Background: There are currently no effective disease-modifying drugs to prevent cartilage loss in osteoarthritis and synovial fluid is a potentially valuable source of biomarkers to understand the pathogenesis of different types of arthritis and identify drug responsiveness. The aim of this study was to compare the differences between SF cytokines and other proteins in patients with OA (n = 21) to those with RA (n = 27) and normal knees (n = 3). Methods: SF was obtained using ultrasound (US) guidance and an external pneumatic compression device. RA patients were categorized as active (n = 20) or controlled (n = 7) based upon SF white blood cell counts (> or <300 cells/mm3). Samples were cryopreserved and analyzed by multiplex fluorescent bead assays (Luminex). Between-group differences of 16 separate biomarker proteins were identified using ANOVA on log10-transformed concentrations with p values adjusted for multiple testing. Results: Only six biomarkers were significantly higher in SF from active RA compared to OA—TNF-α, IL-1-β IL-7, MMP-1, MMP-2, and MMP-3. Only MMP-8 levels in RA patients correlated with SF WBC counts (p < 0.0001). Among OA patients, simultaneous SF IL-4, IL-6, IL-8, and IL-15 levels were higher than serum levels, whereas MMP-8, MMP-9, and IL-18 levels were higher in serum (p < 0.05). Conclusion: These results support the growing evidence that OA patients have a pro-inflammatory/catabolic SF environment. SF biomarker analysis using multiplex testing and US guidance may distinguish OA phenotypes and identify treatment options based upon targeted inflammatory pathways similar to patients with RA.
Skeletal muscle glycogen (SMG) stores in highly glycolytic activities regulate muscle contraction by controlling calcium release and uptake from sarcoplasmic reticulum, which could affect muscle contraction. Historically, the assessment of SMG was performed through invasive and non-practical muscle biopsies. In this study we have utilized a novel methodology to assess SMG through a non-invasive high-frequency ultrasound. Nine MLS professional soccer players (180.4 ± 5.9 cm; 72.4 ± 9.3 kg; 10.4% ± 0.7% body fat) participated. All followed the nutritional protocol 24 h before the official match as well as performing the same practice program the entire week leading to the match. The SMG decreased from 80 ± 8.6 to 63.9 ± 10.2; p = 0.005 on MuscleSound® score (0–100) representing a 20% ± 10.4% decrease in muscle glycogen after match. Inter-individual differences in both starting glycogen content (65–90) and in percentage decrease in glycogen after the match (between 6.2% and 44.5%). Some players may not start the match with adequate SMG while others’ SMG decreased significantly throughout the game. Adequate pre-match SMG should be achieved during half-time and game-play in order to mitigate the decrease in glycogen. Further and more ample studies are needed before the application of this technology.
In our paper published in this journal, we present a pilot study application of a novel way to "indirectly assess" skeletal muscle glycogen based on the methodology that we developed though high-frequency skeletal muscle ultrasound [...].
HISTORY: 12 y/o soccer player presents to family medicine clinic with gradual onset of right hip pain for 1 week. Pain located over left lateral hip worse with walking and abduction movements. Able to play soccer through the pain. Denies a history of sudden onset, injury, trauma or mechanical symptoms. He was initially seen, diagnosed with a gluteus strain, and then returned to the clinic 2 weeks later due to worsening left hip pain, now unable to play soccer. PHYSICAL EXAMINATION: L Hip: TTP over greater trochanter and gluteus muscles. Non-TTP over the ASIS, AIIS. Full, symmetric ROM at hip. 5/5 strength w/ flexion/extension/adduction at the hip. Painful resisted abduction, and w/ contraction of the gluteus medius. Negative FABER, FADIR. Neg ober and snapping hip. Negative SLR, neural slump test. Sensation intact and symmetric over L3, L4, L5 S1 dermatomes. DIFFERENTIAL DIAGNOSIS: 1. Dystrophic soft-tissue calcification 2. Myositis ossificans 3. Extra-skeletal osteosarcoma 4. Soft tissue neoplasm TESTS AND RESULTS: 1. Xray L hip: Loculated calcification of the soft tissue lateral to left hip near AIIS. 2. Labs: CBC wnl. CRP 5.2, Sed Rate 67 2. MRI L hip/pelvis: A 4cm well-circumscribed partially ossified mass in the left deep gluteal compartment with large surrounding edema 3. CT L hip/pelvis: 4cm partially ossified mass. No osseous extension into acetabulum or proximal femur. Appearance favors myositis ossificans. Cannot r/o osteosarcoma. 4. Pathology: Core needle biopsy of L buttock mass: Low grade fibrous lesion with myxoid change. Immunihistory chemistry results recommend FISH to r/o low grade fibromyxoid sarcoma 5. FISH Interphase: No evidence of FUS rearrangement 6. Pathology: Open biopsy of L buttock mass: Most consistent with benign fibro-osseous tumor (myositis ossificans) FINAL WORKING DIAGNOSIS: Myositis Ossificans TREATMENT AND OUTCOMES: The case was reviewed by a multidisciplinary team including orthopedic surgery, oncology, and reading pathologist who concluded that this definitely represents a myositis ossificans with no current evidence of malignancy. -Resume activity and soccer as tolerated -PT to work on gluteus and abductor strengthening -In 4 months plan to repeat XR and MRI of pelvis to ensure findings parallel the natural history of myositis ossificans
Total blood levels of creatine kinase (CK) have been shown to be an effective biomarker to assess the degree of muscle damage in athletes. However, few studies exist in American football during the season and post-game PURPOSE: To study the evolution in total CK levels throughout different periods of the year, including pre-season, in-season and end of season METHODS: 48 Division 1 College level (Pac-12) football players (186.7 ± 7.1 cm, 105.3 ± 18.3 kg) had levels of total CK measured at four different periods. The first blood analysis (T1) was done in July in the midst of pre-season conditioning after student-athletes completed 3 weeks of weight training 3x per week, aerobic conditioning 2x per week, agility drills 2x per week and tactical preparation 2x per week. The second blood analysis (T2) was performed in August at the end of 3-week pre-season training camp when they were practicing 1-2x per day and weight training was done every day except during days with 2 practices. The intensity and volume of training during this period was 15% and 25% respectively lower respect T1. The third blood analysis (T3) was performed in the middle of the season 48h post-game where they practiced 6x per week and maintenance resistance training 2x week. The fourth test (T4) was done at the end of last week of the season with same training regime as T4 RESULTS: CK levels were 725.2 ± 641.8 U/L (normal laboratory reference range up to 250U/L) for T1, 1187.7 ± 827.1 for T2, 992.2 ± 791.7 U/L for T3 and 652.8 ± 453.8 U/L for T4. The percentage of players with CK levels more than 1,000 U/L were 15%, 43.9%, 29.3% and 25% for T1, T2, T3 and T4 respectively CONCLUSIONS: These results suggest that there is considerable degree of muscle damage in football players during pre-season as well as during season, which could result in a decrease in performance and increased injury risk. The standard deviations observed in the four analyses are remarkable, suggesting an important range in variability to the response to training and competition among football players of a same team which could be due to individual differences in assimilation of workload and competition. Our data shows that individualization and monitoring of training is important in college football and that monitoring for CK could be a useful method to monitor and prevent muscle injuries in NCAA football players
INTRODUCTION: Proper glycogen stores are an essential element in athletic performance as shown in the scientific literature for many years. Recently, the role of glycogen in controlling muscle contraction has been shown as glycogen regulates calcium release from sarcoplasmic reticulum which could interfere with performance. However, regular assessment of glycogen content in athletes has not been possible due to the invasive nature of muscle biopsies or the cost of nuclear magnetic resonance spectroscopy (NMRS). Recently, we have developed and validated a novel methodology to assess muscle glycogen through high frequency skeletal muscle ultrasound in a fast, portable and non-invasive manner (1). In this study we evaluated the changes in skeletal muscle glycogen content in professional (MLS) soccer players after a soccer match. METHODS: 9 professional soccer players (MLS) (189.2 ± 9.1 cm, 74.1 ± 7.6 kg) from different positions were assessed for skeletal muscle glycogen in the rectus femoris (RF) muscle before and after a game (all played the entire game) through high frequency ultrasound scans using MuscleSound® technology. PURPOSE: To assess changes in skeletal muscle glycogen before and after a professional soccer game. RESULTS: Average RF glycogen content decreased from 68.3 ± 7.9 points (MuscleSound® score points) before the game to 55.6 ±9.1 points after the game (p=0.006). All players decreased glycogen content at various rates, -7.2 to -40%. CONCLUSION: During a soccer game skeletal muscle glycogen content decreases at various rates among players which could be attributable to different factors such as metabolic differences in substrate utilization, game demand and/or differences in carbohydrate replacement during the game. The assessment of skeletal muscle glycogen in soccer players could be beneficial to individualize nutrition during the game.
In 2011, the Centers for Disease Control and Prevention reported approximately 25.8 million children and adults in the United States were affected by diabetes mellitus, making diabetes one of the most prevalent chronic diseases in our population.1Centers for Disease Control and PreventionNational Diabetes Fact Sheet: National Estimates and General Information on Diabetes and Prediabetes in the United States, 2011. US Department of Health and Human Services, Atlanta, GA2011Google Scholar Although people with type 1 diabetes mellitus (DM1) constitute a small percentage of this population, the majority of them are involved in various levels of athletic activities, including endurance sports.2Chansky M.E. Corbett J.G. Cohen E. Hyperglycemic emergencies in athletes.Clin Sports Med. 2009; 28: 469-478Abstract Full Text Full Text PDF PubMed Scopus (8) Google Scholar The American Diabetes Association published a position statement in 2004 reinforcing the fact that persons with DM1 can participate in all levels of activity granted that they have no complications of their diabetes and are in good glycemic control.3American Diabetes AssociationPhysical activity/exercise and diabetes.Diabetes Care. 2004; 27: 58-62PubMed Google Scholar Subsequent to this position statement, there have been a few articles discussing the recommended management of glycemic control in diabetic patients participating in endurance sports.2Chansky M.E. Corbett J.G. Cohen E. Hyperglycemic emergencies in athletes.Clin Sports Med. 2009; 28: 469-478Abstract Full Text Full Text PDF PubMed Scopus (8) Google Scholar, 3American Diabetes AssociationPhysical activity/exercise and diabetes.Diabetes Care. 2004; 27: 58-62PubMed Google Scholar, 4Devadoss M. Kennedy L. Herbold N. Endurance athletes and type 1 diabetes.Diabetes Educ. 2011; 37: 193-207Crossref PubMed Scopus (17) Google Scholar However, only a few papers have reported case series of athletes with DM1 in endurance and ultraendurance sports.4Devadoss M. Kennedy L. Herbold N. Endurance athletes and type 1 diabetes.Diabetes Educ. 2011; 37: 193-207Crossref PubMed Scopus (17) Google Scholar, 5Boehncke S. Poettgen K. Maser-Gluth C. Reusch J. Boehncke W.H. Badenhoop K. Endurance capabilities of triathlon competitors with type 1 diabetes mellitus [in German]..Dtsch Med Wochenschr. 2009; 134: 677-682Crossref PubMed Scopus (25) Google Scholar, 6Vlahek P. Car S. Ostroski I. Sweet 452 km—a report on the first type 1 diabetes patient to finish Double Ironman, a 30-hour endurance triathlon race.Croat Med J. 2013; 54: 306-307Crossref PubMed Scopus (15) Google Scholar The purpose of the present study was to report the number and performance of athletes with DM1 who participated in the Leadville 100 races. The Leadville 100 consists of a 161-km mountain bike race and a 161-km ultramarathon in Leadville, Colorado, in August of each year. The courses range in altitude from 2800 m to 3840 m, and the majority are on forest trails with some mountain roads.7Khodaee M. Myers R. Spittler J. Lee J.A. Hill J.C. Yeakel D. Risk factors for injuries in a high-altitude ultramarathon.Br J Sports Med. 2011; 45: 355-356Crossref Google Scholar The Leadville 100 mountain bike race starts at 6:30 am on the second Saturday of each August. Participants should finish the race within 12 hours to be able to successfully complete the race. The Leadville 100 ultramarathon starts at 4:00 am of the third Saturday of each August. Runners should finish the race within 30 hours to be able to successfully complete the race. All Leadville 100 race participants have to report their medical history and medication use through an electronic medical check-in before the race. A medical team reviews the responses for any potential risks for participation before the race. At-risk athletes are counseled during the medical check-in before the race. After reviewing our database, we included all self-described athletes with DM1 who reported being on insulin from 2011 to 2013 in the study. We excluded athletes with type 2 diabetes who reported being on insulin. We performed a descriptive analysis of demographics and unpaired t test to compare our study population to all other athletes of these two races. The Colorado Multiple Institutional Review Board and the Leadville 100 race approved this study. From 2011 to 2013, a total of 7215 athletes competed in the Leadville 100 races. Of these, 5194 athletes (4851 mountain bikers and 2364 runners) were able to successfully complete the races (72%). Nineteen athletes reported having DM1. Only 2 runners with DM1 started the race more than once (2011 and 2012, and 2012 and 2013). Both runners who were not able to finish the race on their first attempt were able to successfully complete the race the next year. The other 15 athletes with DM1 only participated once during the 2011–2013 period. The Figure illustrates the comparison of athletes with DM1 to all other athletes. The majority of the participants with DM1 were male, with average age of 39 years (range 22 to 61 years). The majority (68.4%) of athletes with DM1 were able to successfully complete the race. The average finish time for mountain bike and run for DM1 athletes, respectively, was 10 hours, 36 minutes (range 8 hours, 44 minutes, to 11 hours, 45 minutes), and 27 hours, 54 minutes (range 24 hours, 45 minutes, to 29 hours, 52 minutes). Because of the small number of athletes with DM1, including or excluding them from the entire population did not change any statistics (eg, completion rate). There was no statistically significant difference for successfully completing the races between athletes with DM1 and all other athletes (odds ratio 0.84; 95% confidence interval, 0.32 to 2.22). Ultraendurance events are growing in popularity. It is inevitable that athletes with chronic diseases, including DM1, who desire to push their limits will be encountered. In the retrospective, self-reported enrollment data from an ongoing longitudinal observational study, 0.7% of ultramarathon runners reported having diabetes (type of diabetes was not reported).8Hoffman M.D. Krishnan E. Health and exercise-related medical issues among 1,212 ultramarathon runners: baseline findings from the Ultrarunners Longitudinal Tracking (ULTRA) study.PLoS One. 2014; 9: e83867Crossref PubMed Scopus (79) Google Scholar There have been only a handful of reported cases of athletes with DM1 who completed endurance races.5Boehncke S. Poettgen K. Maser-Gluth C. Reusch J. Boehncke W.H. Badenhoop K. Endurance capabilities of triathlon competitors with type 1 diabetes mellitus [in German]..Dtsch Med Wochenschr. 2009; 134: 677-682Crossref PubMed Scopus (25) Google Scholar, 6Vlahek P. Car S. Ostroski I. Sweet 452 km—a report on the first type 1 diabetes patient to finish Double Ironman, a 30-hour endurance triathlon race.Croat Med J. 2013; 54: 306-307Crossref PubMed Scopus (15) Google Scholar, 9Graveling A.J. Frier B.M. Risks of marathon running and hypoglycaemia in type 1 diabetes.Diabet Med. 2010; 27: 585-588Crossref PubMed Scopus (29) Google Scholar, 10Grimm J.J. Muchnick S. Type I diabetes and marathon running.Diabetes Care. 1993; 16: 1624Crossref PubMed Scopus (10) Google Scholar This number is much smaller for ultraendurance races.5Boehncke S. Poettgen K. Maser-Gluth C. Reusch J. Boehncke W.H. Badenhoop K. Endurance capabilities of triathlon competitors with type 1 diabetes mellitus [in German]..Dtsch Med Wochenschr. 2009; 134: 677-682Crossref PubMed Scopus (25) Google Scholar, 6Vlahek P. Car S. Ostroski I. Sweet 452 km—a report on the first type 1 diabetes patient to finish Double Ironman, a 30-hour endurance triathlon race.Croat Med J. 2013; 54: 306-307Crossref PubMed Scopus (15) Google Scholar To our knowledge, this is the largest number of reported athletes with DM1 who participated in 161-km mountain bike and run races. It appears that athletes with DM1 are able to compete in ultraendurance events. Owing to its retrospective nature, our report has limitations connected to this type of study. When planning medical coverage for these ultraendurance events—which frequently have remote, difficult-to-access courses over a single track, mountain passes, and densely wooded areas—medical teams should be prepared to manage unusual, but serious circumstances such as hypoglycemia.11Khodaee M. Ansari M. Common ultramarathon injuries and illnesses: race day management.Curr Sports Med Rep. 2012; 11: 290-297Crossref PubMed Scopus (36) Google Scholar Many athletes with DM1 use insulin pumps and frequent or continuous glucose monitoring to stay on top of their insulin and caloric needs, and they can complete these ultraevents with few issues. However, that should not be assumed, because often athletes with DM1 are not aware of guidelines on how to manage glycemic fluctuations during long exercises and can run into serious problems with glycemic control.4Devadoss M. Kennedy L. Herbold N. Endurance athletes and type 1 diabetes.Diabetes Educ. 2011; 37: 193-207Crossref PubMed Scopus (17) Google Scholar Close glycemic and dietary monitoring before and during the race is the key to avoid complications.12Marcason W. Is there a recommended target range for blood glucose for the type 1 diabetic endurance athlete?.J Acad Nutr Diet. 2012; 112: 2092Abstract Full Text Full Text PDF PubMed Scopus (6) Google Scholar Further prospective studies focusing on metabolic and physiologic changes as a result of these extreme exercises among athletes with DM1 are required. We would like to thank Mr Joshua Colley and Lifetime Fitness for allowing us to conduct this study, and we also thank our study participants.
The letter by Khodaee et al1Khodaee M. Riederer M. VanBaak K. Hill J.C. Ultraendurance athletes with type 1 diabetes: Leadville 100 experience.Wilderness Environ Med. 2015; 26: 273-275Abstract Full Text Full Text PDF PubMed Scopus (11) Google Scholar nicely describes the performance of 19 athletes with type 1 diabetes (DM1) out of 7215 total athletes competing in the 2011–2013 Leadville 100, a 161-km mountain bike race and 161-km ultramarathon run. There was no statistical difference between the 68.4% completion rate of the DM1 athletes and the other endurance athletes. However, concern was expressed in this letter about awareness of, or adherence to, diabetes management guidelines. Education for DM1 patients on multiple daily injections or pumps usually (or should) include exercise instructions for reduced insulin basal needs, carbohydrate boluses, and correction boluses as well as increased use of glucose monitoring, target ranges of glucose to avoid hypoglycemia, and calorie intake. All of this is labor-intensive. Insulin adjustments are highly individualized and involve some trial and error, but are helped especially by the ever-increasing sophistication of insulin pumps, pump trainer/educators, and pump users. Guidelines by the American Diabetes Association2American Diabetes AssociationStandards of medical care in diabetes—2014.Diabetes Care. 2014; 37: S14-S80Crossref PubMed Scopus (3680) Google Scholar are expectedly generalized. More specifics are available, for example, from other sources about endurance athletes with DM1.3Devadoss M. Kennedy L. Herbold N. Endurance athletes and type 1 diabetes.Diabetes Educ. 2011; 37: 193-207Crossref PubMed Scopus (17) Google Scholar In the arduous Leadville 100, perhaps the patient-provider(s) relationship, the Internet, social media, and personal experience offered detailed advice for individual insulin management. Or perhaps information was available from Team Novo Nordisk, a global all-diabetes sports team of cyclists, triathletes, and runners, spearheaded by the world’s first all-diabetes professional cycling team and sponsored by the Danish insulin manufacturer Novo Nordisk.4Team Novo Nordisk. Racing with diabetes. Available at: http://www.teamnovonordisk.com/. Accessed July 13, 2015.Google Scholar I agree with the authors that further studies are needed, but they are hard to come by in such a setting. Until that day arrives, are there any practical tips that can be gleaned from their review? For example, was there any prerace diabetes planning vs actual implementation to change doses of insulin before, during, and after the event when hypoglycemia can still strike? As most were probably pump users, were pump basal infusions reduced and by how much, or temporarily suspended? Were carb boluses cut, say, in half? Were square-wave profiles used rather than simple boluses? Were insertion site set failures common? Were continuous glucose-monitoring systems that measure interstitial glucose levels accurate or useful in this dynamic setting? This was a retrospective study with limitations, and such information may not be available from the entire group, but even individual or anecdotal information would be helpful for both providers and athletes with DM1. Thank you.
Serum biomarkers fluctuate as a result of running marathons, but their changes during ultramarathons have not been adequately studied. We collected blood samples from 20 participants before and 21 participants after the 161-km ultramarathon in Leadville, Colorado in August 2013. Using a portable analyzer, we measured cardiac troponin I (cTnl), hematologic, and metabolic biomarkers. Out of 10 runners for whom we collected both pre- and post-race samples, 8 were able to successfully complete the race. Mean cTnl increased from 0.001 to 0.047ng/mL (p=0.005). Mean sodium decreased from 141 to 138mmol/L (p<0.01). However, all runners had a sodium of 135 mmol/L post-race (reference range 138-146mmol/L). Mean creatinine increased from 0.93 to 1.17mg/dL (p<0.05). Only one out of 10 runners had an abnormal creatinine level of 1.8 mg/dL post-race (reference range 0.6-1.3mg/dL). The other parameters did not reach statistical significance. Analyzing the samples from 21 runners after the race revealed that runners who finished the race in faster time had higher cTnl levels compared to those who finished the race close to the 30-hour cut-off finish time (P=0.005). Running an ultramarathon caused significant changes in cardiac and metabolic parameters. Ultramarathon running intensity and finish time may have effects on post-race cTnl level.
INTRODUCTION: Glycogen stores are a key element in athletic performance. Scientific literature shows the classic role of glycogen depletion in performance. Furthermore, recent research shows that glycogen controls muscle contraction by regulating calcium release from sarcoplasmic reticulum. However, regular assessment of glycogen content in athletes has not been possible due to the invasive nature of muscle biopsies or the cost of nuclear magnetic resonance spectroscopy (NMRS). Recently, we have developed and validated a novel methodology to assess muscle glycogen through high frequency skeletal muscle ultrasound in a fast, portable and non-invasive manner (1). In this study we evaluated the changes in skeletal muscle glycogen content in football players after a division 1 collegiate football game. METHODS: 10 college (Pac12) American football players (189.2 ± 9.1 cm, 122.6 ± 27.3 kg) from different positions were assessed for skeletal muscle glycogen in the rectus femoris (RF) muscle before and after a game through high frequency ultrasound scans using MuscleSound® technology. PURPOSE: To assess changes in skeletal muscle glycogen before and after a collegiate level football game. RESULTS: Average RF glycogen content decreased from 72.5 ± 7.9 points (MuscleSound® score points) before the game to 63 ±11.6 points after the game (p<0.05). Only 3 players were able to maintain pre-game RF glycogen content while 7 players decreased glycogen content at various rates, -6.2 to -40%. CONCLUSIONS: Skeletal muscle glycogen content decreases at various rates among players during a football game. This could be attributable to different factors such as metabolic differences in substrate utilization, game demand and/or differences in carbohydrate replacement during the game. The assessment of skeletal muscle glycogen in football players could be beneficial to individualize nutrition during the game.
We read with enthusiasm the letter from Dr Lankford1Lankford HV. In response to Ultraendurance athletes with type 1 diabetes: Leadville 100 experience, by Khodaee et al. Wilderness Environ Med. 2015;26:588Google Scholar in response to our recently published letter to the editor “Ultraendurance athletes with type 1 diabetes: Leadville 100 experience.”2Khodaee M. Riederer M. VanBaak K. Hill J.C. Ultraendurance athletes with type 1 diabetes: Leadville 100 experience.Wilderness Environ Med. 2015; 26: 273-275Abstract Full Text Full Text PDF PubMed Scopus (11) Google Scholar We are pleased that our findings have started to generate discussion among clinicians and researchers. As Dr Lankford mentioned in his letter, there is a lack of specific guidelines for endurance athletes with type 1 diabetes mellitus (DM1).1Lankford HV. In response to Ultraendurance athletes with type 1 diabetes: Leadville 100 experience, by Khodaee et al. Wilderness Environ Med. 2015;26:588Google Scholar Anecdotally, most of our athletes with DM1 did not use insulin pumps. Although we had glucose monitoring capabilities at our medical aid stations, most of our athletes with DM1 used their own glucose monitors. Unfortunately, we are unable to answer any other specific questions raised by Dr Lankford owing to the retrospective nature of our study. We hope this reply has made it clear that until we have large-scale prospective studies, an individualized and well-thought-out plan designed and reviewed by the athletes with DM1, the athletes’ physicians, and the race medical team should be used to achieve optimal glycemic control during these long races. In addition to the standard medical alert bracelets, we recommend using medical wristbands for each athlete highlighting the information about pertinent medical conditions, medications, and allergies.3Hoffman M.D. Pasternak A. Rogers I. et al.Medical services at ultra-endurance foot races in remote environments: medical issues and consensus guidelines.Sports Med. 2014; 44: 1055-1069Crossref PubMed Scopus (80) Google Scholar
Introduction While exertional rhabdomyolysis (ER) can occur with any strenuous exercise, it is more common with exercise involving repetitive eccentric contractions than with concentric contractions (5). ER is the result of the breakdown of skeletal muscle fibers due to overexertion with muscle destruction, necrosis, loss of cell membrane integrity, and displacement of intracellular contents into the extracellular space (1). ER is a syndrome entailing muscle soreness, weakness, and possibly brown urine (13). Complications of ER may include acute kidney injury (AKI), compartment syndrome, hyperkalemia, disseminated intravascular coagulation (DIC), and hypocalcemia (1). Diagnosis of rhabdomyolysis is made by clinical evidence of muscle damage and the presence of circulatory muscle cell content including creatine kinase (CK) and myoglobin (16). Elevation in serum myoglobin declines rapidly and may not be present at the time of presentation. Urine myoglobin test may take several days so it cannot be relied upon for treatment decisions. It is generally acknowledged that an increase in CK of five times the upper limit of normal, with symptoms of muscle pain or muscle weakness, and dark urine in the setting of strenuous activity are indicative of ER (3,14). Case Presentation A sedentary 32-year-old Caucasian woman presented with bilateral upper extremity swelling 4 d after initiating a new exercise program. The patient’s workout was supervised by a personal trainer and consisted of intense upper body eccentric exercises, which included multiple sets of pull ups. The patient noted dull achy pain localized from her mid-upper arms to lower forearms beginning 2 h postworkout and gradual swelling at the same locations that progressed over the following 4 d. Over the course of the 4 d, her pain abated, but she developed upper extremity stiffness and slight intermittent tingling in her hands. She did not notice color changes over the affected area, cramping, or weakness. She did report a few episodes of mild swelling localized to her shoulders following previous workouts. The patient denied any trauma, immunizations, extraordinary events, or changes to her routine over the week leading up to her symptoms. She was in good health with no recent history of fevers and malaise. She was not taking any supplements or medications. She had normal stools and bowel movements with no recent nausea and vomiting. She reported no decrease in urine output and no urine color changes. The patient’s physical examination was positive for bilateral upper extremity nonpitting edema from her mid-upper arms to the distal forearms (Fig. 1a and b). The right side was more pronounced than the left. There was no tenderness to palpation over the affected area. She had full painless passive and active range of motion of her wrists, elbows, and shoulders bilaterally. No upper extremity muscle weakness was appreciated. Sensation was intact to light touch and pin prick throughout the upper extremities. Triceps, biceps, and brachioradialis deep tendon reflexes were 2+ and equal bilaterally. Bilateral brachial and radial pulses were regular, strong, and symmetric.Figure 1: (A and B) Bilateral upper extremity edema from mid-upper arms to distal forearm bilaterally 4 d postexercise. (C) Resolution ofedema 14 d postexercise.On the day the patient presented to the clinic, a urine analysis, basic metabolic panel, complete blood count, and CK levels were assessed. The urine dipstick was positive for trace blood. Microscopic urinalysis was negative for red blood cells, which is likely consistent with myoglobinuria. The patient’s CK was 21,300 U·L−1, and liver markers were mildly elevated (Table). The patient’s creatinine and blood urea nitrogen were within normal limits. A diagnostic musculoskeletal ultrasound of the patient’s upper extremities using a linear transducer (Philips L12-3 MHz) revealed subcutaneous edema that was more significant on the right side (Fig. 2). The ultrasound appearance of the upper extremity musculature was normal with organized fascicular architectures (Fig. 2). There were no hypoechoic or hyperechoic foci in any of the muscles examined. Humeral, radial, and ulnar cortexes were normal with no irregularities.Table: Laboratory values.Figure 2: Edema presented in longitudinal view of (A) anterior right arm (epidermis, dermis, and subcutaneous depth of 0.56 cm) and (B) volar aspect of right midforearm (epidermis, dermis, and subcutaneous depth of 0.793 cm).The patient was treated with observation, oral hydration, and restricted physical activity. She was seen in the clinic 10 d after her initial visit. Laboratories were drawn 4 and 10 d following her initial visit. Within 10 d of her first visit, her symptoms had completely abated. On day 10, she had no swelling on examination and her laboratory values returned to normal limits (Fig. 1c). She was able to resume normal activities by day 10, and at 6 months, she reported no further episodes or exacerbations. Discussion There have been only a few reported cases of isolated upper extremity ER (9,10,14,19). Contrary to our case, all of these cases reported pain as a major symptom. Another important feature of this case was the presence of substantial amount of subcutaneous edema. Clinical presentation of edema has been reported in a few cases of rhabdomyolysis (9,10,12,15,18). However pain seemed to be present in all cases (9,10,12,15,18). Other causes of subcutaneous edema like congestive heart failure, cellulitis, thrombosis, myositis, and drug-induced myopathy should be considered in cases with clinical suspicion for ER. Ultrasonic appearance of our case was consistent with a significant subcutaneous edema with no noticeable intramuscular edema or abnormality. Ultrasonic features of rhabdomyolysis include homogenous decreased echogenicity, areas of hyperechogenic foci, disorganized muscle fibers, and edema within the muscle (17,18). Lamminen et al. (11) examined the use of imaging modalities in the diagnosis of rhabdomyolysis and found out that the sensitivities of magnetic resonance imaging (MRI), computed tomography (CT), and ultrasound in the detection of rhabdomyolysis were 100%, 62%, and 42%, respectively. Presence of subcutaneous edema on MRI, CT, and ultrasound has been reported in few cases of rhabdomyolysis (9,11,12,15,18). However all of these cases showed substantial evidence of characteristic muscle damage on imaging modalities (9,11,12,15,18). The complications of rhabdomyolysis can be severe and grave. Severe electrolyte imbalance (e.g., hyperkalemia and hypocalcemia), arrhythmia, and DIC are rare complications of rhabdomyolysis. AKI is a common and important complication of ER. The incidence of AKI in patients with rhabdomyolysis is approximately 5% to 7% (16). AKI occurs in the setting of rhabdomyolysis as a result of serum myoglobin levels exceeding 100 mg·dL−1 (16). At this level, tubule epithelial myoglobin metabolization capacity is overwhelmed and filtered myoglobin accumulates in the tubules leading to tubule damage, AKI, and myoglobinuria (1). Serum CK levels correlate with myoglobin levels, and CK is the preferred marker over myoglobin because of its longer half-life, cost, and laboratory properties (4,5,16). Myoglobinuria occurs when CK levels approach 70,000 U·L−1 (16). The risk of AKI from any form of rhabdomyolysis is low when serum CK levels are less than 20,000 U·L−1 (4,6,7). Most reported cases of ER that result in AKI have occurred in patients with coexisting medical conditions (4,6,7). Underlying conditions that may increase the risk of AKI include dehydration, nonsteroidal anti-inflammatory drug (4) use, heat, and genetic conditions (1,4–7). Sickle cell trait is a major risk factor for ER (4,13). Repetitive sprints or timed laps may cause exertional sickling and eventually ischemia in athletes with sickle cell traits (7). Levels of serum CK up to 100,000 U·L−1 have been reported in healthy individuals with no renal complications (4). These findings suggest that elevated or extremely elevated CK levels in the setting of ER in healthy individuals may not be predictive of renal failure (1,4–6). There is no consensus on the CK serum level that will precipitate AKI and warrant hospital admission (1,2,4,6). It remains unclear why the incidence of ER is relatively high among untrained individuals performing repetitive eccentric exercise (4). ER is a potential life-threatening syndrome that may present with nonspecific clinical features like muscle pain, tenderness, and swelling. Screening is performed with urine dipstick and microscopy. Early recognition and prompt management are critical to prevent potential complications. More scientific studies are needed to further understand the clinical course of ER. Conclusion Patients with ER can present variably, sometimes including minimal pain and normal renal function. Musculoskeletal ultrasound is an inexpensive rapid office diagnostic tool that can aid in evaluation of a patient suspected of having ER. Severe complications from ER in patients with no coexisting medical conditions are rare (8). Patients presenting with ER with no comorbidity can be managed in the outpatient setting, with close serial monitoring, oral hydration, and restricted physical activity. Complications of rhabdomyolysis can be severe in patients with underlying medical conditions, and clinical judgment must be exercised on a case-by-case basis when determining the management of a patient presenting with ER. The authors declare no conflicts of interest and do not have any financial disclosures.
UNLABELLED:Glycogen storage is essential for exercise performance. The ability to assess muscle glycogen levels should be an important advantage for performance. However, skeletal muscle glycogen assessment has only been available and validated through muscle biopsy. We have developed a new methodology using high-frequency ultrasound to assess skeletal muscle glycogen content in a rapid, portable, and noninvasive way using MuscleSound (MuscleSound, LCC, Denver, CO) technology. PURPOSE:To validate the utilization of high-frequency musculoskeletal ultrasound for muscle glycogen assessment and correlate it with histochemical glycogen quantification through muscle biopsy. METHODS:Twenty-two male competitive cyclists (categories: Pro, 1-4; average height, 183.7 ± 4.9 cm; average weight, 76.8 ± 7.8 kg) performed a steady-state test on a cyclergometer for 90 minutes at a moderate to high exercise intensity, eliciting a carbohydrate oxidation of 2-3 g·min⁻¹ and a blood lactate concentration of 2 to 3 mM. Pre- and post-exercise glycogen content from rectus femoris muscle was measured using histochemical analysis through muscle biopsy and through high-frequency ultrasound scans using MuscleSound technology. RESULTS:Correlations between muscle biopsy glycogen histochemical quantification (mmol·kg⁻¹) and high-frequency ultrasound methodology through MuscleSound technology were r = 0.93 (P < 0.0001) pre-exercise and r = 0.94 (P < 0.0001) post-exercise. The correlation between muscle biopsy glycogen quantification and high-frequency ultrasound methodology for the change in glycogen from pre- and post-exercise was r = 0.81 (P < 0.0001). CONCLUSION:These results demonstrate that skeletal muscle glycogen can be measured quickly and noninvasively through high-frequency ultrasound using MuscleSound technology.
An increasing participation in ultra-endurance foot races is cause for greater need to ensure the presence of appropriate medical care at these events. Unique medical challenges result from the extreme physical demands these events place on participants, the often remote settings spanning broad geographical areas, and the potential for extremes in weather conditions and various environmental hazards. Medical issues in these events can adversely affect race performance, and there is the potential for the presentation of life-threatening issues such as exercise-associated hyponatremia, severe altitude illnesses, and major trauma from falls or animal attacks. Organization of a medical support system for ultra-endurance foot races starts with a determination of the level of medical support that is appropriate and feasible for the event. Once that is defined, various legal considerations and organizational issues must be addressed, and medical guidelines and protocols should be developed. While there is no specific or universal standard of medical care for ultra-endurance foot races since a variety of factors determine the level and type of medical services that are appropriate and feasible, the minimum level of services that each event should have in place is a plan for emergency transport of injured or ill participants, pacers, spectators and event personnel to local medical facilities.
BackgroundLittle is known about the effect of injuries during training on ultramarathon performance.ObjectiveDetermine effects of injuries during training on race performance.DesignObservational study using a self-administered pre-race survey. Finish times were obtained from race results posted online.SettingThe 2013 Leadville Trail 100 (LT100) and Western States Endurance Run (WSER).ParticipantsParticipants of LT100 and WSER 161 km ultramarathons.Risk factor assessmentAge, gender, educational level, prior completion of a 161 km ultramarathon, shoe type, self-report of foot strike pattern, and injuries or illnesses interfering with training in the past year were considered.Main outcome measurementsThe primary outcome measure was whether sustaining an injury or illness resulting in missed training days affected successful completion of an ultramarathon.ResultsOut of 1206 LT100 and 408 WSER entrants, 893 and 368 completed the pre-race survey (73.9% and 90.1%, respectively). Most participants were male (82%) with average age of 41 years. 52.3% of LT100 and 72.3% of WSER starters finished the races under the 30 hour cutoff time. Among respondents, 40% had masters or higher degrees and 45% reported using dietary supplements on a regular basis. Respondents reported 1432 (multiple answers per runner) injury episodes causing less than a week of missed training and 641 injury episodes causing a week or longer of missed training in the past year. Pain in Achilles (n=196), lower iliotibial band (n=164), upper hamstring (n=115), and groin pain (n=106) were the most common reported issues interfering with training. Only 45 (2.8%) of respondents reported sustaining a stress fracture during training in the past year. Of these, 27 (60%) involved the metatarsals and 10 (22%) involved the tibia. Using a binary logistic regression model, sustaining an injury during the training, age, gender, educational level, prior completion of a 161 km ultramarathon, shoe type, and self-report of foot strike pattern did not affect finish status (P>.05).ConclusionsMany ultramarathon runners sustain injuries and illnesses interfering with training schedule, but this does not seem to be a predictor of successfully completing the race.
Background Despite increased ultramarathon participation in recent years, little is known about causes of race incompletion. This study surveyed runners of three 161–168 km ultramarathons in Europe and North America to explore characteristics and issues that affected race performance. Objective Determine human and environmental factors related to failure to complete ultramarathons of ∼161 km in the previous year. Design Observational study using surveys prior to the race. Setting The 2013 Ultra-Trail du Mont-Blanc ® (UTMB ® ) in Europe; Leadville Trail 100 (LT100) and Western States Endurance Run (WSER) in North America. Participants Out of 4 110 race entrants, 2 794 (69%) completed the pre-race survey. Risk factor assessment In this epidemiologic study, we report the incidence of intrinsic and extrinsic factors related to failure to finish of at least one ∼161 km race in the previous year. Main outcome measurements The main outcome measurements were self-reported reasons for not finishing the race. Results Among respondents, about 30% had masters or higher degrees. Out of 2,469 UTMB ® , 1206 LT 100, and 408 WSER entrants, the majority successfully completed the race (68%, 52% and 72%, respectively). Among participants who responded, 18.3% reported they failed to complete an ultramarathon of ∼161km in the past year. The main reasons for dropping out were inability to make the cut off time (23.1%), nausea and/or vomiting (16.5%), injury during the race (16.5%), and an ongoing injury (13.3%). Conclusions We conclude that primary performance-limiting issues in 161–168 km ultramarathons include inability to make the cut off time, nausea and/or vomiting, and injury before and during the race.
Background: The purpose of this paper was to assess the feasibility of Micro-Mobile Compression (R) (MMC) on lactate clearance following exhaustive exercise and on subsequent exercise performance.Methods: Elite male cyclists were randomized to MMC (n = 8) or passive recovery (control, n = 8). MMC is incorporated into a sandal that intermittently compresses the venous plexus during non-weight bearing to augment venous return. On day 1, subjects performed a graded exercise test on a cycle ergometer followed by 60 minutes of seated recovery, with or without MMC. Blood lactate concentration ([La-]) was measured during exercise and recovery. Subjects returned home for 3 more hours of seated recovery, with or without MMC. On days 2 and 3, subjects exercised to exhaustion in a fixed-load cycle ergometer test at 85% peak power and then repeated the day 1 post-exercise recovery procedures. Lactate clearance data after the time to exhaustion tests on days 2 and 3 were averaged to adjust for interday variation.Results: On the day after MMC or control recovery, mean time to exhaustion was 15% longer (mean difference, 2.1 minutes) in the MMC group (P = 0.30). The standardized mean difference of MMC for time to exhaustion was 0.55, defined as a moderate treatment effect. Following the graded exercise test, area under the 60-minute lactate curve was nonsignificantly lower with MMC (3.2 +/- 0.4 millimolar [mM]) versus control (3.5 +/- 0.4 mM, P = 0.10) and times from end of exercise to 4mM and 2mM were 2.1 minutes (P = 0.58) and 7.2 minutes (P = 0.12) shorter, although neither achieved statistical significance. Following time to exhaustion testing, the area under the 60-minute lactate curve was lower with MMC (3.2 +/- 0.2 mM) versus control (3.5 +/- 0.2 mM, P = 0.02) and times from end of exercise to 4mM and 2mM were 4.4 minutes (P = 0.02) and 7.6 minutes (P < 0.01) faster. The standardized mean difference of MMC on most lactate clearance parameters was >0.8, defined as a large treatment effect.Conclusion: MMC yields large treatment effects on lactate clearance following high-intensity exercise and moderate treatment effects on subsequent exercise performance in elite male cyclists.