BACKGROUND AND OBJECTIVES. Methane (CH₄) from ruminant livestock is a major contributor to global greenhouse gas (GHG) emissions. Early-lactation cows experience negative energy balance, leading to mobilization of body reserves. Subclinical ketosis (SCK) is a common metabolic disorder immediately after calving that can compromise feed efficiency, productivity, and rumen fermentation. The aim of the study was to investigate the impact of SCK on GHG output and production efficiency. MATERIALS AND METHODS. A total of 60 multiparous Holstein-Friesian cows were monitored from 3 to 28 days in milk. Blood β-hydroxybutyrate (BHB) concentrations were measured at 7, 14, 21, and 28 DIM to divide cows as healthy controls (CTR; BHB < 1.0 mmol/L at all time points; n = 43) or affected by SCK (KET; BHB ≥ 1.0 mmol/L at least once; n = 17). Individual CH₄, CO₂, and H₂ emissions were recorded daily using an automated system during voluntary feeding, which allowed cows to access the measurement unit without restraint. Emission data were expressed both as absolute daily production and normalized per kilogram of milk or DMI to assess efficiency-related effects. Statistical analysis was performed using linear mixed-effects models, with health status, time, and their interaction as fixed effects and cow as a random effect. Differences were considered significant at p ≤ 0.05. RESULTS. Cows affected by SCK produced 65.2% more CH₄ than healthy cows (402.8 ± 26.6 vs. 243.8 ± 17.7 g/day), corresponding to 10.96 ± 0.72 kg CO₂-equivalents/day compared with 6.60 ± 0.48 kg/day in CTR cows. When normalized per kilogram of milk, CH₄ output was nearly doubled in KET cows (12.8 ± 1.2 vs. 7.7 ± 0.8 g/kg), indicating reduced feed-to-milk conversion efficiency. Total CO₂ emissions were lower in KET cows (11,035 ± 593 vs. 12,225 ± 416 g/day), but including CH₄-derived CO₂ equivalents showed an overall higher GHG footprint for diseased animals. The H₂ emissions were reduced in KET cows, reflecting greater utilization by methanogenic archaea in the rumen. Temporal analysis revealed that CH₄ emissions increased suddenly following SCK onset. The dry matter intake was consistently lower in KET cows, confirming reduced feed efficiency. CONCLUSIONS. The SCK significantly affects enteric CH₄ emissions and the overall carbon footprint of early-lactation dairy cows. Preventing or mitigating SCK could provide dual benefits, improving both metabolic health and milk production. These findings highlight the importance of integrated metabolic and nutritional management strategies to enhance both animal welfare and the sustainability of dairy systems.
Subclinical ketosis in early-lactation dairy cows increases greenhouse gas emissions
Taio Giorgia;Lisuzzo Anastasia;Cecchini Francesca;Gianesella Matteo;Michele Berlanda;Fiore Enrico
2026
Abstract
BACKGROUND AND OBJECTIVES. Methane (CH₄) from ruminant livestock is a major contributor to global greenhouse gas (GHG) emissions. Early-lactation cows experience negative energy balance, leading to mobilization of body reserves. Subclinical ketosis (SCK) is a common metabolic disorder immediately after calving that can compromise feed efficiency, productivity, and rumen fermentation. The aim of the study was to investigate the impact of SCK on GHG output and production efficiency. MATERIALS AND METHODS. A total of 60 multiparous Holstein-Friesian cows were monitored from 3 to 28 days in milk. Blood β-hydroxybutyrate (BHB) concentrations were measured at 7, 14, 21, and 28 DIM to divide cows as healthy controls (CTR; BHB < 1.0 mmol/L at all time points; n = 43) or affected by SCK (KET; BHB ≥ 1.0 mmol/L at least once; n = 17). Individual CH₄, CO₂, and H₂ emissions were recorded daily using an automated system during voluntary feeding, which allowed cows to access the measurement unit without restraint. Emission data were expressed both as absolute daily production and normalized per kilogram of milk or DMI to assess efficiency-related effects. Statistical analysis was performed using linear mixed-effects models, with health status, time, and their interaction as fixed effects and cow as a random effect. Differences were considered significant at p ≤ 0.05. RESULTS. Cows affected by SCK produced 65.2% more CH₄ than healthy cows (402.8 ± 26.6 vs. 243.8 ± 17.7 g/day), corresponding to 10.96 ± 0.72 kg CO₂-equivalents/day compared with 6.60 ± 0.48 kg/day in CTR cows. When normalized per kilogram of milk, CH₄ output was nearly doubled in KET cows (12.8 ± 1.2 vs. 7.7 ± 0.8 g/kg), indicating reduced feed-to-milk conversion efficiency. Total CO₂ emissions were lower in KET cows (11,035 ± 593 vs. 12,225 ± 416 g/day), but including CH₄-derived CO₂ equivalents showed an overall higher GHG footprint for diseased animals. The H₂ emissions were reduced in KET cows, reflecting greater utilization by methanogenic archaea in the rumen. Temporal analysis revealed that CH₄ emissions increased suddenly following SCK onset. The dry matter intake was consistently lower in KET cows, confirming reduced feed efficiency. CONCLUSIONS. The SCK significantly affects enteric CH₄ emissions and the overall carbon footprint of early-lactation dairy cows. Preventing or mitigating SCK could provide dual benefits, improving both metabolic health and milk production. These findings highlight the importance of integrated metabolic and nutritional management strategies to enhance both animal welfare and the sustainability of dairy systems.
Pubblicazioni consigliate
I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
