aerobic+training

=Aerobic Exercise Training and Hyperlipidaemia= For many decades, researchers have been reporting differences in lipid profiles between subjects who engage in regular aerobic exercise training and less active subjects. A fundamental question facing researchers in this field is the extent to which the observed improvements in lipid profiles are due to specific training adaptations or simply to the reductions in body fat percentage and adipose tissue characteristic of those who undertake regular aerobic training. Certainly, those exercise studies that result in weight loss are more likely to show improvement in lipid profile attributes.

Williams et al (1990) sought to investigate this fundamental question - they felt it was "unclear from previous studies whether, in men, weight loss by calorie restriction alone has the same effects on lipoprotein metabolism as weight loss by exercise". In this study of moderately overweight men aged 30 to 59, they found comparable mean changes in the mass of small LDL and of VLDL particles through exercise-induced and diet-induced weight loss. But they found that the anti-arthrogenic HDL2 sub-fraction increased significantly less in dieters than in exercisers.

[|rapid weight loss]

Aerobic Exercise Training as a Preventative for Hyperlipidaemia
Numerous studies have sought to determine if aerobic exercise training can prevent the emergence of the hyperlipidaemia that is commonly observed with aging (see Prevalence). Some of these studies have particularly sought to determine the volume and intensity required to achieve a preventative effect, whether there's a necessary "threshold" activity level or a more continuous dose-response relationship and others have sought to identify the longevity of the observed treatment effect of aerobic exercise training.

Thompson et al (1991) compared the lipid profiles of endurance trained and sedentary men before and after a period of controlled dietary intake. The study group spanned a broad age range. The endurance trained men had significantly lower body fat percentage at baseline than the sedentary subjects. At commencement of the study, the endurance trained men had HDL-C concentrations that were 41% higher and triglyceride levels 45% lower than the sedentary control. But this study did not examine the extent to which these differences could be attributed to the exercise regimen or to the differences in adiposity at commencement of the study.

These authors applied a controlled but conventional US diet to both subject groups for a 28 day period. Subjects maintained traditional activity levels and the caloric content was designed to match estimated energy expenditure. The authors found even further improvements in HDL2-C levels in the endurance trained men, but no significant changes in the sedentary men. So, Thompson et al (1991) clearly suggests there is a preventative effect of chronic aerobic exercise training.

In 1998, Ferguson et al studied the acute effect of aerobic training on a group of healthy, trained men. They found that aerobic training at 70% of VO 2 max could elicit significantly increased HDL-C and lipoprotein lipase concentrations, but only from a session that involved energy expenditure in excess of 1,100 kcal.

The durability of the preventative effect of aerobic training was examined in a study of healthy young women by LeMura et al (2000). After 16 weeks of aerobic exercise training (up to 4 times/week for 45 minutes at up to 85% HRmax), they found that triglycerides were reduced by 14% and HDL-C was increased by 29%. However, after a 6 week detraining period, they found that both HDL-C and VO 2 max had returned to baseline levels while triglyceride levels were increasing more slowly toward baseline, but still remained significantly below baseline after the 6 week detraining period. The authors speculate that the effect of aerobic exercise on triglyceride levels follows from a increase in the amount of lipoprotein lipase (LPL) in adipose and muscle tissue. LPL facilitates the clearance of triglycerides from the bloodstream. It would appear from this study that the stimulus to LPL activity may be more durable than the other positive effects of the aerobic exercise program.

In an attempt to better isolate the preventative effect of exercise, Petridou et al (2005) compared the lipidaemic profile of young lean male athletes and non-athletes matched for body fat percentage. They found no significant difference in triglycerides, total cholesterol, LDL-C or HDL-C between the groups. This finding of Petridou et al (2005) is not inconsistent with the observations of Durstine et al (2001). They undertook a comprehensive review of cross-sectional studies which found that blood lipid profiles do not differ significantly between physically active and sedentary individuals of similar body fat. Unfortunately, the numbers of sedentary individuals with low body fat percentage has been rapidly decreasing over recent decades (see Obesity Prevalence data).

Not all research has found a preventative effect of aerobic exercise leading to a reduction in both adiposity and the associated adverse blood lipid and lipoprotein levels. In a study of healthy middle-aged men and women, Ring-Dimitrou et al (2007) found no effect of 9 months of aerobic exercise training on blood lipids or body fat percentage. The duration and intensity of aerobic training was similar to other intervention studies, and a comparable effect on VO 2 max was achieved. However, this subject pool commenced with an unusually healthy average HDL-C level of 63mg/dL which may explain its failure to elicit the positive effect on HDL-C that has been seen in numerous other studies in this age group. This unexpected result could also be explained by the failure to regulate diet. Subjects were free to up-regulate caloric intake to match increased energy expenditure and their food choices may have been inconsistent with the TLC diet messages of reducing saturated fat and cholesterol intake.

In an interesting study, Angelopoulos et al (2007) observed a significant but unexpected increase in LDL-C following 6 months of moderate intensity aerobic training, but only in the sub-sample of participants with normal LDL-C levels at commencement of the study period. Those participants with initially elevated LDL-C levels responded positively to exercise training with a significant decrease in LDL-C levels. The authors note that a similar short term effect of a moderate intensity exercise regimen has previously been observed, but in that case the effect was not chronic. Angelopoulos et al (2007) observed the significantly elevated LDL-C level persisting for more than 72 hours after the final exercise session.

Aerobic Exercise Training as a Therapeutic Intervention for Hyperlipidemia
In a review of the effectiveness of aerobic exercise training in improving blood lipid profiles, Leon and Sanchez (2001) considered 51 studies. They found that cross-sectional observational studies, involving men and women of all ages performing a variety of aerobic activities, consistently demonstrate what appears to be a positive dose-response association between volume and intensity of aerobic activities and plasma HDL-C levels and inverse associations with TG levels. However, they note that causative relationships cannot be proven by such studies because of numerous potential confounding variables.

From the 28 randomised controlled trials considered by Leon and Sanchez (2001) they found that moderate- to hard-intensity aerobic exercise training inconsistently results in an improvement in the blood lipid profile, but with insufficient data to establish dose-response relationships. In the studies evaluated, the authors found that exercise was generally performed at a moderate to hard intensity, three to five times per week for 30 min or more per session, consistent with current ACSM guidelines for improving cardiorespiratory endurance in healthy adults. The aerobic exercise interventions involved weekly energy expenditures ranging from 2,000 to >20,000 kcal. They found that the increase in HDL-C with aerobic exercise training was inversely associated with its baseline level, but no significant associations were found with age, gender, weekly volume of exercise, or with exercise-induced changes in body weight or VO 2 max. The reviewers note that no significant associations were observed with weekly energy expenditure during the exercise programs, because in almost all of the studies the training volume exceeded the weekly threshold of 800–1,000 kcal - regarded prior to 2001 as the threshold required to raise HDL-C (see Durstine et al (2001)).

Of particular note, Leon and Sanchez (2001) observe that all lipid parameters generally improved in studies in which there was a substantial weight loss (greater than or equal to 4 kg). Such weight loss was usually associated with a concomitant hypocaloric diet.

In a study of men and women with mild to moderate dyslipidemia, Kraus et al (2002) found that a significant effect on HDL-C only occurred with high intensity aerobic exercise involving more that 3.5 hours/week. There was a significant effect of high intensity exercise on the more arthrogenic LDL2 subfraction; and, in overweight symptomatic individuals in the study, they observed positive effects on blood lipids without any weight loss. However, there may well have been body composition changes as a result of the exercise interventions without weight loss.

Kraus et al (2002) examined 11 lipid profile attributes and ranked the observed effect of exercise amounts and intensities on the 11 attributes.

The amounts of aerobic exercise training were defined as The high exercise amount consistently had the best effect on the lipid profile attributes, ahead of low amount and control.
 * "high amount" = 23 kcal per kilogram of body weight per week, and
 * "low amount" = 14 kcal per kilogram of body weight per week.

The intensities in this study were defined as The authors found no clear effect of the intensity of the exercise treatment on blood lipid profile.
 * High = 65 to 80% of peak oxygen consumption
 * Moderate = 40 to 55% of peak oxygen consumption

This and many others studies have found an effect of aerobic exercise on HDL-C and some other lipid profile attributes, but not consistently enough to establish a dose-response relationship. Instead, the concept of a threshold weekly exercise volume of 1200 to 2200 kcal per week has persisted (see Durstine et al (2001)). More recently, Durstine et al (2009) has suggested that 1200 to 1500 kcal/week of aerobic exercise for at least 12 weeks is required to realise beneficial outcomes for lipids and lipoproteins.

In another more recent literature review related to exercise, lipids and lipoproteins, Tambalis et al (2009) found that with aerobic exercise of moderate and high intensity only a small percentage of trials reported significant reductions in total cholesterol, triglycerides and LDL-C; and only 21% of trials found significant improvements in HDL-C.


 * //So certainly the situation isn't crystal clear! But it's probably safe to conclude that targeting exercise to reduce body fat% is advantageous both as a preventative measure and a therapeutic measure to avoid or reduce the impacts of hyperlipidemias.//**

Novelty Interventions
There are two emerging fields of research that hold some promise for treatment of hyperlipidemias - aerobic interval training and endurance exercise training in the fasted state. They're mentioned here for those with special interest in this field, they're not necessarily for general application in exercise prescription at this stage.

Aerobic interval training - (aka HIIT - high intensity intermittent training)
A number of researchers have recently published studies on the utility of high intensity intermittent exercise in weight loss and lipid profiles. Tjonna et al (2008) found in a study, of subjects diagnosed with metabolic syndrome, that a 16 week intervention of aerobic interval training had superior effect on HDL-C than did continuous moderate aerobic exercise (CME). After a warm-up, the interval training protocol required the subjects to do 4 blocks * [4 mins @90% of HRmax followed by 3 mins active recovery at 70% of HRmax] and for CME to exercise continuously at 70% of HRmax. The authors sought to match the energy expenditures of the two treatments by manipulation of the duration of exercise sessions. Papers from this team at Trondheim extend beyond simply observing effect of exercise on lipid and lipoprotein levels and tend to explore mechanisms. The authors conclude that high intensity exercise interventions show promise for those diagnosed with metabolic syndrome but caution that the injury risk of intense training protocols has not been assessed.

More locally, researchers from the University of New South Wales have also been experimenting with aerobic interval training - see Boutcher (2011). While the focus of the studies of Boutcher's team is on weight loss and particularly on insulin sensitvity, many of the muscular adaptations that they are observing are relevant to hyperlipidemias. The training protocols employed by Boutcher and colleagues are much more intense than those used by Tjonna et al at Trondheim. Boutcher (2011) reports using 4 to 6 repetitions of 30 seconds maximal followed by a 4 minute recovery in one study and in another reported by Trapp et al (2007) they've used 8 seconds on, followed by 12 seconds recovery, repeated for a total of 20 minutes in a study of overweight and obese young women. Future studies from this Research Group are likely to report effects on lipid profiles.

Endurance exercise training in the fasted state
There is a growing literature describing aerobic exercise interventions undertaken in a fasted state (see van Proeyen et al (2011) ). Although none of the recent papers particularly target hyperlipidemic subjects nor the effect of exercise in a fasted state on blood lipid profiles, the interest in enhanced fat metabolism and associated processes is such that future research into aerobic exercise in a fasted state is likely to reveal insights into processes that regulate blood lipid levels.

A final word of warning!
Another recent paper, from Boutcher's research group at UNSW, provides a useful review of factors that reduce the ability of exercise to bring about weight loss. All of the papers regarding exercise interventions mentioned above, present the effect of the intervention as the mean response of each treatment group. It's worth remembering that an individual patient's response to an exercise intervention is most unlikely to match the mean response of the published interventions. This paper by Boutcher and Dunn (2009) describe a variety of factors that may play a determining role in the exercise–body composition relationship - factors that can be grouped into - Every exercise physiologists is likely to be met with disappointments - response to exercise interventions that fail to meet expectations. This paper may provide some solace.
 * behavioural,
 * inherited and
 * physiological categories

Exercise Training

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