Prescribing the frequency, duration, or volume of training is simple as these factors can be altered by manipulating the number of exercise sessions per week, the duration of each session, or the ...total work performed in a given time frame (e.g., per week). However, prescribing exercise intensity is complex and controversy exists regarding the reliability and validity of the methods used to determine and prescribe intensity. This controversy arises from the absence of an agreed framework for assessing the construct validity of different methods used to determine exercise intensity. In this review, we have evaluated the construct validity of different methods for prescribing exercise intensity based on their ability to provoke homeostatic disturbances (e.g., changes in oxygen uptake kinetics and blood lactate) consistent with the moderate, heavy, and severe domains of exercise. Methods for prescribing exercise intensity include a percentage of anchor measurements, such as maximal oxygen uptake (Formula: see text), peak oxygen uptake (Formula: see text), maximum heart rate (HR
), and maximum work rate (i.e., power or velocity-Formula: see text or Formula: see text, respectively), derived from a graded exercise test (GXT). However, despite their common use, it is apparent that prescribing exercise intensity based on a fixed percentage of these maximal anchors has little merit for eliciting distinct or domain-specific homeostatic perturbations. Some have advocated using submaximal anchors, including the ventilatory threshold (VT), the gas exchange threshold (GET), the respiratory compensation point (RCP), the first and second lactate threshold (LT
and LT
), the maximal lactate steady state (MLSS), critical power (CP), and critical speed (CS). There is some evidence to support the validity of LT
, GET, and VT to delineate the moderate and heavy domains of exercise. However, there is little evidence to support the validity of most commonly used methods, with exception of CP and CS, to delineate the heavy and severe domains of exercise. As acute responses to exercise are not always predictive of chronic adaptations, training studies are required to verify whether different methods to prescribe exercise will affect adaptations to training. Better ways to prescribe exercise intensity should help sport scientists, researchers, clinicians, and coaches to design more effective training programs to achieve greater improvements in health and athletic performance.
A sedentary lifestyle has been linked to a number of metabolic disorders that have been associated with sub-optimal mitochondrial characteristics and an increased risk of premature death. Endurance ...training can induce an increase in mitochondrial content and/or mitochondrial functional qualities, which are associated with improved health and well-being and longer life expectancy. It is therefore important to better define how manipulating key parameters of an endurance training intervention can influence the content and functionality of the mitochondrial pool. This review focuses on mitochondrial changes taking place following a series of exercise sessions (training-induced mitochondrial adaptations), providing an in-depth analysis of the effects of exercise intensity and training volume on changes in mitochondrial protein synthesis, mitochondrial content and mitochondrial respiratory function. We provide evidence that manipulation of different exercise training variables promotes specific and diverse mitochondrial adaptations. Specifically, we report that training volume may be a critical factor affecting changes in mitochondrial content, whereas relative exercise intensity is an important determinant of changes in mitochondrial respiratory function. As a consequence, a dissociation between training-induced changes in mitochondrial content and mitochondrial respiratory function is often observed. We also provide evidence that exercise-induced changes are not necessarily predictive of training-induced adaptations, we propose possible explanations for the above discrepancies and suggestions for future research.
Background To determine the validity of the lactate threshold (LT) and maximal oxygen uptake () determined during graded exercise test (GXT) of different durations and using different LT ...calculations. Trained male cyclists (n = 17) completed five GXTs of varying stage length (1, 3, 4, 7 and 10 min) to establish the LT, and a series of 30-min constant power bouts to establish the maximal lactate steady state (MLSS). was assessed during each GXT and a subsequent verification exhaustive bout (VEB), and 14 different LTs were calculated from four of the GXTs (3, 4, 7 and 10 min)—yielding a total 56 LTs. Agreement was assessed between the highest measured during each GXT () as well as between each LT and MLSS. and LT data were analysed using mean difference (MD) and intraclass correlation (ICC). Results The value from GXT1 was 61.0 ± 5.3 mL.kg-1.min-1 and the peak power 420 ± 55 W (mean ± SD). The power at the MLSS was 264 ± 39 W. from GXT3, 4, 7, 10 underestimated by ~1–5 mL.kg-1.min-1. Many of the traditional LT methods were not valid and a newly developed Modified Dmax method derived from GXT4 provided the most valid estimate of the MLSS (MD = 1.1 W; ICC = 0.96). Conclusion The data highlight how GXT protocol design and data analysis influence the determination of both and LT. It is also apparent that and LT cannot be determined in a single GXT, even with the inclusion of a VEB.
Physical inactivity represents the fourth leading risk factor for mortality, and it has been linked with a series of chronic disorders, the treatment of which absorbs ~ 85% of healthcare costs in ...developed countries. Conversely, physical activity promotes many health benefits; endurance exercise in particular represents a powerful stimulus to induce mitochondrial biogenesis, and it is routinely used to prevent and treat chronic metabolic disorders linked with sub-optimal mitochondrial characteristics. Given the importance of maintaining a healthy mitochondrial pool, it is vital to better characterize how manipulating the endurance exercise dose affects cellular mechanisms of exercise-induced mitochondrial biogenesis. Herein, we propose a definition of mitochondrial biogenesis and the techniques available to assess it, and we emphasize the importance of standardizing biopsy timing and the determination of relative exercise intensity when comparing different studies. We report an intensity-dependent regulation of exercise-induced increases in nuclear peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) protein content, nuclear phosphorylation of p53 (serine 15), and PGC-1α messenger RNA (mRNA), as well as training-induced increases in PGC-1α and p53 protein content. Despite evidence that PGC-1α protein content plateaus within a few exercise sessions, we demonstrate that greater training volumes induce further increases in PGC-1α (and p53) protein content, and that short-term reductions in training volume decrease the content of both proteins, suggesting training volume is still a factor affecting training-induced mitochondrial biogenesis. Finally, training-induced changes in mitochondrial transcription factor A (TFAM) protein content are regulated in a training volume-dependent manner and have been linked with training-induced changes in mitochondrial content.
Mitochondrial defects are implicated in multiple diseases and aging. Exercise training is an accessible, inexpensive therapeutic intervention that can improve mitochondrial bioenergetics and quality ...of life. By combining multiple omics techniques with biochemical and in silico normalisation, we removed the bias arising from the training-induced increase in mitochondrial content to unearth an intricate and previously undemonstrated network of differentially prioritised mitochondrial adaptations. We show that changes in hundreds of transcripts, proteins, and lipids are not stoichiometrically linked to the overall increase in mitochondrial content. Our findings suggest enhancing electron flow to oxidative phosphorylation (OXPHOS) is more important to improve ATP generation than increasing the abundance of the OXPHOS machinery, and do not support the hypothesis that training-induced supercomplex formation enhances mitochondrial bioenergetics. Our study provides an analytical approach allowing unbiased and in-depth investigations of training-induced mitochondrial adaptations, challenging our current understanding, and calling for careful reinterpretation of previous findings.
Autophagy is a key intracellular mechanism by which cells degrade old or dysfunctional proteins and organelles. In skeletal muscle, evidence suggests that exercise increases autophagosome content and ...autophagy flux. However, the exercise-induced response seems to differ between rodents and humans, and little is known about how different exercise prescription parameters may affect these results. The present study utilised skeletal muscle samples obtained from four different experimental studies using rats and humans. Here, we show that, following exercise, in the soleus muscle of Wistar rats, there is an increase in LC3B-I protein levels immediately after exercise (+109%), and a subsequent increase in LC3B-II protein levels 3 h into the recovery (+97%), despite no change in
mRNA levels. Conversely, in human skeletal muscle, there is an immediate exercise-induced decrease in LC3B-II protein levels (-24%), independent of whether exercise is performed below or above the maximal lactate steady state, which returns to baseline 3.5 h following recovery, while no change in LC3B-I protein levels or
mRNA levels is observed.
/p62 protein and mRNA levels did not change in either rats or humans following exercise. By employing an ex vivo autophagy flux assay previously used in rodents we demonstrate that the exercise-induced decrease in LC3B-II protein levels in humans does not reflect a decreased autophagy flux. Instead, effect size analyses suggest a modest-to-large increase in autophagy flux following exercise that lasts up to 24 h. Our findings suggest that exercise-induced changes in autophagosome content markers differ between rodents and humans, and that exercise-induced decreases in LC3B-II protein levels do not reflect autophagy flux level.
Background
Inadequate sleep is associated with many detrimental health effects, including increased risk of developing insulin resistance and type 2 diabetes. These effects have been associated with ...changes to the skeletal muscle transcriptome, although this has not been characterised in response to a period of sleep restriction. Exercise induces a beneficial transcriptional response within skeletal muscle that may counteract some of the negative effects associated with sleep restriction. We hypothesised that sleep restriction would down-regulate transcriptional pathways associated with glucose metabolism, but that performing exercise would mitigate these effects.
Methods
20 healthy young males were allocated to one of three experimental groups: a Normal Sleep (NS) group (8 h time in bed per night (TIB), for five nights (11 pm – 7 am)), a Sleep Restriction (SR) group (4 h TIB, for five nights (3 am – 7 am)), and a Sleep Restriction and Exercise group (SR+EX) (4 h TIB, for five nights (3 am – 7 am) and three high-intensity interval exercise (HIIE) sessions (performed at 10 am)). RNA sequencing was performed on muscle samples collected pre- and post-intervention. Our data was then compared to skeletal muscle transcriptomic data previously reported following sleep deprivation (24 h without sleep).
Results
Gene set enrichment analysis (GSEA) indicated there was an increased enrichment of inflammatory and immune response related pathways in the SR group post-intervention. However, in the SR+EX group the direction of enrichment in these same pathways occurred in the opposite directions. Despite this, there were no significant changes at the individual gene level from pre- to post-intervention. A set of genes previously shown to be decreased with sleep deprivation was also decreased in the SR group, but increased in the SR+EX group.
Conclusion
The alterations to inflammatory and immune related pathways in skeletal muscle, following five nights of sleep restriction, provide insight regarding the transcriptional changes that underpin the detrimental effects associated with sleep loss. Performing three sessions of HIIE during sleep restriction attenuated some of these transcriptional changes. Overall, the transcriptional alterations observed with a moderate period of sleep restriction were less evident than previously reported changes following a period of sleep deprivation.
The maximal oxygen uptake (VO2max) is deemed the highest predictor for all-cause mortality, and therefore, an ability to assess VO2max is important. The YMCA submaximal test is one of the most widely ...used tests to estimate VO2max; however, it has questionable validity.
We validated a customized submaximal test that accounts for the nonlinear rise in VO2 relative to power output and compared its accuracy against the YMCA protocol.
Fifty-six men and women performed a graded exercise test with a subsequent exhaustive, square wave bout for the verification of "true" VO2max. In counterbalanced order, subjects then completed the YMCA test and our new Mankato submaximal exercise test (MSET). The MSET consisted of a 3-min stage estimated at 35% VO2max and a second 3-min stage estimated at either 65% or 70% VO2max, where VO2max was estimated with a regression equation using sex, body mass index, age, and self-reported PA-R.
VO2 values from the graded exercise test and square wave verification bout did not differ with the highest value used to identify "true" VO2max (45.1 ± 8.89 mL · kg(-1) · min(-1)). The MSET (43.6 ± 8.6 mL · kg(-1) · min(-1)) did not differ from "true" VO2max, whereas the YMCA test (41.1 ± 9.6 mL · kg(-1) · min(-1)) yielded an underestimation (P = 0.002). The MSET was moderately correlated with "true" VO2max (ICC = 0.73, CV of 11.3%). The YMCA test was poorly correlated with "true" VO2max (ICC = 0.29, CV of 15.1%).
To our knowledge, this is the first study to examine submaximal exercise protocols versus a verified VO2max protocol. The MSET yielded better estimates of VO2max because of the protocol including a stage exceeding gas exchange threshold.
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