Durability of the moderate-to-heavy-intensity transition is related to the effects of prolonged exercise on severe-intensity performance.

PURPOSE: Power output at the moderate-to-heavy-intensity transition decreases during prolonged exercise, and resilience to this has been termed 'durability'. The purpose of this study was to assess the relationship between durability and the effect of prolonged exercise on severe-intensity performance, and explore intramuscular correlates of durability. METHODS: On separate days, 13 well-trained cyclists and triathletes (V̇O2peak, 57.3 ± 4.8 mL kg-1 min-1; training volume, 12 ± 2.1 h week-1) undertook an incremental test and 5-min time trial (TT) to determine power output at the first ventilatory threshold (VT1) and severe-intensity performance, with and without 150-min of prior moderate-intensity cycling. A single resting vastus lateralis microbiopsy was obtained. RESULTS: Prolonged exercise reduced power output at VT1 (211 ± 40 vs. 198 ± 39 W, ∆ -13 ± 16 W, ∆ -6 ± 7%, P = 0.013) and 5-min TT performance (333 ± 75 vs. 302 ± 63 W, ∆ -31 ± 41 W, ∆ -9 ± 10%, P = 0.017). The reduction in 5-min TT performance was significantly associated with durability of VT1 (rs = 0.719, P = 0.007). Durability of VT1 was not related to vastus lateralis carnosine content, citrate synthase activity, or complex I activity (P > 0.05). CONCLUSION: These data provide the first direct support that durability of the moderate-to-heavy-intensity transition is an important performance parameter, as more durable athletes exhibited smaller reductions in 5-min TT performance following prolonged exercise. We did not find relationships between durability and vastus lateralis carnosine content, citrate synthase activity, or complex I activity.

Locally applied heat stress during exercise training may promote adaptations to mitochondrial enzyme activities in skeletal muscle.

There is some evidence for temperature-dependent stimulation of mitochondrial biogenesis; however, the role of elevated muscle temperature during exercise in mitochondrial adaptation to training has not been studied in humans in vivo. The purpose of this study was to determine the role of elevating muscle temperature during exercise in temperate conditions through the application of mild, local heat stress on mitochondrial adaptations to endurance training. Eight endurance-trained males undertook 3 weeks of supervised cycling training, during which mild (~ 40 °C) heat stress was applied locally to the upper-leg musculature of one leg during all training sessions (HEAT), with the contralateral leg serving as the non-heated, exercising control (CON). Vastus lateralis microbiopsies were obtained from both legs before and after the training period. Training-induced increases in complex I (fold-change, 1.24 ± 0.33 vs. 1.01 ± 0.49, P = 0.029) and II (fold-change, 1.24 ± 0.33 vs. 1.01 ± 0.49, P = 0.029) activities were significantly larger in HEAT than CON. No significant effects of training, or interactions between local heat stress application and training, were observed for complex I-V or HSP70 protein expressions. Our data provides partial evidence to support the hypothesis that elevating local muscle temperature during exercise augments training-induced adaptations to mitochondrial enzyme activity.

Power output at the moderate-to-heavy intensity transition decreases in a non-linear fashion during prolonged exercise.

PURPOSE: The aims of this study were to: (i) describe the time course of the decrease in power output at the moderate-to-heavy intensity transition during prolonged exercise; (ii) investigate the association between durability of the moderate-to-heavy intensity transition and exercise capacity; and (iii) explore physiological correlates of durability of the moderate-to-heavy intensity transition. METHODS: Twelve trained cyclists (age: 40 ± 8 y, V ˙ O2peak: 52.3 ± 5.2 mL·min-1·kg-1) performed an exhaustive cycling protocol involving alternating incremental exercise tests to determine power output at the moderate-to-heavy intensity transition via the first ventilatory threshold (VT1), and 30-min bouts at 90% of the power output at the previously estimated VT1 in the rested state. The individual time course of VT1 was modelled using linear and second-order polynomial functions, and time to a 5% decrease in VT1 (Δ5%VT1) was estimated using the best-fitting model. RESULTS: Power output at VT1 decreased according to a second-order polynomial function in 11 of 12 participants. Time-to-task failure (234 ± 66 min) was correlated with Δ5%VT1 (139 ± 78 min, rs = 0.676, p = 0.016), and these were strongly correlated with absolute and relative rates of fat oxidation at specific exercise intensities measured during the incremental test performed in the rested state. CONCLUSIONS: These data: (i) identify a non-linear time course of decreases in the moderate-to-heavy intensity transition during prolonged exercise; (ii) support the importance of durability of the moderate-to-heavy intensity transition in prolonged exercise capacity; and (iii) suggest durability of the moderate-to-heavy intensity transition is related to fat oxidation rates.

Prolonged exercise shifts ventilatory parameters at the moderate-to-heavy intensity transition.

PURPOSE: To quantify the effects of prolonged cycling on the rate of ventilation ([Formula: see text]), frequency of respiration (FR), and tidal volume (VT) associated with the moderate-to-heavy intensity transition. METHODS: Fourteen endurance-trained cyclists and triathletes (one female) completed an assessment of the moderate-to-heavy intensity transition, determined as the first ventilatory threshold (VT1), before (PRE) and after (POST) two hours of moderate-intensity cycling. The power output, [Formula: see text], FR, and VT associated with VT1 were determined PRE and POST. RESULTS: As previously reported, power output at VT1 significantly decreased by ~ 10% from PRE to POST. The [Formula: see text] associated with VT1 was unchanged from PRE to POST (72 ± 12 vs. 69 ± 13 L.min-1, ∆ - 3 ± 5 L.min-1, ∆ - 4 ± 8%, P = 0.075), and relatively consistent (within-subject coefficient of variation, 5.4% [3.7, 8.0%]). The [Formula: see text] associated with VT1 was produced with increased FR (27.6 ± 5.8 vs. 31.9 ± 6.5 breaths.min-1, ∆ 4.3 ± 3.1 breaths.min-1, ∆ 16 ± 11%, P = 0.0002) and decreased VT (2.62 ± 0.43 vs. 2.19 ± 0.36 L.breath-1, ∆ - 0.44 ± 0.22 L.breath-1, ∆ - 16 ± 7%, P = 0.0002) in POST. CONCLUSION: These data suggest prolonged exercise shifts ventilatory parameters at the moderate-to-heavy intensity transition, but [Formula: see text] remains stable. Real-time monitoring of [Formula: see text] may be a useful means of assessing proximity to the moderate-to-heavy intensity transition during prolonged exercise and is worthy of further research.

Kinetic Analysis, Potentiation, and Fatigue During Vertical and Horizontal Plyometric Training: An In-Depth Investigation Into Session Volume.

Despite previous support for plyometric training, optimal dosing strategies remain unclear. PURPOSE: To investigate vertical and horizontal jump kinetic performance following a low-volume plyometric stimulus with progressively increased session jump volume. METHODS: Sixteen academy rugby players (20.0 [2.0] y; 103.0 [17.6] kg; 184.3 [5.5] cm) volunteered for this study. Vertical and horizontal jump sessions were conducted 1 week apart and consisted of a 40-jump low-volume plyometric stimulus using 4 exercises, after which volume was progressively increased to 200 jumps, using countermovement jump (CMJ) for vertical sessions and horizontal broad jump (HBJ) for horizontal sessions. Jump performance was assessed via force-plate analysis at baseline (PRE-0), following the low-volume plyometric stimulus (P-40), and every subsequent 10 jumps until the end of the session (P-50, P-60, P-70, ... P-200). RESULTS: The low-volume stimulus was effective in potentiating HBJ (2% to 5%) but not CMJ (0% to -7%) performance (P < .001). The HBJ performance enhancements were maintained throughout the entire high-volume session, while CMJ realized small but significant decrements (-5% to -7%) in jump height P-50 to P-80 before recovering to presession values. Moreover, increases in eccentric impulse (5% to 24%; P < .001) in both sessions were associated with decreased or maintained concentric impulse, indicating a breakdown in performance-augmenting mechanisms and less effective power transfer concentrically after moderate volumes. CONCLUSION: Practitioners should consider kinetic differences between HBJ and CMJ with increasing volume to better inform and understand session dosing strategies.

The Weekly Periodization of Top 5 Tour de France General Classification Finishers: A Multiple Case Study.

PURPOSE: The aim of this study was to describe individual training characteristics, racing strategies, and periodization in preparation for the Tour de France in 2 world-class road cyclists finishing in the top 5 of the general classification. METHODS: Week-by-week power meter training and racing data of 2 (A and B) road cyclists (age: 29 and 23 y; maximum oxygen consumption: 83 and 81 mL·min-1·kg-1; and relative 20-min record power output: 6.9 and 6.5 W·kg-1) in the preparation phase (December-July/August) leading up to the Tour de France were retrospectively analyzed. Weekly volume and intensity distribution in power zones were considered. RESULTS: Cyclists A and B completed 46 and 19 races, 22.5 (6.3) and 18.2 (5.1) h·wk-1, with a pyramidal intensity distribution of 81.0%-13.3%-5.7%, and 88.8%-7.9%-3.3% in zone 1-zone 2-zone 3. Cyclist B spent 14 days at altitude. Increased high-intensity volume and polarization index occurred during race weeks. During periods without racing, training intensity progressively increased. Strength training was performed during November and December but not during the following months. During tapering, total exercise volume and time at high intensity decreased. CONCLUSION: These data provide novel insights into the periodization of world-class road cyclists in advance of a top 5 placing in the Tour de France general classification.

Skeletal muscle proteins involved in fatty acid transport influence fatty acid oxidation rates observed during exercise.

Several proteins are implicated in transmembrane fatty acid transport. The purpose of this study was to quantify the variation in fatty acid oxidation rates during exercise explained by skeletal muscle proteins involved in fatty acid transport. Seventeen endurance-trained males underwent a (i) fasted, incremental cycling test to estimate peak whole-body fatty acid oxidation rate (PFO), (ii) resting vastus lateralis microbiopsy, and (iii) 2 h of fed-state, moderate-intensity cycling to estimate whole-body fatty acid oxidation during fed-state exercise (FO). Bivariate correlations and stepwise linear regression models of PFO and FO during 0-30 min (early FO) and 90-120 min (late FO) of continuous cycling were constructed using muscle data. To assess the causal role of transmembrane fatty acid transport in fatty acid oxidation rates during exercise, we measured fatty acid oxidation during in vivo exercise and ex vivo contractions in wild-type and CD36 knock-out mice. We observed a novel, positive association between vastus lateralis FATP1 and PFO and replicated work reporting a positive association between FABPpm and PFO. The stepwise linear regression model of PFO retained CD36, FATP1, FATP4, and FABPpm, explaining ~87% of the variation. Models of early and late FO explained ~61 and ~65% of the variation, respectively. FATP1 and FATP4 emerged as contributors to models of PFO and FO. Mice lacking CD36 had impaired whole-body and muscle fatty acid oxidation during exercise and muscle contractions, respectively. These data suggest that substantial variation in fatty acid oxidation rates during exercise can be explained by skeletal muscle proteins involved in fatty acid transport.

Carbohydrate, but not fat, oxidation is reduced during moderate-intensity exercise performed in 33 vs. 18 °C at matched heart rates.

PURPOSE: Exposure to environmental heat stress increases carbohydrate oxidation and extracellular heat shock protein 70 (HSP70) concentrations during endurance exercise at matched absolute, external work rates. However, a reduction in absolute work rate typically occurs when unacclimated endurance athletes train and/or compete in hot environments. We sought to determine the effect of environmental heat stress on carbohydrate oxidation rates and plasma HSP70 expression during exercise at matched heart rates (HR). METHODS: Ten endurance-trained, male cyclists performed two experimental trials in an acute, randomised, counterbalanced cross-over design. Each trial involved a 90-min bout of cycling exercise at 95% of the HR associated with the first ventilatory threshold in either 18 (TEMP) or 33 °C (HEAT), with ~ 60% relative humidity. RESULTS: Mean power output (17 ± 11%, P < 0.001) and whole-body energy expenditure (14 ± 8%, P < 0.001) were significantly lower in HEAT. Whole-body carbohydrate oxidation rates were significantly lower in HEAT (19 ± 11%, P = 0.002), while fat oxidation rates were not different between-trials. The heat stress-induced reduction in carbohydrate oxidation was associated with the observed reduction in power output (r = 0.64, 95% CI, 0.01, 0.91, P = 0.05) and augmented sweat rates (r = 0.85, 95% CI, 0.49, 0.96, P = 0.002). Plasma HSP70 and adrenaline concentrations were not increased with exercise in either environment. CONCLUSION: These data contribute to our understanding of how moderate environmental heat stress is likely to influence substrate oxidation and plasma HSP70 expression in an ecologically-valid model of endurance exercise.

Natural killer cell subset count and antigen-stimulated activation in response to exhaustive running following adaptation to a ketogenic diet.

NEW FINDINGS: What is the central question of this study? Does a ketogenic diet (KD) modulate circulating counts of natural killer (NK) cells, including CD56bright and CD56dim subsets, and their ability to activate (CD69 expression) following in vitro antigen stimulation in response to exhaustive moderate-intensity exercise? What is the main finding and its importance? The KD amplified the biphasic exercise-induced NK cell response due to a greater mobilisation of the cytotoxic CD56dim subset but did not alter NK cell CD69 expression. The KD appears to modulate exercise-induced circulating NK cell mobilisation and egress, but not antigen-stimulated circulating NK cell activation. ABSTRACT: We investigated the effect of a 31-day ketogenic diet (KD) compared with a habitual, carbohydrate (CHO)-based diet on total circulating natural killer (NK) CD3- CD56+ , dim and bright subset count, and antigen-stimulated CD3- CD56+ cell activation (CD69+ ) in response to exhaustive running. In a randomised, repeated-measures, cross-over study, eight trained, male endurance athletes ingested a 31-day low-CHO KD or their habitual diet (HD). On day 31, participants ran to exhaustion at 70% V ̇ O 2 max $\dot{V}_{{\rm{O}}_{2}{\rm{max}}}$ (∼3.5-4 h, ∼45-50 km). A low-CHO (<10 g) meal was ingested prior to the KD trial, with fat ingested during exercise. A high-CHO (2 g kg-1 ) meal was ingested prior to the HD trial, with CHO (∼55 g h-1 ) ingested during exercise. Venous blood samples were collected at pre-exercise, post-exercise and 1 h post-exercise. The KD amplified the classical exercise-induced biphasic CD3- CD56+ cell response by increasing the post-exercise counts (P = 0.0004), which appeared to be underpinned by the cytotoxic CD3- CD56dim subset (main effect of time point, P < 0.0001). The KD had no effect on NK cells' expression of CD69 or their geometric mean fluorescence intensity of CD69 expression, either for unstimulated or for antigen-stimulated NK cells (all P > 0.05). In conclusion, adaptation to a KD may alter the number of circulating NK cells but not their ability to activate to an antigenic challenge.

Prolonged cycling reduces power output at the moderate-to-heavy intensity transition.

PURPOSE: To determine the effect of prolonged exercise on moderate-to-heavy intensity transition power output and heart rate. METHODS: Fourteen endurance-trained cyclists and triathletes took part in the present investigation (13 males, 1 female, V·O2peak 59.9 ± 6.8 mL.kg-1.min-1). Following a characterisation trial, participants undertook a five-stage incremental step test to determine the power output and heart rate at the moderate-to-heavy intensity transition before and after two hours of cycling at 90% of the estimated power output at first ventilatory threshold (VT1). RESULTS: Power output at the moderate-to-heavy intensity transition significantly decreased following acute prolonged exercise when determined using expired gases (VT1, 217 ± 42 W vs. 196 ± 42 W, P < 0.0001) and blood lactate concentrations (LoglogLT, 212 ± 47 W vs. 190 ± 47 W, P = 0.004). This was attributable to loss of efficiency (VT1, -8 ± 10 W; LoglogLT, - 7 ± 9 W) and rates of metabolic energy expenditure at the transition (VT1, - 14 ± 11 W; LoglogLT, - 15 ± 22 W). The heart rate associated with the moderate-to-heavy intensity transition increased following acute prolonged exercise (VT1, 142 ± 9 beats.min-1 vs. 151 ± 12 beats.min-1, P < 0.001; LoglogLT, 140 ± 13 beats.min-1 vs. 150 ± 15 beats.min-1, P = 0.006). CONCLUSION: These results demonstrate the external work output at the moderate-to-heavy intensity transition decreases during prolonged exercise due to decreased efficiency and rates of metabolic energy expenditure, but the associated heart rate increases. Therefore, individual assessments of athlete 'durability' are warranted.

A three-minute all-out test performed in a remote setting does not provide a valid estimate of the maximum metabolic steady state.

PURPOSE: The three-minute all-out test (3MT), when performed on a laboratory ergometer in a linear mode, can be used to estimate the heavy-severe-intensity transition, or maximum metabolic steady state (MMSS), using the end-test power output. As the 3MT only requires accurate measurement of power output and time, it is possible the 3MT could be used in remote settings using personal equipment without supervision for quantification of MMSS. METHODS: The aim of the present investigation was to determine the reliability and validity of remotely performed 3MTs (3MTR) for estimation of MMSS. Accordingly, 53 trained cyclists and triathletes were recruited to perform one familiarisation and two experimental 3MTR trials to determine its reliability. A sub-group (N = 10) was recruited to perform three-to-five 30 min laboratory-based constant-work rate trials following completion of one familiarisation and two experimental 3MTR trials. Expired gases were collected throughout constant-work rate trials and blood lactate concentration was measured at 10 and 30 min to determine the highest power output at which steady-state [Formula: see text] (MMSS-[Formula: see text]) and blood lactate (MMSS-[La-]) were achieved. RESULTS: The 3MTR end-test power (EPremote) was reliable (coefficient of variation, 4.5% [95% confidence limits, 3.7, 5.5%]), but overestimated MMSS (EPremote, 283 ± 51 W; MMSS-[Formula: see text], 241 ± 46 W, P = 0.0003; MMSS-[La-], 237 ± 47 W, P = 0.0003). This may have been due to failure to deplete the finite work capacity above MMSS during the 3MTR. CONCLUSION: These results suggest that the 3MTR should not be used to estimate MMSS in endurance-trained cyclists.

Decoupling of Internal and External Workload During a Marathon: An Analysis of Durability in 82,303 Recreational Runners.

AIM: This study characterised the decoupling of internal-to-external workload in marathon running and investigated whether decoupling magnitude and onset could improve predictions of marathon performance. METHODS: The decoupling of internal-to-external workload was calculated in 82,303 marathon runners (13,125 female). Internal workload was determined as a percentage of maximum heart rate, and external workload as speed relative to estimated critical speed (CS). Decoupling magnitude (i.e., decoupling in the 35-40 km segment relative to the 5-10 km segment) was classified as low (< 1.1), moderate (≥ 1.1 but < 1.2) or high (≥ 1.2). Decoupling onset was calculated when decoupling exceeded 1.025. RESULTS: The overall internal-to-external workload decoupling experienced was 1.16 ± 0.22, first detected 25.2 ± 9.9 km into marathon running. The low decoupling group (34.5% of runners) completed the marathon at a faster relative speed (88 ± 6% CS), had better marathon performance (217.3 ± 33.1 min), and first experienced decoupling later in the marathon (33.4 ± 9.0 km) compared to those in the moderate (32.7% of runners, 86 ± 6% CS, 224.9 ± 31.7 min, and 22.6 ± 7.7 km), and high decoupling groups (32.8% runners, 82 ± 7% CS, 238.5 ± 30.7 min, and 19.1 ± 6.8 km; all p < 0.01). Compared to females, males' decoupling magnitude was greater (1.17 ± 0.22 vs. 1.12 ± 0.16; p < 0.01) and occurred earlier (25.0 ± 9.8 vs. 26.3 ± 10.6 km; p < 0.01). Marathon performance was associated with the magnitude and onset of decoupling, and when included in marathon performance models utilising CS and the curvature constant, prediction error was reduced from 6.45 to 5.16%. CONCLUSION: Durability characteristics, assessed as internal-to-external workload ratio, show considerable inter-individual variability, and both its magnitude and onset are associated with marathon performance.

Peak fat oxidation is positively associated with vastus lateralis CD36 content, fed-state exercise fat oxidation, and endurance performance in trained males.

PURPOSE: Whole-body fat oxidation during exercise can be measured non-invasively during athlete profiling. Gaps in understanding exist in the relationships between fat oxidation during incremental fasted exercise and skeletal muscle parameters, endurance performance, and fat oxidation during prolonged fed-state exercise. METHODS: Seventeen endurance-trained males underwent a (i) fasted, incremental cycling test to assess peak whole-body fat oxidation (PFO), (ii) resting vastus lateralis microbiopsy, and (iii) 30-min maximal-effort cycling time-trial preceded by 2-h of fed-state moderate-intensity cycling to assess endurance performance and fed-state metabolism on separate occasions within one week. RESULTS: PFO (0.58 ± 0.28 g.min-1) was associated with vastus lateralis citrate synthase activity (69.2 ± 26.0 µmol.min-1.g-1 muscle protein, r = 0.84, 95% CI 0.58, 0.95, P < 0.001), CD36 abundance (16.8 ± 12.6 µg.g-1 muscle protein, rs = 0.68, 95% CI 0.31, 1.10, P = 0.01), pre-loaded 30-min time-trial performance (251 ± 51 W, r = 0.76, 95% CI 0.40, 0.91, P = 0.001; 3.2 ± 0.6 W.kg-1, r = 0.62, 95% CI 0.16, 0.86, P = 0.01), and fat oxidation during prolonged fed-state cycling (r = 0.83, 95% CI 0.57, 0.94, P < 0.001). Addition of PFO to a traditional model of endurance (peak oxygen uptake, power at 4 mmol.L-1 blood lactate concentration, and gross efficiency) explained an additional ~ 2.6% of variation in 30-min time-trial performance (adjusted R2 = 0.903 vs. 0.877). CONCLUSION: These associations suggest non-invasive measures of whole-body fat oxidation during exercise may be useful in the physiological profiling of endurance athletes.

Effects of short-term graded dietary carbohydrate intake on intramuscular and whole body metabolism during moderate-intensity exercise.

Altering dietary carbohydrate (CHO) intake modulates fuel utilization during exercise. However, there has been no systematic evaluation of metabolic responses to graded changes in short-term (< 1 wk) dietary CHO intake. Thirteen active men performed interval running exercise combined with isocaloric diets over 3 days before evaluation of metabolic responses to 60-min running at 65% V̇O2max on three occasions. Diets contained lower [LOW, 2.40 ± 0.66 g CHO·kg-1·day-1, 21.3 ± 0.5% of energy intake (EI)], moderate (MOD, 4.98 ± 1.31 g CHO·kg-1·day-1, 46.3 ± 0.7% EI), or higher (HIGH, 6.48 ± 1.56 g CHO·kg-1·day-1, 60.5 ± 1.6% EI) CHO. Preexercise muscle glycogen content was lower in LOW [54.3 ± 26.4 mmol·kg-1 wet weight (ww)] compared with MOD (82.6 ± 18.8 mmol·kg -1 ww) and HIGH (80.4 ± 26.0 mmol·kg-1 ww, P < 0.001; MOD vs. HIGH, P = 0.85). Whole body substrate oxidation, systemic responses, and muscle substrate utilization during exercise indicated increased fat and decreased CHO metabolism in LOW [respiratory exchange ratio (RER): 0.81 ± 0.01] compared with MOD (RER 0.86 ± 0.01, P = 0.0005) and HIGH (RER: 0.88 ± 0.01, P < 0.0001; MOD vs. HIGH, P = 0.14). Higher basal muscle expression of genes encoding proteins implicated in fat utilization was observed in LOW. In conclusion, muscle glycogen availability and subsequent metabolic responses to exercise were resistant to increases in dietary CHO intake from ∼5.0 to ∼6.5 g CHO·kg-1·day-1 (46% to 61% EI), while muscle glycogen, gene expression, and metabolic responses were sensitive to more marked reductions in CHO intake (∼2.4 g CHO·kg-1·day-1, ∼21% EI).NEW & NOTEWORTHY The data presented here suggest that metabolic responses to steady-state aerobic exercise are somewhat resistant to short-term changes in dietary carbohydrate (CHO) intake within the 5-6.5 g CHO·kg-1·day-1 [46-61% energy intake (EI)] range. In contrast, reduction in short-term dietary CHO intake to ∼2.4 g CHO·kg-1·day-1 (21% EI) evoked clear changes indicative of increased fat and decreased CHO metabolism during exercise.

Temperate performance and metabolic adaptations following endurance training performed under environmental heat stress.

Endurance athletes are frequently exposed to environmental heat stress during training. We investigated whether exposure to 33°C during training would improve endurance performance in temperate conditions and stimulate mitochondrial adaptations. Seventeen endurance-trained males were randomly assigned to perform a 3-week training intervention in 18°C (TEMP) or 33°C (HEAT). An incremental test and 30-min time-trial preceded by 2-h low-intensity cycling were performed in 18°C pre- and post-intervention, along with a resting vastus lateralis microbiopsy. Training was matched for relative cardiovascular demand using heart rates measured at the first and second ventilatory thresholds, along with a weekly "best-effort" interval session. Perceived training load was similar between-groups, despite lower power outputs during training in HEAT versus TEMP (p < .05). Time-trial performance improved to a greater extent in HEAT than TEMP (30 ± 13 vs. 16 ± 5 W, N = 7 vs. N = 6, p = .04), and citrate synthase activity increased in HEAT (fold-change, 1.25 ± 0.25, p = .03, N = 9) but not TEMP (1.10 ± 0.22, p = .22, N = 7). Training-induced changes in time-trial performance and citrate synthase activity were related (r = .51, p = .04). A group × time interaction for peak fat oxidation was observed (Δ 0.05 ± 0.14 vs. -0.09 ± 0.12 g·min-1 in TEMP and HEAT, N = 9 vs. N = 8, p = .05). Our data suggest exposure to moderate environmental heat stress during endurance training may be useful for inducing adaptations relevant to performance in temperate conditions.

The Importance of 'Durability' in the Physiological Profiling of Endurance Athletes.

Profiling physiological attributes is an important role for applied exercise physiologists working with endurance athletes. These attributes are typically assessed in well-rested athletes. However, as has been demonstrated in the literature and supported by field data presented here, the attributes measured during routine physiological-profiling assessments are not static, but change over time during prolonged exercise. If not accounted for, shifts in these physiological attributes during prolonged exercise have implications for the accuracy of their use in intensity regulation during prolonged training sessions or competitions, quantifying training adaptations, training-load programming and monitoring, and the prediction of exercise performance. In this review, we argue that current models used in the routine physiological profiling of endurance athletes do not account for these shifts. Therefore, applied exercise physiologists working with endurance athletes would benefit from development of physiological-profiling models that account for shifts in physiological-profiling variables during prolonged exercise and quantify the 'durability' of individual athletes, here defined as the time of onset and magnitude of deterioration in physiological-profiling characteristics over time during prolonged exercise. We propose directions for future research and applied practice that may enable better understanding of athlete durability.

Autonomic and Perceptual Responses to Induction of a Ketogenic Diet in Free-Living Endurance Athletes: A Randomized, Crossover Trial.

PURPOSE: Considerable interindividual heterogeneity has been observed in endurance performance responses following induction of a ketogenic diet (KD). It is plausible that a physiological stress response in the period following the dramatic dietary shift associated with transition to a KD may explain this heterogeneity. METHODS: In a randomized, crossover study design, 8 trained male runners completed an incremental exercise test and ran to exhaustion at 70%VO2max before and after a 31-day rigorously controlled habitual diet or KD intervention, and recorded heart rate variability (root mean square of the sum of successive differences in R-R intervals [rMSSD]) upon waking each morning along with the recovery-stress questionnaire for athletes each week. Data were analyzed using linear mixed models. RESULTS: A significant reduction in rMSSD was observed in the KD (-9.77 [4.03] ms, P = .02), along with an increase in day-to-day variability in rMSSD (2.1% [1.0%], P = .03). The reduction in rMSSD in the KD for the subgroup of individuals exhibiting impaired exercise capacity following induction of the KD approached significance (Δ -22 [15] ms, P = .06, N = 4); whereas no effect was observed in those who exhibited unchanged exercise capacity (Δ 5 [18] ms, P = .61, N = 4). No main effects were observed for recovery-stress questionnaire for athletes. CONCLUSIONS: Our data suggest those working with endurance athletes transitioning onto a KD may consider using noninvasive, inexpensive resting heart rate variability measures to gain individual-level insights into the likely short-term effects on exercise capacity.

Stability of Heart Rate at Physiological Thresholds Between Temperate and Heat Stress Environments in Endurance-Trained Males.

Many endurance athletes perform specific blocks of training in hot environments in "heat stress training camps." It is not known if physiological threshold heart rates measured in temperate conditions are reflective of those under moderate environmental heat stress. A total of 16 endurance-trained cyclists and triathletes performed incremental exercise assessments in 18°C and 35°C (both 60% relative humidity) to determine heart rates at absolute blood lactate and ventilatory thresholds. Heart rate at fixed blood lactate concentrations of 2, 3, and 4 mmol·L-1 and ventilatory thresholds were not significantly different between environments (P > .05), despite significant heat stress-induced reductions in power output of approximately 10% to 17% (P < .05, effect size = 0.65-1.15). The coefficient of variation for heart rate at these blood lactate concentrations (1.4%-2.9%) and ventilatory thresholds (2.3%-2.7%) between conditions was low, with significant strong positive correlations between measurements in the 2 environments (r = .92-.95, P < .05). These data indicate heart rates measured at physiological thresholds in temperate environments are reflective of measurements taken under moderate environmental heat stress. Therefore, endurance athletes embarking on heat stress training camps can use heart rate-based thresholds ascertained in temperate environments to prescribe training under moderate environmental heat stress.

Racing and Training Physiology of an Elite Ultra-Endurance Cyclist: Case Study of 2 Record-Setting Performances.

PURPOSE: To present a case report of an elite ultra-endurance cyclist, who was the winner and course record holder of 2 distinct races within a 4-month span: a 24-hour solo cycling race and a 2-man team multiday race (Race Across America). METHODS: The athlete's raw data (cycling power, heart rate [HR], speed, and distance) were obtained and analyzed for 2 ultra-endurance races and 11 weeks of training in between. RESULTS: For the 24-hour race, the athlete completed 861.6 km (average speed 35.9 km·h-1, average power 210 W [2.8 W·kg-1], average HR 121 beats per minute) with a 37% decrease in power and a 22% decrease in HR throughout the race. During the 11 weeks between the 24-hour race and Race Across America, training intensity distribution (Zone 1/2/3) based on HR was 51%/39%/10%. For the Race Across America, total team time to complete the 4939-km race was 6 days, 10 hours, 39 minutes, at an average speed of 31.9 km·h-1. Of this, the athlete featured in this case study rode 75.2 hours, completing 2532 km (average speed 33.7 km·h-1, average power 203 W [2.7 W·kg-1]), with a 12% decrease in power throughout the race. Power during daytime segments was greater than nighttime (212 [25] vs 189 [18] W, P < .001, ηp2=.189). CONCLUSIONS: This case report highlights the performance requirements of elite ultra-endurance cycling. Although average power was similar when riding for 24 hours continuously and 75 hours intermittently over 6.5 days, there were large differences in pacing strategies and within-day power-output changes.