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| 2. |
- Bakkman, Linda, et al.
(författare)
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Hälsosegrar : Den vetenskapliga vägen till ett friskare liv
- 2021
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Bok (populärvet., debatt m.m.)abstract
- Forskning visar att det vi aktivt ägnar oss åt - våra medvetna livsstilsval - kan påverka så mycket som 40 % av vårt välbefinnande. Vi har med andra ord stora möjligheter att själva göra en skillnad i hur vi mår. Hälsosegrarna är inom räckhåll!Här presenteras den allra senaste forskningen om hur rörelse, mat och återhämtning påverkar vår hälsa. Vi får veta vad som händer i kroppen och i hjärnan när vi till exempel stressar för mycket, sover dåligt, sitter för länge eller inte får i oss tillräckligt med näring. Men också hur vi faktiskt kan omsätta den kunskapen i praktiken och ändra våra beteenden. Hur vilar man hjärnan? Vad är egentligen "nyttig" mat? Och vilken funktion fyller vardagsmotionen? Fokus ligger på de vardagliga utmaningarna och de små men hållbara förändringar som kan göra stor skillnad.Med gedigen kunskap och ett motiverande tilltal varvar de tre författarna vetenskapliga fakta och studier med konkreta tips. Sammantaget blir det ett inspirerande smörgåsbord av fullt genomförbara livsstilsförändringar som kan göra stor skillnad för hur vi mår.[Text från förlaget]
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| 3. |
- Bakkman, Linda
(författare)
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Mitochondrial function adaptations to changed metabolic conditions
- 2010
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- The skeletal muscle mitochondria play a decisive role for the metabolic capacity of the body. A capability to adapt to changed metabolic conditions and energy demands is crucial for weight control and physical exercise. The aim of this thesis was to describe how the mitochondria adapt its function to different environmental conditions and changed metabolic demands. In study I, the aim was to evaluate mitochondrial adaptations to hypoxic exercise. The effect of one-legged cycle training at hypoxia was compared to equivalent normoxic training, performed at the same relative intensity. Eight untrained volunteers performed one-legged cycle training during 4 weeks. Muscle biopsies were taken before and after the exercise period. The leg trained during normoxia increased its mitochondrial population (+20.8%, P<0.05) and there was a trend towards increased respiratory capacity (+31.2%, P<0.08), while adaptations were absent in the hypoxically trained leg. Altitude training might thus be disadvantageous for mitochondrial adaptations and muscle oxidative function. In study II, the aim was to investigate the effect of ultra endurance exercise on mitochondrial function. Elite ultra endurance athletes performed running, kayaking, and cycling at 60% of their maximal oxygen consumption for 24 h. Muscle biopsies were taken preexercise, postexercise, and after 28 h of recovery. We found that mitochondrial efficiency was reduced, while the mitochondrial capacity to utilize fat was up regulated (+40%, P<0.05) after exercise. This increase in fat oxidation was reflected at whole body level substrate utilization, thus it might benefit performance during prolonged exercise. In study III and IV, the aims were to study mitochondrial function in obesity and effects of weight loss, respectively. Weight gain varies among individuals despite equal calorie overconsumption. Furthermore, weight loss resulting from low calorie diets is often less than expected and long-term success is low. This suggests differences and changes in metabolic efficiency and basal metabolism. Since mitochondrial uncoupling accounts for a substantial portion of the basal metabolic rate, we compared mitochondrial respiration in obese subjects to normal weight reference groups (study III). In study IV, we studied how mitochondrial capacity was affected by calorie restriction. Muscle biopsies were taken from 11 obese women, with an average BMI of 39 kg/m2, in conjunction with their gastric bypass surgery and at 6-months of follow-up. We found that obese subjects had a decreased oxidative capacity (-47%, P<0.01) per mitochondrial volume, compared to the to normal weight reference groups. A low capacity for fuel oxidation could play a role in the predisposition for obesity. Six months after the gastric bypass surgery, the subjects had lost on average 25.5 kg of their body weight. Coupled, ADP generating respiration, had increased significantly (+69%, P≤0.01), while the uncoupled respiration was not significantly altered. Mitochondrial efficiency increased significantly. An increased mitochondrial efficiency could partly explain the reduced basal metabolism and thus the reduced inclination for weight loss at calorie restriction. The reduced capacity among the obese is thus suggested to rather be an effect of the obesity than a casual factor.
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| 4. |
- Bakkman, Linda, et al.
(författare)
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Quantitative and qualitative adaptation of human skeletal muscle mitochondria to hypoxic compared to
- 2007
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Ingår i: Acta Physiologica. - : Wiley. - 1748-1708 .- 1748-1716. ; 190:3, s. 243-251
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Tidskriftsartikel (refereegranskat)abstract
- AIM: To investigate if training during hypoxia (H) improves the adaptation of muscle oxidative function compared with normoxic (N) training performed at the same relative intensity. METHOD: Eight untrained volunteers performed one-legged cycle training during 4 weeks in a low-pressure chamber. One leg was trained under N conditions and the other leg under hypobaric hypoxia (526 mmHg) at the same relative intensity as during N (65% of maximal power output, W(max)). Muscle biopsies were taken from vastus lateralis before and after the training period. Muscle samples were analysed for the activities of oxidative enzymes [citrate synthase (CS) and cytochrome c oxidase (COX)] and mitochondrial respiratory function. RESULTS: W(max) increased with more than 30% over the training period during both N and H. CS activity increased significantly after training during N conditions (+20.8%, P < 0.05) but remained unchanged after H training (+4.5%, ns) with a significant difference between conditions (P < 0.05 H vs. N). COX activity was not significantly changed by training and was not different between exercise conditions [+14.6 (N) vs. -2.3% (H), ns]. Maximal ADP stimulated respiration (state 3) expressed per weight of muscle tended to increase after N (+31.2%, P < 0.08) but not after H training (+3.2%, ns). No changes were found in state four respiration, respiratory control index, P/O ratio, mitochondrial Ca(2+) resistance and apparent Km for oxygen. CONCLUSION: The training-induced increase in muscle oxidative function observed during N was abolished during H. Altitude training may thus be disadvantageous for adaptation of muscle oxidative function.
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| 5. |
- Bakkman, Linda, et al.
(författare)
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Reduced respiratory capacity in muscle mitochondria of obese subjects.
- 2010
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Ingår i: Obesity Facts. - : S. Karger AG. - 1662-4025 .- 1662-4033. ; 3:6, s. 371-5
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND/AIMS: The extent of weight gain varies among individuals despite equal calorie overconsumption. Furthermore, weight gain is often less than expected from energy excess. This suggests differences in metabolic efficiency and basal metabolism. Since mitochondrial uncoupling accounts for a substantial portion of the basal metabolic rate, we compared skeletal muscle mitochondrial respiration in obese subjects to normal-weight reference groups with various degrees of physical activity.METHODS: Muscle biopsies were taken from the vastus lateralis muscle of 9 healthy obese subjects (BMI 40 ± 3). Mitochondria were isolated and analyzed for coupled (state 3) and uncoupled (state 4) respirations as well as mitochondrial efficiency (P/O ratio) using pyruvate as a substrate. Respiratory data were compared to reference groups A, normal-weight untrained (BMI 24 ± 0.7), and B, normal-weight trained (BMI 24 ± 0.6).RESULTS: Obese subjects had a decreased respiratory capacity per mitochondrial volume compared to the reference groups: this was evident in state 4 (65% and 35% of reference group A and B, respectively) and state 3 (53% and 29% of A and B, respectively) (p < 0.05).CONCLUSION: Obese subjects had a low capacity for fuel oxidation, which may play a role in the predisposition of obesity. However, whether lower mitochondrial capacity is a cause or a consequence of obesity requires further research.
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| 6. |
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| 7. |
- Enqvist, Jonas K, et al.
(författare)
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Energy turnover during 24 hours and 6 days of adventure racing.
- 2010
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Ingår i: Journal of Sports Sciences. - : Routledge. - 0264-0414 .- 1466-447X. ; 28:9, s. 947-955
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Tidskriftsartikel (refereegranskat)abstract
- 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.
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| 8. |
- Fernström, Maria, 1960-, et al.
(författare)
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Improved Muscle Mitochondrial Capacity Following Gastric Bypass Surgery in Obese Subjects
- 2016
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Ingår i: Obesity Surgery. - New York, USA : Springer. - 0960-8923 .- 1708-0428. ; 26:7, s. 1391-1397
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Tidskriftsartikel (refereegranskat)abstract
- Background: Weight loss resulting from low-calorie diets is often less than expected. We hypothesized that energy restriction would influence proton leakage and improve mitochondrial efficiency, leading to reduced energy expenditure, partly explaining the difficulties in weight loss maintenance.Methods: Eleven women with a median BMI of 38.5 kg/m(2) (q-range 37-40), and referred to gastric bypass surgery participated. Before surgery, and at 6 months of follow-up, muscle biopsies were collected from the vastus lateralis muscle. Mitochondria were isolated and analyzed for coupled (state 3) and uncoupled (state 4) respiration and mitochondrial capacity (P/O ratio).Results: At follow-up, the participants had a median BMI of 29.6 kg/m(2) (28.3-32.0). State 3 increased from 20.6 (17.9-28.9) to 34.9 nmol O2/min/U citrate synthase (CS) (27.0-49.0), p = 0.01, while state 4 increased from 2.8 (1.8-4.2) to 4.2 nmol O2/min/U CS (3.1-6.1), although not statistically significant. The P/O ratio increased from 2.7 (2.5-2.8) to 3.2 (3.0-3.4), p = 0.02, indicating improved mitochondrial efficiency.Conclusions: Six months after gastric bypass surgery, the mitochondrial capacity for coupled, i.e., ATP-generating, respiration increased, and the P/O ratio improved. Uncoupled respiration was not enhanced to the same extent. This could partly explain the decreased basal metabolism and the reduced inclination for weight loss during energy restriction.
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| 9. |
- Fernström, Maria, et al.
(författare)
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Reduced efficiency, but increased fat oxidation, in mitochondria from human skeletal muscle after 24-h ultraendurance exercise.
- 2007
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Ingår i: Journal of applied physiology. - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 102:5, s. 1844-1849
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Tidskriftsartikel (refereegranskat)abstract
- 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.
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| 10. |
- Fernström, Maria, et al.
(författare)
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Skeletal muscle mitochondrial function and ROS production in response to extreme endurance exercise in athletes.
- 2006
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Ingår i: 14 European bioenergetic conference, Moscow, Russia, 22-27 July, 2006.
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
- Although it is well known that endurance exercise induces oxidative stress (1) there is no evidence of deteriorated mitochondrial function after 1-2 hours intensive exercise (2). However, the effects of extreme endurance exercise on mitochondrial function and mitochondrial ROS production have not been investigated previously. Nine healthy well-trained men (age 27.1 ± 0.87 (mean ± SE), BMI 24.2 ± 0.64 and VO2 peak 62.5 ± 1.78 ml/kg. min) performed 24 hours exercise, consisting of equal parts running, cycling and paddling. Muscle biopsies were taken from vastus lateralis pre-exercise (PreEx), immediately post-exercise (PostEx) and after 28 hours of recovery (PostEx-28). Mitochondria were isolated and mitochondrial respiration was analyzed with palmitoyl-carnitine (PC) and pyruvate (Pyr). Mitochondrial H2O2 release was measured with the Amplex Red-horseradish peroxide method. The reaction was initiated by addition of succinate with following addition of antimycin A (reversed electron flow). UCP3 protein expression, evaluated with western blot technique, was not changed by exercise. Both state 3 (Pyr and PC) and state 4 (PC) rates of oxygen consumption (estimated per maximal ETC-activity) were increased PostEx (+29%, +11% and +18%). State 3 remained elevated PostEx-28, whereas state 4 (Pyr) decreased below that at PreEx (-18%). Mitochondrial efficiency (P/O) decreased PostEx (Pyr -8.9%, PC -6.1%) and remained reduced PostEx-28. The relative substrate oxidation (state 3 PC/Pyr) increased after exercise PreEx: (0.71 ± 0.06 vs. PostEx (0.90 ±0.04) and (0.77 ±0.06) PostEx-28. Mitochondrial H2O2 release (succinate) increased dramatically after exercise (+189 ± 64%). Treatment with Antimycin A resulted in a twofold-increased rate of mitochondrial H2O2 release PreEx but a decreased rate in PostEx samples. The exercise-induced changes in mitochondrial ROS production was totally abolished PostEx-28. In conclusion extreme endurance exercise decreases mitochondrial efficiency and increases mitochondrial ROS production. Both of these changes would increase the oxygen demand during exercise. Relative fatty acid oxidation as measured in isolated mitochondria increased after exercise indicating that the capacity to oxidize fat is improved during prolonged exercise.1. Mastaloudis, A., S.W. Leonard, and M.G. Traber, Oxidative stress in athletes during extreme endurance exercise. Free Radic Biol Med, 2001. 31(7): p. 911-22.2. Tonkonogi, M., et al., Mitochondrial function and antioxidative defence in human muscle: effects of endurance training and oxidative stress. J Physiol, 2000. 528 Pt 2: p. 379-88.
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