Exercise and Health: Coursework 1

Metabolic syndrome is the termed used to define a cluster of associated pathologies that stem from insulin resistance. Using relevant research literature discuss the following:

  1. The process by which insulin resistance develops.

Insulin resistance is described as insensitivity to plasma glucose, which therefore lowers the effects of insulin (Borghouts and Keizer 2000). An important factor in the development of insulin resistance is the type of the fibre in an individual’s skeletal muscle. Research has given evidence to suggest that reduced proportions of slow-twitch and oxidative fibres and increased proportions of fast twitch fibres are associated with development of insulin resistance in men and women (Lillioja et al., 1987 cited by Simoneau and Kelley 1997). Age and physical activity are both associated with insulin resistance, as they are both related with a reduction in oxidative capacity of the skeletal muscle. A lack of exercise is associated with decreased insulin sensitivity and is more common with an increase in age. Although further research (Zavaroni et al., 1986 cited by Ivy 1997) found that the effect of aging was secondary to changes in body composition and a sedentary lifestyle.

It is seen that the development of insulin resistance is associated with changes in the glycolytic and oxidative capacities of the skeletal muscle. Simoneau and Kelley (1997) conducted a study on glucose tolerant obese individuals and found that insulin resistance was related to a decrease in the activity of oxidative enzymes and a disproportionate increase in glycolytic enzymes.

        Obesity is an important factor that contributes to the development of insulin resistance. Evidence to support this is in a study on women by Simoneau, et al., (1995, cited in Simoneau and Kelley, 1997), which found that visceral obesity had a direct association with an increased ratio of glycolytic to oxidative enzyme capacity in skeletal muscle.

        Research has shown that insulin resistance can also be caused by defects in the liver that lead to a decrease in hepatic glucose uptake and consequently prolonged hyperglycemia (Defronzo, Ferrannini and Koivisto 1983). This results in a sustained basal hyperinsulinemia and therefore decreased insulin building, which is also contributed too by alterations to the beta cells.

  1. How insulin resistance results in the development of hypertension, hyperlipidaemia, diabetes and therefore increased risk of CHD.

The altered sensitivity and responsiveness of the tissues to circulating insulin is a factor in the contribution to hypertension. Insulin resistance will result in a decrease in the insulin-induced vasodilation of the vessel and therefore a reduction in the amount of blood flow to the skeletal muscles. This decrease in glucose uptake results in an increased need for insulin, which is required to maintain normal blood glucose levels. But because there is continued resistance to insulin there are insufficient levels in order to maintain normal blood glucose, which is known as Hyperinsulinaemia. An increase in vascular smooth muscle growth will increase vascular resistance and will therefore result in the development of hypertension. Research has shown that in hypertensive individuals there is a greater fraction of total limb blood flow is directed to insulin-resistant fibres (Ferrannini and Natali 1991). These abnormalities are seen to affect the efficiency of insulin and substrate delivery to target tissues. The increased levels of insulin in the blood can also cause the kidneys to react by increasing the volume of the blood. This in turn results in an increase in blood pressure.

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Insulin resistance can cause an abnormal ratio of high-density lipoproteins (HDL) to low-density lipoproteins (LDL). HDL’s remove excess lipids from the arterial wall and transport it to the liver, whilst LDL’s transport lipids from the liver to the tissues. The syndrome results in a reduced ratio of HDL in relation to LDL because the insulin has less effect on inhibiting the free fatty acids release from the adipocytes. This increases the amount of free fatty acids in the blood and to compensate the liver repackages the lipids into LDL’s. Reaven (1993) also stated that the resistance to glucose stimulated uptake ...

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