Purpose: Acute cold exposure (ACE) stimulates metabolism but data evaluating inflammatory and lipid biomarkers related to cardiovascular disease in response to ACE are lacking. Therefore, we investigated the relationship between ACE and inflammatory and lipid biomarkers.Methods: Twenty subjects underwent 30 min of ACE with blood drawn: 1) pre-ACE (baseline), 2) at 30 min ACE, and 3) 2 h post-ACE. Plasma was analyzed for 10 cytokines (monocyte chemoattractant protein-1 (CCL2), interleukin (IL)-1β, IL-2, IL-4, IL-6, IL-8, IL-10, granulocyte-macrophage colony stimulating factor (GM-CSF), tumor necrosis factor-alpha (TNF-α), interferon-gamma (INFγ)), 9 acute phase proteins (ferritin, fibrinogen, procalcitonin, serum amyloid A, serum amyloid P, tissue plasminogen, C-reactive protein, haptoglobin, α-2-macroglobin), and 5 lipid biomarkers (triglycerides, nonesterified fatty acids (NEFA), low-and high-density lipoprotein (LDL, HDL), and total cholesterol). Heart rate, whole body oxygen consumption (VO 2 ), energy expenditure (EE), shivering sensations, and pain were measured prior and during ACE.Results: ACE increased heart rate by 11%, shivering sensations by 4-fold, pain by 2-fold, VO2 by 50%, and EE by 52%. IL-1β increased after 30 min ACE by 24% (p=0.048) and 2 h post ACE by 65% (p=0.01). Alpha-2-macroglobin increased after 30 min ACE by 16% (p=0.005) and returned to baseline levels 2 h post-ACE. HDL increased at 2 h post-ACE by 15% (p=0.034). Sex differences were noted between IL-2, IL-6, IL-8, ferritin, α-2-macroglobin and HDL.Conclusions: These findings indicate ACE increases EE and modifies inflammation, the acute phase response, and lipid metabolism. Long-term risk of CVD needs further exploration to assess the risks or benefits of ACE. Future studies with diverse subjects varying in age and body composition and studies aimed to determine the effectiveness of ACE as compared to diet and exercise are warranted.

Acute cold exposure (ACE) stimulates metabolism but data evaluating inflammatory and lipid biomarkers related to cardiovascular disease in response to ACE are lacking. Therefore, we investigated the relationship between ACE and inflammatory and lipid biomarkers. Methods: Twenty subjects underwent 30 min of ACE with blood drawn: 1) pre-ACE (baseline), 2) at 30 min ACE, and 3) 2 h post-ACE. Plasma was analyzed for 10 cytokines (monocyte chemoattractant protein-1 (CCL2), interleukin (IL)-1β, IL-2, IL-4, IL-6, IL-8, IL-10, granulocyte-macrophage colony stimulating factor (GM-CSF), tumor necrosis factor-alpha (TNF-α), interferon-gamma (INFγ)), 9 acute phase proteins (ferritin, fibrinogen, procalcitonin, serum amyloid A, serum amyloid P, tissue plasminogen, C-reactive protein, haptoglobin, α-2-macroglobin), and 5 lipid biomarkers (triglycerides, nonesterified fatty acids (NEFA), low-and high-density lipoprotein (LDL, HDL), and total cholesterol). Heart rate, whole body oxygen consumption (VO2), energy expenditure (EE), shivering sensations, and pain were measured prior and during ACE. Results: ACE increased heart rate by 11%, shivering sensations by 4-fold, pain by 2-fold, VO2 by 50%, and EE by 52%. IL-1β increased after 30 min ACE by 24% (p=0.048) and 2 h post ACE by 65% (p=0.01). Alpha-2-macroglobin increased after 30 min ACE by 16% (p=0.005) and returned to baseline levels 2 h post-ACE. HDL increased at 2 h post-ACE by 15% (p=0.034). Sex differences were noted between IL-2, IL-6, IL-8, ferritin, α-2-macroglobin and HDL. Conclusions: These findings indicate ACE increases EE and modifies inflammation, the acute phase response, and lipid metabolism.