Purpose Whole-body fat oxidation during exercise can be measured non-invasively during athlete profiling. Gaps in understanding exist in the relationships between fat oxidation during incremental fasted exercise and skeletal muscle parameters, endurance performance, and fat oxidation during prolonged fed-state exercise. Methods Seventeen endurance-trained males underwent a (i) fasted, incremental cycling test to assess peak whole-body fat oxidation (PFO), (ii) resting vastus lateralis microbiopsy, and (iii) 30-min maximal-effort cycling time-trial preceded by 2-h of fed-state moderate-intensity cycling to assess endurance performance and fed-state metabolism on separate occasions within one week. Results PFO (0.58 ± 0.28 g . min −1 ) was associated with vastus lateralis citrate synthase activity (69.2 ± 26.0 μmol . min −1. g −1 muscle protein, r = 0.84, 95% CI 0.58, 0.95, P < 0.001), CD36 abundance (16.8 ± 12.6 μg . g −1 muscle protein, r s = 0.68, 95% CI 0.31, 1.10, P = 0.01), pre-loaded 30-min time-trial performance (251 ± 51 W, r = 0.76, 95% CI 0.40, 0.91, P = 0.001; 3.2 ± 0.6 W . kg −1 , r = 0.62, 95% CI 0.16, 0.86, P = 0.01), and fat oxidation during prolonged fed-state cycling ( r = 0.83, 95% CI 0.57, 0.94, P < 0.001). Addition of PFO to a traditional model of endurance (peak oxygen uptake, power at 4 mmol . L −1 blood lactate concentration, and gross efficiency) explained an additional ~ 2.6% of variation in 30-min time-trial performance (adjusted R 2 = 0.903 vs. 0.877). Conclusion These associations suggest non-invasive measures of whole-body fat oxidation during exercise may be useful in the physiological profiling of endurance athletes.

Lettuce necrotic yellows virus (LNYV) is the type member of the genus Cytorhabdovirus, family Rhabdoviridae, and causes a severe disease of lettuce (Lactuca sativa L.). This virus has been described as endemic to Australia and New Zealand, with sporadic reports of a similar virus in Europe. Genetic variability studies of plant-infecting rhabdoviruses are scarce. We have extended a previous study on the variability of the LNYV nucleocapsid gene, comparing sequences from isolates sampled from both Australia and New Zealand, as well as analysing symptom expression on Nicotiana glutinosa. Phylogenetic and BEAST analyses confirm separation of LNYV isolates into two subgroups (I and II) and suggest that subgroup I is slightly older than subgroup II. No correlation was observed between isolate subgroup and disease symptoms on N. glutinosa. The origin of LNYV remains unclear; LNYV may have moved between native and weed hosts within Australia or New Zealand before infecting lettuce or may have appeared as a result of at least two incursions, with the first coinciding with the beginning of European agriculture in the region. The apparent extinction of subgroup I in Australia may have been due to less-efficient dispersal than that which has occurred for subgroup II - possibly a consequence of suboptimal interactions with plant and/or insect hosts. Introduction of subgroup II to New Zealand appears to be more recent. More-detailed epidemiological studies using molecular tools are needed to fully understand how LNYV interacts with its hosts and to determine where the virus originated.

We present the first complete genome of vanilla mosaic virus (VanMV). The VanMV genomic structure is consistent with that of a potyvirus, containing a single open reading frame (ORF) encoding a polyprotein of 3139 amino acids. Motif analyses indicate the polyprotein can be cleaved into the expected ten individual proteins; other recognised potyvirus motifs are also present. As expected, the VanMV genome shows high sequence similarity to the published Dasheen mosaic virus (DsMV) genome sequences; comparisons with DsMV continue to support VanMV as a vanilla infecting strain of DsMV. Phylogenetic analyses indicate that VanMV and DsMV share a common ancestor, with VanMV having the closest relationship with DsMV strains from the South Pacific.

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Several proteins are implicated in transmembrane fatty acid transport. The purpose of this study was to quantify the variation in fatty acid oxidation rates during exercise explained by skeletal muscle proteins involved in fatty acid transport. Seventeen endurance-trained males underwent a (i) fasted, incremental cycling test to estimate peak whole-body fatty acid oxidation rate (PFO), (ii) resting vastus lateralis microbiopsy, and (iii) 2 h of fed-state, moderate-intensity cycling to estimate whole-body fatty acid oxidation during fed-state exercise (FO). Bivariate correlations and stepwise linear regression models of PFO and FO during 0–30 min (early FO) and 90–120 min (late FO) of continuous cycling were constructed using muscle data. To assess the causal role of transmembrane fatty acid transport in fatty acid oxidation rates during exercise, we measured fatty acid oxidation during in vivo exercise and ex vivo contractions in wild-type and CD36 knock-out mice. We observed a novel, positive association between vastus lateralis FATP1 and PFO and replicated work reporting a positive association between FABPpm and PFO. The stepwise linear regression model of PFO retained CD36, FATP1, FATP4, and FABPpm, explaining ~87% of the variation. Models of early and late FO explained ~61 and ~65% of the variation, respectively. FATP1 and FATP4 emerged as contributors to models of PFO and FO. Mice lacking CD36 had impaired whole-body and muscle fatty acid oxidation during exercise and muscle contractions, respectively. These data suggest that substantial variation in fatty acid oxidation rates during exercise can be explained by skeletal muscle proteins involved in fatty acid transport.