Exercise Can Reverse Cardiac Secondary Aging Resulting from a Sedentary Lifestyle
It is never too late to exercise in order to obtain benefits to health - there are any number of studies showing beneficial outcomes to result from structured exercise, especially resistance exercise, even for people in very late life. That said, the study of exercise noted here suggests that at some point in middle age it does become too late to reverse consequences of secondary cardiac aging such as hypertrophy, stiffening of heart muscle leading to diastolic heart failure, and the like. Up until that point, however, even the earnestly idle among us can choose to undo some of the portion of overall loss of function that results from a sedentary lifestyle.
What is secondary aging? There is no bright dividing line between primary aging and secondary aging, but one possible definition is that primary aging results from the normal operation of cellular metabolism in a healthy individual in an optimal environment, while secondary aging results from detrimental environmental factors: long-term exposure to toxins or pathogens, lingering latent viral infections, poor diet leading to excess fat tissue, a smoking habit, lack of exercise, and so forth. The reason I say that there is no bright dividing line is that if you look under the hood at the types of damage and molecular mechanisms involved, there is considerable overlap between primary and secondary aging. Chronic inflammation and common ways in which cells can malfunction feature prominently on both sides, for example. Aging is damage, and for many forms of that damage it is a matter of origin and semantics as to whether we consider it a part of aging, the pathology of a disease, a self-inflicted injury, or something else.
Exercise can only take you so far. Given that it is essentially free, and reliably produces benefits, of course everyone should exercise if capable of doing so. But three quarters of the fittest, most diligent people nonetheless die from age-related disease, largely cardiovascular disease, before reaching 90 years of age, and those still alive at 90 are pale shadows of their former, youthful selves. The gains of exercise are small when considered against the bigger picture of what will become possible though near future medical technology. So exercise by all means, but also put some thought towards supporting the development of rejuvenation therapies capable of repairing and reversing the various forms of cell and tissue damage that cause aging. Success in that line of work is the only way forward to live in good health, and with a youthful physiology, for far longer than is presently possible.
Middle-aged couch potatoes may reverse heart effects of a sedentary life with exercise training
The researchers analyzed the hearts of 53 adults ages 45-64 who were healthy but sedentary at the start of the study - meaning they tended to sit most of the time. Study participants received either two years of training, including high- and moderate-intensity aerobic exercise four or more days a week (exercise group), or they were assigned to a control group, which engaged in regular yoga, balance training, and weight training three times a week for two years.
The exercise group committed to a progressive exercise program which monitored participants' recorded heart rates. People in this group worked up to doing exercises, such as four-by-fours - foue sets of four minutes of exercise at 95 percent of their maximum heart rate, followed by three minutes of active recovery at 60 percent to 75 percent peak heart rate. In this study, maximum heart rate was defined as the hardest a person could exercise and still complete the four-minute interval. Active recovery heart rate is the speed at which the heart beats after exercise.
They found that, overall, the committed exercise intervention made people fitter, increasing VO2max, the maximum amount of energy used during exercise, by 18 percent. There was no improvement in oxygen uptake in the control group. The committed exercise program also notably decreased cardiac stiffness. There was no change in cardiac stiffness among the controls. Sedentary behaviors - such as sitting or reclining for long periods of time - increase the risk of the heart muscle shrinking and stiffening in late-middle age and increases heart failure risk.
Previous studies have shown that elite athletes, who spent a lifetime doing high-intensity exercise, had significantly fewer effects of aging on the heart and blood vessels. However, the six to seven days a week of intense exercise training that many elite athletes perform throughout their life isn't a reality for many middle-aged adults, which led researchers to study different exercise doses, including casual exercise at two to three days a week and "committed exercise" at four to five days a week. "We found that exercising only two or three times a week didn't do much to protect the heart against aging. But committed exercise four to five times a week was almost as effective at preventing sedentary heart aging as the more extreme exercise of elite athletes. We've also found that the 'sweet spot' in life to get off the couch and start exercising is in late-middle age, when the heart still has plasticity."
Sedentary aging is strongly associated with deleterious changes in cardiovascular function, including an increase in left ventricular (LV) stiffness. Sedentary seniors have small stiff LVs, which are comparable to patients with heart failure with a preserved ejection fraction (HFpEF). In contrast, competitive athletes have large, compliant LVs equivalent to much younger individuals, suggesting that exercise training, performed at a very high level over a lifetime, may counteract the detrimental effects of aging and inactivity on the LV.
Although competitive athletes are a useful model for characterizing the upper limits of cardiovascular protection from prolonged exercise training, the volume of training performed by these individuals (≥6 days/wk plus competitions) is not feasible for the general population. Although it appears that 4 to 5 days of committed exercise training over decades is adequate to achieve most of this benefit, it is unclear whether exercise training can restore or improve LV compliance in previously sedentary individuals, and if so, when is the optimal stage of life to intervene.
Epidemiological studies show that a measurement of fitness in middle age is the strongest predictor of future heart failure. Moreover, in observational studies, the dose of exercise associated with reduced heart failure incidence is much higher than that associated with reduced mortality. However, if exercise is started too late in life (i.e. after 65 years) in sedentary individuals, there is little effect on LV stiffness. Thus, a lifetime of sedentary aging is associated with a reduction of cardiac plasticity, which cannot be overcome with a year of moderate-intensity exercise training. We recently documented that this LV stiffening begins to be identifiable during middle age with a leftward shift in the LV end-diastolic pressure volume curve. We hypothesize that middle-aged hearts retain some degree of cardiac plasticity and may represent a more optimal time to intervene with aggressive lifestyle modification aimed at improving cardiac stiffness.
This study is the longest, prospective randomized controlled trial that has documented the physiological effects of supervised, structured exercise training in a group of sedentary but healthy middle-aged adults. The key finding is that 2 years of exercise training performed for at least 30 minutes, 4 to 5 days per week, and including at least 1 high-intensity interval session per week results in a significant reduction in LV chamber and myocardial stiffness. The use of high-resolution, invasively measured LV pressure-volume curves and comparison with an attention control group enhances the confidence in this conclusion. This study also demonstrated that exercise training can be adhered to by middle-aged adults over a prolonged period, suggesting that this may be an effective strategy to mitigate the deleterious effects of sedentary aging on the heart and forestall the development of HFpEF.