Six sessions of high-intensity interval training (HIT) are sufficient to improve exercise capacity. The mechanisms explaining such improvements are unclear. Accordingly, the aim of this study was to perform a comprehensive evaluation of physiologically relevant adaptations occurring after six sessions of HIT to determine the mechanisms explaining improvements in exercise performance. Sixteen untrained (43 ± 6 ml·kg(-1)·min(-1)) subjects completed six sessions of repeated (8-12) 60 s intervals of high-intensity cycling (100% peak power output elicited during incremental maximal exercise test) intermixed with 75 s of recovery cycling at a low intensity (30 W) over a 2-wk period. Potential training-induced alterations in skeletal muscle respiratory capacity, mitochondrial content, skeletal muscle oxygenation, cardiac capacity, blood volumes, and peripheral fatigue resistance were all assessed prior to and again following training. Maximal measures of oxygen uptake (Vo2peak; ∼8%; P = 0.026) and cycling time to complete a set amount of work (∼5%; P = 0.008) improved. Skeletal muscle respiratory capacities increased, most likely as a result of an expansion of skeletal muscle mitochondria (∼20%, P = 0.026), as assessed by cytochrome c oxidase activity. Skeletal muscle deoxygenation also increased while maximal cardiac output, total hemoglobin, plasma volume, total blood volume, and relative measures of peripheral fatigue resistance were all unaltered with training. These results suggest that increases in mitochondrial content following six HIT sessions may facilitate improvements in respiratory capacity and oxygen extraction, and ultimately are responsible for the improvements in maximal whole body exercise capacity and endurance performance in previously untrained individuals.

Key pointsr This study assessed the respective contributions of haematological and skeletal muscle adaptations to any observed improvement in peak oxygen uptake (V O 2 peak ) induced by endurance training (ET).rV O 2 peak , peak cardiac output (Q peak ), blood volumes and skeletal muscle biopsies were assessed prior (pre) to and after (post) 6 weeks of ET. Following the post-ET assessment, red blood cell volume (RBCV) reverted to the pre-ET level following phlebotomy andV O 2 peak andQ peak were determined again.r We speculated that the contribution of skeletal muscle adaptations to an ET-induced increase inV O 2 peak could be identified when offsetting the ET-induced increase in RBCV.rV O 2 peak ,Q peak , blood volumes, skeletal muscle mitochondrial volume density and capillarization were increased after ET. Following RBCV normalization,V O 2 peak andQ peak reverted to pre-ET levels.r These results demonstrate the predominant contribution of haematological adaptations to any increase inV O 2 peak induced by ET.Abstract It remains unclear whether improvements in peak oxygen uptake (V O 2 peak ) following endurance training (ET) are primarily determined by central and/or peripheral adaptations. Herein, we tested the hypothesis that the improvement inV O 2 peak following 6 weeks of ET is mainly determined by haematological rather than skeletal muscle adaptations. Sixteen untrained healthy male volunteers (age = 25 ± 4 years,V O 2 peak = 3.5 ± 0.5 l min −1 ) underwent supervised ET (6 weeks, 3-4 sessions per week).V O 2 peak , peak cardiac output (Q peak ), haemoglobin mass (Hb mass ) and blood volumes were assessed prior to and following ET. Skeletal muscle biopsies were analysed for mitochondrial volume density (Mito VD ), capillarity, fibre types and respiratory capacity (OXPHOS). After the post-ET assessment, red blood cell volume (RBCV) was re-established at the pre-ET level by phlebotomy andV O 2 peak andQ peak were measured again. We speculated that the contribution of skeletal muscle adaptations to the ET-induced increase inV O 2 peak would be revealed when controlling for haematological adaptations.V O 2 peak andQ peak were increased (P < 0.05) following ET (9 ± 8 and 7 ± 6%, respectively) and decreased (P < 0.05) after phlebotomy (−7 ± 7 and −10 ± 7%). RBCV, plasma volume and Hb mass all increased (P < 0.05) after ET (8 ± 4, 4 ± 6 and 6 ± 5%). As for skeletal muscle adaptations, capillary-to-fibre ratio and total Mito VD increased (P < 0.05) following ET (18 ± 16 and 43 ± 30%), but OXPHOS remained unaltered. Through stepwise multiple regression analysis,Q peak , RBCV and Hb mass were found to be independent predictors ofV O 2 peak . In conclusion, the improvement inV O 2 peak following 6 weeks of ET is primarily attributed to increases inQ peak and oxygen-carrying capacity of blood in untrained healthy young subjects.

Mito increased with 55 ± 9% (P < 0.001), whereas the number of mitochondrial profiles per area of skeletal muscle remained unchanged following training. Citrate synthase activity (CS) increased (44 ± 12%, P < 0.001); however, there were no functional changes in oxidative phosphorylation capacity (OXPHOS, CI+II ) or cytochrome c oxidase (COX) activity. Correlations were found between Mito and CS (P = 0.01; r = 0.58), OXPHOS, CI+CIIP (P = 0.01; R = 0.58) and COX (P = 0.02; R = 0.52) before training; after training, a correlation was found between Mito and CS activity only (P = 0.04; R = 0.49). Intrinsic respiratory capacities decreased (P < 0.05) with training when respiration was normalized to Mito This was not the case when normalized to CS activity although the percentage change was comparable CONCLUSIONS: Mito was increased by inducing mitochondrial enlargement rather than de novo biogenesis. CS activity may be appropriate to track training-induced changes in Mito

This study investigated if well-trained cyclists improve VO 2max and performance in cool conditions following heat acclimatization through natural outdoor training in hot conditions. Eighteen trained male cyclists were tested for physiological adaptations, VO 2max , peak aerobic power output, exercise efficiency, and outdoor time trial (TT) performance (43.4 km in cool environment, ∼5-13°C) before and after 2 weeks of training in a cool (CON, n = 9) or hot (∼35°C, HA, n = 9) environment. After heat acclimatization, TT performance in the heat was improved by 16%; however, there was no change in the HA group in VO 2max (4.79 ± 0.21 L/min vs 4.82 ± 0.35 L/min), peak aerobic power output (417 ± 16 W vs 422 ± 17 W), and outdoor TT performance in cool conditions (300 ± 14 W/69 ± 3 min vs 302 ± 9 W/69 ± 4 min). The present study shows that 2 weeks of heat acclimatization was associated with marked improvements in TT performance in the heat. However, for the well-trained endurance athletes, this did not transfer to an improved aerobic exercise capacity or outdoor TT performance in cool conditions.

With this study we tested the hypothesis that 6 wk of endurance training increases maximal cardiac output (Qmax) relatively more by elevating blood volume (BV) than by inducing structural and functional changes within the heart. Nine healthy but untrained volunteers (Vo2max 47 ± 5 ml·min(-1)·kg(-1)) underwent supervised training (60 min; 4 times weekly at 65% Vo2max for 6 wk), and Qmax was determined by inert gas rebreathing during cycle ergometer exercise before and after the training period. After the training period, blood volume (determined in duplicates by CO rebreathing) was reestablished to pretraining values by phlebotomy and Qmax was quantified again. Resting echography revealed no structural heart adaptations as a consequence of the training intervention. After the training period, plasma volume (PV), red blood cell volume (RBCV), and BV increased (P< 0.05) by 147 ± 168 (5 ± 5%), 235 ± 64 (10 ± 3%), and 382 ± 204 ml (7 ± 4%), respectively. Vo2max was augmented (P < 0.05) by 10 ± 7% after the training period and decreased (P < 0.05) by 8 ± 7% with phlebotomy. Concomitantly, Qmax was increased (P < 0.05) from 18.9 ± 2.1 to 20.4 ± 2.3 l/min (9 ± 6%) as a consequence of the training intervention, and after normalization of BV by phlebotomy Qmax returned to pretraining values (18.1 ± 2.5 l/min; 12 ± 5% reversal). Thus the exercise training-induced increase in BV is the main mechanism increasing Qmax after 6 wk of endurance training in previously untrained subjects.

The aim of this study was to determine the time course of physiological adaptations and their relationship with performance improvements during 2 weeks of heat acclimatization. Nine trained cyclists completed 2 weeks of training in naturally hot environment (34 ± 3°C; 18 ± 5% relative humidity). On days 1, 6, and 13, they performed standardized heat response tests (HRT-1, 2, 3), and 43.4-km time trials in the heat (TTH-1, 2, 3) were completed on days 2, 7, and 14. Within the first 5-6 days, sweat sodium concentration decreased from 75 ± 22 mmol/L to 52 ± 24 mmol/L, sweat rate increased (+20 ± 15%), and resting hematocrit decreased (−5.6 ± 5.4%), with no further changes during the remaining period. In contrast, power output during TTHs gradually improved from TTH-1 to TTH-2 (+11 ± 8%), and from TTH-2 to TTH-3 (+5 ± 4%). Individual improvements in performance from TTH-1 to TTH-2 correlated with individual changes in hematocrit (assessed after the corresponding HRT; r = −0.79, P < 0.05), however, were not related to changes in performance from TTH-2 to TTH-3. In trained athletes, sudomotor and hematological adaptations occurred within 5-6 days of training, whereas the additional improvement in performance after the entire acclimatization period did not relate to changes in these parameters.

The impact of altitude training on haematological parameters and the Athlete Biological Passport (ABP) was evaluated in international-level elite athletes. One group of swimmers lived high and trained high (LHTH, n = 10) for three to four weeks at 2130 m or higher whereas a control group (n = 10) completed a three-week training camp at sea-level. Haematological parameters were determined weekly three times before and four times after the training camps. ABP thresholds for haemoglobin concentration ([Hb]), reticulocyte percentage (RET%), OFF score and the abnormal blood profile score (ABPS) were calculated using the Bayesian model. After altitude training, six swimmers exceeded the 99% ABP thresholds: two swimmers exceeded the OFF score thresholds at day +7; one swimmer exceeded the OFF score threshold at day +28; one swimmer exceeded the threshold for RET% at day +14; and one swimmer surpassed the ABPS threshold at day +14. In the control group, no values exceeded the individual ABP reference range. In conclusion, LHTH induces haematological changes in Olympic-level elite athletes which can exceed the individually generated references in the ABP. Training at altitude should be considered a confounding factor for ABP interpretation for up to four weeks after altitude exposure but does not consistently cause abnormal values in the ABP.

The aim of the present study was to examine whether improvements in pulmonary oxygen uptake (V̇o2) kinetics following a short period of high-intensity training (HIT) would be associated with improved skeletal muscle mitochondrial function. Ten untrained male volunteers (age 26 ± 2 yr; mean ± SD) performed six HIT sessions (8-12 × 60 s at incremental test peak power; 271 ± 52 W) over a 2-wk period. Before and after the HIT period, V̇o2 kinetics was modeled during moderate-intensity cycling (110 ± 19 W). Mitochondrial function was assessed with high-resolution respirometry (HRR), and maximal activities of oxidative enzymes citrate synthase (CS) and cytochrome c oxidase (COX) were accordingly determined. In response to HIT, V̇o2 kinetics became faster (τ: 20.4 ± 4.4 vs. 28.9 ± 6.1 s; P < 0.01) and fatty acid oxidation (ETFP) and leak respiration (LN) both became elevated (P < 0.05). Activity of CS and COX did not increase in response to training. Both before and after the HIT period, fast V̇o2 kinetics (low τ values) was associated with large values for ETFP, electron transport system capacity (ETS), and electron flow specific to complex II (CIIP) (P < 0.05). Collectively, these findings support that selected measures of mitochondrial function obtained with HRR are important for fast V̇o2 kinetics and better markers than maximal oxidative enzyme activity in describing the speed of the V̇o2 response during moderate-intensity exercise.