Michael R. Deschenes

Quantity and Quality of Exercise for Developing and Maintaining Cardiorespiratory, Musculoskeletal, and Neuromotor Fitness in Apparently Healthy Adults: Guidance for Prescribing Exercise

SUMMARYThe purpose of this Position Stand is to provide guidance to professionals who counsel and prescribe individualized exercise to apparently healthy adults of all ages. These recommendations also may apply to adults with certain chronic diseases or disabilities, when appropriately evaluated and

Effects of aging on muscle fibre type and size

Aging has been associated with a loss of muscle mass that is referred to as ‘sarcopenia’. This decrease in muscle tissue begins around the age of 50 years, but becomes more dramatic beyond the 60th year of life. Loss of muscle mass among the aged directly results in diminished muscle function. Decreased strength and power contribute to the high incidence of accidental falls observed among the elderly and can compromise quality of life. Moreover, sarcopenia has been linked to several chronic afflictions that are common among the aged, including osteoporosis, insulin resistance and arthritis. Loss of muscle fibre number is the principal cause of sarcopenia, although fibre atrophy — particularly among type II fibres — is also involved. Several physiological mechanisms have been implicated in the development of sarcopenia. Denervation results in the loss of motor units and thus, muscle fibres. A decrease in the production of anabolic hormones such as testosterone, growth hormone and insulin-like growth factor-1 impairs the capacity of skeletal muscle to incorporate amino acids and synthesise proteins. An increase in the release of catabolic agents, specifically interleukin-6, amplifies the rate of muscle wasting among the elderly. Given the demographic trends evident in most western societies, i.e. increased number of those considered aged, management interventions for sarcopenia must become a major goal of the healthcare profession.

Remodeling of the neuromuscular junction precedes sarcopenia related alterations in myofibers

Several mechanisms contributing to the etiology of sarcopenia (age-related loss of muscle size) have been postulated. One of these attributes the loss of muscle mass to a preceding age-related denervation of myofibers. The aim of this study was to determine if signs of denervation were apparent at the neuromuscular junction (NMJ) before fiber atrophy, or fiber type conversion could be documented, and to reveal if a muscles activity level impacts its sensitivity to age-related denervation. Plantaris and soleus muscles were obtained from young adult (10 months) and early aged (21 months) rats. Pre- and post-synaptic NMJ morphology was quantified with cytofluorescent staining of nerve terminal branches and endplate regions, respectively. Myofiber profiles (fiber size and fiber type composition) were assessed with histochemical procedures. Results show that in the lightly recruited plantaris, significant (P<0.05) signs of denervation were noted in aged rats, while the same muscles displayed no change in myofiber profile. In the heavily recruited soleus, however, there was little evidence of denervation, and again no alterations in myofiber profile. These results indicate that age-related denervation occurs before myofiber atrophy, and that high amounts of neuromuscular activity may delay the onset of age-related denervation and sarcopenia.

Androgen receptor content following heavy resistance exercise in men

The purpose of the present investigation was to examine androgen receptor (AR) content in the vastus lateralis following two resistance exercise protocols of different volume. Nine resistance-trained men (age=24.3+/-4.4 years) performed the squat exercise for 1 (SS) and 6 sets (MS) of 10 repetitions in a random, counter-balanced order. Muscle biopsies were performed at baseline, and 1h following each protocol. Blood was collected prior to, immediately following (IP), and every 15 min after each protocol for 1h. No acute elevations in serum total testosterone were observed following SS, whereas significant 16-23% elevations were observed at IP, 15, and 30 min post-exercise following MS. No acute elevations in plasma cortisol were observed following SS, whereas significant 31-49% elevations were observed for MS at IP, 15, and 30 min post-exercise. Androgen receptor content did not change 1h following SS but significantly decreased by 46% following MS. These results demonstrated that a higher volume of resistance exercise resulted in down-regulation of AR content 1h post-exercise. This may have been due to greater protein catabolism associated with the higher level of stress following higher-volume resistance exercise.

Motor unit and neuromuscular junction remodeling with aging.

The neuromuscular system is one of the largest and most vital organ systems of the body. The function and mass of the neuromuscular system gradually deteriorate during the natural process of aging. The neuromuscular system is comprised of individual motor units, each of which features a single motor neuron and all the muscle fibers it innervates. Motor units also demonstrate age-related remodeling such as reduced number, muscle fiber atrophy, but an increased number of fibers per motor unit. Enabling communication between motor neurons and the muscle fibers they innervate is a specialized synapse known as the neuromuscular junction. Aging, too, elicits remodeling of this synapse joining motor nerve terminal endings with a small ( < 0.1%) area of the muscle fibers surface called the endplate. Aged neuromuscular junctions exhibit elevations in pre-synaptic nerve terminal branching, and in the post-synaptic distribution of receptor sites for neurotransmitter. This anatomical remodeling is coupled with age-related neurophysiological alterations including increased quantal content, with a more rapid rundown of endplate potential strength during continuous stimulation of the pre-synaptic neuron. Moreover, there is a growing body of evidence indicating that aging impacts the capacity of the NMJ to adapt to increased, as well as decreased physical activity. Because of the marked increase in the number of people considered to be aged in industrialized countries, it is essential to expand our understanding of the influence of aging on the neuromuscular system, its constituent motor units, and the neuromuscular junctions which allow neural cells and muscle fibers to effectively work together.

Biorhythmic influences on functional capacity of human muscle and physiological responses.

UNLABELLED Previously, this laboratory has demonstrated that exhaustive aerobic exercise performance is not subject to significant chronobiological variation between 0800 and 2000 h, but certain physiological responses to maximal aerobic effort do fluctuate significantly within that time frame. PURPOSE The purpose of the present investigation was to determine whether muscle performance, and selected physiological responses to resistance exercise, was significantly influenced by time of day effects. METHODS Ten healthy, but untrained, men (21.1+/-0.6 yr, mean +/- SE) volunteered to participate in the study. In a balanced and randomized study design, each subject performed resistance exercise protocols on an isokinetic dynamometer with maximal effort at 0800 h, 1200 h, 1600 h, and 2000 h. Selected physiological and hormonal data were recorded before and immediately following the exercise stimulus. RESULTS The data demonstrated significant chronobiological oscillation in peak torque, average power, maximal work in a single repetition, and total work per set. Interestingly, this oscillation was manifested only at the fastest velocities of limb movement utilized. Pre- and postexercise rectal temperature exhibited significant time of day fluctuation, as did postexercise blood pressure. Plasma levels of testosterone and cortisol also displayed significant biorhythmicity under both pre- and postexercise conditions. However, exercise-induced responses (pre- to postexercise differences) of those steroid hormones did not exhibit significant biorythmic variation. Although plasma concentrations of both testosterone and cortisol were highest at 0800 h, testosterone to cortisol ratios were greatest at 2000 h. CONCLUSIONS In summary, these data suggest that maximal muscle performance does vary within the segment of the day when exercise typically occurs (0800-2000 h) but that this variation is specific to speed of movement.

Chronobiological effects on exercise performance and selected physiological responses.

Abstract Previous studies investigating the impact of circadian rhythms on physiological variables during exercise have yielded conflicting results. The purpose of the present investigation was to examine maximal aerobic exercise performance, as well as the physiological and psychophysiological responses to exercise, at four different intervals (0800 hours, 1200 hours, 1600 hours, and 2000 hours) within the segment of the 24-h day in which strenuous physical activity is typically performed. Ten physically fit, but untrained, male university students served as subjects. The results revealed that exercise performance was unaffected by chronobiological effects. Similarly, oxygen uptake, minute ventilation and heart rate showed no time of day influences under pre-, submaximal, and maximal exercise conditions. Ratings of perceived exertion were unaffected by time of day effects during submaximal and maximal exercise. In contrast, rectal temperature exhibited a significant chronobiological rhythm under all three conditions. Under pre- and submaximal exercise conditions, significant time of day effects were noted for respiratory exchange ratio, while a significant rhythmicity of blood pressure was evident during maximal exercise. However, none of these physiological variables exhibited significant differential responses (percent change from pre-exercise values) to the exercise stimulus at any of the four time points selected for study. Conversely, resting plasma lactate levels and lactate responses to maximal exercise were found to be significantly sensitive to chronobiological influences. Absolute post-exercise plasma norepinephrine values, and norepinephrine responses to exercise (percent change from pre-exercise values), also fluctuated significantly among the time points studied. In summary, these data suggest that aerobic exercise performance does not vary during the time frame within which exercise is normally conducted, despite the fact that some important physiological responses to exercise do fluctuate within that time period.

Neuromuscular disturbance outlasts other symptoms of exercise-induced muscle damage

This study examined the biochemical, immunological, functional, and neuromuscular responses associated with exercise-induced muscle damage in the quadriceps of untrained men. Muscle damage and soreness was elicited with maximal concentric/eccentric muscle actions at 0.53 rads s(-1). Significant (P<0.05) soreness was evident 1, 2, and 3 days following muscle insult, while plasma creatine kinase, a marker of muscle damage, was elevated 3 and 5 days post-insult. Plasma interleukin-Ibeta was significantly increased within 5 min, and remained elevated 1, 2, 5, and 7 days post-insult. Maximal isometric quadriceps function was impaired (P<0. 05) for 5 days following muscle challenge. Maximal isokinetic performance at 1.09 rads s(-1) was diminished (P<0.05) for 2 days post-insult; no significant decrements at 3.14 rads s(-1) were noted. Average electrical activation (iEMG) of the quadriceps was unaltered, but iEMG activity of the rectus femoris - where soreness was focused - was significantly increased. Neuromuscular efficiency (torque/iEMG) was compromised throughout the 10-day post-insult period investigated. While other symptoms of exercise-induced muscle damage dissipate within 7 days, neuromuscular perturbation persists for at least 10 days.

Degeneration of neuromuscular junction in age and dystrophy.

Functional denervation is a hallmark of aging sarcopenia as well as of muscular dystrophy. It is thought to be a major factor reducing skeletal muscle mass, particularly in the case of sarcopenia. Neuromuscular junctions (NMJs) serve as the interface between the nervous and skeletal muscular systems, and thus they may receive pathophysiological input of both pre- and post-synaptic origin. Consequently, NMJs are good indicators of motor health on a systemic level. Indeed, upon sarcopenia and dystrophy, NMJs morphologically deteriorate and exhibit altered characteristics of primary signaling molecules, such as nicotinic acetylcholine receptor and agrin. Since a remarkable reversibility of these changes can be observed by exercise, there is significant interest in understanding the molecular mechanisms underlying synaptic deterioration upon aging and dystrophy and how synapses are reset by the aforementioned treatments. Here, we review the literature that describes the phenomena observed at the NMJ in sarcopenic and dystrophic muscle as well as to how these alterations can be reversed and to what extent. In a second part, the current information about molecular machineries underlying these processes is reported.

The neuromuscular junction: Anatomical features and adaptations to various forms of increased, or decreased neuromuscular activity

The neuromuscular junction (NMJ) allows communication between motor neurons and muscle fibers. During development, marked morphological changes occur as the functional NMJ is formed. During the postnatal period of rapid growth and muscle enlargement, endplate size concurrently increases. Even beyond this period of pronounced plasticity, the NMJ undergoes subtle morphological remodeling—expansion and retraction—although its overall dimensions remain stable. This natural, continual NMJ remodeling is amplified with alterations in neuromuscular activity. Increased activity, presented by exercise training, typically results in expansion of NMJ size. Disuse, brought about by neurotoxins, denervation, or spaceflight, also elicits substantial reconfiguring of the endplate.