Showing papers by "Michael Kjaer published in 2006"

Muscle and blood metabolites during a soccer game: implications for sprint performance.

Abstract: Purpose: To examine muscle and blood metabolites during soccer match play and relate it to possible changes in sprint performance. Methods: Thirty-one Danish fourth division players took part in three friendly games. Blood samples were collected frequently during the game, and muscle biopsies were taken before and after the game as well as immediately after an intense period in each half. The players performed five 30-m sprints interspersed by 25-s recovery periods before the game and immediately after each half (N = 11) or after an intense exercise period in each half (N = 20). Results: Muscle lactate was 15.9 ± 1.9 and 16.9 ± 2.3 mmol·kg-1 d.w. during the first and second halves, respectively, with blood lactate being 6.0 ± 0.4 and 5.0 ± 0.4 mM, respectively. Muscle lactate was not correlated with blood lactate (r2 = 0.06-0.25, P >0.05). Muscle glycogen decreased (P < 0.05) from 449 ± 23 to 255 ± 22 mmol·kg-1 d.w. during the game, with 47 ± 7% of the muscle fibers being completely or almost empty of glycogen after the game. Blood glucose remained elevated during the game, whereas plasma FFA increased (P < 0.05) from 0.45 ± 0.05 to 1.37 ± 0.23 mM. Mean sprint time was unaltered after the first half, but longer (P < 0.05) after the game (2.8 ± 0.7%) as well as after intense periods in the first (1.6 ± 0.6%) and second halves (3.6 ± 0.5%). The decline in sprint performance during the game was not correlated with muscle lactate, muscle pH, or total glycogen content. Conclusion: Sprint performance is reduced both temporarily during a game and at the end of a soccer game. The latter finding may be explained by low glycogen levels in individual muscle fibers. Blood lactate is a poor indicator of muscle lactate during soccer match play.

Creatine supplementation augments the increase in satellite cell and myonuclei number in human skeletal muscle induced by strength training

Abstract: The present study investigated the influence of creatine and protein supplementation on satellite cell frequency and number of myonuclei in human skeletal muscle during 16 weeks of heavy-resistance training. In a double-blinded design 32 healthy, male subjects (19-26 years) were assigned to strength training (STR) while receiving a timed intake of creatine (STR-CRE) (n=9), protein (STR-PRO) (n=8) or placebo (STR-CON) (n=8), or serving as a non-training control group (CON) (n=7). Supplementation was given daily (STR-CRE: 6-24 g creatine monohydrate, STR-PRO: 20 g protein, STR-CON: placebo). Furthermore, timed protein/placebo intake were administered at all training sessions. Muscle biopsies were obtained at week 0, 4, 8 (week 8 not CON) and 16 of resistance training (3 days per week). Satellite cells were identified by immunohistochemistry. Muscle mean fibre (MFA) area was determined after histochemical analysis. All training regimes were found to increase the proportion of satellite cells, but significantly greater enhancements were observed with creatine supplementation at week 4 (compared to STR-CON) and at week 8 (compared to STR-PRO and STR-CON) (P<0.01-0.05). At week 16, satellite cell number was no longer elevated in STR-CRE, while it remained elevated in STR-PRO and STR-CON. Furthermore, creatine supplementation resulted in an increased number of myonuclei per fibre and increases of 14-17% in MFA at week 4, 8 and 16 (P<0.01). In contrast, STR-PRO showed increase in MFA only in the later (16 week, +8%) and STR-CON only in the early (week 4, +14%) phases of training, respectively (P<0.05). In STR-CRE a positive relationship was found between the percentage increases in MFA and myonuclei from baseline to week 16, respectively (r=0.67, P<0.05). No changes were observed in the control group (CON). In conclusion, the present study demonstrates for the first time that creatine supplementation in combination with strength training amplifies the training-induced increase in satellite cell number and myonuclei concentration in human skeletal muscle fibres, thereby allowing an enhanced muscle fibre growth in response to strength training.

Eccentric rehabilitation exercise increases peritendinous type I collagen synthesis in humans with Achilles tendinosis.

Abstract: It has been shown that 12 weeks of eccentric heavy resistance training can reduce pain in runners suffering from chronic Achilles tendinosis, but the mechanism behind the effectiveness of this treatment is unknown. The present study investigates the local effect of an eccentric training regime on elite soccer players suffering from chronic Achilles tendinosis on the turnover of the peritendinous connective tissue. Twelve elite male soccer players, of whom six suffered from unilateral tendinosis and six were healthy controls, participated in this study. All participants performed 12 weeks of heavy-resistance eccentric training apart from their regular training and soccer activity. Before and after the training period the tissue concentration of indicators of collagen turnover was measured by the use of the microdialysis technique. After training, collagen synthesis was increased in the initially injured tendon (n=6; carboxyterminal propeptide of type I collagen (PICP): pre 3.9+/-2.5 microg/L to post 19.7+/-5.4 microg/L, P 0.05). Collagen degradation, measured as carboxyterminal telopeptide region of type I collagen (ICTP), was not affected by training neither in the injured nor in the healthy tendons. The clinical effect of the 12 weeks of eccentric training was determined by using a standardized loading procedure of the Achilles tendons showing a decrease in pain in all the chronic injured tendons (VAS before 44+/-9, after 13+/-9; P<0.05), and all subjects were back playing soccer following the eccentric training regime. The present study demonstrates that chronically injured Achilles tendons respond to 12 weeks of eccentric training by increasing collagen synthesis rate. In contrast, the collagen metabolism in healthy control tendons seems not to be affected by eccentric training. These findings could indicate a relation between collagen metabolism and recovery from injury in human tendons.

Enhanced satellite cell proliferation with resistance training in elderly men and women

Abstract: In addition to the well-documented loss of muscle mass and strength associated with aging, there is evidence for the attenuating effects of aging on the number of satellite cells in human skeletal ...

Expression of insulin-like growth factor I, insulin-like growth factor binding proteins, and collagen mRNA in mechanically loaded plantaris tendon

Abstract: Insulin-like growth factor I (IGF-I) is known to exert an anabolic effect on tendon fibroblast production of collagen. IGF-I's regulation is complex and involves six different IGF binding proteins (IGFBPs). Of these, IGFBP-4 and -5 could potentially influence the effect of IGF-I in the tendon because they both are produced in fibroblast; however, the response of IGFBP-4 and -5 to mechanical loading and their role in IGF-I regulation in tendinous tissue are unknown. A splice variant of IGF-I, mechano-growth factor (MGF) is upregulated and known to be important for adaptation in loaded muscle. However, it is not known whether MGF is expressed and upregulated in mechanically loaded tendon. This study examined the effect of mechanical load on tendon collagen mRNA in relation to changes in the IGF-I systems mRNA expression. Data were collected at 2, 4, 8 and 16 days after surgical removal of synergistic muscle to the plantaris muscle of the rat, thus increasing the load to plantaris muscle and tendon. Nearly a doubling of the tendon mass was observed after 16 days of loading. A rapid rise in tendon procollagen III mRNA was seen after 2 days whereas the increase in procollagen I mRNA was significant from day 8. MGF was expressed and upregulated in loaded tendon tissue with a faster response than IGF-I, which was increased from day 8. Finally, IGFBP-4 mRNA was increased with a time pattern similar to procollagen III, whereas IGFBP-5 decreased at day 8. In conclusion, loading of tendon tissue results in an upregulation of IGF-I, IGFBP-4, and procollagen and is associated with an increase in tendon mass. Also, MGF is expressed with an early upregulation in loaded tendon tissue. We suggest that the IGF-I system could be involved in collagen synthesis in tendon in response to mechanical loading.

No effect of menstrual cycle on myofibrillar and connective tissue protein synthesis in contracting skeletal muscle

Abstract: We tested the hypothesis that acute exercise would stimulate synthesis of myofibrillar protein and intramuscular collagen in women and that the phase of the menstrual cycle at which the exercise took place would influence the extent of the change. Fifteen young, healthy female subjects were studied in the follicular (FP, n=8) or the luteal phase (LP, n=7, n=1 out of phase) 24 h after an acute bout of one-legged exercise (60 min of kicking at 67% W(max)), samples being taken from the vastus lateralis in both the exercised and resting legs. Rates of synthesis of myofibrillar and muscle collagen proteins were measured by incorporation of [(13)C]leucine. Myofibrillar protein synthesis (means+/-SD; rest FP: 0.053+/-0.009%/h, LP: 0.055+/-0.013%/h) was increased at 24-h postexercise (FP: 0.131+/-0.018%/h, P<0.05, LP: 0.134+/-0.018%/h, P< 0.05) with no differences between phases. Similarly, muscle collagen synthesis (rest FP: 0.024+/- 0.017%/h, LP: 0.021+/- 0.006%/h) was elevated at 24-h postexercise (FP: 0.073+/- 0.016%/h, P<0.05, LP: 0.072+/- 0.015%/h, P<0.05), but the responses did not differ between menstrual phases. Therefore, there is no effect of menstrual cycle phase, at rest or in response to an acute bout of exercise, on myofibrillar protein synthesis and muscle collagen synthesis in women.

The possible role of myostatin in skeletal muscle atrophy and cachexia

Abstract: The presence of sufficient skeletal muscle is of paramount importance for body function. Cachexia can be defined as a wasting syndrome describing the progressive loss of both adipose and skeletal muscle tissue in concert with severe injury, chronic or end-stage malignant and infectious diseases. Generally, cachexia predisposes to poor prognosis, co-morbidities and death. One signaling pathway possibly involved in muscle atrophy and cachexia is the myostatin cascade. This transforming growth factor-beta superfamily member myostatin is a strong candidate for regulating muscle mass, and is shown to inhibit muscle growth in different in vivo mammalian models. Overall, the modulation of the myostatin pathway seems interesting from the perspective of both pathology and sports medicine. Hence, myostatin signaling components and post-translational modulators are possible targets of pharmacological and other treatments against muscle loss, thus potentially contributing to the understanding and mitigation of muscle atrophies associated with inactivity, senescence and disease.

Corticosteroids Reduce the Tensile Strength of Isolated Collagen Fascicles

Abstract: BackgroundOveruse tendon injuries are frequent. Corticosteroid injections are commonly used as treatment, although their direct effects on the material properties of the tendon are poorly understood.PurposeTo examine the influence of corticosteroids on the tensile strength of isolated collagen fascicles.Study DesignControlled laboratory study.MethodsSingle strands (300-500 [.mu]m) of rat-tail collagen fascicles were incubated in either high (1 mL of 40 mgmL-1 mixed with 0.5 mL saline 9%) or low (1 mL of 40 mgmL-1 mixed with 2 mL saline 9%) concentration of methylprednisolone acetate (Depomedrol) for 3 or 7 days, while the control segment from the same fascicle was kept in saline (N = 64). After the incubation period, the fascicles underwent displacement to failure in a mechanical test rig at 0.13 mm/s, and thereafter hydroxylysyl pyridinoline and lysyl pyridinoline cross-link content was evaluated in a high-performance liquid chromatography system. Data for each group were analyzed with a 2-way analysis o...

Nitric oxide and prostaglandins influence local skeletal muscle blood flow during exercise in humans: coupling between local substrate uptake and blood flow

Abstract: Synergic action of nitric oxide (NO) and prostaglandins (PG) in the regulation of muscle blood flow during exercise has been demonstrated In the present study, we investigated whether these vasodi

Expression, content, and localization of insulin-like growth factor I in human achilles tendon.

Abstract: In animals insulin-like growth factor I (IGF-I) stimulates collagen production by fibroblasts and is expressed in tendons together with its binding protein 4 (IGFBP-4). However, the presence of IGF-I and IGFBP-4 in human tendon tissue is not described. Tissue IGF-I content was examined by immunoflourometric assay, real-time PCR, and immunohistochemistry used to localize and determine expression of IGF-I and IGFBP-4 in 6 postmortem human Achilles tendons. Tendon tissue concentrations of IGF-I were found to be 0.53 ± 0.10 ng/g. Furthermore, we demonstrated that IGF-I and IGFBP-4 are localized around the tendon fibroblasts and that mRNA for IGF-I and IGFBP-4 can be determined in human tendon tissue. The present study adds support for the roles of IGF-I and IGFBP-4 in the regulation of tendon adaptive responses to mechanical loading.

Passive knee joint range of motion is unrelated to the mechanical properties of the patellar tendon.

Abstract: The physiological factors that govern passive joint range of motion (ROM) are poorly understood. The present study investigated the relation between passive knee joint ROM and the mechanical properties of the patellar tendon. Knee joint ROM was assessed in 43 individuals, and the subjects with the greatest ROM (flexible group, n=10) and lowest ROM (inflexible group, n=10) were selected for further analysis. In these groups an overall "lower extremity joint ROM score" was determined with 11 clinical tests. The elongation of the patellar tendon was assessed during graded maximal isometric knee extensor contractions using ultrasonography, and the mechanical properties of the patellar tendon were determined from corresponding load and tendon deformation data. The two groups were similar with respect to weight, height, tendon cross-sectional area and length, and were, furthermore, equally physically active. The knee joint ROM and lower extremity joint ROM score was significantly different between the groups (flexible: 136+/-7 degrees vs inflexible: 76+/-16 degrees , P<0.001 and flexible: -4.7+/-1.3 vs inflexible: 3.1+/-4.1, P<0.001). There was no difference between groups in maximal knee extensor force or the corresponding tendon deformation. The tendon stiffness (flexible: 3269+/-1591 vs inflexible: 3185+/-1457 N/mm), stress (flexible: 22.4+/-6.5 vs inflexible: 34.0+/-17.6 N/mm(2)), strain (flexible; 6.5+/-1.6 vs inflexible: 7.2+/-1.9%) and Young's modulus (flexible: 0.81+/-0.35 vs inflexible: 1.22+/-0.52 GPa) were not different between the two groups of subjects. These data suggest that differences in knee joint ROM cannot be explained by the mechanical properties of the patellar tendon.

Sudden cardiac death associated with sports in young individuals: is screening the way to avoid it ?

Abstract: Worldwide the problem of sudden cardiac death associated with exercise in children, adolescents and young adults is currently debated, and individual cases are receiving marked media attention and will often result in a public demand to introduce measures to avoid further cases. Evidently such events of sudden cardiac deaths are unfortunate and tragic, and should be avoided as much as possible. The question is only, can they be avoided and what measures should be taken? It is important to underline that the long-term beneficial effects of regular physical training by far outweigh the acute risk for sudden cardiac death in the general population. Physical inactivity is one of the most important factors behind the development of life-style-associated diseases such as ischaemic heart disease, hypertension, diabetes, osteoporosis, obesity and metabolic syndrome. But evidently the occurrence of sudden death in young individuals during sports is alarming. Despite increased media attention in several countries there is no documentation that the number of cardiac deaths in young individuals should be increasing, and depending upon which country one looks at, the frequency is from 0.5 to 2 cases per 100 000 athletes per year (Corrado et al., 1998, 2003, 2005; Maron et al., 1998, 2003, 2005). Where complications to coronary vessel disease is the most common cause for sudden death in adults 435 years, the causes for exercise-associated cardiac death in individuals under 35 are related to inheritable hypertrophic cardiomyopathy, arythmogenic right ventricular dysplasia/cardiomyopathy (ARVD), myocarditis, contusio cordis and inborn abnormal coronary vessel position and rhythmic disturbances (Maron et al., 1998, 2003; Corrado et al., 2003). Evidently, the occurrence of sudden cardiac deaths calls for action, and in many countries its debated whether screening of young athletes is the answer. In Italy a systematic screening of young individuals participating in sports has existed for more than 20 years. In order to introduce screening several questions arise. First, although only one study has convincingly shown that because of some individuals being at risk, the immediate overall risk among exercising youths is somewhat higher than in nonexercising counterparts (Corrado et al., 2003), the question arises: Can this increased mortality be avoided by identifying diseases (e.g. cardiomyopathy) through screening ? Only few studies have solid documentation for the cause of these deaths, but in general hypertrophic cardiomyopathy represents a major fraction (8–30%), although it cannot be excluded that physiological athletic trained hypertrophic hearts have been falsely interpreted as hypertrophic cardiomyopathy (Maron et al., 1998, 2003; Corrado et al., 2003). A major problem in using, e.g. electrocardiogram (ECG) for screening, is that the well-trained athletic heart demonstrate a major overlap into pathological findings (Maron et al., 2005), and requires specialists interested in this area to distinguish differences between extreme physiological adaptation and pathology. Of the other causes for sudden death, only in an Italian investigation the fraction of individuals with ARVD has been shown to be very high (15–20%) (Corrado et al., 2003). The question now arises, whether screening tools for these diseases are valid. There are unfortunately no good documentation for sensitivity or specificity of the screening methods. The frequency of identified hypertrofic cardiomyopathy through screening (using anamnesis, ECG, echo-cardiography) is found to be between 0.07% and 0.17% (Maron et al., 1995, 2005; Corrado et al., 1998). A general screening of all individuals under 35 years that participate in competition sports – as done in Italy – has not been able to screen effectively for ARVD so far, and has not convincingly shown any ‘‘protective effect’’ toward diminishing the number of sudden cardiac deaths in young athletes (Corrado et al., 1998, 2003). It is important to note, that the mandatory screening system in Italy causes a high number of false-positive results. Based upon ECG screening, around 2% of all athletes were excluded from sports until further investigations had justified that they did in fact not suffer from a cardiac disease (Corrado et al., 2003). For identification of individuals at risk and the avoidance of one cardiac death, 4500 individuals were ‘‘grounded’’ from sports with Scand J Med Sci Sports 2006: 16: 1–3 COPYRIGHT & 2006 The Author Journal Compilation

Determination of markers for collagen type I turnover in peritendinous human tissue by microdialysis: effect of catheter types and insertion trauma

Abstract: Objectives: Previous results from our group have shown that loading of human tendon elevates tendinous type I collagen production measured by microdialysis. However, exclusion of the observed elevation as a response to trauma from inserting the microdialysis catheters or a possible influence from the collagen production in skin was not determined.Methods: Using the microdialysis method we measured the tissue levels of type I collagen metabolism markers [procollagen I COOH‐terminal propeptide (PICP) and COOH‐terminal telopeptide of type I collagen (ICTP)] in peritendinous tissue of the Achilles tendon in volunteers at two time points, 0 and 72 h. Using two different catheter types, an investigation of the contribution from the skin in the collagen results obtained was also examined.Results: The data showed no significant changes in the dialysate levels for PICP or ICTP (p>0.05) in either of the catheters.Conclusion: Inserting microdialysis fibres around the Achilles tendon twice does not increase the colla...

[The physically-inactive surgical patient].

Abstract: Major surgery is associated with a decrease in muscle strength, muscle mass and functional performance. However, early intervention with intensive physical training seems to counteract the loss in muscle mass and muscle function as well as to shorten the postoperative length of stay in hospital. In addition, a sufficient intake of protein seems to be a central element in the treatment of postoperative patients to reduce the protein degradation normally seen with immobilisation and surgery. Knowledge regarding the potential effect of preoperative physical activity is sparse.