Daniela Flück

Improvements in exercise performance with high-intensity interval training coincide with an increase in skeletal muscle mitochondrial content and function

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.

Haematological rather than skeletal muscle adaptations contribute to the increase in peak oxygen uptake induced by moderate endurance training

This study assessed the respective contributions of haematological and skeletal muscle adaptations to any observed improvement in peak oxygen uptake ( V̇O2 peak ) induced by endurance training (ET). V̇O2 peak , peak cardiac output ( Q̇ 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 and V̇O2 peak and Q̇ peak were determined again. We speculated that the contribution of skeletal muscle adaptations to an ET‐induced increase in V̇O2 peak could be identified when offsetting the ET‐induced increase in RBCV. V̇O2 peak , Q̇ peak , blood volumes, skeletal muscle mitochondrial volume density and capillarization were increased after ET. Following RBCV normalization, V̇O2 peak and Q̇ peak reverted to pre‐ET levels. These results demonstrate the predominant contribution of haematological adaptations to any increase in V̇O2 peak induced by ET.

Phlebotomy eliminates the maximal cardiac output response to six weeks of exercise training

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.

Twenty-eight days of exposure to 3454 m increases mitochondrial volume density in human skeletal muscle.

It is generally accepted that mitochondrial volume density in human skeletal muscle diminishes with chronic high altitude exposure. All data supporting this concept were collected during mountaineering expeditions, which are associated with the confounding effects of whole body negative energy balance. Here we examine the effect of 28 days of exposure to 3454 m on skeletal muscle mitochondrial volume density in a setting where whole body weight, whole body composition, leg lean mass, skeletal muscle fibre area and maximal power output were preserved. Our results demonstrate that total skeletal muscle mitochondrial volume density increases in response to high altitude exposure secondary to a preferential increase in intermyofibrillar mitochondrial populations. This study provides direct evidence contradicting the notion that high altitude exposure diminishes skeletal muscle mitochondrial volume density, highlighting an inconsistent understanding of the role of hypoxia on skeletal muscle mitochondria.

Heat training increases exercise capacity in hot but not in temperate conditions: a mechanistic counter-balanced cross-over study

The aim was to determine the mechanisms facilitating exercise performance in hot conditions following heat training. In a counter-balanced order, seven males (V̇o2max 61.2 ± 4.4 ml·min(-1)·kg(-1)) were assigned to either 10 days of 90-min exercise training in 18 or 38°C ambient temperature (30% relative humidity) applying a cross-over design. Participants were tested for V̇o2max and 30-min time trial performance in 18 (T18) and 38°C (T38) before and after training. Blood volume parameters, sweat output, cardiac output (Q̇), cerebral perfusion (i.e., middle cerebral artery velocity [MCAvmean]), and other variables were determined. Before one set of exercise tests in T38, blood volume was acutely expanded by 538 ± 16 ml with an albumin solution (T38A) to determine the role of acclimatization induced hypervolemia on exercise performance. We furthermore hypothesized that heat training would restore MCAvmean and thereby limit centrally mediated fatigue. V̇o2max and time trial performance were equally reduced in T38 and T38A (7.2 ± 1.6 and 9.3 ± 2.5% for V̇o2max; 12.8 ± 2.8 and 12.9 ± 2.8% for time trial). Following heat training both were increased in T38 (9.6 ± 2.1 and 10.4 ± 3.1%, respectively), whereas both V̇o2max and time trial performance remained unchanged in T18. As expected, heat training augmented plasma volume (6 ± 2%) and mean sweat output (26 ± 6%), whereas sweat [Na(+)] became reduced by 19 ± 7%. In T38 Q̇max remained unchanged before (21.3 ± 0.6 l/min) to after (21.7 ± 0.5 l/min) training, whereas MCAvmean was increased by 13 ± 10%. However, none of the observed adaptations correlated with the concomitant observed changes in exercise performance.

Hypoxic training: effect on mitochondrial function and aerobic performance in hypoxia.

PURPOSE The effects of hypoxic training on exercise performance remain controversial. Here, we tested the hypotheses that i) hypoxic training possesses ergogenic effects at sea level and altitude and ii) the benefits are primarily mediated by improved mitochondrial function of the skeletal muscle. METHODS We determined aerobic performance (incremental test to exhaustion and time trial for a set amount of work) in moderately trained subjects undergoing 6 wk of endurance training (3-4 times per week, 60 min per session) in normoxia (placebo, n = 8) or normobaric hypoxia (FIO2 = 0.15, n = 9) using a double-blind and randomized design. Exercise tests were performed in normoxia and acute hypoxia (FIO2 = 0.15). Skeletal muscle mitochondrial respiratory capacities and electron coupling efficiencies were measured via high-resolution respirometry. Total hemoglobin mass was assessed by carbon monoxide rebreathing. RESULTS Skeletal muscle respiratory capacity was not altered by training or hypoxia; however, electron coupling control respective to fat oxidation slightly diminished with hypoxic training. Hypoxic training did increase total hemoglobin mass more than the placebo (8.4% vs 3.3%, P = 0.02). In normoxia, hypoxic training had no additive effect on maximal measures of oxygen uptake or time trial performance. In acute hypoxia, hypoxic training conferred no advantage on maximal oxygen uptake but tended to enhance time trial performance more than normoxic training (52% vs 32%, P = 0.09). CONCLUSIONS Our data suggest that, in moderately trained subjects, 6 wk of hypoxic training possesses no ergogenic effect at sea level. It is not excluded that hypoxic training might facilitate endurance capacity at moderate altitude; however, this issue is still open and needs to be further examined.

Exercise training increases skeletal muscle mitochondrial volume density by enlargement of existing mitochondria and not de novo biogenesis

(i) To determine whether exercise‐induced increases in muscle mitochondrial volume density (MitoVD) 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 MitoVD.

A short period of high-intensity interval training improves skeletal muscle mitochondrial function and pulmonary oxygen uptake kinetics

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.

Parasympathetic withdrawal increases heart rate after 2 weeks at 3454 m altitude

Heart rate is increased in chronic hypoxia and we tested whether this is the result of increased sympathetic nervous activity, reduced parasympathetic nervous activity, or a non‐autonomic mechanism. In seven lowlanders, heart rate was measured at sea level and after 2 weeks at high altitude after individual and combined pharmacological inhibition of sympathetic and/or parasympathetic control of the heart. Inhibition of parasympathetic control of the heart alone or in combination with inhibition of sympathetic control abolished the high altitude‐induced increase in heart rate. Inhibition of sympathetic control of the heart alone did not prevent the high altitude‐induced increase in heart rate. These results indicate that a reduced parasympathetic nervous activity is the main mechanism underlying the elevated heart rate in chronic hypoxia.

Passive heat stress reduces circulating endothelial and platelet microparticles

What is the central question of this study? Does passive heat stress of +2°C oesophageal temperature change concentrations of circulating arterial endothelial‐ and platelet‐derived microparticles in healthy adults? What is the main finding and its importance? Concentrations of circulating endothelial‐ and platelet‐derived microparticles were markedly decreased in heat stress. Reductions in circulating microparticles might indicate favourable vascular changes associated with non‐pathological hyperthermia.