Repercussions of training and detraining by water‐based exercise on functional fitness and quality of life: a short‐term follow‐up in healthy older women
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Abstract
OBJECTIVE:
To evaluate the effects of short‐term exercise detraining on the functional fitness
of older women after a 12‐week water‐based exercise (WE) program.
METHODS:
Healthy older women (trained (TR) group) were submitted to 12 weeks WE (three 45 min
sessions per week) followed by a 6‐week detraining period. A group of aged‐matched
women without any exercise training (UN group) were evaluated during the same period.
The aerobic power, measured by VO
2max and 800 meters performance, and the neuromuscular fitness and quality of life
were evaluated. All assessments were made at baseline, after 12 weeks of training
and after 4 and 6 weeks of detraining.
RESULTS:
No changes were found for the UN group during the follow‐up study, but WE induced
significant improvement in aerobic capacity, neuromuscular fitness and quality of
life score. However, the upper and lower body strength, agility, flexibility, and
body balance returned to UN levels (p>0.05) after 6 weeks of detraining.
CONCLUSIONS:
The results confirmed that 12 weeks of WE improves the functional fitness parameters
and quality of life of older women. However, after a short detraining period of 4–6 weeks,
the neuromuscular parameters and the quality of life score returns to baseline or
untrained subject levels.
Recent studies provide clear and convincing evidence that psychosocial factors contribute significantly to the pathogenesis and expression of coronary artery disease (CAD). This evidence is composed largely of data relating CAD risk to 5 specific psychosocial domains: (1) depression, (2) anxiety, (3) personality factors and character traits, (4) social isolation, and (5) chronic life stress. Pathophysiological mechanisms underlying the relationship between these entities and CAD can be divided into behavioral mechanisms, whereby psychosocial conditions contribute to a higher frequency of adverse health behaviors, such as poor diet and smoking, and direct pathophysiological mechanisms, such as neuroendocrine and platelet activation. An extensive body of evidence from animal models (especially the cynomolgus monkey, Macaca fascicularis) reveals that chronic psychosocial stress can lead, probably via a mechanism involving excessive sympathetic nervous system activation, to exacerbation of coronary artery atherosclerosis as well as to transient endothelial dysfunction and even necrosis. Evidence from monkeys also indicates that psychosocial stress reliably induces ovarian dysfunction, hypercortisolemia, and excessive adrenergic activation in premenopausal females, leading to accelerated atherosclerosis. Also reviewed are data relating CAD to acute stress and individual differences in sympathetic nervous system responsivity. New technologies and research from animal models demonstrate that acute stress triggers myocardial ischemia, promotes arrhythmogenesis, stimulates platelet function, and increases blood viscosity through hemoconcentration. In the presence of underlying atherosclerosis (eg, in CAD patients), acute stress also causes coronary vasoconstriction. Recent data indicate that the foregoing effects result, at least in part, from the endothelial dysfunction and injury induced by acute stress. Hyperresponsivity of the sympathetic nervous system, manifested by exaggerated heart rate and blood pressure responses to psychological stimuli, is an intrinsic characteristic among some individuals. Current data link sympathetic nervous system hyperresponsivity to accelerated development of carotid atherosclerosis in human subjects and to exacerbated coronary and carotid atherosclerosis in monkeys. Thus far, intervention trials designed to reduce psychosocial stress have been limited in size and number. Specific suggestions to improve the assessment of behavioral interventions include more complete delineation of the physiological mechanisms by which such interventions might work; increased use of new, more convenient "alternative" end points for behavioral intervention trials; development of specifically targeted behavioral interventions (based on profiling of patient factors); and evaluation of previously developed models of predicting behavioral change. The importance of maximizing the efficacy of behavioral interventions is underscored by the recognition that psychosocial stresses tend to cluster together. When they do so, the resultant risk for cardiac events is often substantially elevated, equaling that associated with previously established risk factors for CAD, such as hypertension and hypercholesterolemia.
The adaptation of muscle structure, power output, and mass-specific rate of maximal O2 consumption (VO2max/Mb) with endurance training on bicycle ergometers was studied for five male and five female subjects. Biopsies of vastus lateralis muscle and VO2max determinations were made at the start and end of 6 wk of training. The power output maintained on the ergometer daily for 30 min was adjusted to achieve a heart rate exceeding 85% of the maximum for two-thirds of the training session. It is proposed that the observed preferential proliferation of subsarcolemmal vs. interfibrillar mitochondria and the increase in intracellular lipid deposits are two possible mechanisms by which muscle cells adapt to an increased use of fat as a fuel. The relative increase of VO2max/Mb (14%) with training was found to be smaller by more than twofold than the relative increase in maximal maintained power (33%) and the relative change in the volume density of total mitochondria (+40%). However, the calculated VO2 required at an efficiency of 0.25 to produce the observed mass-specific increase in maximal maintained power matched the actual increase in VO2max/Mb (8.0 and 6.5 ml O2 X min-1 X kg-1, respectively). These results indicate that despite disparate relative changes the absolute change in aerobic capacity at the local level (maintained power) can account for the increase in aerobic capacity observed at the general level (VO2max).
Although strength training (ST) enhances physical function in the elderly, little is known about the effect of training intensity on training and detraining adaptations in musculoskeletal fitness. To determine the effect of exercise intensity on strength, anaerobic power, and mobility of older men subjected to a 24 week ST protocol followed by prolonged detraining. Fifty two healthy but inactive older men (mean (SD) age 71.2 (4.1) years) were assigned to a control (n = 14), low intensity training (LIST; n = 18; 55% 1RM), or high intensity training (HIST; n = 20; 82% 1RM) group. They carried out a 24 week, whole body (10 exercises, two to three sets/exercise) ST programme followed by a 48 week detraining period. Upper and lower body strength, anaerobic power (Wingate testing), and mobility (timed up and go, walking, climbing stairs) were measured at baseline and immediately after training and during detraining. Although low intensity training improved (p<0.05) strength (42-66%), anaerobic power (10%), and mobility (5-7%), high intensity training elicited greater (p<0.05) gains (63-91% in strength, 17-25% in anaerobic power, 9-14% in mobility). All training induced gains in the LIST group had been abolished after four to eight months of detraining, whereas in the HIST group strength and mobility gains were maintained throughout detraining. However, anaerobic power had returned to baseline levels after four months of detraining in both groups. Higher intensity training protocols induce greater gains in strength, anaerobic power, and whole body physical function of older men. Moreover, higher intensity training may maintain the gains for more prolonged periods after training ceases.
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