Effects of acute,intermittent exercise in hypoxic environments on the release of cardiac troponin

The purpose of this study was to examine the effects of acute, intermittent exercise performed in hypoxic environments on the release of cardiac troponin (cTn). Ten well‐trained, male marathon runners (22.1 ± 2.6 years, 64.0 ± 4.9 kg and 177.3 ± 3.9 cm) completed three intermittent exercise protocols under normoxic (trial N) and hypoxic (trial AH and RH) conditions. In trial N, the fraction of inspiration oxygen (FIO₂) was 21.0% and exercise intensity was 90% and 50% normoxic velocity of VO_2max (vVO_2max). In trial AH, FIO₂ was 14.4% (simulated altitude of 3000 m) and exercise intensity was 90% and 50% normoxic vVO_2max. In trial RH, FIO₂ was 14.4% and exercise intensity was 90% and 50% hypoxic vVO_2max. High‐sensitivity cardiac troponin T (hs‐cTnT) and cardiac troponin I (cTnI) were measured pre‐ and 0, 2, 4, and 24 h post‐exercise. Hs‐cTnT was elevated in all three trials, peaking at 2 to 4 h and returning to the baseline 24 h post‐exercise. CTnI increased in trial AH, peaking at 2 to 4 h and returning below the detection limit 24 h post‐exercise. It is concluded that the stimulus of hypoxia did not in and of itself induce more cTn to be released, but exercise intensity could affect this response in hypoxic environments.     

The impact of remote ischemic preconditioning on cardiac biomarker and functional response to endurance exercise

Remote ischemic preconditioning (RIPC; repeated short reversible periods of ischemia) protects the heart against subsequent ischemic injury. We explored whether RIPC can attenuate post‐exercise changes in cardiac troponin T (cTnT) and cardiac function in healthy individuals. In a randomized, crossover design, 14 participants completed 1‐h cycling time trials (TT) on two separate visits; preceded by RIPC (arms/legs, 4 × 5‐min 220 mmHg), or SHAM‐RIPC (20 mmHg). Venous blood was sampled before and 0‐, 1‐, and 3‐h post‐exercise to assess high sensitivity (hs‐)cTnT and brain natriuretic peptide (NT‐proBNP). Echocardiograms were performed at the same time points to assess left and right ventricular systolic (ejection fraction; EF and right ventricular fractional area change; RVFAC, respectively) and diastolic (early transmitral flow velocities; E) function. Baseline hs‐cTnT was not different between RIPC and SHAM. Post‐exercise hs‐cTnT levels were consistently lower following RIPC (18 ± 3 vs 21 ± 3; 19 ± 3 vs 23 ± 3; and 20 ± 2 vs 25 ± 2 ng/L at 0, 1 and 3‐h post‐exercise, respectively; P < 0.05). There was no main effect of time, trial, or interaction for NT‐proBNP and left ventricular EF or RVFAC (all P < 0.05). A main effect of time was evident for E which transiently declined immediately after exercise to a similar level in both trials (0.85 ± 0.04 vs 0.74 ± 0.04 m/s, respectively; P < 0.05). In summary, RIPC was associated with lower hs‐cTnT levels after exercise but there was no independent effect of RIPC for NT‐proBNP or LV systolic and diastolic function. The lower hs‐cTnT levels after RIPC suggests that further research should evaluate the role of ischemia in exercise‐induced elevation in hs‐cTnT.     

Serum cardiac troponin T, troponin I, plasma BNP and left ventricular mass index in professional football players

Concentrations of cardiac troponins (cTn) in serum or plasma may be elevated in several disease states other than acute coronary syndromes. In heart failure and end stage renal disease, cardiac troponin T (cTnT) correlates positively with left ventricular mass index (LVMI). Exercise-induced elevation of cardiac troponins in well-trained athletes has been confirmed by several reports but the aetiology and clinical significance is unclear. In the present study, we measured baseline concentrations of cardiac markers and investigated whether or not serum cTnT is associated with left ventricular hypertrophy (LVH) in professional football players. METHODS: Twenty-three male professional football players with a mean age of 23 years (range 18-32) were studied. Echocardiography and blood sampling were carried out approx 24h after a training session. Serum cTnT, other cardiac markers and plasma brain natriuretic peptide (BNP) were compared with LVMI. RESULTS: cTnT was only detectable in one subject. The prevalence of elevated cardiac troponin I (cTnI), creatine kinase MB (CKMB) and creatine kinase was higher than for cTnT. cTnI concentrations were higher in football players than in controls. LVMI did not correlate with any of the cardiac markers. Plasma BNP concentrations were normal in all subjects. CONCLUSION: Serum cTnT concentrations were not elevated in healthy professional football players with LVH. This argues against the hypothesis that LVH per se may cause increased cTnT. The finding of higher cTnI in football players than in non-athletic controls should be confirmed and the aetiology elucidated.     

Serum cardiac troponin response in adolescents playing basketball

Cardiac troponin release is generally found in adult athletes after continuous-type endurance exercises or sport competitions. The purpose of this study was to investigate whether the physical stress experienced by adolescents while playing basketball, an intense, intermittent-type sport, could induce transient elevations of the serum cardiac troponin T (cTnT) and I (cTnI). Serum cTnT and cTnI levels in 10 male adolescent players (age 15.0 +/- 0.7 yr) were assessed immediately before and at 2, 4 and 24 h after a game randomly selected from a preseason basketball-training program. At 4 h following the game, serum cTnT levels in four of the ten subjects were above the cutoff of 0.01 ng . ml (-1) for myocardial injury. Two of these four subjects had values higher than the acute myocardial infarction cutoff of 0.05 ng . ml (-1). In three of the four subjects, the serum cTnI was above the cutoff of 0.06 ng . ml (-1) for myocardial injury. Nevertheless, serum cardiac troponins at 24 h had returned to pre-exercise levels. These findings suggest that the physical stress encountered during intense, intermittent-type sports could cause release of cardiac troponins in some adolescents at low risk for cardiac disease.     

High‐sensitivity troponin T in marathon runners,marathon runners with heart disease and collapsed marathon runners

Endurance exercise is an established cause of cardiac troponin (cTn) elevation, of further interest is whether this rise represents clinical significance. This study compared cTnT rise in three cohorts of marathon runners using a high‐sensitivity assay; control runners, those with known heart disease and runners who collapsed at the finish line. Control runners (n = 126) and runners with heart disease (n = 12) were prospectively recruited with cTnT levels measured pre‐race and at race completion. Collapsed runners (n = 15) were retrospectively recruited. A mixed model ANCOVA was used to compare the three groups. Pre‐race median cTnT for the control group and heart disease groups was 3.9 ng/L (IQR 3.1 ng/L) and 4.1 ng/L (IQR 3.4 ng/L). Post‐race values for the three groups were control 45.6 ng/L (IQR 42.5 ng/L), heart disease 41.2 ng/L (IQR 36.1 ng/L), and collapsed 41.9 ng/L (IQR 57.8 ng/L). Post‐race cTnT and cTnT change were significantly correlated with pre‐race cTnT within the control group (r = 0.38 and 0.30, P < 0.01). There was no difference in post‐race cTnT (adjusted for pre‐race cTnT) between the three groups. None of the runners reported symptoms suggestive of acute myocardial infarction on follow‐up. These results demonstrate that marathon running is associated with an asymptomatic cTnT rise for all runners, and this rise is significantly correlated to baseline cTnT levels, in addition, marathon runners with pre‐existing cardiac pathology or who collapse at the finish line do not exhibit an increased cTnT rise compared to healthy runners.     

Evidence of exercise-induced cardiac dysfunction and elevated cTnT in separate cohorts competing in an ultra-endurance mountain marathon race

Cardiac damage has recently been implicated in the aetiology of "exercise induced cardiac dysfunction". The humoral markers of cardiac damage that have been utilised to date are not sufficiently cardio-specific to investigate this hypothesis. The aim of the present study was to examine cardiac function following prolonged exercise, and investigate the contention of cardiac damage utilising a new highly cardio-specific marker. Thirty-seven competitors in the 2-day Lowe Alpine Mountain Marathon 2000 volunteered for the study. Competitors were sub-divided into 2 groups. Group 1 (n = 11) were examined using echocardiography pre and post the event, examining left ventricular diastolic and systolic function. Group 2 (n = 26) had venous blood samples drawn prior to the event and immediately following day-1 and day-2. Blood samples were analysed for total creatine kinase activity (CK), creatine kinase isoenzyme MB(mass) (CK-MB(mass)), and cardiac troponin T. Echocardiographic results indicated left ventricular diastolic and systolic dysfunction following cessation of exercise. CK and CK-MB(mass) were both elevated following day-1, and immediately following race completion. Cardiac troponin T levels were below the 99th percentile (0.01 microg/L) in all subjects prior to the event, following day-1 cTnT was elevated above 0.01 microg/L in 13 subjects, but returned to below 0.01 microg/L following race completion on day-2. However, no individual data reached clinical cut-off levels for acute myocardial infarction (AMI) (0.1 microg/L). Two days arduous exercise over mountainous terrain resulted in cardiac dysfunction, and significant skeletal muscular degradation. The elevation of cTnT above the 99th percentile in the present study is suggestive of minimal myocardial damage. The clinical significance of and exact mechanism responsible for such damage remains to be elucidated.     

Elevation of serum N-terminal pro-brain natriuretic peptide after exercise is an index of myocardial damage or a cytoprotective reflection?

AIM: Recent investigations have suggested the occurrence of transient cardiac dysfunction and reversible myocardial injury in healthy individuals after heavy exercise. Our purpose was to examine if the release of N-terminal pro-brain natriuretic peptide (NT-proBNP) after intense exercise in obviously healthy participants may have cytoprotective and growth-regulating effects or may result from myocardial dysfunction/damage with changes in cTnT as a marker for myocardial cell necrosis during exercise. METHODS: In 43 highly-trained male athletes <35 years old, who were examined immediately after exercising as well as 2 days later, 21 age-matched male patients classified as stage-B according to ACC/AHA guidelines and 35 healthy age-matched males, we evaluated NT-proBNP and 3rd generation's cTnT by electrochemiluminescence immunoassay. All participants underwent a detailed cardiac protocol including echocardiography and electrocardiogram (ECG). RESULTS: In athletes, cTnT consistently remained <0.01 mg/L after exercising as well as after 2 days. NTproBNP immediately after exercising was 58.27+/-19.48 ng/L, without reaching pathological levels, decreasing 2 days later to 22.93+/-10.22 ng/L. Our patients maintained high levels of NTproBNP, as much as a six-fold increase with reference to the levels of our study's control group and with cTnT <0.01 mg/L. In the control group, cTnT and NTproBNP levels were statistically similar with those of the athletes 2 days after exercising. NT-proBNP as a biological marker can reliably discriminate pathological from physiological cardiac hypertrophy. CONCLUSION: A normal plasma concentration of NT-proBNP in consecutive routine check-up, before and after exercise, could minimize the possibility of cardiac dysfunction, whereas persistent elevated plasma concentrations warrant further cardiological evaluation.     

高原肺水肿治疗前后血清心肌肌钙蛋白T的变化

目的 探讨诊断和判别高原肺水肿（ＨＡＰＥ）状态的新指标。方法 在海拔３７００ｍ处对８例ＨＡＰＥ患者在治疗前及临床治愈后分别测定血清肌酸激酶同功酶（ＣＫ－ＭＢ）和ｃＴｎＴ两项指标。结果 ＨＡＰＥ患者血清ＣＫ－ＭＢ和ｃＴｎＴ临床治愈后较治疗前均降低,二者间的差别有非常显著性意义（Ｐ〈０．０１）。结论 ＨＡＰＥ时存在心肌损伤,血清ｃＴｎＴ是一项具有高灵敏度、高特异性的血清心肌损伤标志物,对ＨＡＰＥ的诊断、病情分析有一定的价值。     

Exercise-induced cardiac troponin T release: a meta-analysis

PURPOSE: Cardiac troponin T (cTnT) is a highly specific marker of myocardial damage and used clinically in the diagnosis of acute myocardial infarction (AMI). Release of cTnT has been demonstrated in several small studies after endurance exercise. The purpose of this study was to explore, using a meta-analytic approach, the incidence of postexercise cTnT release after endurance exercise. METHODS: Articles identified via Pubmed, SportDiscus, and Embase (1997-2006) searches using the key words cardiac troponin T, cTnT, cardiac biomarkers, and exercise; a search of bibliographies; and consultation with experts in the field were entered into a random-effects meta-analysis. We identified 26 relevant studies (1120 cases). Age, gender, and body mass of participants, as well as exercise mode and duration, were explored as possible moderator variables with meta-regressions. RESULTS: Postexercise cTnT levels exceeded the assay detection limit in 47% of participants (95% CI = 39-56%). The detection of postexercise cTnT after cycling events was approximately half that of running events (27 vs 52%, P = 0.042). The detection of postexercise cTnT decreased slightly as event duration increased (P = 0.022) and mean body mass decreased (P = 0.0033). Postexercise detection of cTnT was not affected by age (P= 0.309) and was only slightly higher for studies with more males in the sample (P = 0.028). CONCLUSIONS: Exercise-induced cTnT release is apparent in almost half of the endurance athletes who have been studied to date. Relatively heavy individuals competing in shorter endurance events, primarily running marathons, are slightly more likely to demonstrate elevated cTnT postexercise than other athletes. These data are useful for clinicians evaluating athletes with cTnT elevations after competitive endurance exercise events.     

The standing knee lift test is not a useful screening tool for time loss from low back pain in youth basketball and floorball players

ObjectivesThe aim of this study was to investigate the association between pelvic kinematics during the standing knee lift (SKL) test and low back pain (LBP) in youth floorball and basketball players.DesignA prospective cohort study.SettingFinnish elite youth floorball and basketball players.ParticipantsFinnish elite youth female and male floorball and basketball players (n = 258, mean age 15.7 ± 1.8).Main outcome measuresLBP resulting in time loss from practice and games was recorded over a 12-month period and verified by a study physician. Associations between LBP and sagittal plane pelvic tilt and frontal plane pelvic obliquity during the SKL test as measured at baseline were investigated. Individual training and game hours were recorded, and Cox’s proportional hazard models with mixed effects were used for the analysis.ResultsCox analyses revealed that sagittal plane pelvic tilt and frontal plane pelvic obliquity were not associated with LBP in floorball and basketball players during the follow-up. The hazard ratios for pelvic tilt and pelvic obliquity ranged between 0.93 and 1.08 (95% CIs between 0.91 and 1.07 and 0.83 and 1.29), respectively.ConclusionsPelvic movement during the SKL test is not associated with future LBP in youth floorball and basketball players.     

Exercise-associated increases in cardiac biomarkers

At present, the risk of myocardial damage by endurance exercise is under debate because of reports on exercise-associated increases in cardiac biomarkers troponin and B-type natriuretic peptide (BNP); these markers are typically elevated in patients with acute myocardial infarction and chronic heart failure, respectively. Exercise-associated elevations of cardiac biomarkers can be present in elite and in recreational athletes, especially after prolonged and strenuous endurance exercise bouts (e.g., marathon and ultratriathlon). However, in contrast to cardiac patients, it is still unclear if the exercise-associated appearance or increase in cardiac biomarkers in obviously healthy athletes represents clinically significant cardiac insult or is indeed part of the physiological response to endurance exercise. In addition, elevations in cardiac biomarkers in athletes after exercise may generate difficulties for clinicians in terms of differential diagnosis and may result in inappropriate consequences. Therefore, the aim of this article is to provide an overview of exercise-associated alterations of the cardiac biomarkers troponin T and I, ischemia-modified albumin, BNP, and its cleaved inactive fragment N-terminal pro BNP for the athlete, coach, scientist, and clinician.     

Resting and post‐exercise serum biomarkers of cardiac and skeletal muscle damage in adolescent runners

This study examined the response of serum biomarkers of cardiac and skeletal muscle damage at rest and after a routine workout of 21 km run in 12 male adolescent (16.2±0.6 years) long‐distance runners. Biomarkers of cardiac [troponins (cTnT, cTnI), creatine kinase MB mass (CK‐Mbmass)] and skeletal muscle [creatine kinase (CK), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and hydroxybutyrate dehydrogenase (HBD)] damage were assayed at rest, 2, 4 and 24 h post‐exercise. At rest, cTnT and cTnI were not detectable; however, CK, CK‐MBmass, AST, ALT and HBD were above corresponding clinical cut‐off values. Post‐exercise significant elevations above rest were observed for all biomarkers, except ALT, 2 and 4 h following the run, and remained elevated in cTnI, CK, CK‐MBmass, LDH and AST 24 h post‐workout. A significant increase in data points above clinical cut‐off values from rest to post‐exercise was reported for cTnT, cTnI and CK at 2 and 4 h, and in cTnI and CK 24 h post‐exercise. In conclusion, a 21 km run in adolescent runners increased post‐exercise biomarkers of cardiac and skeletal muscle damage.     

The impact of exercise duration and intensity on the release of cardiac biomarkers

Numerous studies have observed cardiac biomarker release with prolonged exercise. Despite this, we are unsure as to the constituent aspects of any given exercise bout that may be important in promoting cardiac biomarker release. This study examined the influence of exercise duration and intensity on the appearance of cardiac biomarkers. Twenty‐one subjects ran for 45, 90 and 180 min at 85% and 95% of their individual anaerobic threshold on six different days randomized. Cardiac troponin I (cTnI) and N‐terminal pro‐brain natiuretic peptide (NT‐proBNP) were assayed from blood samples collected before, 30 min and 3 h post‐exercise. NT‐proBNP was elevated after all exercise trials (range before: 21–32; range post: 38–67 ng/L). Peak post‐exercise concentrations of NT‐proBNP were associated with exercise duration (P=0.049), but not exercise intensity (P=0.451). cTnI was elevated after all exercise trials (range before: 0.007–0.011; range post: 0.008–0.021 μg/L). Peak post‐exercise concentrations of cTnI were associated with exercise duration (P=0.003) and intensity (P=0.037). Data suggest that while both cTnI and NT‐proBNP increased after all exercise trials, the mediating effect of duration influenced both NT‐proBNP and cTnI while intensity influenced only cTnI.     

Changes in serum cardiac troponins following a 21-km run in junior male runners

AIM: This study was designed to examine the appearance and clearance characteristics of serum cardiac troponin T (cTnT) and I (cTnI) in junior runners after an exhaustive 21-km run. The dependence of the alternations of the cardiac troponins on the runners' training status reflected in training years, running ability and physiological profile at ventilatory threshold (Th(vent)) was also examined. METHODS: Ten trained male adolescents (16.2+/-0.6 years) performed 21-km run and graded treadmill exercise with maximum effort on two different days. cTnT and cTnI immediately before and 2, 4 and 24 hours after exercise were measured in the 21-km trial. The parameters at Thvent including the running speed (Th(vent)-Speed) and VO2 (Th(vent)-VO2) were identified in the graded exercise trial. RESULTS: Serum cTnT and cTnI in 6 of the 10 subjects measured 4 hours after the 21-km run were above the myocardial injury cutoffs of 0.03 and 0.09 ng x mL(-1), respectively, but returned towards pre-exercise levels within 24 hours that were not in the same manner observed in the clinical situation of myocardial infraction. The 6 subjects' training status was generally lower than that of the rest 4. Further, subjects' 4-h serum cTnT and cTnI were negatively related to their training years, Th(vent)-Speed and Th(vent)-VO2, and positively related to their personal best in half- and full-marathon races (r2 = or > 36%, n = 10). CONCLUSIONS: Such findings implied that clinicians based the diagnosis of long-distance run-induced myocardial infraction in novice junior runners upon the transient postexercise elevations of cardiac troponins alone should be with caution.     

Myocardial stress after competitive exercise in professional road cyclists

PURPOSE: Based on the determination of cardiac troponin (cTnT), brain natriuretic peptide (BNP), and echocardiographic measurements, recent investigations have reported myocardial damage and reversible cardiac dysfunction after prolonged endurance exercise in apparently healthy subjects. In the present study, we investigated the myocardial stress reaction in professional endurance athletes after strenuous competitive physical exercise. METHODS: Eleven highly trained male professional road cyclists (age 27 +/- 4 yr; .VO2peak 67 +/- 5 mL.kg-1.min-1; training workload 34,000 +/- 2,500 km.yr-1) were examined. The following parameters were determined before and after one stage of a 5-d professional cycling race: BNP, cTnT (third-generation assay that shows no cross reactivity with skeletal TnT), creatine kinase (CK), creatine kinase MB (CKMB), myoglobin (Myo), and urea. All participants were submitted to a careful cardiac examination including echocardiography and stress ECG. RESULTS: None of the athletes showed pathological findings in the cardiac examination. CK (P < 0.01), CKMB (P < 0.05), and Myo (P < 0.01) were increased after the race. Normal postexercise cTnT levels indicate that the increase in CK, CKMB, and Myo was of noncardiac origin. In contrast, BNP rose significantly from 47.5 +/- 37.5 to 75.3 +/- 55.3 pg.mL-1 (P < 0.01). Pre- and postexercise values of BNP as well as the individual exercise-induced increase in BNP were significantly correlated with age (R2 = 0.68, R2 = 0.66, and R2 = 0.58, respectively; P < 0.05). CONCLUSION: Strenuous endurance exercise in professional road cyclists does not result in structural myocardial damage. The rise in BNP in older athletes may reflect a reversible, mainly diastolic left ventricular dysfunction. This needs to be confirmed by larger trials including different intensities, sports, and age groups.     

Cardiac troponin T release after prolonged strenuous exercise

Over the past 2 decades, there has been a large interest in cardiac troponin T (cTnT) elevations, which are often seen following endurance sport events. There have been many reports on this topic, although sometimes with different approaches. We reviewed the available literature on cTnT elevations after prolonged strenuous exercise and discovered profound differences in the percentage of subjects reported to have elevated cTnT concentrations. This could partly be attributed to differences in immunoassay characteristics, such as cross-reactivity with skeletal troponin T, and the use of different cut-off values used in the different studies. The elevations were transient, with levels decreasing to pre-event concentrations within 24-48 hours. This might be explained by the relatively short half-life of cTnT, or water imbalance during and after the event. The release mechanism of cTnT, as well as the long-term positive or negative effects, remains unclear. Future research should therefore be aimed at clarifying the release mechanism of cTnT. Furthermore, the benefits and the possible long-term negative aspects of prolonged exercise should be evaluated.     

Allopurinol prevents cardiac and skeletal muscle damage in professional soccer players

Xanthine oxidase (XO), a free radical‐generating enzyme, is involved in tissue damage produced during exhaustive exercise. Our aim was to test whether allopurinol, a powerful inhibitor of XO, may be effective in preventing exercise‐induced tissue damage in soccer players. Twelve soccer players were randomized into two experimental groups. One received allopurinol, before a match of the premier Spanish Football League, and the other placebo. Allopurinol prevented the exercise‐induced increase in all the markers of skeletal muscle damage analyzed: creatine kinase, lactate dehydrogenase, aspartate aminotransferase, and myoglobin. Creatine kinase‐MB isoenzyme and highly sensitive troponin T, specific biomarkers of myocardial injury, increased significantly in the placebo but not in the allopurinol‐treated group after the football match. We also found that the exercise‐induced lipid peroxidation, as reflected by malondialdehyde measurements, was prevented after allopurinol administration. However, inhibition of XO did not prevent the increment in the activity of alanine aminotransferase found after the match. No changes in the serum gamma glutamyltransferase activity was found after the match on either the placebo and the allopurinol groups. These two enzymes were determined as biomarkers of liver injury. Allopurinol represents an effective and inexpensive pharmacological agent to prevent tissue damage in soccer players.     

Injury risk in female floorball: a prospective one-season follow-up

The purpose of this prospective study was to examine the incidence, nature, causes, and severity of injuries in female floorball. Three hundred and seventy-four licensed female floorball players from Finnish top leagues were observed prospectively for one season (6 months). The practice and game hours of floorball were recorded on an exercise diary. All injuries were registered with a structured questionnaire and verified by a physician. During the study period, 133 out of the 374 (35%) players sustained 172 injuries. The injury incidence was 1.8 per 1000 practice hours and 40.3 per 1000 game hours. Of all injuries, 70% were traumatic and 30% were from overuse. The most common injury type was joint sprain (27%). The most commonly injured sites were the knee (27%) and ankle (22%). Twenty-one of the knee injuries (46%) were serious including 10 anterior cruciate ligament (ACL) ruptures. Eight of ACL ruptures occurred during floorball games, giving an ACL rupture incidence of 3.6 per 1000 game hours. Eleven injuries (6%) needed hospital admission. The study attested that injury rate in floorball game is very high. Injury prevention strategies in female floorball should be targeted at injuries occurring at the knee and ankle.     

Injuries in Swedish floorball: a cost analysis

The epidemiology of sport injuries is well documented. However, the costs are rarely discussed. Previous studies have presented such costs in specific sports or localization. No study has investigated the costs related to injuries in elite floorball. Thus, the aim of this study was to estimate cost of injuries in Swedish elite floorball players. During 1 year, 346 floorball players were prospectively followed. All time‐loss injures were recorded. The injured players were asked to complete a questionnaire regarding their costs tied to the injury. Mean costs were calculated by multiplying the total resource use with the collected unit costs and dividing these total costs with the number of injuries as well as players. The results showed that the average cost per injury increased with the level of severity and ranged from 332 to 2358 Euros. The mild and moderate overuse injuries were costlier than the corresponding traumatic injuries. However, the severe traumatic injuries were associated with higher costs than overuse injuries. Knee injuries were the costliest. Our results indicate that there are costs to be saved, if floorball injuries can be avoided. They should be of interest to decision makers deciding whether to invest in preventive interventions.