| 1. |
- Björkman, Frida, et al.
(author)
-
Regular moist snuff dipping does not affect endurance exercise performance
- 2017
-
In: Plos One. - : Public Library of Science (PLoS). - 1932-6203. ; 12:7
-
Journal article (peer-reviewed)abstract
- Physiological and medical effects of snuff have previously been obtained either in cross-sectional studies or after snuff administration to non-tobacco users. The effects of snuff cessation after several years of daily use are unknown. 24 participants with >2 years of daily snuff-use were tested before and after >6 weeks snuff cessation (SCG). A control group (CO) of 11 snuff users kept their normal habits. Resting heart rate (HR) and blood pressure (BP) were significantly lower in SCG after snuff cessation, and body mass was increased by 1.4 +/- 1.7 kg. Total cholesterol increased from 4.12 +/- 0.54 (95% CI 3.89-4.35) to 4.46 +/- 0.70 (95% CI 4.16-4.75) mM L-1 in SCG, due to increased LDL, and this change was significantly different from CO. Resting values of HDL, C-reactive protein, and free fatty acids (FFA) remained unchanged in both groups. In SCG group, both HR and BP were reduced during a four-stage incremental cycling test (from 50 to 80% of VO(2)max) and a prolonged cycling test (60 min at 50% of VO(2)max). Oxygen uptake (VO2), respiratory exchange ratio, blood lactate (bLa) and blood glucose (bGlu) concentration, and rate of perceived exertion (RPE) were unchanged. In CO group, all measurements were unchanged. During the prolonged cycling test, FFA was reduced, but with no significant difference between groups. During the maximal treadmill running test peak values of VO2, pulmonary ventilation (VE), time to exhaustion and bLa were unchanged in both groups. In conclusion, endurance exercise performance (VO(2)dmax and maximal endurance time) does not seem to be affected by prolonged snuff use, while effects on cardiovascular risk factors are contradictory. HR and BP during rest and submaximal exercise are reduced after cessation of regular use of snuff. Evidently, the long-time adrenergic stress on circulation is reversible.
|
|
| 2. |
- Boushel, Robert, et al.
(author)
-
Maintained peak leg and pulmonary VO2 despite substantial reduction in muscle mitochondrial capacity.
- 2015
-
In: Scandinavian Journal of Medicine and Science in Sports. - : Wiley. - 0905-7188 .- 1600-0838. ; 25:Suppl 4, s. 135-143
-
Journal article (peer-reviewed)abstract
- We recently reported the circulatory and muscle oxidative capacities of the arm after prolonged low-intensity skiing in the arctic (Boushel et al., 2014). In the present study, leg VO2 was measured by the Fick method during leg cycling while muscle mitochondrial capacity was examined on a biopsy of the vastus lateralis in healthy volunteers (7 male, 2 female) before and after 42 days of skiing at 60% HR max. Peak pulmonary VO2 (3.52 ± 0.18 L.min(-1) pre vs 3.52 ± 0.19 post) and VO2 across the leg (2.8 ± 0.4L.min(-1) pre vs 3.0 ± 0.2 post) were unchanged after the ski journey. Peak leg O2 delivery (3.6 ± 0.2 L.min(-1) pre vs 3.8 ± 0.4 post), O2 extraction (82 ± 1% pre vs 83 ± 1 post), and muscle capillaries per mm(2) (576 ± 17 pre vs 612 ± 28 post) were also unchanged; however, leg muscle mitochondrial OXPHOS capacity was reduced (90 ± 3 pmol.sec(-1) .mg(-1) pre vs 70 ± 2 post, P < 0.05) as was citrate synthase activity (40 ± 3 μmol.min(-1) .g(-1) pre vs 34 ± 3 vs P < 0.05). These findings indicate that peak muscle VO2 can be sustained with a substantial reduction in mitochondrial OXPHOS capacity. This is achieved at a similar O2 delivery and a higher relative ADP-stimulated mitochondrial respiration at a higher mitochondrial p50. These findings support the concept that muscle mitochondrial respiration is submaximal at VO2max , and that mitochondrial volume can be downregulated by chronic energy demand.
|
|
| 3. |
|
|
| 4. |
- Cardinale, Daniele A., 1982-, et al.
(author)
-
Influence of Hyperoxic-Supplemented High-Intensity Interval Training on Hemotological and Muscle Mitochondrial Adaptations in Trained Cyclists.
- 2019
-
In: Frontiers in Physiology. - : Frontiers Media S.A.. - 1664-042X. ; 10
-
Journal article (peer-reviewed)abstract
- Background: Hyperoxia (HYPER) increases O2 carrying capacity resulting in a higher O2 delivery to the working muscles during exercise. Several lines of evidence indicate that lactate metabolism, power output, and endurance are improved by HYPER compared to normoxia (NORM). Since HYPER enables a higher exercise power output compared to NORM and considering the O2 delivery limitation at exercise intensities near to maximum, we hypothesized that hyperoxic-supplemented high-intensity interval training (HIIT) would upregulate muscle mitochondrial oxidative capacity and enhance endurance cycling performance compared to training in normoxia. Methods: 23 trained cyclists, age 35.3 ± 6.4 years, body mass 75.2 ± 9.6 kg, height 179.8 ± 7.9 m, and VO2max 4.5 ± 0.7 L min-1 performed 6 weeks polarized and periodized endurance training on a cycle ergometer consisting of supervised HIIT sessions 3 days/week and additional low-intensity training 2 days/week. Participants were randomly assigned to either HYPER (FIO2 0.30; n = 12) or NORM (FIO2 0.21; n = 11) breathing condition during HIIT. Mitochondrial respiration in permeabilized fibers and isolated mitochondria together with maximal and submaximal VO2, hematological parameters, and self-paced endurance cycling performance were tested pre- and posttraining intervention. Results: Hyperoxic training led to a small, non-significant change in performance compared to normoxic training (HYPER 6.0 ± 3.7%, NORM 2.4 ± 5.0%; p = 0.073, ES = 0.32). This small, beneficial effect on the self-paced endurance cycling performance was not explained by the change in VO2max (HYPER 1.1 ± 3.8%, NORM 0.0 ± 3.7%; p = 0.55, ES = 0.08), blood volume and hemoglobin mass, mitochondrial oxidative phosphorylation capacity (permeabilized fibers: HYPER 27.3 ± 46.0%, NORM 16.5 ± 49.1%; p = 0.37, ES = 3.24 and in isolated mitochondria: HYPER 26.1 ± 80.1%, NORM 15.9 ± 73.3%; p = 0.66, ES = 0.51), or markers of mitochondrial content which were similar between groups post intervention. Conclusions: This study showed that 6 weeks hyperoxic-supplemented HIIT led to marginal gain in cycle performance in already trained cyclists without change in VO2max, blood volume, hemoglobin mass, mitochondrial oxidative phosphorylation capacity, or exercise efficiency. The underlying mechanisms for the potentially meaningful performance effects of hyperoxia training remain unexplained and may raise ethical questions for elite sport.
|
|
| 5. |
- Cardinale, Daniele A., 1982-, et al.
(author)
-
Muscle mass and inspired oxygen influence oxygen extraction at maximal exercise : role of mitochondrial oxygen affinity.
- 2019
-
In: Acta Physiologica. - : Wiley-Blackwell. - 1748-1708 .- 1748-1716. ; 225:1
-
Journal article (peer-reviewed)abstract
- AIM:We examined the Fick components together with mitochondrial O2 affinity (p50mito ) in defining O2 extraction and O2 uptake during exercise with large and small muscle mass during normoxia (NORM) and hyperoxia (HYPER).METHODS:Seven individuals performed two incremental exercise tests to exhaustion on a bicycle ergometer (BIKE) and two on a one-legged knee extension ergometer (KE) in NORM or HYPER. Leg blood flow and VO2 were determined by thermodilution and the Fick method. Maximal ADP-stimulated mitochondrial respiration (OXPHOS) and p50mito were measured ex vivo in isolated mitochondria. Mitochondrial excess capacity in the leg was determined from OXPHOS in permeabilized fibers and muscle mass measured with magnetic resonance imaging in relation to peak leg O2 delivery.RESULTS:The ex vivo p50mito increased from 0.06±0.02 to 0.17±0.04 kPa with varying substrate supply and O2 flux rates from 9.84±2.91 to 16.34±4.07 pmol O2 ·s-1 ·μg-1 respectively. O2 extraction decreased from 83% in BIKE to 67% in KE as a function of a higher O2 delivery, and lower mitochondrial excess capacity. There was a significant relationship between O2 extraction and mitochondrial excess capacity and p50mito that was unrelated to blood flow and mean transit time.CONCLUSION:O2 extraction varies with mitochondrial respiration rate, p50mito and O2 delivery. Mitochondrial excess capacity maintains a low p50mito which enhances O2 diffusion from microvessels to mitochondria during exercise. This article is protected by copyright. All rights reserved.
|
|
| 6. |
- Cardinale, Daniele A, et al.
(author)
-
Reliability of maximal mitochondrial oxidative phosphorylation in permeabilized fibers from the vastus lateralis employing high-resolution respirometry.
- 2018
-
In: Physiological Reports. - : Wiley. - 2051-817X. ; 6:4
-
Journal article (peer-reviewed)abstract
- The purpose was to assess the impact of various factors on methodological errors associated with measurement of maximal oxidative phosphorylation (OXPHOS) in human skeletal muscle determined by high-resolution respirometry in saponin-permeabilized fibers. Biopsies were collected from 25 men to assess differences in OXPHOS between two muscle bundles and to assess the correlation between OXPHOS and the wet weight of the muscle bundle. Biopsies from left and right thighs of another five subjects were collected on two occasions to compare limbs and time-points. A single muscle specimen was used to assess effects of the anesthetic carbocaine and the influence of technician. The difference in OXPHOS between two fiber-bundles from the same biopsy exhibited a standard error of measurement (SEM) of 10.5 pmol · s-1 · mg-1 and a coefficient of variation (CV) of 15.2%. The differences between left and right thighs and between two different time-points had SEMs of 9.4 and 15.2 pmol · s-1 · mg-1 and CVs of 23.9% and 33.1%, respectively. The average (±SD) values obtained by two technicians monitoring different bundles of fibers from the same biopsy were 31.3 ± 7.1 and 26.3 ± 8.1 pmol · s-1 · mg-1 . The time that elapsed after collection of the biopsy (up to a least 5 h in preservation medium), wet weight of the bundle (from 0.5 to 4.5 mg) and presence of an anesthetic did not influence OXPHOS. The major source of variation in OXPHOS measurements is the sample preparation. The thigh involved, time-point of collection, size of fiber bundles, and time that elapsed after biopsy had minor or no effect.
|
|
| 7. |
- Cardinale, Daniele A., et al.
(author)
-
Resistance Training with Co-ingestion of Anti-inflammatory Drugs Attenuates Mitochondrial Function
- 2017
-
In: Frontiers in Physiology. - : Frontiers Media SA. - 1664-042X. ; 8
-
Journal article (peer-reviewed)abstract
- Aim: The current study aimed to examine the effects of resistance exercise with concomitant consumption of high versus low daily doses of non-steroidal anti-inflammatory drugs (NSAIDs) on mitochondrial oxidative phosphorylation in skeletal muscle. As a secondary aim, we compared the effects of eccentric-overload with conventional training. Methods: Twenty participants were randomized to either a group taking high doses (3 x 400 mg/day) of ibuprofen (IBU; 27±5 yr; n=11) or a group ingesting a low dose (1 x 75 mg/day) of acetylsalicylic acid (ASA; 26±4 yr; n=9) during 8 weeks of supervised knee extensor resistance training. Each of the subject’s legs were randomized to complete the training program using either a flywheel (FW) device emphasizing eccentric-overload, or a traditional weight stack machine (WS). Maximal mitochondrial oxidative phosphorylation (CI+IIP) from permeabilized skeletal muscle bundles was assessed using high-resolution respirometry. Citrate synthase (CS) activity was assessed using spectrophotometric techniques and mitochondrial protein content using western blotting. Results: After training, CI+IIP decreased (P<0.05) in both IBU (23%) and ASA (29%) with no difference across medical treatments. Although CI+IIP decreased in both legs, the decrease was greater (interaction p = 0.015) in WS (33%, p = 0.001) compared with FW (19%, p = 0.078). CS activity increased (p = 0.027) with resistance training, with no interactions with medical treatment or training modality. Protein expression of ULK1 increased with training in both groups (p < 0.001). The increase in quadriceps muscle volume was not correlated with changes in CI+IIP (R=0.16). Conclusion: These results suggest that 8 weeks of resistance training with co-ingestion of anti-inflammatory drugs reduces mitochondrial function but increases mitochondrial content. The observed changes were not affected by higher doses of NSAIDs consumption, suggesting that the resistance training intervention was the prime mediator of the decreased mitochondrial phosphorylation. Finally, we noted that flywheel resistance training, emphasizing eccentric overload, rescued some of the reduction in mitochondrial function seen with conventional resistance training.
|
|
| 8. |
- Cardinale, Daniele A., 1982-, et al.
(author)
-
Superior Intrinsic Mitochondrial Respiration in Women Than in Men.
- 2018
-
In: Frontiers in Physiology. - : Frontiers Media SA. - 1664-042X. ; 9
-
Journal article (peer-reviewed)abstract
- Sexual dimorphism is apparent in humans, however, to date no studies have investigated mitochondrial function focusing on intrinsic mitochondrial respiration (i.e., mitochondrial respiration for a given amount of mitochondrial protein) and mitochondrial oxygen affinity (p50mito) in relation to biological sex in human. A skeletal muscle biopsy was donated by nine active women, and ten men matched for maximal oxygen consumption (VO2max) and by nine endurance trained men. Intrinsic mitochondrial respiration, assessed in isolated mitochondria, was higher in women compared to men when activating complex I (CIP) and complex I+II (CI+IIP) (p < 0.05), and was similar to trained men (CIP, p = 0.053; CI+IIP, p = 0.066). Proton leak and p50mito were higher in women compared to men independent of VO2max. In conclusion, significant novel differences in mitochondrial oxidative function, intrinsic mitochondrial respiration and p50mito exist between women and men. These findings may represent an adaptation in the oxygen cascade in women to optimize muscle oxygen uptake to compensate for a lower oxygen delivery during exercise.
|
|
| 9. |
- Cardinale, Daniele A., 1982-
(author)
-
The significance of mitochondrial respiratory function in regulating oxygen uptake and performance in humans
- 2018
-
Doctoral thesis (other academic/artistic)abstract
- The mitochondrion is one of the most fascinating organelles of our cells which has kept and keeps researchers busy in studying its origin, the complex morphology, the numerous functions, the rapid adaptations to a variety of stimuli and its role in health and disease. Exercise challenges cellular homeostasis and skeletal muscle mitochondria greatly adapt to repeated bouts of exercise by increasing mitochondrial respiratory function and content to match energy requirements and to better sustain future perturbations induced by muscle contractions. The oxidative capacity of mitochondria has been shown to exceed the capacity of the cardiorespiratory system to supply oxygen to active muscle at maximal exercise intensity. Despite this, exercise training further increases this overcapacity. Little is known about the role of this excess oxidative capacity of mitochondria in regulating oxygen consumption, the role of oxygen delivery in determining exercise-induced skeletal muscle adaptations, and whether any sex-related differences exist. The assessment of mitochondrial respiratory function in high resolution respirometer is largely used for clinical and scientific purposes. However, the reliability of this method has not been systematically investigated and warrant further investigation.With this background, specific measures of reliability associated with repeated determination of maximal mitochondrial oxidative phosphorylation in saponin-permeabilized fibres, comparison of the right and left legs, variability with measurements at different time-points and over time, as well as influence of the local anesthetic and wet weight of the fiber bundle on determined maximal mitochondrial oxidative phosphorylation were investigated in paper I. The importance of having the same technicians in preparing the samples, and that the major source of variation in measuring mitochondrial oxidative capacity is the sample preparation per se were shown. Furthermore, other factors such as the possible difference between left and right limbs, two time points of sample collection, fibres bundle weight, time that elapsed after collection of the biopsy, and the use of an anesthetic have only a minor impact on the standard error of the measurement.In paper II the physiological significance of having a mitochondrial oxidative capacity in excess of the capacity of the central circulation to deliver oxygen to the tissue was shown by integrating measures of ex vivo mitochondrial respiratory function with direct in vivo measure of oxygen consumption when performing two-legged cycling and one-legged knee extension exercise while inspiring atmospheric air and oxygen enriched air in the same participants. Excess capacity of mitochondria allows submaximal mitochondrial activation at maximal oxygen delivery, thereby maintaining a high mitochondrial oxygen affinity and a high oxygen extraction peripherally. Considering the widespread and increasing sedentary behavior in a society plagued by diseases often linked to mitochondrial dysfunction, these results suggest the importance of preserving a high muscle oxidative capacity throughout life, which can be of significance in patients with heart, circulatory, and overall metabolic diseases.Despite known sex-specific metabolic differences in human skeletal muscle and that animal models have consistently shown females having a superior mitochondrial function compare to males, data in humans are lacking. In paper III the first evidence that women possess higher mitochondrial quality compared to men with equal cardiorespiratory fitness and endurance performance was provided. Mitochondrial oxygen affinity varied with the degree of mitochondrial respiration rate and was lower in women compared to men. These results indicate that the higher mitochondrial quality in women may be an important physiological adaptation that compensates for the lower mitochondrial oxygen affinity allowing a higher oxygen extraction peripherally. Moreover, these results could possibly be linked to the difference in life expectancy, disease occurrence and aging between women and men.Lastly, in paper IV it was shown that increasing oxygen delivery and exercise intensity by means of breathing hyperoxia during high-intensity exercise did not enhance cardiorespiratory fitness and exercise-induced skeletal muscle adaptations but still resulted in a small beneficial effect on performance in trained cyclists. This small positive effect on performance can be exploited in elite athletes; however, considering the cost/benefit, the unknown health-related problems, and ethical issues of performing hyperoxic-supplemented endurance training, it is arguable if the use of this strategy to maximize endurance performance is worthwhile.Overall, this thesis provides useful information for future research on various factors influencing the error of the measurement when assessing mitochondrial respiratory function. Moreover, this thesis sheds light on novel factors that regulate oxygen consumption during exercise, highlighting the importance of maintaining a good mitochondrial function. This thesis also provides possible directions for future studies on mitochondrial function, metabolism and exercise-induced adaptations.
|
|
| 10. |
- Cardinale, Daniele, et al.
(author)
-
Resistance Exercise Attenuates Mitochondrial Function : Effects Of NSAID Intake And Eccentric-Overload Training
- 2017
-
In: Medicine & Science in Sports & Exercise. 49(5S):329, MAY 2017. - : Ovid Technologies (Wolters Kluwer Health). ; , s. 329-329
-
Conference paper (peer-reviewed)abstract
- Although nonsteroidal antiinflammatorydrugs (NSAIDs) have been shown to modulate skeletal muscle adaptations and protein metabolism in response toresistance exercise, little is known about the effects of NSAIDs on mitochondrial function. Thus, the current study aimed to examine the effects of resistanceexercise with concomitant NSAID consumption on mitochondrial oxidative phosphorylation in skeletal muscle. Twenty participants were randomized in asingleblindedfashion to either an experimental group receiving ibuprofen (IBU: 27±5 yr; n=11; 1200 mg/d) or a control group receiving a lowdoseacetylsalicylic acid (CON: 26±4 yr; n=9; 75 mg/d) During this period, subjects performed 8 weeks of supervised resistance exercise involving the kneeextensors muscles. Each of the subject’s legs were randomized to complete the training program using either a flywheel (FW) device emphasizing eccentricoverload,or a traditional weight stack machine (WS). Maximal mitochondrial oxidative phosphorylation (OXPHOS) from permeabilized skeletal muscle bundleswas assessed using high resolution respirometry before and after the training intervention. Citrate synthase activity was assessed using spectrophotometrictechniques. After training, OXPHOS decreased (P<0.05) in both IBU (23%) and CON (29%) with no difference across medical treatments. Although OXPHOSdecreased in both legs, the decrease was greater (interaction P= 0.015) in WS (33%, P= 0.015) than in FW (19%, P= 0.078). Citrate synthase (CS) did notchange after the intervention. The increase in quadriceps muscle volume was not significantly correlated with the change in OXPHOS (R=0.15). These resultssuggest that 1) eight weeks of resistance training reduces mitochondrial function but not mitochondrial content, 2) The decreased mitochondrial function withresistance exercise was not affected by ibuprofen consumption, 3) flywheel resistance training, emphasizing eccentric overload, rescues some of thereduction in mitochondrial function seen with conventional resistance training.
|
|
