Key points: In human skeletal muscles, the current view is that the capacity for mitochondrial energy production, and thus endurance capacity, is set by the mitochondria volume. However, increasing the mitochondrial inner membrane surface comprises an alternative mechanism for increasing the energy production capacity. In the present study, we show that mitochondrial inner membranes in leg muscles of endurance‐trained athletes have an increased ratio of surface per mitochondrial volume. We show a positive correlation between this ratio and whole body oxygen uptake and muscle fibre mitochondrial content. The results obtained in the present study help us to understand modulation of mitochondrial function, as well as how mitochondria can increase their oxidative capacity with increased demand. Mitochondrial energy production involves the movement of protons down a large electrochemical gradient via ATP synthase located on the folded inner membrane, known as cristae. In mammalian skeletal muscle, the density of cristae in mitochondria is assumed to be constant. However, recent experimental studies have shown that respiration per mitochondria varies. Modelling studies have hypothesized that this variation in respiration per mitochondria depends on plasticity in cristae density, although current evidence for such a mechanism is lacking. In the present study, we confirm this hypothesis by showing that, in human skeletal muscle, and in contrast to the current view, the mitochondrial cristae density is not constant but, instead, exhibits plasticity with long‐term endurance training. Furthermore, we show that frequently recruited mitochondria‐enriched fibres have significantly increased cristae density and that, at the whole‐body level, muscle mitochondrial cristae density is a better predictor of maximal oxygen uptake rate than muscle mitochondrial volume. Our findings establish an elevating mitochondrial cristae density as a regulatory mechanism for increasing metabolic power in human skeletal muscle. We propose that this mechanism allows evasion of the trade‐off between cell occupancy by mitochondria and other cellular constituents, as well as improved metabolic capacity and fuel catabolism during prolonged elevated energy requirements.

The aim of the present study was to investigate the influence of muscle glycogen content on sarcoplasmic reticulum (SR) function and peak power output (Wpeak) in elite endurance athletes. Fourteen highly trained male triathletes (V˙O2max = 66.5 ± 1.3 mL O2·kg−1·min−1), performed 4 h of glycogen-depleting cycling exercise (HRmean = 73% ± 1% of maximum). During the first 4 h of recovery, athletes received either water (H2O) or carbohydrate (CHO), separating alterations in muscle glycogen content from acute changes affecting SR function and performance. Thereafter, all subjects received CHO-enriched food for the remaining 20-h recovery period. Immediately after exercise, muscle glycogen content and SR Ca2+ release rate was reduced to 32% ± 4% (225 ± 28 mmol·kg−1 dw) and 86% ± 2% of initial levels, respectively (P < 0.01). Glycogen markedly recovered after 4 h of recovery with CHO (61% ± 2% of preexercise) and SR Ca2+ release rate returned to preexercise level. However, in the absence of CHO during the first 4 h of recovery, glycogen and SR Ca2+ release rate remained depressed, with the normalization of both parameters at the end of the 24 h of recovery after receiving a CHO-enriched diet. Linear regression demonstrated a significant correlation between SR Ca2+ release rate and muscle glycogen content (P < 0.01, r2 = 0.30). The 4 h of cycling exercise reduced Wpeak by 5.5%–8.9% at different cadences (P < 0.05), and Wpeak was normalized after 4 h of recovery with CHO, whereas Wpeak remained depressed (P < 0.05) after water provision. Wpeak was fully recovered after 24 h in both the H2O and the CHO group. In conclusion, the present results suggest that low muscle glycogen depresses muscle SR Ca2+ release rate, which may contribute to fatigue and delayed recovery of Wpeak 4 h postexercise.

The present study investigated the effects of periodic carbohydrate (CHO) restriction on endurance performance and metabolic markers in elite endurance athletes. Twenty-six male elite endurance athletes (maximal oxygen consumption (V˙O2max), 65.0 mL O2·kg−1·min−1) completed 4 wk of regular endurance training while being matched and randomized into two groups training with (low) or without (high) CHO manipulation 3 d·wk−1. The CHO manipulation days consisted of a 1-h high-intensity bike session in the morning, recovery for 7 h while consuming isocaloric diets containing either high CHO (414 ± 2.4 g) or low CHO (79.5 ± 1.0 g), and a 2-h moderate bike session in the afternoon with or without CHO. V˙O2max, maximal fat oxidation, and power output during a 30-min time trial (TT) were determined before and after the training period. The TT was undertaken after 90 min of intermittent exercise with CHO provision before the training period and both CHO and placebo after the training period. Muscle biopsies were analyzed for glycogen, citrate synthase (CS) and β-hydroxyacyl-coenzyme A dehydrogenase (HAD) activity, carnitine palmitoyltransferase (CPT1b), and phosphorylated acetyl-CoA carboxylase (pACC). The training effects were similar in both groups for all parameters. On average, V˙O2max and power output during the 30-min TT increased by 5% ± 1% (P < 0.05) and TT performance was similar after CHO and placebo during the preload phase. Training promoted overall increases in glycogen content (18% ± 5%), CS activity (11% ± 5%), and pACC (38% ± 19%; P < 0.05) with no differences between groups. HAD activity and CPT1b protein content remained unchanged. Superimposing periodic CHO restriction to 4 wk of regular endurance training had no superior effects on performance and muscle adaptations in elite endurance athletes.

Endurance athletes typically consume carbohydrate-rich diets to allow for optimal performance during competitions and intense training. However, acute exercise studies have revealed that training or recovery with low muscle glycogen stimulates factors of importance for mitochondrial biogenesis in addition to favourable metabolic adaptations in trained athletes. Compromised training quality and particularly lower intensities in peak intervals seem to be a major drawback from dietary interventions with chronic carbohydrate (CHO) restriction. Therefore, the concept of undertaking only selected training sessions with restricted CHO availability (periodized CHO restriction) has been proposed for endurance athletes. However, the overall performance effect of this concept has not been systematically reviewed in highly adapted endurance-trained athletes. We therefore conducted a meta-analysis of training studies that fulfilled the following criteria: a) inclusion of females and males demonstrating a VO2max ≥ 55 and 60 ml · kg− 1 · min− 1, respectively; b) total intervention and training periods ≥ 1 week, c) use of interventions including training and/or recovery with periodized carbohydrate restriction at least three times per week, and d) measurements of endurance performance before and after the training period. The literature search resulted in 407 papers of which nine studies fulfilled the inclusion criteria. The subsequent meta-analysis demonstrated no overall effect of CHO periodization on endurance performance compared to control endurance training with normal (high) CHO availability (standardized mean difference = 0.17 [− 0.15, 0.49]; P = 0.29). Based on the available literature, we therefore conclude that periodized CHO restriction does not per se enhance performance in endurance-trained athletes. The review discusses different approaches to CHO periodization across studies with a focus on identifying potential physiological benefits.