Thomas Christian Bonne

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 points This study assessed the respective contributions of haematological and skeletal muscle adaptations to any observed improvement in peak oxygen uptake ( ) induced by endurance training (ET). , peak cardiac output ( ), 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 and and were determined again. We speculated that the contribution of skeletal muscle adaptations to an ET‐induced increase in could be identified when offsetting the ET‐induced increase in RBCV. , , blood volumes, skeletal muscle mitochondrial volume density and capillarization were increased after ET. Following RBCV normalization, and reverted to pre‐ET levels. These results demonstrate the predominant contribution of haematological adaptations to any increase in induced by ET. Abstract It remains unclear whether improvements in peak oxygen uptake ( ) following endurance training (ET) are primarily determined by central and/or peripheral adaptations. Herein, we tested the hypothesis that the improvement in following 6 weeks of ET is mainly determined by haematological rather than skeletal muscle adaptations. Sixteen untrained healthy male volunteers (age = 25 ± 4 years, = 3.5 ± 0.5 l min −1 ) underwent supervised ET (6 weeks, 3–4 sessions per week). , peak cardiac output ( ), 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 and and were measured again. We speculated that the contribution of skeletal muscle adaptations to the ET‐induced increase in would be revealed when controlling for haematological adaptations. and 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, , RBCV and Hb mass were found to be independent predictors of . In conclusion, the improvement in following 6 weeks of ET is primarily attributed to increases in and oxygen‐carrying capacity of blood in untrained healthy young subjects.

Abstract Aims (i) To determine whether exercise‐induced increases in muscle mitochondrial volume density (Mito VD ) are related to enlargement of existing mitochondria or de novo biogenesis and (ii) to establish whether measures of mitochondrial‐specific enzymatic activities are valid biomarkers for exercise‐induced increases in Mito VD . Method Skeletal muscle samples were collected from 21 healthy males prior to and following 6 weeks of endurance training. Transmission electron microscopy was used for the estimation of mitochondrial densities and profiles. Biochemical assays, western blotting and high‐resolution respirometry were applied to detect changes in specific mitochondrial functions. Result Mito VD 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 P ) or cytochrome c oxidase ( COX ) activity. Correlations were found between Mito VD 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 VD 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 VD. This was not the case when normalized to CS activity although the percentage change was comparable . Conclusions Mito VD was increased by inducing mitochondrial enlargement rather than de novo biogenesis. CS activity may be appropriate to track training‐induced changes in Mito VD.

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.

This study investigated if well-trained cyclists improve V ˙ O 2 m a x and performance in cool conditions following heat acclimatization through natural outdoor training in hot conditions. Eighteen trained male cyclists were tested for physiological adaptations, V ˙ O 2 m a x , 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 V ˙ O 2 m a x (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.