Methods of monitoring training load and their relationships to changes in fitness and performance in competitive road cyclists

Purpose: The aim of this study was to assess the dose-response relationships between different training load methods and aerobic fitness and performance in competitive road cyclists. Method: Training data from 15 well-trained competitive cyclists were collected during a 10-week (December – March) pre-season training period. Before and after the training period, participants underwent a laboratory incremental exercise test with gas exchange and lactate measures and a performance assessment using an 8-min time trial (8MT). Internal training load was calculated using Banister’s TRIMP (bTRIMP), Edwards’ TRIMP (eTRIMP), individualized TRIMP (iTRIMP), Lucia’s TRIMP (luTRIMP) and session-RPE (sRPE). External load was measured using Training Stress Score™ (TSS). Results: Large to very large relationships (r = 0.54-0.81) between training load and changes in submaximal fitness variables (power at 2 and 4 mmol·L-1) were observed for all training load calculation methods. The strongest relationships with changes in aerobic fitness variables were observed for iTRIMP (r = 0.81 [95% CI: 0.51 to 0.93, r = 0.77 [95% CI 0.43 to 0.92]) and TSS (r = 0.75 [95% CI 0.31 to 0.93], r = 0.79 [95% CI: 0.40 to 0.94]). The highest dose-response relationships with changes in the 8MT performance test were observed for iTRIMP (r = 0.63 [95% CI 0.17 to 0.86]) and luTRIMP (r = 0.70 [95% CI: 0.29 to 0.89). Conclusions: The results show that training load quantification methods that integrate individual physiological characteristics have the strongest dose-response relationships, suggesting this to be an essential factor in the quantification of training load in cycling

The effect of UCP3 overexpression on mitochondrial ROS production in skeletal muscle of young versus aged mice

AbstractUncoupling protein 3 (UCP3) is suggested to protect mitochondria against aging and lipid-induced damage, possibly via modulation of reactive oxygen species (ROS) production. Here we show that mice overexpressing UCP3 (UCP3Tg) have a blunted age-induced increase in ROS production, assessed by electron spin resonance spectroscopy, but only after addition of 4-hydroxynonenal (4-HNE). Mitochondrial function, assessed by respirometry, on glycolytic substrate was lower in UCP3Tg mice compared to wild types, whereas this tended to be higher on fatty acids. State 4o respiration was higher in UCP3Tg animals. To conclude, UCP3 overexpression leads to increased state 4o respiration and, in presence of 4-HNE, blunts the age-induced increase in ROS production

Differences in Performance Assessments Conducted Indoors and Outdoors in Professional Cyclists

Purpose: The purpose of this study was to assess the relationship between typical performance tests amongst elite and professional cyclists when conducted indoors and outdoors. Methods: 14 male cyclists of either UCI Continental or UCI World Tour level (mean ± SD: age 20.9 ± 2.8 y, mass 68.13 ± 7.25 kg) were recruited to participate in 4 test sessions (2 test sessions indoors, 2 test sessions outdoors) within a 14-day period, consisting of maximum mean power (MMP) testing for durations of 60s, 180s, 300s and 840s. Results: Across all MMP test durations, the trimmed mean power was higher outdoors compared to indoor testing (p < 0.05). Critical Power (CP) was higher outdoors compared to indoors (+19 W, p = 0.005) whilst no difference was observed for the work capacity above CP (W’). Self-selected cadence was 6 rev∙min-1 higher indoors versus outdoors for test durations of 60s (p = 0.038) and 300s (p = 0.002). Conclusions: These findings suggest that maximal power testing in indoor and outdoor settings cannot be used interchangeably. Furthermore, there was substantial individual variation in the difference between indoor and outdoor MMPs, across all time durations, further highlighting the difficulty of translating results from indoor testing to outdoor, on an individual level in elite populations

Human uncoupling protein-3 and obesity: An update

The cloning of the uncoupling protein (UCP)1 homologs UCP2 and UCP3 has raised considerable interest in the mechanism. The expression of UCP3 mainly in skeletal muscle mitochondria and the potency of the skeletal muscle as a thermogenic organ made UCP3 an attractive target for studies toward manipulation of energy expenditure to fight disorders such as obesity and type 2 diabetes. Overexpressing UCP3 in mice resulted in lean, hyperphagic mice. However, the lack of an apparent phenotype in mice lacking UCP3 triggered the search for alternative functions of UCP3. The observation that fatty acid levels significantly affect UCP3 expression has given UCP3 a position in fatty acid handling and/or oxidation. Emerging data indicate that the primary physiological role of UCP3 may be the mitochondrial handling of fatty acids rather than the regulation of energy expenditure through thermogenesis. It has been proposed that UCP3 functions to export fatty acid anions away from the mitochondrial matrix. In doing so, fatty acids are exchanged with protons, explaining the uncoupling activity of UCP3. The exported fatty acid anions may originate from hydrolysis of fatty acid esters by a mitochondrial thioesterase, or they may have entered the mitochondria as nonesterified fatty acids by incorporating into and flip-flopping across the mitochondrial inner membrane. Regardless of the origin of the fatty acid anions, this putative function of UCP3 might be of great importance in protecting mitochondria against fatty acid accumulation and may help to maintain muscular fat oxidative capacity

Physical Activity Energy Expenditure in Dutch Adolescents: Contribution of Active Transport to School, Physical Education and Leisure Time Activities

In dit artikel is het energieverbruik van adolescenten gedurende een schoolweek en een weekend in kaart gebracht. Hierbij is gebruik gemaakt van gecombineerde hartslag-versnellingsmeters. Doordat deelnemers gelijktijdig een beweegdagboek bij hebben gehouden kon ook de afzonderlijke bijdrage aan het totale energievebruik van lichamelijke opvoeding, actief transport naar school en sporten in de vrije tijd bepaald worden

Mechanical efficiency in chronic obstructive pulmonary disease

The primary aims of this study were (1) to evaluate whole-body mechanical efficiency (ME) in a large group of chronic obstructive pulmonary disease (COPD) patients with a wide range of degrees of illness and (2) to examine how ME in COPD is related to absolute work rate and indices of disease severity during exercise testing. A total of 569 patients (301 male patients; GOLD stage I: 28, GOLD stage II: 166, GOLD stage III: 265, and GOLD stage IV: 110) with chronic obstructive pulmonary disease (COPD) were included in the data analysis. Individual maximal workload (watt), peak minute ventilation ((Equation is included in full-text article.)E, L/min body temperature and pressure, saturated), and peak oxygen uptake ((Equation is included in full-text article.)O2, mL/min standard temperature and pressure, dry) were determined from a maximal incremental cycle ergometer test. Ventilatory and metabolic response parameters were collected during a constant work rate test at 75% of the individual maximal workload. From the exercise responses of the constant work rate test, the gross ME was calculated. The mean whole-body gross ME was 11.0 ± 3.5% at 75% peak power. The ME declined significantly (P < .001) with increasing severity of the disease when measured at the same relative power. Log-transformed absolute work rate (r = .87, P < .001) was the strongest independent predictor of gross ME. Body mass was the single other variable that contributed significantly to the linear regression model. Gross ME in COPD was largely predicted by the absolute work rate (r = .87; P < .001) while indices of the severity of the disease did not predict ME in COPD

The effect of high-fat feeding on intramuscular lipid and lipid peroxidation levels in UCP3-ablated mice

AbstractUncoupling protein-3 (UCP3) has been suggested to protect against lipid-induced oxidative damage. Therefore, we studied intramuscular lipid peroxide levels and high-fat diet induced alterations in muscle lipid metabolism of UCP3-ablated mice.UCP3−/− mice showed ∼3-fold higher levels of intramuscular lipid peroxides upon standard chow feeding, compared to wild-type littermates. Remarkably, this difference was no longer apparent on the high-fat diet. However, upon high-fat feeding, intramuscular triacylglycerol levels were ∼50% lower in UCP3−/− mice, in comparison to UCP3+/+ animals. Succinate dehydrogenase activity, and total protein content of the muscle fatty acid transporter FAT/CD36 were however similar between UCP3−/− and UCP3+/+ mice

Twenty-four hour rhythmicity in mitochondrial network connectivity and mitochondrial respiration; a study in human skeletal muscle biopsies of young lean and older individuals with obesity

Objective: Mitochondrial network dynamics may play role in metabolic homeostasis. Whether mitochondrial network dynamics are involved in adaptations to day–night fluctuations in energy supply and demand is unclear. Here we visualized and quantified the mitochondrial network morphology in human skeletal muscle of young healthy lean and older individuals with obesity over the course of 24 h Methods: Muscle biopsies taken at 5 timepoints over a 24-hour period obtained from young healthy lean and older metabolically impaired obese males were analyzed for mitochondrial network integrity with confocal laser scanning microscopy. Variation of level of fragmentation over the course of the day were aligned with variation of mitochondrial respiration over the day Results: Young healthy lean individuals displayed a day–night rhythmicity in mitochondrial network morphology, which aligned with the day–night rhythmicity of mitochondrial respiratory capacity, with a more fused network coinciding with higher mitochondrial respiratory capacity. In the older individuals with obesity, the mitochondrial network was more fragmented overall compared to young healthy lean individuals and completely lacked 24 h rhythmicity, which was also true for the mitochondrial respiratory capacity Conclusions: Our data shows a paralleled rhythmicity between mitochondrial network morphology and mitochondrial oxidative capacity, which oscillates over the course of a mimicked real-life day in human skeletal muscle of young, healthy lean individuals. In older individuals with obesity, the lack of a 24-hour rhythmicity in mitochondrial network connectivity was also aligned with a lack in respiratory capacity. This suggests that 24-hour rhythmicity in mitochondrial network connectivity is a determinant of rhythmicity in mitochondrial respiratory capacity. Thus, restoring mitochondrial network integrity may promote mitochondrial respiratory capacity and hence contribute to blunting the metabolic aberrations in individuals with a disturbed 24-hour rhythmicity in metabolism, like older individuals with obesity