In addition to its effect on muscle growth, exercise upregulates a range of maintenance processes, such as autophagy, that improve tissue function when maintained over the long term. Lack of exercise in later life accelerates the decline in muscle mass and strength, an issue that appears reversible to a degree that might surprise most people. A similar situation occurs with respect to stiffening of blood vessels, in that while much of this depends on mechanisms such as cross-linking and presence of senescent cells, some of the decline is a matter of being sedentary.
The interesting finding in the open access study noted here is that while long term physical exercise is associated with lower blood pressure and lesser degrees of arterial stiffness, having sedentary people undertake short term exercise programs doesn't help in this matter. This can be compared with other studies in which exercise very rapidly improves matters, such as in the case of memory function.
We can speculate as to what this tells us about the importance of various different causes of arterial stiffness, and the authors of the paper do just that. For our part, we might also think of this in the context of data that shows interventions such as nicotinamide riboside and MitoQ, approaches that improve smooth muscle cell function, act to reduce arterial stiffness somewhat. Smooth muscle is the tissue responsible for contraction and dilation of blood vessels, and some fraction of stiffness arises from dysfunction in this tissue. One would certainly expect exercise to act through a similar improvement in smooth muscle function, but apparently that isn't the case in the short term.
Cardiovascular diseases are responsible for the majority of deaths in western countries and age has been identified as a main risk factor. Vascular tissue biomarkers such as arterial stiffness (AST) provide a means of optimized risk assessment to detect individual subclinical organ damage. Commonly measured as central pulse wave velocity (PWV), AST has gained clinical importance and has been proven to be a reliable predictor for cardiovascular (CV) risk in the general population. Altered PWV indicates subclinical target organ damage and may be used to quantify cumulative damaging effects of CV risk factors on the aging arterial wall integrity.
Previous studies on the effect of regular physical activity and exercise on indices of AST in the elderly have reported conflicting results. High-intensity interval training (HIIT) is an exercise modality that has attracted attention for its potency to increase cardiorespiratory fitness and reduce CV risk in patients, for example, with metabolic syndrome. Data on HIIT and its effects on PWV are scarce. Previous evidence suggests that HIIT may be superior regarding reductions in AST compared to moderate aerobic training in young patients with increased CV risk. However, a recent meta-analysis could not detect differences in AST reduction between the two training regimens.=
Our aim was to investigate the associations between long-term physical activity and central PWV in healthy and diseased elderly. Our study results demonstrate the importance of long-term physical activity and the limited impact of short-term exercise training on large artery stiffness in an older population. Long-term physical activity was associated with lower central PWV even in the absence of CV risk factors. Most importantly, 12-weeks of HIIT did not reduce PWV in elderly at increased CV risk.
Aging is characterized by continuous remodeling of the arterial wall, and higher cardiorespiratory fitness may mitigate stiffening of the aging arterial tree. In our study, with every 10 ml/min/kg increase in VO2max, PWV dropped by 0.8 m/s. Active participants presented with 0.5 m/s lower central PWV than their sedentary counterparts. An increase of 1 m/s in central PWV has been associated with a 15% risk increase in CV and all-cause mortality. Thus, our cross-sectional findings indicate an 8% risk increase attributable to a sedentary lifestyle even in healthy elderly.
Our results demonstrate that long-term active compared to sedentary lifestyle is associated with lower AST even in healthy elderly. This suggests that age- and disease-related vascular stiffening and the associated worse CV outcome can be postponed by long-term regular physical exercise. Short-term exercise, even at higher intensities, cannot improve arterial stiffening in sedentary elderly with increased CV risk. Exercise-induced reductions of AST seem to depend on a concomitant decrease of blood pressure.