By increasing fruit exposure to sunlight and influencing fruit development, leaf thinning in the fruit zone can improve grape quality and lower disease incidence; however, further investigations on the timing, varietal response and intensity are needed to optimize results and to better understand underlying physiologic responses. Fruit zone leaf thinning was applied at different timing and intensities to evaluate its effect on cluster health and fruit composition in Cabernet Sauvignon and Chardonnay. Treatments consisted of control (C), pre-bloom leaf thinning (PB) and two levels of fruit-set leaf thinning (three leaves, PF3 and six leaves, PF6). In an additional project on Cabernet Sauvignon, two levels of hedging (17th node, NH and 12th node, H) were integrated with no leaf thinning (L) and fruit set leaf thinning (LR, three leaves).

All leaf thinning treatments consistently reduced disease incidence compared to control vines in both varieties, with the reduction extent varying between 2017 and 2018. Yield was not negatively affected by leaf thinning treatments, even though PB reduced cluster compactness by decreasing the number of berries per cluster of Chardonnay in 2017. Control vines tended to have greater titratable acidity than defoliated vines, while Brix and pH responses varied between seasons. No direct positive correlation was found between sunlight exposure and norisoprenoids concentration. Post fruit set leaf thinning PF6 consistently increase free norisoprenoids at harvest, while pre-bloom defoliation never did. Heterogeneous responses were observed for bound and total norisoprenoids. In Cabernet Sauvignon free, bound and total 1,1,6-trimethyl-1,2-dihydronaphtalene (TDN) was consistently increased by PF3. Hedging negatively influenced Brix and anthocyanins accumulation in 2017, and increased free norisoprenoids while decreasing the bound and total fraction. Results revealed that a high level of stress possiblt caused by excess sunlight and/or reduced photosynthesis might negatively affect norisoprenoids glycosylation.