Biomedical subjects

Lars Nybo

Publications and source records attributed to Lars Nybo.

14 recordsLinked to original sources

PubMed2006

Effect of two different intense training regimens on skeletal muscle ion transport proteins and fatigue development.

This study examined the effect of two different intense exercise training regimens on skeletal muscle ion transport systems, performance, and metabolic response to exercise. Thirteen subjects performed either sprint training [ST; 6-s sprints (n = 6)], or speed endurance training [SET; 30-s runs approximately 130% Vo(2 max), n = 7]. Training in the SET group provoked higher (P < 0.05) plasma K(+) levels and muscle lactate/H(+) accumulation. Only in the SET group was the amount of the Na(+)/H(+) exchanger isoform 1 (31%) and Na(+)-K(+)-ATPase isoform alpha(2) (68%) elevated (P < 0.05) after training. Both groups had higher (P < 0.05) levels of Na(+)-K(+)-ATPase beta(1)-isoform and monocarboxylate transporter 1 (MCT1), but no change in MCT4 and Na(+)-K(+)-ATPase alpha(1)-isoform. Both groups had greater (P < 0.05) accumulation of lactate during exhaustive exercise and higher (P < 0.05) rates of muscle lactate decrease after exercise. The ST group improved (P < 0.05) sprint performance, whereas the SET group elevated (P < 0.05) performance during exhaustive continuous treadmill running. Improvement in the Yo-Yo intermittent recovery test was larger (P < 0.05) in the SET than ST group (29% vs. 10%). Only the SET group had a decrease (P < 0.05) in fatigue index during a repeated sprint test. In conclusion, turnover of lactate/H(+) and K(+) in muscle during exercise does affect the adaptations of some but not all related muscle ion transport proteins with training. Adaptations with training do have an effect on the metabolic response to exercise and specific improvement in work capacity.

Exercise↗

PubMed2006

Capillary-oxygenation-level-dependent near-infrared spectrometry in frontal lobe of humans.

Brain function requires oxygen and maintenance of brain capillary oxygenation is important. We evaluated how faithfully frontal lobe near-infrared spectroscopy (NIRS) follows haemoglobin saturation (SCap) and how calculated mitochondrial oxygen tension (PMitoO2) influences motor performance. Twelve healthy subjects (20 to 29 years), supine and seated, inhaled O2 air-mixtures (10% to 100%) with and without added 5% carbon dioxide and during hyperventilation. Two measures of frontal lobe oxygenation by NIRS (NIRO-200 and INVOS) were compared with capillary oxygen saturation (SCap) as calculated from the O2 content of brachial arterial and right internal jugular venous blood. At control SCap (78%+/-4%; mean+/-s.d.) was halfway between the arterial (98%+/-1%) and jugular venous oxygenation (SvO2; 61%+/-6%). Both NIRS devices monitored SCap (P<0.001) within approximately 5% as SvO2 increased from 39%+/-5% to 79%+/-7% with an increase in the transcranial ultrasound Doppler determined middle cerebral artery flow velocity from 29+/-8 to 65+/-15 cm/sec. When SCap fell below approximately 70% with reduced flow and inspired oxygen tension, PMitoO2 decreased (P<0.001) and brain lactate release increased concomitantly (P<0.001). Handgrip strength correlated with the measured (NIRS) and calculated capillary oxygenation values as well as with PMitoO2 (r>0.74; P<0.05). These results show that NIRS is an adequate cerebral capillary-oxygenation-level-dependent (COLD) measure during manipulation of cerebral blood flow or inspired oxygen tension, or both, and suggest that motor performance correlates with the frontal lobe COLD signal.

Adult↗

PubMed2006

Environmental heat stress, hyperammonemia and nucleotide metabolism during intermittent exercise.

This study investigated the influence of environmental heat stress on ammonia (NH3) accumulation in relation to nucleotide metabolism and fatigue during intermittent exercise. Eight males performed 40 min of intermittent exercise (15 s at 306+/-22 W alternating with 15 s of unloaded cycling) followed by five 15 s all-out sprints. Control trials were conducted in a 20 degrees C environment while heat stress trials were performed at an ambient temperature of 40 degrees C. Muscle biopsies and venous blood samples were obtained at rest, after 40 min of exercise and following the maximal sprints. Following exercise with heat stress, the core and muscle temperatures peaked at 39.5+/-0.2 and 40.2+/-0.2 degrees C to be approximately 1 degrees C higher (P<0.05) than the corresponding control values. Mean power output during the five maximal sprints was reduced from 618+/-12 W in control to 558+/-14 W during the heat stress trial (P<0.05). During the hot trial, plasma NH3 increased from 31+/-2 microM at rest to 93+/-6 at 40 min and 151+/-15 microM after the maximal sprints to be 34% higher than control (P<0.05). In contrast, plasma K+ and muscle H+ accumulation were lower (P<0.05) following the maximal sprints with heat stress compared to control, while muscle glycogen, CP, ATP and IMP levels were similar across trials. In conclusion, altered levels of "classical peripheral fatiguing agents" does apparently not explain the reduced capacity for performing repeated sprints following intermittent exercise in the heat, whereas the augmented systemic NH3 response may be a factor influencing fatigue during exercise with superimposed heat stress.

Adult↗

PubMed2006

The Yo-Yo IR2 test: physiological response, reliability, and application to elite soccer.

PURPOSE: To examine the physiological response, reliability, and validity of the Yo-Yo intermittent recovery level 2 test (Yo-Yo IR2). METHODS: Thirteen normally trained male subjects carried out four Yo-Yo IR2 tests, an incremental treadmill test (ITT), and various sprint tests. Muscle biopsies and blood samples were obtained, and heart rate was measured before, during, and after the Yo-Yo IR2 test. Additionally, 119 Scandinavian elite soccer players carried out the Yo-Yo IR2 test on two to four occasions. RESULTS: Yo-Yo IR2 performance was 591 +/- 43 (320-920) m or 4.3 (2.6-7.9) min. Test-retest coefficient of variation in distance covered was 9.6% (N = 29). Heart rate (HR) at exhaustion was 191 +/- 3 bpm, or 98 +/- 1% HRmax. Muscle lactate was 41.7 +/- 5.4 and 68.5 +/- 7.6 mmol x kg(-1) d.w. at 85 and 100% of exhaustion time, respectively, with corresponding muscle CP values of 40.4 +/- 5.2 and 29.4 +/- 4.7 mmol x kg(-1) d.w. Peak blood lactate was 13.6 +/- 0.5 mM. Yo-Yo IR2 performance was correlated to ITT performance (r = 0.74, P < 0.05) and VO2max (r = 0.56, P < 0.05) but not to 30- and 50-m sprint performance. Yo-Yo IR2 performance was better (P < 0.05) for international elite soccer players than for moderate elite players (1059 +/- 35 vs 771 +/- 26 m) and better (P < 0.05) for central defenders (N = 21), fullbacks (N = 20), and midfielders (N = 48) than for goalkeepers (N = 6) and attackers (N = 24). Fifteen elite soccer players improved (P < 0.05) Yo-Yo IR2 performance by 42 +/- 8% during 8 wk of preseasonal training. CONCLUSION: This study demonstrates that the Yo-Yo IR2 test is reproducible and can be used to evaluate an athlete's ability to perform intense intermittent exercise with a high rate of aerobic and anaerobic energy turnover. Specifically, the Yo-Yo IR2 test was shown to be a sensitive tool to differentiate between intermittent exercise performance of soccer players in different seasonal periods and at different competitive levels and playing positions.

Adult↗

PubMed2004

Cerebral ammonia uptake and accumulation during prolonged exercise in humans.

We evaluated whether peripheral ammonia production during prolonged exercise enhances the uptake and subsequent accumulation of ammonia within the brain. Two studies determined the cerebral uptake of ammonia (arterial and jugular venous blood sampling combined with Kety-Schmidt-determined cerebral blood flow; n = 5) and the ammonia concentration in the cerebrospinal fluid (CSF; n = 8) at rest and immediately following prolonged exercise either with or without glucose supplementation. There was a net balance of ammonia across the brain at rest and at 30 min of exercise, whereas 3 h of exercise elicited an uptake of 3.7 +/- 1.3 micromol min(-1) (mean +/-s.e.m.) in the placebo trial and 2.5 +/- 1.0 micromol min(-1) in the glucose trial (P < 0.05 compared to rest, not different across trials). At rest, CSF ammonia was below the detection limit of 2 microm in all subjects, but it increased to 5.3 +/- 1.1 microm following exercise with glucose, and further to 16.1 +/- 3.3 microm after the placebo trial (P < 0.05). Correlations were established between both the cerebral uptake (r2 = 0.87; P < 0.05) and the CSF concentration (r2 = 0.72; P < 0.05) and the arterial ammonia level and, in addition, a weaker correlation (r2 = 0.37; P < 0.05) was established between perceived exertion and CSF ammonia at the end of exercise. The results let us suggest that during prolonged exercise the cerebral uptake and accumulation of ammonia may provoke fatigue, e.g. by affecting neurotransmitter metabolism.

Adult↗

PubMed2004

Cerebral perturbations provoked by prolonged exercise.

This review addresses cerebral metabolic and neurohumoral alterations during prolonged exercise in humans with special focus on associations with fatigue. Global energy turnover in the brain is unaltered by the transition from rest to moderately intense exercise, apparently because exercise-induced activation of some brain regions including cortical motor areas is compensated for by reduced activity in other regions of the brain. However, strenuous exercise is associated with cerebral metabolic and neurohumoral alterations that may relate to central fatigue. Fatigue should be acknowledged as a complex phenomenon influenced by both peripheral and central factors. However, failure to drive the motorneurons adequately as a consequence of neurophysiological alterations seems to play a dominant role under some circumstances. During exercise with hyperthermia excessive accumulation of heat in the brain due to impeded heat removal by the cerebral circulation may elevate the brain temperature to >40 degrees C and impair the ability to sustain maximal motor activation. Also, when prolonged exercise results in hypoglycaemia, perceived exertion increases at the same time as the cerebral glucose uptake becomes low, and centrally mediated fatigue appears to arise as the cerebral energy turnover becomes restricted by the availability of substrates for the brain. Changes in serotonergic activity, inhibitory feed-back from the exercising muscles, elevated ammonia levels, and alterations in regional dopaminergic activity may also contribute to the impaired voluntary activation of the motorneurons after prolonged and strenuous exercise. Furthermore, central fatigue may involve depletion of cerebral glycogen stores, as signified by the observation that following exhaustive exercise the cerebral glucose uptake increases out of proportion to that of oxygen. In summary, prolonged exercise may induce homeostatic disturbances within the central nervous system (CNS) that subsequently attenuates motor activation. Therefore, strenuous exercise is a challenge not only to the cardiorespiratory and locomotive systems but also to the brain.

Animals↗

PubMed2003

Minor amounts of plasma medium-chain fatty acids and no improved time trial performance after consuming lipids.

Medium-chain triacylglycerols (MCT) have a potential glycogen-saving effect during exercise due to rapid hydrolysis and oxidation. However, studies comparing intake of carbohydrates (CHO) plus 80-90 g MCT with intake of CHO alone have revealed different results. The present study tested performance after consumption of specific structured triacylglycerol, consisting of a mixture of medium-chain fatty acids and long-chain fatty acids, to prevent the adverse effects observed by MCT (pure medium-chain fatty acids) regarding gastrointestinal distress. Seven well-trained subjects cycled 3 h at 55% of maximum O2 uptake during which they ingested CHO or CHO plus specific structured triacylglycerols. Immediately after the constant-load cycling, the subjects performed a time trial of approximately 50-min duration. Breath and blood samples were obtained regularly during the experiment. Fatty acid composition of plasma triacylglycerols, fatty acids, and phospholipids was determined. Performance was similar after administration of CHO plus specific structured triacylglycerol [medium-, long-, and medium-chain fatty acid (MLM)] compared with CHO (50.0 +/- 1.8 and 50.8 +/- 3.6 min, respectively). No plasma 8:0 was detected in the plasma lipid classes, but the amount of phospholipid fatty acids was significantly higher after CHO+MLM compared with CHO intake. The lacking time trial improvement after intake of medium-chain fatty acids might be due to no available 8:0 in the systemic circulation. A higher level of plasma phospholipid fatty acids in the CHO+MLM compared with the CHO group was probably due to endogenous phospholipid release into chylomicrons.

Adult↗

PubMed2003

Neurohumoral responses during prolonged exercise in humans.

This study examined neurohumoral alterations during prolonged exercise with and without hyperthermia. The cerebral oxygen-to-carbohydrate uptake ratio (O2/CHO = arteriovenous oxygen difference divided by arteriovenous glucose difference plus one-half lactate), the cerebral balances of dopamine, and the metabolic precursor of serotonin, tryptophan, were evaluated in eight endurance-trained subjects during exercise randomized to be with or without hyperthermia. The core temperature stabilized at 37.9 +/- 0.1 degrees C (mean +/- SE) in the control trial, whereas it increased to 39.7 +/- 0.2 degrees C in the hyperthermic trial, with a concomitant increase in perceived exertion (P < 0.05). At rest, the brain had a small release of tryptophan (arteriovenous difference of -1.2 +/- 0.3 micromol/l), whereas a net balance was obtained during the two exercise trials. Both the arterial and jugular venous dopamine levels became elevated during the hyperthermic trial, but the net release from the brain was unchanged. During exercise, the O2/CHO was similar across trials, but, during recovery from the hyperthermic trial, the ratio decreased to 3.8 +/- 0.3 (P < 0.05), whereas it returned to the baseline level of approximately 6 within 5 min after the control trial. The lowering of O2/CHO was established by an increased arteriovenous glucose difference (1.1 +/- 0.1 mmol/l during recovery from hyperthermia vs. 0.7 +/- 0.1 mmol/l in control; P < 0.05). The present findings indicate that the brain has an increased need for carbohydrates during recovery from strenuous exercise, whereas enhanced perception of effort as observed during exercise with hyperthermia was not related to alterations in the cerebral balances of dopamine or tryptophan.

Adult↗

PubMed2003

Cerebral metabolism is influenced by muscle ischaemia during exercise in humans.

Maximal exercise reduces the cerebral metabolic ratio (O2/(glucose + 1/2 lactate)) to < 4 from a resting value close to 6, and only part of this decrease is explained by the 'intent' to exercise. This study evaluated whether sensory stimulation of brain by muscle ischaemia would reduce the cerebral metabolic ratio. In 10 healthy human subjects the cerebral arterial-venous differences (a-v differences) for O2, glucose and lactate were assessed before, during and after three bouts of 10 min cycling with equal workload: (1) control exercise at light intensity, (2) exercise that elicited a high rating of perceived exertion due to a 100 mmHg thigh cuff, and (3) exercise followed by 5 min of post-exercise muscle ischaemia that increased blood pressure by approximately 20 %. Control exercise did not significantly affect the a-v differences. However, during the recovery from exercise with thigh cuffs the cerebral metabolic ratio decreased from a resting value of 5.4 +/- 0.2 to 4.0 +/- 0.4 (mean +/- S.E.M.; P < 0.05) as a discrete lactate efflux from the brain at rest shifted to a slight uptake. Also, following post-exercise muscle ischaemia, the cerebral metabolic ratio decreased to 4.5 +/- 0.3 (P < 0.05). The results support the hypothesis that during exercise, cerebral metabolism is influenced both by the mental effort to exercise and by sensory input from skeletal muscles.

Adult↗

PubMed2003

CNS fatigue and prolonged exercise: effect of glucose supplementation.

INTRODUCTION: Ingestion of carbohydrates during prolonged exercise may improve endurance, whereas an insufficient supply of glucose results in hypoglycemia and fatigue. Fatigue, defined as a loss of force-generating capacity, may develop for a variety of reasons and involve both central and peripheral factors. This study investigated whether CNS activation of the skeletal muscles was affected by prolonged exercise with or without glucose supplementation. METHODS: Voluntary force production and central activation ratios, assessed by the twitch interpolation technique, were determined during a 2-min sustained maximal knee extension in eight endurance-trained males in a baseline condition and immediately after 3 h of cycling randomized to be with or without glucose supplementation. RESULTS: The exercise bout without glucose supplementation (placebo trial) reduced the blood glucose concentration from 4.5 +/- 0.2 to 3.0 +/- 0.2 mM, whereas blood glucose homeostasis was maintained during the glucose trial. The average force during the sustained maximal voluntary muscle contraction was 248 +/- 23 N at baseline, 222 +/- 20 N in the glucose trial, and 197 +/- 21 N in the placebo trial (P < 0.05 between conditions). In the placebo trial, the lowered force production was accompanied by a reduced level of CNS activation compared with the other two conditions (P < 0.05), whereas the central activation ratios were similar in the glucose trial as compared with baseline. CONCLUSION: Exercise-induced hypoglycemia attenuates CNS activation during a sustained maximal muscle contraction, whereas central activation appears to be unaffected by 3 h of moderately intense exercise in endurance-trained athletes when euglycemia is maintained by carbohydrate ingestion.

Adult↗

PubMed2003

Cerebral changes during exercise in the heat.

This review focuses on cerebral changes during combined exercise and heat stress, and their relation to fatigue. Dynamic exercise can elevate the core temperature rapidly and high internal body temperatures seem to be an independent cause of fatigue during exercise in hot environments. Thus, in laboratory settings, trained participants become exhausted when they reach a core temperature of approximately 40 degrees C. The observation that exercise-induced hyperthermia reduces the central activation percentage during maximal isometric muscle contractions supports the idea that central fatigue is involved in the aetiology of hyperthermia-induced fatigue. Thus, hyperthermia does not impair the ability of the muscles to generate force, but sustained force production is lowered as a consequence of a reduced neural drive from the CNS. During ongoing dynamic exercise in hot environments, there is a gradual slowing of the electroencephalogram (EEG) whereas hyperthermia does not affect the electromyogram. The frequency shift of the EEG is highly correlated with the participants' perception of exertion, which furthermore may indicate that alterations in cerebral activity, rather than peripheral fatigue, are associated with the hyperthermia-induced development of fatigue. Cerebral blood flow is reduced by approximately 20% during exercise with hyperthermia due to hyperventilation, which causes a lowering of the arterial CO(2) pressure. However, in spite of the reduced blood flow, cerebral glucose and oxygen uptake does not seem to be impaired. Removal of heat from the brain is also an important function of the cerebral blood flow and the lowered perfusion of the brain during exercise and heat stress appears to reduce heat removal by the venous blood. Heat is consequently stored in the brain. The causal relationship between the circulatory changes, the EEG changes and the hyperthermia-induced central fatigue is at the present not well understood and future studies should focus on this aspect.

Body Temperature Regulation↗

PubMed2002

Inadequate heat release from the human brain during prolonged exercise with hyperthermia.

Brain temperature appears to be an important factor affecting motor activity, but it is not known to what extent brain temperature increases during prolonged exercise in humans. Cerebral heat exchange was therefore evaluated in seven males during exercise with and without hyperthermia. Middle cerebral artery mean blood velocity (MCA V(mean)) was continuously monitored while global cerebral blood flow (CBF) and cerebral energy turnover were determined at the end of the two exercise trials in three subjects. The arterial to venous temperature difference across the brain (v-aD(temp)) was determined via thermocouples placed in the internal jugular vein and in the aorta. The jugular venous blood temperature was always higher than that of the arterial blood, demonstrating that heat was released via the CBF during the normothermic as well as the hyperthermic exercise condition. However, heat removal via the jugular venous blood was 30 +/- 6 % lower during hyperthermia compared to the control trial. The reduced heat removal from the brain was mainly a result of a 20 +/- 6 % lower CBF (22 +/- 9 % reduction in MCA V(mean)), because the v-aD(temp) was not significantly different in the hyperthermic (0.20 +/- 0.05 degrees C) compared to the control trial (0.22 +/- 0.05 degrees C). During hyperthermia, the impaired heat removal via the blood was combined with a 7 +/- 2 % higher heat production in the brain and heat was consequently stored in the brain at a rate of 0.20 +/- 0.06 J g(-1) min(-1). The present results indicate that the average brain temperature is at least 0.2 degrees C higher than that of the body core during exercise with or without hyperthermia.

Adult↗

PubMed2002

Interleukin-6 release from the human brain during prolonged exercise.

Interleukin (IL)-6 is a pleiotropic cytokine, which has a variety of physiological roles including functions within the central nervous system. Circulating IL-6 increases markedly during exercise, partly due to the release of IL-6 from the contracting skeletal muscles, and exercise-induced IL-6 may be linked with central fatigue, which is enhanced by hyperthermia. Exercise-induced IL-6 may also stimulate hepatic glycogenolysis, which is important during prolonged and repeated exercise. Thus, in a randomised order and separated by 60 min of rest, eight young male subjects completed two 60 min exercise bouts: one bout with a normal (38 degrees C) and the other with an elevated (39.5 degrees C) core temperature. The cerebral IL-6 response was determined on the basis of internal jugular venous to arterial IL-6 differences and global cerebral blood flow. There was no net release or uptake of IL-6 in the brain at rest or after 15 min of exercise, but a small release of IL-6 was observed after 60 min of exercise in the first bout (0.06 +/- 0.03 ng min(-1)). This release of IL-6 from the brain was five-fold greater at the end of the second bout (0.30 +/- 0.08 ng min(-1); P < 0.05) with no separate influence of hyperthermia. In conclusion, IL-6 is released from the brain during prolonged exercise in humans and it appears that the duration of the exercise rather than the increase in body temperature dictates the cerebral IL-6 response.

Adult↗

PubMed2002

Effects of hyperthermia on cerebral blood flow and metabolism during prolonged exercise in humans.

The development of hyperthermia during prolonged exercise in humans is associated with various changes in the brain, but it is not known whether the cerebral metabolism or the global cerebral blood flow (gCBF) is affected. Eight endurance-trained subjects completed two exercise bouts on a cycle ergometer. The gCBF and cerebral metabolic rates of oxygen, glucose, and lactate were determined with the Kety-Schmidt technique after 15 min of exercise when core temperature was similar across trials, and at the end of exercise, either when subjects remained normothermic (core temperature = 37.9 degrees C; control) or when severe hyperthermia had developed (core temperature = 39.5 degrees C; hyperthermia). The gCBF was similar after 15 min in the two trials, and it remained stable throughout control. In contrast, during hyperthermia gCBF decreased by 18% and was therefore lower in hyperthermia compared with control at the end of exercise (43 +/- 4 vs. 51 +/- 4 ml. 100 g(-1). min(-1); P < 0.05). Concomitant with the reduction in gCBF, there was a proportionally larger increase in the arteriovenous differences for oxygen and glucose, and the cerebral metabolic rate was therefore higher at the end of the hyperthermic trial compared with control. The hyperthermia-induced lowering of gCBF did not alter cerebral lactate release. The hyperthermia-induced reduction in exercise cerebral blood flow seems to relate to a concomitant 18% lowering of arterial carbon dioxide tension, whereas the higher cerebral metabolic rate of oxygen may be ascribed to a Q(10) (temperature) effect and/or the level of cerebral neuronal activity associated with increased exertion.

Adult↗