Gymnastik- och idrottshögskolan, GIH

The insulin-like growth factor (IGF)-IGF binding proteins (BP) and the pituitary-gonadal axes were investigated during ultra endurance exercise in 16 endurance-trained athletes (seven women). Median duration of the race was 6.3 days. Although food and drink were ad libitum, energy balance was negative. Blood samples were drawn before (PRE), at the end of (END) and 24 h after (POST24h) the race. Serum concentrations of total IGF-I (t-IGF-I) and free IGF-I (f-IGF-I) decreased by 33 (SD 38)% and 54 (19)%, respectively. The decrease in t-IGF-I appeared to be associated to the total energy deficit during the race. At END, the IGFBP-3 fragmentation and IGFBP-1 were increased but these changes did not predict changes in f-IGF-I. An increase in POST24h IGFBP-2 levels in women was the only sex difference. Testosterone was decreased by 67 (12)% in the men and estradiol became undetectable in the women without any detectable increase in LH and/or FSH. In conclusion ultra endurance exercise results in similar IGF-IGFBP responses in men and women reflecting a catabolic state. IGFBP-2 was the only exception, with increased levels in women after exercise. A concomitant decrease in gonadal hormones was not related to endocrine changes in the IGF-IGFBP axis but may be related to local changes in IGF-I expression.

This investigation was designed to evaluate changes in plasma and muscle levels of free amino acids during an ultra-endurance exercise and following recovery. Nine male ultra-endurance trained athletes participated in a 24-h standardized endurance trial with controlled energy intake. The participants performed 12 sessions of running, kayaking and cycling (4 x each discipline). Blood samples were collected before, during and after exercise, as well as after 28 h of recovery. Muscle biopsies were taken 1 week before the test and after exercise, as well as after 28 h of recovery. During the 24-h exercise, plasma levels of branched-chain (BCAA), essential amino acids (EAA) and glutamine fell 13%, 14% and 19% (P<0.05) respectively, whereas their concentrations in muscle were unaltered. Simultaneously, tyrosine and phenylalanine levels rose 38% and 50% (P<0.05) in the plasma and 66% and 46% (P<0.05) in muscle, respectively. After the 24-h exercise, plasma levels of BCAA were positively correlated with muscle levels of glycogen (r2=0.73, P<0.05), as was the combined concentrations of muscle tyrosine and phenylalanine with plasma creatine kinase (r2=0.55, P<0.05). Following 28-h of recovery, plasma and muscle levels of amino acids had either returned to their initial levels or were elevated. In conclusion, ultra-endurance exercise caused significant changes elevations in plasma and muscle levels of tyrosine and phenylalanine, which suggest an increase in net muscle protein breakdown during exercise. There was a reduction in plasma concentrations of EAA and glutamine during exercise, whereas no changes were detected in their muscle concentration after exercise.

INTRODUCTION: Stiffness (k) describes a material's resistance to deformation and is useful for understanding neuromuscular function, performance, and injury risk. The aim of this study is to compare the lower limb stiffness method (k_LLS), which uses only force plate data, with methods combining force plate and motion capture data to calculate stiffness during the eccentric phase of a countermovement.

MATERIAL AND METHODS: Twelve resistance-trained males: age 24.9 (4.4) years, height 1.81 (0.05) m, weight 88.2 (14) kg) performed three maximal effort countermovement jumps (CMJ). Data were collected synchronously using three-dimensional (3D) kinematic and kinetic data (dual force plate setup). Lower limb stiffness (z), joint stiffness (x, y, and z), and leg stiffness (linear, sagittal plane, and 3D) were calculated for the eccentric phase of all CMs.

RESULTS: k_LLS showed high concurrent validity with strong correlations to kinetic-kinematic methods (r = 0.90-0.97, p < 0.05). A linear mixed model revealed no significant differences in k-values between k_LLS and leg stiffness, indicating high concurrent validity.

DISCUSSION: k_LLS offers valid and valuable information affecting performance, injury risk, and return-to-sport decisions.

CONCLUSION: The findings suggest that k_LLS is a valid method for calculating stiffness in CMJs and equal to 3D leg stiffness.

Energy turnover was assessed in two conditions of mixed ultra-endurance exercise. In Study 1, energy expenditure and intake were measured in nine males in a laboratory over 24 h. In Study 2, energy expenditure was assessed in six males during an 800-km Adventure race (mean race time 152.5 h). Individual correlations between heart rate and oxygen uptake ([Vdot]O(2)) were established during pre-tests when kayaking, cycling, and running. During exercise, energy expenditure was estimated from continuous heart rate recordings. Heart rate and [Vdot]O(2) were measured regularly during fixed cycling work rates to correct energy expenditure for drift in oxygen pulse. Mean energy expenditure was 18,050 +/- 2,390 kcal (750 +/- 100 kcal . h(-1)) and 80,000 +/- 18,000 kcal (500 +/- 100 kcal . h(-1)) in Study 1 and Study 2 respectively, which is higher than previously reported. Energy intake in Study 1 was 8,450 +/- 1,160 kcal, resulting in an energy deficit of 9,590 +/- 770 kcal. Body mass decreased in Study 1 (-2.3 +/- 0.8 kg) but was unchanged in Study 2. Fat mass decreased in Study 2 (-2.3 +/- 1.5 kg). In Study 1, muscle glycogen content decreased by only 60%. Adventure racing requires a high energy expenditure, with large inter-individual variation. A large energy deficit is caused by inadequate energy intake, possibly due to suppressed appetite and gastrointestinal problems. The oxygen pulse, comparing start to 12 h of exercise and beyond, increased by 10% and 5% in Study 1 and Study 2 respectively. Hence, estimations of energy expenditure from heart rate recordings should be corrected according to this drift.

The hypothesis that ultraendurance exercise influences muscle mitochondrial function has been investigated. Athletes in ultraendurance performance performed running, kayaking, and cycling at 60% of their peak O(2) consumption for 24 h. Muscle biopsies were taken preexercise (Pre-Ex), postexercise (Post-Ex), and after 28 h of recovery (Rec). Respiration was analyzed in isolated mitochondria during state 3 (coupled to ATP synthesis) and state 4 (noncoupled respiration), with fatty acids alone [palmitoyl carnitine (PC)] or together with pyruvate (Pyr). Electron transport chain activity was measured with NADH in permeabilized mitochondria. State 3 respiration with PC increased Post-Ex by 39 and 41% (P < 0.05) when related to mitochondrial protein and to electron transport chain activity, respectively. State 3 respiration with Pyr was not changed (P > 0.05). State 4 respiration with PC increased Post-Ex but was lower than Pre-Ex at Rec (P < 0.05 vs. Pre-Ex). Mitochondrial efficiency [amount of added ADP divided by oxygen consumed during state 3 (P/O ratio)] decreased Post-Ex by 9 and 6% (P < 0.05) with PC and PC + Pyr, respectively. P/O ratio remained reduced at Rec. Muscle uncoupling protein 3, measured with Western blotting, was not changed Post-Ex but tended to decrease at Rec (P = 0.07 vs. Pre-Ex). In conclusion, extreme endurance exercise decreases mitochondrial efficiency. This will increase oxygen demand and may partly explain the observed elevation in whole body oxygen consumption during standardized exercise (+13%). The increased mitochondrial capacity for PC oxidation indicates plasticity in substrate oxidation at the mitochondrial level, which may be of advantage during prolonged exercise.

During prolonged exercise at fixed work rate heart rate (HR) increases slowly with concomitant decrease in stroke volume (SV) in order to maintain cardiac output. Simultaneously, an increased oxygen uptake (VO2) occurs. In this paper we report an unexpected and previously not observed cardiovascular response to ultra-endurance exercise. Nine well-trained male athletes performed 24-h exercise in a controlled laboratory setting, with altering blocks of kayaking, running and cycling. Each block consisted of 110 min of exercise and 10 min of rest. Measurements (HR, VO2 and blood samples) were conducted during cycling at fixed work rate every 6th hour. The average work intensity was approximately 55 % of respective VO2peak. HR was increased at 6 h with 15 beats/min (13 %) compared to pre-exercise (Pre-Ex), but thereafter unexpectedly returned towards initial values. VO2 on the other hand was increased with 0.22 l/min (10 %) at 6 h and 0.37 l/min (17 %) at 12 h compared to Pre-Ex, and thereafter remained stable. This implies an increased oxygen pulse (VO2/HR) with approximately 10 % compared to Pre-Ex at the later half of the exercise. The cardiovascular drift did not progress continuously, but instead changed drastically when duration exceeded 6 hours. The changes in HR and VO2 might have different and complex explanations. HR drift might be explained mainly by central circulatory adaptation (e.g. desensitisation of cardiac adrenergic receptors) whereas drift in VO2 may depend upon peripheral changes (e.g. decreased mitochondrial efficiency). Consequently, using solely HR for determining exercise intensity and energy expenditure becomes invalid during ultra-endurance exercise, if the cardiovascular drift is not measured and taken into account.

Introduction: In clinical medicine, natriuretic peptides, including N-terminal B-type natriuretic peptide (NT-proBNP), are used to detect increased myocardial wall tension in conditions such as heart failure. Tachycardia, arrhythmias and physical exercise may also increase these peptides. The clinical reference value is <100 ng/l, and in clinical practice values >300 ng/l are a strong indicators of heart failure, and values >5000 ng/l highly significant for mortality within 3 months.

Methods: We examined the levels of NT-proBNP after ultra-endurance exercise, and also made an attempt to relate NT-proBNP to performance. The subjects (12 males and 3 females) participated in the Adventure Racing World Championship, a 5-6 days non-stop competition open for mixed gender team of four athletes. They were all healthy, well-trained athletes with experience from several years of competitions at international elite level. Blood samples for determination of NT-proBNP were drawn before exercise (Pre-Ex), at the end of the race (End-Ex) and 24 hours after exercise (Post-Ex). Each athlete rated his/her own performance at the end of the race (i.e. the last 12 hours) on a scale from 1 (good, stronger than teammates), 2 (intermediate) and 3 (poor, got towed in, needed help from teammates). In addition, each athlete was also rated according to the same scale by the other three members of his/her team. Thereafter the four rates were pooled. Note that the rating is in relation to the team rather than the result of the competition.

Results: The average exercise duration was approx. 150 hours, and the calculated average work intensity was 40 % (in percent of respective VO2peak), including time for rest, change of equipment, and food intake. The levels of NT-proBNP increased from 31 ± 14 (10-56) [mean ± SD (min-max)] at Pre-Ex to 487 ± 648 (52-2480) at End-Ex. At Post-Ex the corresponding levels were 224 ± 219 (12-634). At End-Ex seven subjects had NT-proBNP below the reference value. The rated performance for four of them was 1, and the remaining three were rated as 2. Three of the subjects had markedly higher levels than previously reported (>900 ng/l) and they were rated 3, 3 and 2, respectively.

Discussion: Extreme levels of NT-proBNP, up to 2500 ng/l, are present after ultra-endurance exercise in healthy athletes without any clinical signs or symptoms of heart failure. On the other hand, these extreme values may be an indicator of cardiac fatigue, previously described after endurance exercise. Furthermore, in this study high levels of NT-proBNP seem to be associated with decreased exercise performance.

In this paper we report a reversed drift in heart rate (HR) but increased oxygen uptake (VO(2)) during ultra-endurance exercise. Nine well-trained male athletes performed 24-h exercise in a controlled laboratory setting, with alternating blocks of kayaking, running and cycling. Each block included 110 min of exercise and 10 min of rest, with an average work intensity of approximately 55% of respective VO(2peak). Blood samples were taken and HR and VO(2) measured every 6th hour during steady-state cycling at fixed work rate. As assumed HR was increased at 6 h by 15 +/- 6 beats/min compared with initial level (0 h). Thereafter the drift did not progress continuously, but instead unexpectedly returned toward initial values, although the plasma levels of catecholamines increased continuously during exercise. VO(2) was increased by 0.22 +/- 0.15 L/min (10%) at 6 h and 0.37 +/- 0.18 L/min (17%) at 12 h compared with 0 h, and thereafter remained stable. This implies an increased oxygen pulse (VO(2)/HR) by approximately 10% at the last half of the 24-h exercise compared with 0 h. Consequently, sole use of HR would give inaccurate estimates of exercise intensity and energy expenditure during endurance exercise lasting more than 6 h, and different patterns of cardiovascular drift need to be taken into account.

Purpose: The aim of this study was to investigate if extreme workload would induce signs of cardiac fatigue similar to that in skeletal muscle, e.g. decreased velocity of contraction.

Methods: The subjects were 12 men and 3 women who participated in the Adventure Racing World Championship, a 5-7 days non-stop competition open for mixed gender teams of four. All subjects were healthy, well-trained ultra-endurance athletes with experince from several years of training and competition at international elite level. Measurements of the heart's contraction velocities were conducted using tissue Doppler imaging (VIVID7) in a resting situation at baseline, immediately after the race, and after 24 hours of recovery.

Results: Characteristics for the subjects were at baseline (mean ± SD, for men and women): age 30±3 and 27±4; interventricular septal thickness 10.5±0.7 and 8.0±0.0 mm; left ventricular end-diastolic diameter 54.4±3.4 and 45.0±3.0 mm; posterior wall thickness 10.4±0.9 and 8.0±1.0 mm; early to late diastolic filling velocity (E/A) 2.3±0.6 and 2.2±0.2. Exercise duration was approx. 150 hours, and the calculated average work intensity was 40% of respective VO2peak, including time for rest, change of equipment, and food intake. Values of contraction velocities are presented in the table.

Conclusions: All athletes had normally sized hearts. Based on contraction velocities we found no evidence of cardiac fatigue after ultra-endurance exercise. A difference compared to studies that found cardiac fatigue in other sports (e.g. marathon, triathlon) is that even though our population exercised for an extreme duration the average intensity was low. This might point towards that exercise intensity, not duration, is the primary source for cardiac fatigue.

Exercise-induced oxidative stress is important for the muscular adaptation to training but may also cause muscle damage. We hypothesized that prolonged exercise would increase mitochondrial production of reactive oxygen species (ROS) measured in vitro and that this correlates with oxidative damage. Eight male athletes (24-32 years) performed ultra-endurance exercise (kayaking/running/cycling) with an average work intensity of 55% VO2peak for 24 h. Muscle biopsies were taken from vastus lateralis before exercise, immediately after exercise and after 28 h of recovery. The production of H2O2 was measured fluorometrically in isolated mitochondria with the Amplex red and peroxidase system. Succinate-supported mitochondrial H2O2 production was significantly increased after exercise (73% higher, P=0.025) but restored to the initial level at recovery. Plasma level of free fatty acids (FFA) increased 4-fold and exceeded 1.2 mmol l(-1) during the last 6 h of exercise. Plasma FFA at the end of exercise was significantly correlated to mitochondrial ROS production (r=0.74, P<0.05). Mitochondrial content of 4-hydroxy-nonenal-adducts (a marker of oxidative damage) was increased only after recovery and was not correlated with mitochondrial ROS production. Total thiol-group level and glutathione peroxidase activity were elevated after recovery. In conclusion: ultra-endurance exercise increases ROS production in isolated mitochondria but this is reversed after 28 h recovery. Mitochondrial ROS production was not correlated with oxidative damage of mitochondrial proteins, which was increased at recovery but not immediately after exercise. Key words: antioxidative defence, fatty acids, oxidative stress.

Interleukin 6 (IL-6) response was studied during two ultra endurance events – one laboratory 24 h protocol (9 men) with exercise intensity set to 60 % of VO_2max and one Adventure Race over 6 days (12 men/6 women) with a self-selected race pace, including rests, of about 38 % of VO_2max. In the 24 h protocol IL-6 level was elevated from 0.76 ± 0.48 pg mL^-1 at rest to 7.16 ± 2.70 pg mL^-1 at 6 h, and increased further to 10.58 ± 1.04 pg mL^-1 at 12 h, but remained thereafter unchanged at 24 h, (10.89±0.36 pg mL^-1). All participants had nearly identical values at 12 and 24 h, supporting intensity as main determinant in the IL-6 response since exercise duration did not increase IL-6 level after 12 h. Possible confounding factors do not seem to influence the IL-6 concentration during the longer races (>12h), but might very well do so during shorter exercise bouts. In the 6-day race IL-6 increased from rest to 24 h, but thereafter there was no change in plasma IL-6 value until the end of the race (140 h). There was no elevation of TNF-α in any of the protocols, suggesting that the competitors were free from systemic inflammation. During endurance exercise lasting >12 h intensity and not duration is the main determinant of the IL-6 response, while during shorter exercise bouts both intensity and duration contribute to the accumulation of IL-6 in plasma.