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Acute ketone monoester (KE) supplementation can alter exercise responses, but the performance effect is unclear. The limited and equivocal data to date are likely related to factors including the KE dose, test conditions, and caliber of athletes studied. We tested the hypothesis that mean power output during a 20-min cycling time trial (TT) would be different after KE ingestion compared to a placebo (PL). A sample size of 22 was estimated to provide 80% power to detect an effect size dz of 0.63 at an alpha level of.05 with a two-tailed paired t test. This determination considered 2.0% as the minimal important difference in performance. Twenty-three trained cyclists (N = 23; peak oxygen uptake: 65 ± 12 ml·kg−1 min−1; M ± SD), who were regularly cycling >5 hr/week, completed a familiarization trial followed by two experimental trials. Participants self-selected and replicated their diet and exercise for ∼24 hr before each trial. Participants ingested either 0.35 g/kg body mass of (R)-3-hydroxybutyl (R)-3-hydroxybutyrate KE or a flavor-matched PL 30 min before exercise in a randomized, triple-blind, crossover manner. Exercise involved a 15-min warm-up followed by the 20-min TT on a cycle ergometer. The only feedback provided was time elapsed. Preexercise venous [β-hydroxybutyrate] was higher after KE versus PL (2.0 ± 0.6 vs. 0.2 ± 0.1 mM, p <.0001). Mean TT power output was 2.4% (0.6% to 4.1%; mean [95% confidence interval]) lower after KE versus PL (255 ± 54 vs. 261 ± 54 W, p <.01; dz = 0.60). The mechanistic basis for the impaired TT performance after KE ingestion under the present study conditions remains to be determined. [ABSTRACT FROM AUTHOR]

Background: High‐intensity interval training (HIIT) is characterized by repeated bouts of relatively intense exercise interspersed with recovery periods. Previous studies have evaluated this exercise strategy with various population subgroups, regimens, and comparator groups, limiting the generalizability of findings. We performed a novel umbrella review to generate an up‐to‐date synthesis of the available evidence regarding the effect of HIIT on cardiorespiratory fitness (CRF) in adults as compared to non‐exercise control and traditional continuous forms of exercise such as moderate‐intensity continuous training (MICT). Methods: An umbrella review was conducted in accordance with the Preferred Reporting Items for Overviews of Reviews guideline. Seven databases (MEDLINE, EMBASE, Cochrane Database, CINAHL, Scopus, SPORTDiscus, and Web of Science) were searched until February 2024. Systematic reviews with meta‐analyses comparing HIIT and active/non‐active control conditions were included. Literature search, data extraction, and methodological quality assessment (AMSTAR‐2) were conducted independently by two reviewers. Results: Twenty‐four systematic reviews with meta‐analyses, representing 429 primary studies and 12 967 unique participants, met the inclusion criteria. Most of the systematic reviews received moderate‐to‐critically low AMSTAR‐2 scores. The data showed that HIIT, including the particularly intense variant "sprint interval training" (SIT), significantly increases CRF in adults compared to non‐exercise control (standardized mean difference [SMD]: 0.28 to 4.31; weighted mean difference [WMD]: 3.25 to 5.5 mL/kg/min) and MICT (SMD: 0.18 to 0.99; WMD: 0.52 to 3.76 mL/kg/min). This effect was consistently observed across specific groups of individuals (e.g., apparently healthy adults, individuals with overweight/obesity, older adults, and high‐level athletes) and HIIT modalities (e.g., low‐volume HIIT, whole‐body HIIT, home‐based HIIT, aquatic HIIT, and short SIT). Conclusion: Existing evidence from systematic reviews consistently supports the effect of HIIT on enhancing CRF in adults when compared to non‐exercise control and MICT. Our findings offer a comprehensive basis that may potentially contribute to informing physical activity guidelines aimed at improving CRF in the general population. [ABSTRACT FROM AUTHOR]

Peroxisome proliferator-activated receptor gamma coactivator (PGC-1[alpha]) is a transcriptional coactivator that plays a key role in coordinating mitochondrial biogenesis. Recent evidence has linked p38 MAPK and AMPK with activation of PGC-1[alpha]. It was recently shown in rodent skeletal muscle that acute endurance exercise causes a shift in the subcellular localization of PGC-1[alpha] from the cytosol to the nucleus, allowing PGC-1[alpha] to coactivate transcription factors and increase mitochondrial gene expression, but human data are limited and equivocal in this regard. Our purpose was to examine p38 MAPK and AMPK activation, and PGC-1[alpha] protein content in whole muscle, cytosolic, and nuclear fractions of human skeletal muscle following an acute bout of endurance exercise. Eight trained men (29 [+ or -] 3 yr; V[O.sub.2peak] = 55 [+ or -] 2 ml*[kg.sup.-1]*[min.sup.-1]) cycled for 90 min at ~65% of V[O.sub.2peak] and needle biopsy samples (vastus lateralis) were obtained before and immediately after exercise. At rest, the majority of PGC-1[alpha] was detected in cytosolic compared with the nuclear fractions. In response to exercise, nuclear PGC-1[alpha] protein increased by 54% (P < 0.05), yet whole muscle PGC-1[alpha] protein was unchanged compared with rest. Whole muscle and cytosolic p38 MAPK phosphorylation increased several-fold immediately after exercise compared with rest (P < 0.05). Acetyl CoA carboxylase (ACC) phosphorylation, a marker of AMPK activation, was increased by ~5-fold in cytosolic fractions following exercise (P < 0.05). These data provide evidence that, in human skeletal muscle, activation of cytosolic p38 MAPK and AMPK may be potential signals that lead to increased nuclear abundance and activation of PGC-1[alpha] in response to an acute bout of endurance exercise. mitochondrial biogenesis; muscle adaptation; p38 MAPK; AMPK doi: 10.1152/ajpregu.00409.2009.