In the past decades, researchers have extensively studied (elite) athletes' physiological responses to understand how to maximize their endurance performance. In endurance sports, whole-body measurements such as the maximal oxygen consumption, lactate threshold, and efficiency/economy play a key role in performance. Although these determinants are known to interact, it has also been demonstrated that athletes rarely excel in all three. The leading question is how athletes reach exceptional values in one or all of these determinants to optimize their endurance performance, and how such performance can be explained by (combinations of) underlying physiological determinants. In this review, we advance on Joyner and Coyle's conceptual framework of endurance performance, by integrating a meta-analysis of the interrelationships, and corresponding effect sizes between endurance performance and its key physiological determinants at the macroscopic (whole-body) and the microscopic level (muscle tissue, i.e., muscle fiber oxidative capacity, oxygen supply, muscle fiber size, and fiber type). Moreover, we discuss how these physiological determinants can be improved by training and what potential physiological challenges endurance athletes may face when trying to maximize their performance. This review highlights that integrative assessment of skeletal muscle determinants points toward efficient type-I fibers with a high mitochondrial oxidative capacity and strongly encourages well-adjusted capillarization and myoglobin concentrations to accommodate the required oxygen flux during endurance performance, especially in large muscle fibers. Optimisation of endurance performance requires careful design of training interventions that fine tune modulation of exercise intensity, frequency and duration, and particularly periodisation with respect to the skeletal muscle determinants.

V̇o_{2 max}during whole body exercise is presumably constrained by oxygen delivery to mitochondria rather than by mitochondria's ability to consume oxygen. Humans and animals have been reported to exploit only 60-80% of their mitochondrial oxidative capacity at maximal oxygen uptake (V̇o_{2 max}). However, ex vivo quantification of mitochondrial overcapacity is complicated by isolation or permeabilization procedures. An alternative method for estimating mitochondrial oxidative capacity is via enzyme histochemical quantification of succinate dehydrogenase (SDH) activity. We determined to what extent V̇o_{2 max}attained during cycling exercise differs from mitochondrial oxidative capacity predicted from SDH activity of vastus lateralis muscle in chronic heart failure patients, healthy controls, and cyclists. V̇o_{2 max}was assessed in 20 healthy subjects and 28 cyclists, and SDH activity was determined from biopsy cryosections of vastus lateralis using quantitative histochemistry. Similar data from our laboratory of 14 chronic heart failure patients and 6 controls were included. Mitochondrial oxidative capacity was predicted from SDH activity using estimated skeletal muscle mass and the relationship between ex vivo fiber V̇o_{2 max}and SDH activity of isolated single muscle fibers and myocardial trabecula under hyperoxic conditions. Mitochondrial oxidative capacity predicted from SDH activity was related ( r²= 0.89, P < 0.001) to V̇o_{2 max}measured during cycling in subjects with V̇o_{2 max}ranging from 9.8 to 79.0 ml·kg⁻¹·min⁻¹. V̇o_{2 max}measured during cycling was on average 90 ± 14% of mitochondrial oxidative capacity. We conclude that human V̇o_{2 max}is related to mitochondrial oxidative capacity predicted from skeletal muscle SDH activity. Mitochondrial oxidative capacity is likely marginally limited by oxygen supply to mitochondria.

Background: Many sports require maximal strength and endurance performance. Concurrent strength and endurance training can lead to suboptimal training adaptations. However, how adaptations differ between males and females is currently unknown. Additionally, current training status may affect training adaptations. Objective: We aimed to assess sex-specific differences in adaptations in strength, power, muscle hypertrophy, and maximal oxygen consumption ( $$\dot{V}$$V ˙ O_2max) to concurrent strength and endurance training in healthy adults. Second, we investigated how training adaptations are influenced by strength and endurance training status. Methods: A systematic review and meta-analysis was conducted according to PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines, and a Cochrane risk of bias was evaluated. ISI Web of science, PubMed/MEDLINE, and SPORTDiscus databases were searched using the following inclusion criteria: healthy adults aged 18–50 years, intervention period of ≥ 4 weeks, and outcome measures were defined as upper- and lower-body strength, power, hypertrophy, and/or $$\dot{V}$$V ˙ O_2max. A meta-analysis was performed using a random-effects model and reported in standardized mean differences. Results: In total, 59 studies with 1346 participants were included. Concurrent training showed blunted lower-body strength adaptations in males, but not in females (male: − 0.43, 95% confidence interval [− 0.64 to − 0.22], female: 0.08 [− 0.34 to 0.49], group difference: P = 0.03). No sex differences were observed for changes in upper-body strength (P = 0.67), power (P = 0.37), or $$\dot{V}$$V ˙ O_2max (P = 0.13). Data on muscle hypertrophy were insufficient to draw any conclusions. For training status, untrained but not trained or highly trained endurance athletes displayed lower $$\dot{V}$$V ˙ O_2max gains with concurrent training (P = 0.04). For other outcomes, no differences were found between untrained and trained individuals, both for strength and endurance training status. Conclusions: Concurrent training results in small interference for lower-body strength adaptations in males, but not in females. Untrained, but not trained or highly trained endurance athletes demonstrated impaired improvements in $$\dot{V}$$V ˙ O_2max following concurrent training. More studies on females and highly strength-trained and endurance-trained athletes are warranted. Clinical Trial Registration: PROSPERO: CRD42022370894.

Near-infrared spectroscopy (NIRS) measurements of oxygenation reflect O₂ delivery and utilization in exercising muscle and may improve detection of a critical exercise threshold. First, to detect an oxygenation breakpoint (Δ[O₂HbMb-HHbMb]-BP) and compare this breakpoint to ventilatory thresholds during a maximal incremental test across sexes and training status. Second, to assess reproducibility of NIRS signals and exercise thresholds and investigate confounding effects of adipose tissue thickness on NIRS measurements. Forty subjects (10 trained male cyclists, 10 trained female cyclists, 11 endurance trained males and 9 recreationally trained males) performed maximal incremental cycling exercise to determine Δ[O₂HbMb-HHbMb]-BP and ventilatory thresholds (VT1 and VT2). Muscle haemoglobin and myoglobin O₂ oxygenation ([HHbMb], [O₂HbMb], SmO₂) was determined in m. vastus lateralis. Δ[O₂HbMb-HHbMb]-BP was determined by double linear regression. Trained cyclists performed the maximal incremental test twice to assess reproducibility. Adipose tissue thickness (ATT) was determined by skinfold measurements. Δ[O₂HbMb-HHbMb]-BP was not different from VT1, but only moderately related (r = 0.58–0.63, p<0.001). VT1 was different across sexes and training status, whereas Δ[O₂HbMb-HHbMb]-BP differed only across sexes. Reproducibility was high for SmO₂ (ICC = 0.69–0.97), Δ[O₂HbMb-HHbMb]-BP (ICC = 0.80–0.88) and ventilatory thresholds (ICC = 0.96–0.99). SmO₂ at peak exercise and at occlusion were strongly related to adipose tissue thickness (r² = 0.81, p<0.001; r² = 0.79, p<0.001). Moreover, ATT was related to asymmetric changes in Δ[HHbMb] and Δ[O₂HbMb] during incremental exercise (r = -0.64, p<0.001) and during occlusion (r = -0.50, p<0.05). Although the oxygenation threshold is reproducible and potentially a suitable exercise threshold, VT1 discriminates better across sexes and training status during maximal stepwise incremental exercise. Continuous-wave NIRS measurements are reproducible, but strongly affected by adipose tissue thickness.

Optimizing physical performance is a major goal in current physiology. However, basic understanding of combining high sprint and endurance performance is currently lacking. This study identifies critical determinants of combined sprint and endurance performance using multiple regression analyses of physiologic determinants at different biologic levels. Cyclists, including 6 international sprint, 8 team pursuit, and 14 road cyclists, completed a Wingate test and 15‐km time trial to obtain sprint and endurance performance results, respectively. Performance was normalized to lean body mass ^2/3 to eliminate the influence of body size. Performance determinants were obtained from whole‐body oxygen consumption, blood sampling, knee‐extensor maximal force, muscle oxygenation, whole‐muscle morphology, and muscle fiber histochemistry of musculus vastus lateralis. Normalized sprint performance was explained by percentage of fast‐type fibers and muscle volume ( R ² = 0.65; P < 0.001) and normalized endurance performance by performance oxygen consumption (Vo ₂ ), mean corpuscular hemoglobin concentration, and muscle oxygenation ( R ² = 0.92; P < 0.001). Combined sprint and endurance performance was explained by gross efficiency, performance Vo ₂ and likely by muscle volume and fascicle length ( P = 0.056; P = 0.059). High performance Vo ₂ related to a high oxidative capacity, high capillarization x myoglobin, and small physiologic cross‐sectional area ( R ² = 0.67; P < 0.001). Results suggest that fascicle length and capillarization are important targets for training to optimize sprint and endurance performance simultaneously.— Van der Zwaard, S., van derLaarse, W. J., Weide, G., Bloemers, F. W., Hofmijster, M. J., Levels, K., Noordhof, D. A., de Koning, J. J., de Ruiter, C. J., Jaspers, R. T. Critical determinants of combined sprint and endurance performance: an integrative analysis from muscle fiber to the human body. FASEB J. 32, 2110–2123 (2018). www.fasebj.org

Rowers need to combine high sprint and endurance capacities. Muscle morphology largely explains muscle power generating capacity, however, little is known on how muscle morphology relates to rowing performance measures. The aim was to determine how muscle morphology of the vastus lateralis relates to rowing ergometer performance, sprint and endurance capacity of Olympic rowers. Eighteen rowers (12♂, 6♀, who competed at 2016 Olympics) performed an incremental rowing test to obtain maximal oxygen consumption, reflecting endurance capacity. Sprint capacity was assessed by Wingate cycling peak power. M. vastus lateralis morphology (volume, physiological cross-sectional area, fascicle length and pennation angle) was derived from 3-dimensional ultrasound imaging. Thirteen rowers (7♂, 6♀) completed a 2000-m rowing ergometer time trial. Muscle volume largely explained variance in 2000-m rowing performance (R² = 0.85), maximal oxygen consumption (R² = 0.65), and Wingate peak power (R² = 0.82). When normalized for differences in body size, maximal oxygen consumption and Wingate peak power were negatively related in males (r = −0.94). Fascicle length, not physiological cross-sectional area, attributed to normalized peak power. In conclusion, vastus lateralis volume largely explains variance in rowing ergometer performance, sprint and endurance capacity. For a high normalized sprint capacity, athletes may benefit from long fascicles rather than a large physiological cross-sectional area.