Research Publication Title

A Review of Different Diets on Respiration and Cardiac Output

Major

Exercise Science

Faculty Mentor(s)

Dr. Kelly Massey

Keywords

Cardiac Output, Nutrition, Respiration, Diet, Carbohydrate, Fat

Abstract

A Review of Different Diets on Respiration and Cardiac Output Low-Carbohydrate High-fat (LCHF) diets in female mice, after 4 weeks, have resulted in higher fat mass/lean mass ratio. Nilsson et al stated that heart function was impaired in respect to reducing stroke volume and cardiac output, and it also reduced the weight of the liver and lungs compared to the control mice. These results are different than a protein sufficient diet. Lipids are the main energy source in a healthy heart, while excessive lipid amounts can have adverse effects. Nilsson et al mentioned the Natriuretic Protein A (ANP) was significantly lower in the LCHF group but an increased ANP expression is traditionally used as a marker for heart failure. The increase in NPR-A (receptor) has been linked to metabolic dysfunction. The lower liver weight may be due to the degradation of tissues that support gluconeogenesis but did not show an increase in fibrosis or steatosis. The perigonadal adipose tissue showed an increase in leptin with the LCHF diet. Leptin levels may also cause an increase energy expenditure via sympathetic activation. This could explain why mice that were fed the LCHF diet could maintain their body weight despite somewhat lower total energy intake (Nilsson et al.). After 4 weeks on the LCHF diet, cardiac and maximum aerobic capacity was impaired. These effects are unknown in human populations, thus requiring more research. According to the findings in mice it is believed that cardiac function should be carefully evaluated in humans who are on a low-carbohydrate diet.

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A Review of Different Diets on Respiration and Cardiac Output

A Review of Different Diets on Respiration and Cardiac Output Low-Carbohydrate High-fat (LCHF) diets in female mice, after 4 weeks, have resulted in higher fat mass/lean mass ratio. Nilsson et al stated that heart function was impaired in respect to reducing stroke volume and cardiac output, and it also reduced the weight of the liver and lungs compared to the control mice. These results are different than a protein sufficient diet. Lipids are the main energy source in a healthy heart, while excessive lipid amounts can have adverse effects. Nilsson et al mentioned the Natriuretic Protein A (ANP) was significantly lower in the LCHF group but an increased ANP expression is traditionally used as a marker for heart failure. The increase in NPR-A (receptor) has been linked to metabolic dysfunction. The lower liver weight may be due to the degradation of tissues that support gluconeogenesis but did not show an increase in fibrosis or steatosis. The perigonadal adipose tissue showed an increase in leptin with the LCHF diet. Leptin levels may also cause an increase energy expenditure via sympathetic activation. This could explain why mice that were fed the LCHF diet could maintain their body weight despite somewhat lower total energy intake (Nilsson et al.). After 4 weeks on the LCHF diet, cardiac and maximum aerobic capacity was impaired. These effects are unknown in human populations, thus requiring more research. According to the findings in mice it is believed that cardiac function should be carefully evaluated in humans who are on a low-carbohydrate diet.