Exogenous ketosis produced by oral ketone ester ingestion during the early phase of prolonged endurance exercise and against the background of adequate carbohydrate intake neither causes muscle glycogen sparing nor improves performance in the final stage of the event. However, such exogenous ketosis may decrease buffering capacity in the approach of the final episode of the event. Furthermore, ketone ester intake during exercise may reduce appetite immediately after exercise.

Purpose We recently reported that oral ketone ester (KE) intake before and during the initial 30 min of a 3 h 15 min simulated cycling race (RACE) transiently decreased blood pH and bicarbonate without affecting maximal performance in the final quarter of the event. We hypothesized that acid–base disturbances due to KE overrules the ergogenic potential of exogenous ketosis in endurance exercise. Methods Nine well-trained male cyclists participated in a similar RACE consisting of 3 h submaximal intermittent cycling (IMT 180′ ) followed by a 15-min time trial (TT 15′ ) preceding an all-out sprint at 175% of lactate threshold (SPRINT). In a randomized crossover design, participants received (i) 65 g KE, (ii) 300 mg·kg −1 body weight NaHCO 3 (BIC), (iii) KE + BIC, or (iv) a control drink (CON), together with consistent 60 g·h −1 carbohydrate intake. Results KE ingestion transiently elevated blood D-ß-hydroxybutyrate to ~2–3 mM during the initial 2 h of RACE ( P < 0.001 vs CON). In KE, blood pH concomitantly dropped from 7.43 to 7.36 whereas bicarbonate decreased from 25.5 to 20.5 mM (both P < 0.001 vs CON). Additional BIC resulted in 0.5 to 0.8 mM higher blood D-ß-hydroxybutyrate during the first half of IMT 180′ ( P < 0.05 vs KE) and increased blood bicarbonate to 31.1 ± 1.8 mM and blood pH to 7.51 ± 0.03 by the end of IMT 180′ ( P < 0.001 vs KE). Mean power output during TT 15′ was similar between KE, BIC, and CON at ~255 W but was 5% higher in KE + BIC ( P = 0.02 vs CON). Time to exhaustion in the sprint was similar between all conditions at ~60 s ( P = 0.88). Gastrointestinal symptoms were similar between groups. Discussion The coingestion of oral bicarbonate and KE enhances high-intensity performance at the end of an endurance exercise event without causing gastrointestinal distress.

Old skeletal muscle exhibits decreased anabolic sensitivity, eventually contributing to muscle wasting. Besides anabolism, also muscle inflammation and catabolism are critical players in regulating the old skeletal muscle’s sensitivity. Omega-3 fatty acids (ω-3) are an interesting candidate to reverse anabolic insensitivity via anabolic actions. Yet, it remains unknown whether ω-3 also attenuates muscle inflammation and catabolism. The present study investigates the effect of ω-3 supplementation on muscle inflammation and metabolism (anabolism/catabolism) upon resistance exercise (RE). Twenty-three older adults (65–84 years; 8♀) were randomized to receive ω-3 (~3 g/d) or corn oil (placebo [PLAC]) and engaged in a 12-week RE program (3×/wk). Before and after intervention, muscle volume, strength, and systemic inflammation were assessed, and muscle biopsies were analyzed for markers of anabolism, catabolism, and inflammation. Isometric knee-extensor strength increased in ω-3 (+12.2%), but not in PLAC (−1.4%; pinteraction = .015), whereas leg press strength improved in both conditions (+27.1%; ptime &lt; .001). RE, but not ω-3, decreased inflammatory (p65NF-κB) and catabolic (FOXO1, LC3b) markers, and improved muscle quality. Yet, muscle volume remained unaffected by RE and ω-3. Accordingly, muscle anabolism (mTORC1) and plasma C-reactive protein remained unchanged by RE and ω-3, whereas serum IL-6 tended to decrease in ω-3 (pinteraction = .07). These results show that, despite no changes in muscle volume, RE-induced gains in isometric strength can be further enhanced by ω-3. However, ω-3 did not improve RE-induced beneficial catabolic or inflammatory adaptations. Irrespective of muscle volume, gains in strength (primary criterion for sarcopenia) might be explained by changes in muscle quality due to muscle inflammatory or catabolic signaling.

The Achilles tendon has a unique structure-function relationship thanks to its innate hierarchical architecture in combination with the rotational anatomy of the sub-tendons from the triceps surae muscles. Previous research has provided valuable insight in global Achilles tendon mechanics, but limitations with the technique used remain. Furthermore, given the global approach evaluating muscle-tendon junction to insertion, regional differences in tendon mechanical properties might be overlooked. However, recent advancements in the field of ultrasound imaging in combination with speckle tracking have made an intratendinous evaluation possible. This study uses high-frequency ultrasound to allow for quantification of regional tendon deformation. Also, an interactive application was developed to improve clinical applicability. A dynamic ultrasound of both Achilles tendons of ten asymptomatic subjects was taken. The displacement and regional strain in the superficial, middle and deep layer were evaluated during passive elongation and isometric contraction. Building on previous research, results showed that the Achilles tendon displaces non-uniformly with a higher displacement found in the deep layer of the tendon. Adding to this, a non-uniform regional strain behavior was found in the Achilles tendon during passive elongation, with the highest strain in the superficial layer. Further exploration of tendon mechanics will improve the knowledge on etiology of tendinopathy and provide options to optimize existing therapeutic loading programs.

Achilles tendon stiffness determines calf muscle functioning during functional activities. However, contrasting evidence was found in studies comparing Achilles tendon stiffness in older and younger adults. Therefore, this systematic review compares Achilles tendon stiffness and elastic modulus in older and younger adults and reviews functional implications. Studies revealed by systematic bibliographic searches were included if healthy older adults were investigated, and if Achilles tendon stiffness was measured using ultrasound and dynamometry. Meta-analyses were performed to compare Achilles tendon stiffness and elastic modulus in older and younger adults. Achilles tendon stiffness (weighted standardized mean difference = 1.40, 95% confidence intervals [0.42-2.38]) and elastic modulus (weighted standardized mean difference = 1.74, 95% confidence intervals [0.99-2.49]) were decreased in older compared with younger adults. Decreased Achilles tendon stiffness was related to walking performance and balance. Possibly, decreased Achilles tendon stiffness is caused by altered elastic modulus in older adults. Training interventions increasing Achilles tendon stiffness could improve functional capacity.