Erratum: Extremely limited synthesis of long-chain polyunsaturates in adults: implications for their dietary essentiality and use as supplements.
Plourde M, Cunnane SC.
Research Center on Aging, Departments of Medicine, and Physiology and Biophysics, Université de Sherbrooke, 1036 Belvedere St. S., Sherbrooke, QC J1H 4C4, Canada.
The potential benefits of creatine and conjugated linoleic acid as adjuncts to resistance training in older adults.
Human aging is associated with a significant reduction in muscle mass (sarcopenia) resulting in muscle weakness and functional limitations in the elderly. Sarcopenia has been associated with mitochondrial dysfunction and the accumulation of mtDNA deletions. Resistance training increases muscle strength and size and can increase mitochondrial capacity and decrease oxidative stress in older adults. Creatine monohydrate (CrM) and conjugated linoleic acid (CLA) have biological effects that could enhance some of the beneficial effects of resistance training in older adults (i.e., ↑ fat-free mass, ↓ total body fat). We have completed two resistance-training studies with CrM alone and CrM + CLA supplementation in older adults to evaluate the independent effects of exercise and dietary supplements, as well as their interactive effects. Our studies, and several others, have found that CrM enhanced the resistance exercise mediated gains in fat-free mass and strength. More recently, we found that the addition of CLA also lead to a significant reduction of body fat after six months of resistance training in older adults. Older adults have fewer wild-type mtDNA copies and higher amounts of mtDNA deletions as compared with younger adults in mature skeletal muscle; however, these deletions are not seen in the satellite cell-derived myoblast cultures. These findings, and the fact that mtDNA deletions are lower and wild-type mtDNA copy number is higher after resistance training in older adults, suggests that activation of satellite cells secondary to resistance exercise-induced muscle damage can dilute or “shift” the proportion of mtDNA genotype towards that of a younger adult. Recent evidence suggests that CrM supplementation in combination with strength training can enhance satellite cell activation and total myonuclei number per muscle fiber in young men. Future studies are required to determine whether the mitochondrial adaptations to resistance exercise in older adults are further enhanced with CrM supplementation and whether this is due to increased recruitment of satellite cells. It will also be important to determine whether these changes are maintained over a longer time period.
Tarnopolsky MA, Safdar A.
Department of Pediatrics and Medicine, McMaster University, HSC-2H26, 1200 Main St. W., Hamilton, ON L8NÂ 3Z5, Canada.
Effect of estrogenic compounds (estrogen or phytoestrogens) combined with exercise on bone and muscle mass in older individuals.
Exercise has a beneficial effect on bone, possibly by stimulating estrogen receptor α. Because estrogen up-regulates this receptor, estrogen therapy combined with exercise training may be optimal for increasing bone mineral density. Studies combining estrogen therapy and exercise training in postmenopausal women show mixed results, but indicate that the combination of interventions may be more effective for increasing bone mass than either intervention alone. Plant-like estrogens (i.e phytoestrogens such as soy isoflavones) may act as weak estrogen agonists or antagonists, have small beneficial effects on bone, and may interact with exercise for increasing bone mineral density. Phytoestrogen derived from flaxseed (flax lignans) has not been evaluated as extensively as soy isoflavones and thus its effect on bone is difficult to determine. Estrogen or soy isoflavones given to postmenopausal women results in a small increase in lean tissue mass that may be mediated through estrogen receptor α on muscle or through decreased inflammation.
Chilibeck PD, Cornish SM.
College of Kinesiology, University of Saskatchewan, 87 Campus Dr., Saskatoon, SKÂ S7NÂ 5B2.
Resistance training, sarcopenia, and the mitochondrial theory of aging.
Skeletal muscle aging is associated with a significant loss of muscle mass, strength, function, and quality of life. In addition, the healthcare cost of aging and age-related disease is growing, and will continue to grow as a larger proportion of our population reaches retirement age and beyond. The mitochondrial theory of aging has been identified as a leading explanation of the aging process and describes a path leading to cellular senescence that includes electron transport chain deficiency, reactive oxygen species production, and the accumulation of mitochondrial DNA deletions and mutations. It is also quite clear that regular resistance exercise is a potent and effective countermeasure for skeletal muscle aging. In this review, we discuss age-related sarcopenia, the mitochondrial theory of aging, and how resistance exercise may directly affect key components of the mitochondrial theory. It is clear from the data discussed that regular resistance training can effectively disturb processes that contribute to the progression of aging as it pertains to the mitochondrial theory.
Johnston AP, De Lisio M, Parise G.
Department of Kinesiology, McMaster University, Hamilton, ON L8N 3Z5.
Timing of creatine or protein supplementation and resistance training in the elderly.
Muscle loss with age has a negative effect on strength and functional independence. Age-related loss of muscle is the result of decreased muscle fiber number and size, which are functions of altered hormonal status, physical inactivity, and variations in nutritional intake. Resistance training has a positive effect on muscle mass and strength in the elderly. Studies of protein or creatine supplementation for increasing muscle mass and strength in older individuals are equivocal. The timing of nutritional supplementation may be more important than the absolute daily intake of supplements. Protein or creatine ingestion proximate to resistance-training sessions may be more beneficial for increasing muscle mass and strength than ingestion of protein or creatine at other times of the day, possibly because of increased blood flow and therefore increased transport of amino acids and creatine to skeletal muscle.
Candow DG, Chilibeck PD.
Faculty of Kinesiology and Health Studies, University of Regina, Regina, SK S4SÂ 0A2.
The impact of nutritional and exercise strategies for aging bone and muscle.
This symposium addressed recent evidence suggesting that nutritional intervention and resistance-training strategies may be important for aging bone and muscle. The physiological consequences of aging and the potential mechanistic actions of nutritional aids during resistance training were emphasized.
Candow DG.
Faculty of Kinesiology and Health Studies, University of Regina, Regina, SK S4S 0A2 (e-mail: darren.candow@uregina.ca).
Vascular nitric oxide: effects of exercise training in animals.
Exercise training is known to induce several adaptations in the cardiovascular system, one of which is increased skeletal muscle blood flow at maximal exercise. Improved muscle blood flow, in turn, could in part be accounted for by augmented endothelium-dependent, nitric oxide (NO)-mediated vasodilation. Studies have indeed demonstrated that endothelium-dependent, NO-mediated dilation of conductance-type vessels is augmented after endurance exercise training; recently, this adaptation has been extended into resistance-type vessels within rodent skeletal muscle. With the latter, however, it appears that only resistance vessels supplying muscle active during training sessions exhibit this adaptation. These findings in rats are in contrast to those from human studies, in which increased endothelium-dependent dilation has been observed in vasculatures not associated with elevated blood flow during exercise. Increased expression of endothelial NO synthase (eNOS) appears to underlie enhanced endothelium-dependent, NO-mediated dilation of both conductance and resistance vessels. Greater eNOS expression may also underlie the preventive and (or) rehabilitative effect(s) of exercise training on atherosclerosis, given that NO inhibits several steps of the atherosclerotic disease process. Thus, exercise training may induce adaptations that benefit both vasodilation and vascular health.
McAllister RM, Newcomer SC, Laughlin MH.
Department of Biomedical Sciences, University of Missouri, E102 Veterinary Medicine Building, Columbia, MO 65211.
Vascular biology of angiotensin and the impact of physical activity.
The renin-angiotensin system (RAS) is important for regulating blood pressure and extracellular fluid. The concept of the RAS has recently evolved from a classical systemic endocrine system to an appreciation of local RASs functioning in a paracrine manner, including in the vascular wall. Angiotensin II (AII), the main effector of the RAS, is a potent vasoconstrictor formed by the action of angiotensin-converting enzyme (ACE). ACE is multifunctional and also destroys the endogenous vasodilator bradykinin. A recently discovered novel ACE2 enzyme is responsible for forming a vasodilatory compound, angiotensin 1-7, from AII. Thus, the actions of ACE and ACE2 are antagonistic. Tissue actions of AII are mediated by specific receptors, AT1 and AT2, with AT1 mediating the classical actions. AT1-stimulated vasoconstricton occurs via phospholipase-D-mediated second messenger generation directly, and indirectly via the coupling of AT1 to the prooxidant enzyme NADPH oxidase. Since the vascular NADPH oxidase is a major source of vascular reactive oxygen species generation and is responsible for the breakdown of the vasodilator nitric oxide (NO), there is another potential link between RAS and regulation of vasodilatory pathways. AT2 signaling is antagonistic to AT1 signaling, and results in bradykinin and NO formation. Chronic AII signaling induces vascular dysfunction, whereas pharmacological management of the RAS can not only control blood pressure, but also correct endothelial dysfunction in hypertensives. Exercise training can also improve endothelial function in hypertensives, raising the question of whether there is a potential role for RAS in mediating the vascular effects of exercise training. Recent studies have demonstrated reductions in the expression of NADPH oxidase components in the vascular wall in response to exercise training, thus tempering one of the main cellular effectors of AII, and this is associated with reduced vascular ROS production and enhanced NO bioavailability. Importantly, it has now been demonstrated in human arteries that exercise training also tempers vascular AT1 receptor expression and AII-induced vasoconstriction, while enhancing endothelium-dependent dilation. The signals responsible for these chronic adaptations are not clearly understood, and may include changes in RAS components prompted by acute exercise. ACE genotype may have an effect on physical activity levels and on the cardiovascular responses to exercise training, and the II genotype (compared with ID and DD) is associated with the largest endothelium-dependent dilations in athletes compared with those in sedentary individuals. Thus, the tissue location of the RAS, the complement of ACE/ACE2, the receptor expression of AT1/AT2, and the ACE genotype are all variables that could impact the vascular responses to exercise training, but the responses of most of these variables to regular exercise training and the mechanisms responsible have not been systematically studied.
Rush JW, Aultman CD.
Department of Kinesiology, University of Waterloo, Waterloo, ON N2LÂ 3G1, Canada.
Nitric oxide and muscle blood flow in exercise.
Despite being the subject of investigation for well over 100 years, the nature of exercising muscle blood flow control remains, in many respects, poorly understood. In this review we focus on the potential role of nitric oxide in vasodilation of muscle resistance vessels during a bout of exercise. Its contribution is explored in the context of whether it contributes to steady-state exercise hyperemia, the dynamic adjustment of muscle blood flow to exercise, or the modulation of sympathetic vasoconstriction in exercising muscle. It appears that the obligatory role of nitric oxide in all three of these categories is modest at best. The elucidation of the integrated nature of exercise hyperemia control in terms of synergy and redundancy of mechanism interaction remains in its infancy, and much more remains to be learned about the role of nitric oxide in this type of integrated control.
Tschakovsky ME, Joyner MJ.
School of Kinesiology and Health Studies, Queen\’s University, Kingston, ON K7LÂ 3N6.
Introduction to proceedings from the 2005 CSEP symposium “Exercise and the endothelium”
This introduction summarizes the topics addressed in the three companion review papers on various issues surrounding exercise and the endothelium. Leading experts in the field discuss the most recent findings regarding the following: (i) nitric oxide and exercise hyperemia, (ii) the response of the endothelium to exercise training, and (iii) the impact of exercise on the vascular biology of angiotensin as it relates to the vascular endothelium.
Tschakovsky ME.
