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Data Source: Zamparo P, Bonifazi M (2013). Bioenergetics of cycling sports activities in water.

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Brief Swimming Review Volume 1 Edition 5

In an attempt to improve swimming transparency, a brief swimming related literature review will be posted on Saturday. If you enjoy this brief swimming review, consider supporting and purchasing the Swimming Science Research Review

Risk Factors for Shoulder Pain

Walker (2012) took 74 competitive swimmers and took self-reported data over 12 months as well as anthropometric features and swimming characteristics before the competitive season. Shoulder pain was classified as "significant interfering shoulder pain (SIP) defined as pain interfering (causing cessation or modification) with training or competition, or progression in training. A significant shoulder injury (SSI) was any SIP episode lasting for at least 2 weeks (Walker 2012)".

These results found 38% reported SIP and 23% reported SSI. Swimmers with high and low external rotation range of motion were at 8.1 and 12.5 times greater risk for for SIP and 35.4 and 32.5 times greater risk for SSI. Also, those with a history of shoulder pain were 4.1 and 11.3 times greater to sustain a SIP and SSI.

One again, it seems extreme ranges of motion and a history of shoulder pain are predictors of shoulder pain. Unfortunately, I do not have this whole study and am curious about their criteria or specificity for normal range of motion. Nonetheless, screening and acknowledging these features is essential for a proper shoulder injury prevention program. 

Shoulders and Swimming

5 Swimming Shoulder Stresses
Swimmers Shoulder
COR Swimmer's Shoulder System

Asthma and Swimming Training in Children and Adolescents
Beggs (2013) performed a Cochrane review of all the quality research on asthma and swimming in children and adolescents. Overall they analyzed eight studies involving 262 participants with stable, mild to severe asthma. In all the studies, the participants were 5 - 18 in age and swam 30 - 60 minutes 2 -3 times/week.

Swimming training increased exercise capacity compared with usual care or a control group. VO2max increased ~9.67 mL/kg/min.


"Swimming training was associated with small increases in resting lung function parameters of varying statistical significance; mean difference (MD) for FEV1 % predicted 8.07; 95% CI 3.59 to 12.54. In sensitivity analyses, by risk of attrition bias or use of imputed standard deviations, there were no important changes on effect sizes. Unknown chlorination status of pools limited subgroup analyses.Based on limited data, there were no adverse effects on asthma control or occurrence of exacerbations (Beggs 2013)."

Swimming is not associated with any adverse reactions and is well-tolerated in children and adolescents. However, the positive influences on lung function and cardio-vascular fitness may also occur in other forms of training. 
Asthma and Swimming
Asthma and Swimming
Asthma and Swimmers
Asthma and Swimming: Know the Rules
Friday Interview: Giacomo Crivelli on Asthma and β2-Agonists

Warm-up is Better than no Warm-up!
Neiva (2013) had twenty competitive swimmers performed two maximal 100-m freestyle trials with and without a 1000-m warm-up (intermediate swimmers, ~67 100-m time trial). 

The warm-up condition resulted in significantly faster 100-m performance. However, three swimmers swam faster without warm-up. Swimmers who warmed-up had a significantly greater distance per stroke and swimming efficiency (measured by stroke index). Stroke kinematics, blood lactate concentrations, and perceived exertion were similar between trials.

Unfortunately (once again), I don't have this whole article for review, but it brings some interesting notes. For one, could those with a short distance per stroke benefit more from a warm-up than those with a long distance per stroke? Also, what characteristics result in those having greater performance without a warm-up? For this difference warm-ups are necessary for different swimmers.

Other studies have analyzed swimming performance and was discussed in Perfect' Swimming Warm-up (2012). 

This article discussed a study out of Alabama had swimmers perform 50-yard time trials with three different warm-up variations: no warm-up, short warm-up (two 50-yard paces), and regular warm-up. The researcher's concluded "individual data indicated that 19% of participants performed their best 50-yd time after short-, 37% after no-, and 44% after regular warm-up" (Balilionis, 2012).

Once again, individual warm-up is essential for elite performance in sprint swimming. However, more research is necessary on different strokes and longer distance. Until this is achieved, different warm-ups lengths should be considered for each individual.

  1. Walker H, Gabbe B, Wajswelner H, Blanch P, Bennell K.Shoulder pain in swimmers: a 12-month prospective cohort study of incidence and risk factors. Phys Ther Sport. 2012 Nov;13(4):243-9. doi: 10.1016/j.ptsp.2012.01.001. Epub 2012 Feb 29.
  2. Beggs S, Foong YC, Le HC, Noor D, Wood-Baker R, Walters JA.Swimming training for asthma in children and adolescents aged 18 years and under.Cochrane Database Syst Rev. 2013 Apr 30;4:CD009607. doi: 10.1002/14651858.CD009607.pub2.
  3. Neiva HP, Marques MC, Fernandes RJ, Viana JL, Barbosa TM, Marinho DA. Does Warm-Up Have a Beneficial Effect on 100m Freestyle?Int J Sports Physiol Perform. 2013 Apr 9. [Epub ahead of print] 
  4. Balilionis G, Nepocatych S, Ellis CM, Richardson MT, Neggers YH, Bishop PA. Effects of Different Types of Warm-Up on Swimming Performance, Reaction Time, and Dive Distance.J Strength Cond Res. 2012 Jan 10.
By Dr. G. John Mullen received his Doctorate in Physical Therapy from the University of Southern California and a Bachelor of Science of Health from Purdue University. He is the founder of Mullen Physical Therapy, the Center of Optimal Restoration, head strength coach at Santa Clara Swim Club, creator of the Swimmer's Shoulder System, and chief editor of the Swimming Science Research Review.

Friday Interview: Giacomo Crivelli on Asthma and β2-Agonists

1. Please introduce yourself to the readers (how you started in the profession, educa-tion, credentials, experience, etc.). 
Giacomo Crivelli, PhD student at the Institute of Sport Sciences at the University of Lausan-ne, Switzerland. My research is focused on the effects of the β2-adrenoceptor agonists on the skeletal muscle contraction in humans, under supervision of Dr. Fabio Borrani1 and Dr. Nicola A. Maffiuletti2. We use direct non-invasive techniques, which involve the application of percutaneous electrical stimulation to the motor nerve or directly to the muscle, for in vivo assessment of changes in contractile functions of individual muscles.  
1Institute of Sport Sciences, University of Lausanne, Lausanne, Switzerland.
2Neuromuscular Research Laboratory, Schulthess Clinic, Zurich, Switzerland.
2. You recently published an article on the role of β2-agonists and exercise, could you please explain the pertinent findings? 
β2-Adrenergic agonists are powerful bronchodilators that are widely used for treating asthma and exercise-induced asthma (EIA). In addition to their bronchodilatory action, β2-agonists, when administered acutely, have been shown to modulate the contractility of the slow skeletal muscle fibers in the animal models. Thus, we investigated central and peripheral neuromuscular adjustments induced by an acute oral therapeutic administration of the β2-agonist terbutaline (8 mg) on a predominantly slow human muscle, the soleus. We found that acute oral intake of terbutaline diminished the contractile function of the human slow soleus muscle in vivo. The reduction of half-relaxation time in terbutaline condition indicates an ac-celerated muscle relaxation. Moreover, under terbutaline treatment, the force associated to evoked submaximal tetani was decreased, suggesting the presence of a weakening effect in the slow muscle fibres. The increased central motor drive (as estimated from changes in soleus surface EMG activity) to the soleus muscle during submaximal voluntary contractions was interpreted as a compensatory adjustment of central nervous system to counter the weakening action elicited by terbutaline on the slow muscle fibres3.
3Crivelli G, Borrani F, Capt R, Gremion G, Maffiuletti NA. Actions of β2-Adrenoceptor Agonist Drug on Human Soleus Muscle Contraction. Med Sci Sports Exerc. 2013 Jan 4 [Epub ahead of print].
3. A lot of swimmers have exercise induced asthma and use β2-agonists, so what should swimmers take from the results? 
The maximal force generation capacity of the muscle is not impaired by β2-agonists, even though an enhanced neural drive to the muscle would be required to develop submaximal force. The latter effect may increase the energetic cost of the contraction and accelerate muscle fatigability. On the other hand, the faster relaxation rate of the muscle induced by β2-agonists could improve the switch between agonist-antagonist muscles in rapid alternating movements, thus increasing exercise performance in short-lasting and rapid tasks. However, it is important to emphasize the following considerations:
i) The weakening effect on slow muscle fibres can be attributed to the specific action elicited by β2-agonists at the skeletal muscle level. Nevertheless, this weakening action would most likely be influenced by the concomitant and widespread effects that β2-agonists exert at the whole-body level (i.e., on the metabolism activity, cardiac output, blood flow, ions transport).
ii) Asthmatic athletes commonly use inhaled β2-agonists to prevent and treat asthmatic sympoms. To date, however, there is no human evidence of modulation of the contractile function after β2-agonists inhalation. Doses of inhaled β2-agonists are 10- to 20-times smaller than oral doses and mainly act locally within the airway. Thus, the amount of β2-agonist reaching the peripheral muscle may be insufficient after acute inhalation of therapeutic doses to potentially diminish the muscle function, as opposed to an oral administration.
4. Why measure half-relaxation time in muscles as opposed to full relaxation? 
Half-relaxation time, defined as the time to obtain half of the decline in peak force, is widely used to assess changes in rate of force relaxation. This parameter is determined in a mathematical way from the force signal with a high repeatability of the measurements. Conversely, “full relaxation” presents several drawbacks, which could potentially affect its validity. From a methodological standpoint, the exact location of the complete relaxation is hard to define on the force signal. Furthermore, this part of the force signal is strongly influenced by artifacts induced by the discomfort generated from the percutaneous electrical simulations, thus com-promising this measurement.
5. Do β2-agonists occur naturally in any foods? 
β2-Agonists do not occur naturally in any foods. Nevertheless, the β2-agonist clenbuterol, due to its anabolic property, has been used in the livestock industry to improve muscles growth in animals and hence promoting the efficiency of meat production. Clenbuterol has been banned in the meat industry in the U.S. since 1991 and in the EU since 1996 because of health concerns about symptoms noted in consumers (e.g., increased heart rate, muscular tremors, headache and nausea). Although clenbuterol was banned in the last decade, several professional athletes (including Alberto Contador during the Tour de France race 2010) were tested positives in urines to this drug resulting from a possible food contamination. A recent study by the German Sport University Lab in Cologne confirmed that humans can inadvertently ingest clenbuterol from eating meat. Current reports indicate that food contamination with clenbuterol is a serious problem especially in China and Mexico, which had a problem with illegal substance for animal feeding. Therefore, athletes visiting those area take a risk of an inadvertently clenbuterol contamination with food and consequently, unintended doping4.
3 Guddat S, Fußhöller G, Geyer H, Thomas A, Braun H, Haenelt N, Schwenke A, Klose C, Thevis M, Schänzer W. Clenbuterol – regional food contamination a possible source for inadvertent doping in sports. Drug Test Anal 4: 534-8, 2012.  
Furthermore, it must be emphasized that to date there is no human evidence of force potentiation in fast muscle fibres induced by administration of β2-agonists. 

6. What sorts of activities would benefit from having increased rate of slow twitch muscle relaxation? 
The switch between agonist-antagonist muscles in rapid alternating movements should be increased by faster relaxation rate of the slow muscle fibres. Nevertheless, this would only be effective in a short-lasting exercise, because the compensatory adjustment of the central nervous system during submaximal voluntary contractions would be disadvantageous in term of metabolic cost and fatigability. It is not surprising that improvement in exercise performance after acute intake of β2-agonists has been reported almost only in anaerobic and explosive tasks. Therefore, acute oral administration of β2-agonists could potentially have an ergogenic benefit for sprint performance (e.g., 50 m free-style swimming).
7. Given that β2-agonists are restricted via WADA/USADA, how long would it take for these to exit the system?  Are there any recommended protocols that can derive benefits of this research while remaining in compliance with doping rules? 
According to the Prohibited List 2013 published by WADA, “all β2-agonists are prohibited except inhaled salbutamol (maximum 1600 micrograms over 24 h), formoterol (maximum 54 micrograms over 24 h) and salmeterol when taken by inhalation in accordance with the ma-nufacturers’ recommended therapeutic regime. For the use of other β2-agonists, that are not one of the three exceptions listed above, athletes can apply for a Therapeutic Use Exemption. The presence in urine of salbutamol in excess of 1000 ng/mL or formoterol in excess of 40ng/mL is presumed not to be an intended therapeutic use of the substance and will be considered as an Adverse Analytical Finding unless the athlete proves, through a controlled pharmacokinetic study, that the abnormal result was the consequence of the use of the therapeutic inhaled dose up to the maximum indicated above”.
Even though our recent investigation demonstrated a weakening effect of β2-agonists on the contractile function of human slow muscle fibres, such result doesn’t justify any loosening of the restrictions for β2-agonists use by WADA. Indeed, we showed that β2-agonists, after an acute oral therapeutic intake, reach the systemic circulation in a sufficient amount capable to affect the human skeletal muscle contractility. Moreover, our study didn’t investigate the act-ion of chronic therapeutic administration of β2-agonists on contractile function, which could also differ from the effects induced by acute intake. Thus, the restriction for oral administration of this class of drugs must be preserved.
Conversely, on the basis of scientific evidence, inhaled β2-agonists don’t have any relevant ergogenic effect on exercise performance in non-asthmatic competitive athletes. Thus, from the ergogenic standpoint, inhaled β2-agonists should not be prohibited for athletes.  
Considering the possibility to analyze in the urine the quantity of β2-agonists, the current regulation is appropriate to detect misuse of this substance. In addition, it would make sense to include β2-agonists in the Monitoring List of the WADA anti-doping program. The inclusion of β2-agonists in the Monitoring List would permit WADA to detect eventual increase in misuse of this substance, and thus bring back this class of drugs to the Prohibited List. Furthermore, it could significantly reduce the complicated administrative process for athletes and physicians (who are responsible for the treatment) to obtain TUE and diminish the administrative expenses for the handling of these substances by WADA5.
5Wolfarth B, Wuestenfeld JC, Kindermann W. Ergogenic Effects of Inhaled β2-agonists in Non-asthmatic Athletes. Endocrinol Metab Clin North Am 39: 75-87, 2010.
8. Any different recommended protocols for those with asthma already taking β2-agonists? 
The current guidelines for the treatment and prevention of asthma and exercise-induced asthma (EIA) in athletes are valid. According to these recommendations, inhaled short-acting β2-agonists are used before exercise, when bronchoconstriction occurs with exercise, to prevent of attacks of EIA. Instead, long-acting β2-agonists (combined with corticosteroids) are inhaled as a basic treatment for severe cases of asthma.
It is important to raise awareness in the athletes of the risk for the misuse of administration of high doses of  β2-agonists, to avoid adverse effects (such as tachycardia, tremors, headache, hyperglycemia, hypokalaemia) and the weakening action on human skeletal muscle function, which both may affect negatively exercise performance.
9. What mistakes still exist in professional athletes and medical clinics in regards to β2-agonists? 
I think a common mistake is to believe that use of β2-agonists will have a positive ergogenic action on performance in non-asthmatic competitive athletes. Despite β2-agonists administration has been shown to induce a small bronchodilation in healthy athletes, the improved lung function does not induce any enhancement in performance. From my point of view is import-ant to raise awareness in all athletes, trough prevention and education programs, on the appropriate use of β2-agonists to avoid overuse of non-performance enhancing medications. This will ensure that athletes know health consequences of what they put in their bodies, not only for asthma treatment, but also for the adverse effects on physical performance. 

It is important to raise awareness in the athletes of the risk for the misuse of administration of high doses of  β2-agonists, to avoid adverse effects (such as tachycardia, tremors, headache, hyperglycemia, hypokalaemia) and the weakening action on human skeletal muscle function, which both may affect negatively exercise performance.
9. What mistakes still exist in professional athletes and medical clinics in regards to β2-agonists? 
I think a common mistake is to believe that use of β2-agonists will have a positive ergogenic action on performance in non-asthmatic competitive athletes. Despite β2-agonists administration has been shown to induce a small bronchodilation in healthy athletes, the improved lung function does not induce any enhancement in performance. From my point of view is import-ant to raise awareness in all athletes, trough prevention and education programs, on the appropriate use of β2-agonists to avoid overuse of non-performance enhancing medications. This will ensure that athletes know health consequences of what they put in their bodies, not only for asthma treatment, but also for the adverse effects on physical performance.

10. What research or projects are you currently working on or should we look from you in the future?
I am currently concluding an experiment to determine the effects of acute administration of β2-agonists on human skeletal muscle during a fatiguing exercise. The results of the latter study would be divulged in the coming months.

Thanks Dr. Crivelli 

Asthma and Swimming: Know the Rules

Asthma is always a hot topic around the pool, whether formally diagnosed or whether used colloquially to describe a swimmer who habitually runs out of breath.  With many athletes taking asthma medications, it’s important to know the rules, even if you aren’t formally tested by regulatory agencies.   Respiratory issues garner even more attention during these winter months as more swimmers are driven indoors full time.  Asthma is also the most common chronic condition among all Olympic athletes, not only swimmers (Fitch 2012).  

For previous discussion here on asthma see An Interdisciplinary Look at Asthma and Swimming and Asthma and Swimmers.  To sum up previous writings, asthma is a multidimensional condition with biomechanical and psychological factors often neglected in favor of a narrow focus on pulmonary and respiratory elements.  Nonetheless, with many swimmers dutifully puffing from their inhalers to control asthma or even using medicine for performance enhancement, it is important to know the rules.   

While some of this may seem abstract to the average age grouper or masters swimmer, thousands of athletes are only one breakthrough performance away from finding themselves in USADA's national testing list (and if you’re fast enough for the officials to care what you’re putting in your body, that’s a good thing).  It behooves coaches and parents to remain abreast of testing requirements for health, performance, and compliance. 

In this post we’ll cover the basics of World Anti Doping Agency (WADA) requirements for asthma medications.  For complete information visit WADA or USADA.  Rules governing asthma medications have changed in recent years.  Some may cite politics, while others may point to recent studies indicating asthma medications confer no performance benefits on healthy athletes (Pluim 2011).  If there’s a lesson to be learned it’s that medication rules are a moving target … and you as the athlete are responsible for what you ingest.  Don’t make yourself a news item for the wrong reasons!

WADA’s asthma restrictions are simple yet complex: essentially, all beta-2 antagonists are PROHIBITED except “inhaled salbutamol (maximum 1600 micrograms over 24 hours), inhaled formoterol (maximum delivered dose 54 micrograms over 24 hours) and salmeterol when taken by inhalation in accordance with the manufacturers’ recommended therapeutic regimen.”  As for brand names, salbutamol is commonly known as Albuterol; formoterol better known as Foradil or Perforomist; selmeterol is sold as Serevent.
Despite these restrictions, athletes can apply for a Therapeutic Use Exemption, the core of which is a two-step testing process to demonstrate actual need.  A TEU would allow an athlete to legally use a beta-2 antagonist that’s not one of the three exceptions listed above.  First, an athlete must perform spirometry, or airflow testing.  A “12% or higher increase in FEV1 following the use of an inhaled beta-2 agonist is considered to be the standard diagnostic test for the reversibility of bronchospasm.” 

However, because high level athletes can demonstrate normal flow, yet still have asthma, a bronchial provocation test is available as a second layer to detect the condition.  A positive finding on any of the established bronchial provocation tests would qualify the athlete for the exemption, so long as other administrative requirements are met.  If the athlete has a negative result (no asthma diagnosis) on both tests, they may still submit a medical file for review by the agency. 

To complicate things further, the NCAA has its own rules, as it prohibits asthma medications that are otherwise permitted by WADA, but these medications may be allowed via prescription.  Check with department medical staff if in doubt, as the penalty could be loss of eligibility for a failed test and possibly sanctions for the team. 

Know the rules in this potentially thorny area as winter and indoor training oiten aggravate asthma-like symptoms.  Ensure that swimmers know both the legalities and the health consequences of what they put in their bodies, not only for asthma but for all conditions and performance enhancement.   

  1. K. D. Fitch. An overview of asthma and airway hyper-responsiveness in Olympic athletes. British Journal of Sports Medicine, 2012; 46 (6): 413
  2. Pluim BMde Hon OStaal JBLimpens JKuipers HOverbeek SEZwinderman AHScholten RJ.  Β2-Agonists  and physical performance: a systematic review and meta-analysis of randomized controlled trials.  Sports Med. 2011 Jan 1;41(1):39-57. doi: 10.2165/11537540-000000000-00000.

By Allan Phillips. Allan and his wife Katherine are heavily involved in the strength and conditioning community, for more information refer to Pike Athletics.

Nasal and Lung Functions in Swimming

Swimmers commonly have respiratory problems. I can not count the number of asthmatic swimmers on the side of a pool deck throughout my swimming career, huffing and puffing or just huffing...anyway the cause of respiratory disorders in swimming is believed to be caused by the chlorine, but there is limited evidence to support this claim. A recent study out of Italy (no wonder these big schnoz wanted to check nasal functions) looked at pre and post lung functions as well as questionnaires regarding these functions in swimmers and compared their results to visitors of the swimming pool. The results noted 18% of the participants reported nasal-sinusal symptoms following swimming, but there was not significant different in forced expiratory volume following swimming. In fact, the majority 70% of the swimmers experienced opening of the nasal cavity following swimming (most people have seen this in the pool when they have a cold and swimming helps decongest their symptoms) from the humidity and warm air temperature. Opening of the nasal cavity is the opposite affect as asthma since asthma constricts the respiratory system. One flaw of this study is it only looked at short term changes after one day of swimming, because some literature suggesting swimming greater than 30 hours a week increases the likelihood of asthma in swimmers. The authors stated
"Chlorine is a yellow-green gas, responsible for inflammation and oedema of the respiratory system. It is considered dangerous, when used at high concentrations in the industrial field . The irritating effect of chlorine, dissolved in the swimming pool water, is due to trichlorate nitrogen (NCl3) , to a lesser extent, to monochloramines and chloroform. The latter are produced when chlorine, in solution as hypochlorose acid, reacts together with organic contaminants, such as urine and sweat."
In conclusion, the authors saw no correlation between allergic reactions and swimming.

By the way, for all you pool managers here were the settings of their pool:
Humidity and temperature were constant in every evaluation, in particular water and air temperatures were respectively 28° and 27°C.The physicochemical analysis of the swimming-pool water was in the range of the recommended values; in particular.the water pH was constant at 7.6, free chlorine was 0.66 mg Cl2/l, combined chlorine was 0.2 mg Cl2/l and
nitrates were 6.3 mg NO3-/l.The swimming pool was equipped with an Unit Air Treatment.

1. Ondolo C, Aversa S, Passali F, et al. Nasal and lung function in competitive swimmers. Acta Otorhinolaryngol Ital. Jun 2009;29(3):137-143.

Swimming Detrimental to Asthma Suffers?

Take Home Points:

  1. Swimmers have a higher incidence of asthma.
The Journal of Brazil Pneumology investigated the incidence of asthma symptoms among amateur swimmers. In this study, the investigators surveyed and took expiratory volumes of a large group of swimmers on a club team in Brazil. People with asthma have been recommended to stay active to improve their respiratory function, more specifically they have been suggested to swim since the humid climate is believed to help with the brochodilation (however the best mode of exercise has yet to be identified). This study also found that 20% of the swimmers reported asthma symptoms, which is 2 times the rate of children who do not participate in sports in Brazil. This study concluded that their facility that used chlorine-based water elicited more asthma and airway irritation. This study also claims that swimming in a chlorine-based pool does not reduce symptoms of asthma suffers and increases the incidence of asthma like symptoms in amateur swimmers without asthma.

Every swimmer has known an asthma sufferer in practice, lying on the deck struggling to catch their breath. Is it too radical to say participating in swimming (in chlorine-based pools) is
 making their disease worse? I am curious to hear/see if any studies can be made on salt water pools or bromine based pools. What are your experiences in these conditions?


  1. Fiks IN, Santos LC, Antunes T, Gonçalves RC, Carvalho CR, Carvalho CR. Incidence of asthma symptoms and decreased pulmonary function in young amateur swimmers. J Bras Pneumol. 2009 Mar;35(3):206-12.
By G. John Mullen founder of the Center of Optimal Restoration, Swimming World Magazine Columnist, creator of the Swimmer's Shoulder System, and chief editor of the Swimming Science Research Review.