Krafttraining : Strength Training for disease prevention

Insulin Resistance and Abdominal Obesity & Dyslipidemia and Hypertension

von Ph.D. Ben F. Hurley

There is an increasing number of investigations into the use of strength training (ST) as an intervention for the prevention and/or treatment of chronic disease, particularly the metabolic syndrome (MetS), defined as a clustering of interrelated risk factors for the development of atherosclerotic cardiovascular disease (CVD), diabetes mellitus, and hypertension. Based on the relationship between the MetS and CVD, the diagnosis of the MetS is defined by the International Diabetes Federation and the National Institutes of Health in the U.S. as meeting three out of the following five criterion measures: 1) elevated fasting plasma glucose levels, 2) elevated waist circumference, 3) elevated blood pressure, 4) elevated triglycerides, and 5) reduced HDL cholesterol levels. The predominant environmental/behavioral risk factors linked to these series of events include cigarette smoking, age, family history, obesity, atherogenic diets, and physical inactivity.

While it is difficult to precisely quantify the relative contribution of physical inactivity to the development of the MetS, many studies have determined the extent to which increasing physical activity through formal exercise training programs will reduce risk of the MetS. It is often assumed that only aerobic exercise training, i.e., exercise involving primarily aerobic metabolism, can lead to reductions in risk of the MetS. However, epidemiology studies show that muscular strength is inversely related to both MetS and all-cause mortality. Moreover, high insulin levels, low muscle mass, and low strength were the strongest set of factors associated with increased risk of MetS and were independent of abdominal fat and other risk factors in the Florey Adelaide Male Ageing Study (Atlantis et al. 2009). This studyconsisted of 1,195 Australian men between 35 and 81 years of age. The authors concluded that the level of increases in muscle mass and strength needed to eliminate risk factor exposure and prevent approximately 14% to 24% of MetS prevalence could be achieved with a short-term ST program. This conclusion raises the question of whether ST could serve as an effective intervention for the prevention or treatment of MetS. Although data are lacking on the direct effect of ST on MetS, as an outcome measure, there is a large volume of research literature on the effects of ST on risk of the components of MetS, which include, 1) insulin resistance, 2) abdominal obesity, 3) dyslipidemia, and 4) hypertension.

Insulin resistance

In the March 4th 2010 issue of the New England Journal of Medicine, Selven et al. provided evidence from 11,092 nondiabetics that blood levels of glycosylated hemoglobin (A1C) is strongly associated with risk of diabetes, CVD, and death. A recent report from a committee of international experts echoed this sentiment (Nathan, 2009). Even small changes (< 1 % point) in A1C can account for relatively large shifts in morbidity and mortality.

Because of the relationship of A1C to glycemic control, insulin resistance, risk of diabetes, and the MetS, exercise interventions that influence blood A1C levels are of great interest to exercise scientists. Low muscle mass and strength are associated with type 2 diabetes (Park et al., 2006 & Park et al., 2007), providing support to the hypothesis that ST may have a favorable effect on A1C levels. In this context, Castaneda et al. (2002) found that A1C levels were reduced by one full percentage point with ST, resulting in a reduction in the dose of prescribed diabetes medication in 72% of participants, compared to a no exercise control group that showed no significant changes in A1C levels and a 42% increase in diabetes medications. Similar effects of ST on A1C levels in diabetics have been reported by others, with a few showing a slightly reduced level of improvement. Combining aerobic exercise training with ST appears to be more effective than either aerobic or ST alone, but each training modality leads to improvements in A1C levels, independent of the other (Sigal et al. 2007). Collectively, studies generally show more improvement in A1C with ST when baseline values are high and when training programs use relatively heavy resistance protocols lasting longer than two months. One exception to this conclusion, however, was a study by Ishii et al. (1998) who reported a 2.0% reduction in 4–6 weeks without using a particularly heavy resistance protocol. There are many other techniques or biomarkers used to estimate the effects of ST on insulin resistance or sensitivity, but similarly to those that have used A1C, the majority have shown improvements in insulin sensitivity or reductions in insulin resistance with ST, regardless of the technique or biomarker used for assessment.

Abdominal Obesity

For the first time in U.S. history, the majority of older men and women are abdominally obese and this level of prevalence is now greater than it is for general obesity (Li et al., (2007). This places them at high risk for insulin resistance and the MetS. Because abdominal (visceral) obesity is more consistently related to a metabolic profile predictive of CVD risk and to the MetS than general obesity, it is considered even more dangerous than general obesity.
Several studies have examined the effects of ST on visceral fat. Most have found a statistically significant reduction in intra-abdominal fat with ST, but the changes have been relatively small. Thus, from a health perspective, the meaningfulness of these changes arequestionable. Moreover, studies that have reported ST-induced reductions in visceral fat have often not adequately controlled for dietary or other factors that could potentially influence visceral fat changes. There is increasing evidence, however, that ST may prevent age-associated increases in visceral fat. For example, during a one year follow-up period after a weight loss program had ended, Hunter et al. (2009) observed a 38% increase in visceral fat in those who were not compliant to regular exercise. There were no changes after this program in either an aerobic training or ST group that adhered to regular exercise during this same time period. Despite the higher energy expenditure in the aerobic training group, there were no differences in visceral fat change between the aerobic and ST groups. Thus, both training modalities prevented the regain of visceral fat during a period in which all groups gained weight. Similar findings of ST preventing increases in visceral fat over time were reported by Schmitz et al. (2007).

From an energy expenditure perspective, ST would not appear to be the exercise of choice for optimizing fat loss. In this context, we have measured energy expenditure during circuit ST and compared it to that of aerobic exercise (i.e., jogging on a treadmill) in the same people. We found that a single ST exercise session, including recovery periods between exercises, expends only about one-third to one-half the calories as aerobic training for the same time period. This is because much of the energy expenditure is derived from anaerobic (glycolysis) rather than aerobic (oxidative phosphorylation) pathways. Nevertheless, we also reported increases in resting metabolic rate and sympathetic activity with ST, which provides support for a physiological rationale of fat loss with ST.

Dyslipidemia

Almost half of the U.S. population (~ 45%) has lipoprotein-lipid profiles that place them at risk for the development of MetS, atherosclerotic CVD and subsequent mortality. For this reason, abnormal lipoprotein-lipid profiles (dyslipidemia) has important health implications. We concluded a decade ago (Hurley & Roth, 2000) that many studies showed improved lipoprotein-lipid profiles with strength training (ST), but most of them did not use proper controls to adequately address the independent effects of ST. We also concluded that when studies controlled for those factors that may influence lipid profiles, such as diet and diurnal or seasonal variation, improvements in lipid profiles were not generally observed with ST. Similar conclusions were made in a 2006 review by Braith and Stewart and in a subsequent review by Williams et al. in 2007, but a more recent review by Kelley and Kelley (2009) concluded that ST improves all lipoproteins, except HDL cholesterol. They reviewed the research literature from 1955 to 2007. This comprised 1,329 men and women. They concluded that on average, ST reduced total cholesterol (TC) by 2.7%, non-HDL-C by 11.6%, LDL-C by 4.6%, and triglyceride by 6.4%, while increasing TC/HDL-C by 1.4%, with no significant overall changes in HDL-C. Some of the studies they included in their analysis, however, were the same ones we and others identified previously as those that lacked proper control for factors that influence lipid profiles. They later added to this conclusion that alternative non-pharmacologic interventions, such aerobic training, or pharmacologic interventions, such as statins, may be more efficacious that ST for improving lipids and lipoproteins in adults, which supports the conclusions we and others made in our previous reviews on this topic. Despite this overall conclusion, there are reasonably well controlled studies that report significant improvements in lipids or lipoprotein profiles with ST. For example, Fahlman et al. (2002) observed significant reductions in triglycerides and LDL-C levels and increases in HDL-C levels compared to a non exercise control group after 11 wks of ST in 70-87 yr old women. In contrast, Misra et al. (2008) reported significant improvements in total cholesterol, but no improvements in HDL-C or LDL-C in Asian Indians with type 2 diabetes. Similarly to Fahlman et al. (2002), however, Misra et al. (2008) did observe reductions in triglyceride levels with ST. This finding observed independently in these two studies may have important clinical implications for the diagnosis of the MetS, given that elevated triglyceride, but not elevated total cholesterol or LDL cholesterol is used as one of the criterion measures in the diagnosis of MetS.

Hypertension

High blood pressure (BP) is the leading preventable cause of disease-specific death in women and the leading preventable cause of death in men due to CVD in the U.S. Yet, people do not die from hypertension, but rather from its influence on cardiovascular disease and stroke. Because of the well known elevations in BP resulting from the acute effects of heavy muscular exertions, known as the Valsalva maneuver, ST has not previously been recommended as an intervention for BP reduction. The BP adaptations from chronic resistance exercise (ST), however, are quite different from the acute effects of resistance exercise. This paradoxical relationship between acute and chronic effects of exercise is not unique to ST or to BP. For example, heart rate and lactate both go up substantially with aerobic exercise but are reduced substantially with aerobic training when both are compared under the same conditions, such as rest or at the same exercise intensity level.
CVD risk doubles with each increase of 20/10 mm Hg starting at a BP of only 115/75 mm Hg. Thus, BP should be viewed as a continuum rather than having distinct categories of risk. Those who have systolic BP values between 120 and 139 mm Hg and diastolic BP values between 80 and 89 mm Hg were previously considered to have normal BP, but are now considered to be prehypertensive and are likely to develop hypertension within four years, according to evidence from epidemiological studies. For this reason, in recent years more credence has been given to interventions that reduce BP in those with BP values below the level necessary to be considered hypertension. In this context, we demonstrated that a heavy resistance, high volume ST program can reduce resting BP in older men and women who are in the higher range of the prehypertensive stage (i.e., 120 and 139 and/or diastolic BP values between 80 and 89 mm Hg). These reductions were maintained for at least 2 days after exercise. This decreased diastolic BP in men resulted in a shift from the prehypertensive category to the normal range. We also studied the influence of gene profiles (genotypes) on BP response to ST and found that older men and women who have specific gene profiles for genes coding for proteins that regulate BP, experience a greater reduction in their resting BP in response to ST than those with other genotypes at these same loci. Thus, BP response to ST may be genotype dependent.
Although the American College of Sports Medicine’s position stand on exercise and hypertension concludes that ST elicits significant reductions in BP in normotensives, prehypertensives, and hypertensives. Other reports have added more information to this consensus statement. For example, Cornelissen and Fagard pooled data from 9 randomized controlled trials in a meta analysis on the effects of ST on BP. They concluded that ST reduced systolic BP by 3.2 mm Hg (borderline significant) and diastolic BP by 3.5 mm Hg when weighted by the number of participants studied. These reductions were even greater when weighted by the variation of BP change (6.0 mm Hg decline in systolic BP and 4.7 mm Hg decline in diastolic BP). However, smaller reductions were reported in studies using hypertensive patients. Nevertheless, the results in non hypertensives have important health implications because a large proportion of CVD occurs in people with prehypertension, and the overall cardiovascular morbidity and mortality is reduced in the general population with even modest reductions in resting BP.

Conclusions

Low muscle mass and strength are associated with the metabolic syndrome and diabetes. The following conclusions can be made about the effectiveness of strength training as a countermeasure to the metabolic syndrome and its components: 1) It is an effective intervention for reducing insulin resistance and compares favorable to that of aerobic exercise training, 2) It may play a role in delaying the onset of abdominal obesity with aging when combined with aerobic exercise training by preventing or reversing age-related declines in resting metabolic rate. However, because of its relatively low energy cost, it does not appear to be as effective as aerobic exercise training for optimal fat loss, independent of diet, 3) It does not appear to consistently improve lipoprotein lipid profiles, but it does appear to reduce blood triglyceride values, a criterion of the diagnosis of the metabolic syndrome, and 4) It can lead to small to moderate reductions in both systolic and diastolic blood pressure, but these effects may be genotype dependent.

Acknowledgements

Some of the research outlined from the authors’ laboratory in this review was partially supported by NIH research contract AG-42148, NIH research grants AG-018336 and NIH training grant AG-000268.

benhur@umd.edu

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