upper extremity involvement).

So, while VO2max holds limited value as an estimator of performance, it does hold great value as a predictor of overall health and in determining work capacity standards for various occupations. Individuals who are physically active generally have higher VO2max scores and present with lower risks for morbidity and mortality. Likewise, as VO2 reflects work capacity, many physically-demanding occupations (e.g., fire services, military) rely upon these scores to quantity an individual’s capacity to perform work duties safely and competently.

VO2 and Performance in Colder and Higher Environments

Increases in elevation generally reduce ambient temperatures, both of which can negatively impact athletic performance. A common misconception is that at altitude the air holds less oxygen, making breathing harder, which, in turn reduces exercise capacity. However, it is not the concentration of oxygen that presents the problem, but the decreased pressure of ambient air pushing oxygen into the lungs and into the blood that is the issue. Dalton’s law of partial pressures states that the total pressure of a gas is the sum of the partial pressures of the individual gases (e.g., oxygen, carbon dioxide) (1-2). At higher elevations, the total pressure of atmospheric air drops, therefore the partial pressure of oxygen also drops. For example, at sea level, atmospheric air exerts a total pressure of 760 mm Hg and with oxygen comprising 20.93% of that value, it holds a partial pressure of 159 mm Hg (760 x 0.2093 = 159 mm Hg). At 14,000 feet (4,267 meters) however, atmospheric air only exerts a total pressure of 447 mm Hg and with oxygen comprising 20.93% of that value, it holds a partial pressure of 94 mm Hg (447 x 0.2093 = 94 mm Hg). Simply put, this means less oxygen being driven into your lungs and blood.

Lower pressures reduce the ability for oxygen to cross from the lungs into the blood and bind to hemoglobin for transportation to the cells, resulting in less oxygen being available for mitochondrial oxidation. To compensate for this decrease, the body starts to produce additional red blood cells soon after arriving at elevation with mature red blood cells (erythrocytes) appearing in the blood after approximately seven days of altitude exposure (6). This process is called erythropoiesis and is regulated by the hormone erythropoietin (EPO)*. This helps explain why athletes have traditionally traveled to altitude to train, later returning to lower elevations to perform because they have more red blood cells to carry oxygen. This effect usually lasts a few weeks at most because red blood cells only have a lifespan of approximately 4 weeks. The reality, however, is that this technique does not guarantee performance improvements because more than just increased oxygen carrying capacity to the cell is needed to improve performance.

* Synthetic alternatives to EPO are very prevalent in endurance sports – some athletes might opt to use and cheat.

Upon arriving at altitude, our breathing mechanics change dramatically. Air is colder and drier, and it must be warmed and humidified as it enters the body. This results in faster losses of vital fluids and dehydration, as well as potential bronchospasm which may counter the normal bronchodilation effects that occur during exercise with the release of epinephrine and norepinephrine (1). Fluid losses decrease our blood volume which reduces stroke volume, or the volume of blood ejected from the heart with each contraction. To compensate and maintain cardiac output (a measure of how hard the heart is working), the heart beats faster which may limit the capacity for higher intensities of exercise.

Another immediate adaptation experienced at altitude lies in ventilation. To account for lower oxygen partial pressures, we increase our tidal volumes, the volume of air moved with normal breathing. This is accompanied by more forceful expirations (hyperventilation) which pushes more carbon dioxide (CO2) out of our lungs and from the blood. Considering CO2’s role in regulating breathing and blood pH, the body responds by producing more CO2 which it does using our precious lactate buffer and reduces that amount available for high-intensity work. Athletes often experience noticeably higher blood lactate levels and decreased work capacity with high-intensity work when initially training at altitude. This reduced blood lactate buffer can also compromise near maximal performance when the athlete returns to lower elevations. After a few weeks at altitude however, our cardiopulmonary systems undergo several adjustments to try to revert to normal, but the consensus of science is that training at altitude might not be as beneficial as once believed. Subsequent strategies, thanks in part to emerging technologies, optimize many of the elevation training gains without the potential downsides – these include:

  • Hypoxic sleeping chambers where individuals live in quarters simulating altitude by breathing lower oxygen concentrations, but train normally at lower elevations.
  • Intermitted hypoxic exposure (i.e., live high-train low) – commuting 33 miles between Salt Lake City and Park City – a differential of almost 3,000 feet (800 m).
  • Using supplemental oxygen when living at higher elevations, but not when training.

Athletes competing at elevation and in cold must also contend with other physiological factors that may impede overall performance (1):

  • Thermoregulation – the proper application of fabrics and layers to ensure appropriate removal of excess heat, without wet fabrics remaining in contact with the skin which can trigger hypothermia.
  • Decreased free fatty acid mobilization from our subcutaneous fat stores due to peripheral vasoconstriction in cold climates – may reduce the availability of fats as a fuel to muscle cells and force faster glycogen utilization rates and the potential for depletion.
  • Altered nerve and muscle physiological function, altered muscle fiber recruitment patterns, and decreased muscle-shortening speeds and force-generating capacity, all of which can reduce muscle strength and power levels.

So how do these events change the winter athlete in comparison to the summer athlete? It certainly would be hard to make any unequivocal statements, but what is apparent is that the winter athlete appears to face greater obstacles when it comes to their training and performance. They certainly should give more careful thought and consideration to planning their training regimens if they want to succeed. So, in this 2018 Olympiad, let’s appreciate these endurance athletes with a unique perspective that is greater than just being that of a spectator watching the world’s top athletes. With your deeper understanding of what each endurance athlete endured just to get to these games, I hope your appreciation of their efforts are truly admired and respected.



  1. Pocari J, Bryant CX, and Comana F, (2015). Exercise Physiology. Philadelphia, PA. F.A. Davis Company.
  2. Katch VA, McArdle Wd and Katch FI, (2011). Essentials of Exercise Physiology (4th). Baltimore, MD. Lippincott, Williams and Wilkins.
  3. Kenny WL, Wilmore JH, and Costill DL, (2015). Physiology of Sports and Exercise (5th). Champaign, IL. Human Kinetics.
  4. Tipton CM (Ed), (2006). ACSM’s Advanced Exercise Physiology. Baltimore, MD. Lippincott, Williams and Wilkins
  5. Noakes T, (2003). The Lore of Running. (4th ed.). Champaign, IL. Human Kinetics.
  6. Robergs RA, and Roberts SO (1997). Exercise Physiology – Exercise Performance and Clinical Applications. St. Louis, MO., Mosby Year Book, Inc.





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Friday, February 9, 2018

Heart of the Matter: Fit or Not

Fit or not, pay attention to the warning signs your heart is giving you. Your life depends on it. Even as “fit” fitness professionals, we are not immune to heart disease. See how this NASM Master Trainer found out.

Recently I made a trip back home to Western New York. Unfortunately, it was for the passing of my 96 year old grandfather. He lived an amazing and long life, one that I hope to experience as well. During the visit I was approached by many relatives and friends about my current medical situation. They remarked, “You look amazing, how can you be the one with a heart issue?” or “You are the last person that I would think of having two stents.”

My heart issue journey began back in December of 2015. I was visiting family and was running outside. I was having trouble breathing but I just chalked it up to the cold weather. Then when I returned to Florida and was running, I felt an immense pain in my chest and I couldn’t breathe very well. I never felt anything like this before. Of course, I just kept on going and thought nothing of it until a few days later when I started getting tingles down my left arm while indoor cycling. Now I knew something was wrong and thought it would be important to check since I had a family history of heart disease. I had thought if I take care of myself physically, exercise, eat right, there will be no problem right? Wrong! After a few tests and some good speculating by the medical staff, they saw that my widowmaker (left anterior descending coronary artery) was 98% blocked. That was a shock since this could have ended my life. They put in a stent and I was feeling better. 

Looking back, the warning signs were there, I just didn’t know much about them. Add to that the grey facial skin discoloration, irritability, and being tired all the time I was experiencing. I just thought it was part of the aging process and a 50-hour a week personal training business.

The doctors thought that this was, what they called, an “anomaly.” I didn’t fit the profile and it was just a strange thing to happen. Just keep living the way you were, take your meds, check back with doctors periodically and best of luck the rest of your life. I continued to feel great. A booming fitness business, I was eating better than before, everything was on the up and up. My wife and I took a trip to Italy, our family was growing as we welcomed our third daughter and bought a house. Life was good.

Then this past year I noticed that my mood was really starting to slip. My wife was staying home to take care of the baby and I started putting in more hours at work. I was getting that tired all the time feeling again and started to gain extra weight that I couldn’t take off. Stress was really getting the best of me.

Then one morning I woke up and I told my wife that I didn’t feel well. I thought I had indigestion the previous night, plus I had discomfort on my left side. I looked in the mirror and I looked horrible. I went to the emergency room and told them my symptoms and my past heart experience. They said that they would probably do a cardiac catheterization to see how well my heart was working, but they were with me, how can this be? I couldn’t believe the results, the same artery was 98% blocked. They put in another stent and now I have had two stents in less than 3 years. Unbelievable.

I recently read in The New York Times about Bob Harper, one of the trainers from The Biggest Loser, about his heart attack experience. He felt the same way I did, took good care of himself and the next thing you know you he was hooked up to tubes and wires lying in a hospital bed.

The article mentions that his Lipoprotein(a) blood levels were high. Normal values for most people are below 30 mg/dL in the blood.(1) Higher levels are associated with triple the risk of heart attack and stroke at an early age since Lp(a) is a type of cholesterol that can lead to a risk of atherosclerosis.(1) The challenge is that most doctors do not routinely test for Lp(a) like they do for LDL and HDL since it is not recommended unless there is a family history of cardiovascular disease.(2)

According to the Lipoprotein(a) Foundation, 1 in 5 people globally have high levels of Lp(a), above 50mg/dL, in their bloodstream. About 1.1% of our population have above 180 mg/dL, which can be potentially life threatening. When I looked at my Lp(a) levels from a 2015 blood test I was astonished to learn it was 220 mg/dL.

Now I understand the impact of genetics. Studies show diet and exercise have very little impact on Lp(a) levels and genetics mostly determines how much your body produces. The risk factor was present on both sides of my family. My dad and uncle both had major bypass surgeries by the time they were 70. My other uncles all died of massive heart attacks in their 50s and my grandmother died of heart attack at 70. I thought if I ate right, exercised regularly, didn’t smoke, I would be ok. Now I know this is not entirely true, while also realizing that these healthy lifestyle factors are still important to reducing the risk of cardiovascular disease.

I have since taken a different approach to my health. Of course, more visits to the cardiologist and blood work to monitor are a must. I am also seeking a second opinion from a top cardiologists in the country. I have also turned to a more plant-based diet which has been linked to lower total cholesterol levels, including LDL. Every morning I meditate for stress relief and incorporate yoga into my exercise routine five days per week.

If you have a family history of heart disease talk with your doctor about an Lp(a) test. They can then refer you to a specialist if needed. There is also the Lipoprotein(a) Foundation that can help you with questions or refer you to a specialist. Educate yourself on heart attack warning signs and don’t ignore them. Your life may depend on it- mine did. Twice.



  1. Rallidis, Loukianos S. et al. (2018) High levels of lipoprotein (a) and premature acute coronary syndrome. Atherosclerosis , Volume 269 , 29 – 34.
  2. “Lipoprotein-a.” MedlinePlus Medical Encyclopedia, U.S.National Library of Medicine, 5 May 2016,


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