Obesity Risk Among West Point Graduates Later in Life.

ABSTRACT: Szivak, TK, Thomas, MM, Pietrzak, RH, Nguyen, DR, Ryan, DM, and Mazure, CM. Obesity Risk Among West Point Graduates Later in Life. J Strength Cond Res 37(6): 1284-1291, 2023-The purpose of this investigation was to evaluate sex differences in health and fitness outcomes among United States Military Academy (USMA) graduates (class years 1980-2011). Subjects ( n = 701 men, 641 women, age: 45.7 ± 9.3 years) were surveyed as a part of a larger investigation on risk and resiliency factors among USMA graduates. Physical activity was assessed using the International Physical Activity Questionnaire (IPAQ) short form and calculation of weekly metabolic equivalents (METs). Overweight and obesity status were assessed by body mass index (BMI). Significance for the study was set at p ≤ 0.05. Obesity rates for men (30.1%) were significantly higher than for women (16.6%). Men reported significantly higher ( p = 0.01) vigorous METs·wk -1 (1,214.6 ± 1,171.6) than women (1,046.8 ± 1,133.2) despite significantly higher ( p = 0.00) BMI values (28.75 ± 4.53 kg·m -2 ) than women (25.90 ± 5.48 kg·m -2 ). Women were 89% more likely to have ever been on a diet and reported higher (15.2%) Army Body Composition Program enrollment rates than men (6.3%). Obesity rates among men reflect trends seen in the broader military, Veteran, and U.S. adult populations, whereas obesity rates among women were lower. Men may be at a greater risk for obesity later in life despite higher self-reported physical activity; however, lean body mass and self-report bias should be considered. Because lifetime obesity may be influenced by factors other than physical activity, health initiatives should use a comprehensive approach early in the career of military officers.

Neuromuscular manifestations of work-related myalgia in women specific to extensor carpi radialis brevis.

This study assessed neuromuscular function in the extensor carpi radialis brevis (ECRB) of female workers diagnosed with work-related myalgia (WRM, n = 14, age 45.2 ± 1.9 years) and the ECRB of healthy controls (CON, n = 10, age 34.6 ± 2.5 years). Groups were compared on voluntary and electrically evoked functional responses at rest (Pre), immediately following a 5 min repetitive task (Post-0) performed at 60% maximal voluntary contraction (MVC), and after 5 min of recovery (Post-5). Despite near complete motor unit activation (MUA) (CON 98% ± 1% vs. WRM 99% ± 1%), at Pre, WRM produced 26% less (P < 0.05) MVC force than CON. Following an MVC, twitch force was increased (P < 0.05) by 94% ± 13% and 54% ± 11% in CON and WRM, respectively (CON vs. WRM; P < 0.05). The peak force and the maximal rates of force development and decline of electrically evoked contractions (10-100 Hz) were generally depressed (P < 0.05) at Post-0 and Post-5 relative to Pre. The response pattern to increasing frequencies of stimulation was not different (P > 0.05) between groups and MUA was not impaired (CON 97% ± 1% vs. WRM 97% ± 1%; P > 0.05). In conclusion, the peripheral weakness observed in the ECRB in WRM at rest does not result in abnormal fatigue or recovery responses after performing a task controlled for relative demand (60% MVC).

Muscle-specific AMPK ß1ß2-null mice display a myopathy due to loss of capillary density in nonpostural muscles.

AMP-activated protein kinase (AMPK) is a master regulator of metabolism. While muscle-specific AMPK ß1ß2 double-knockout (ß1ß2M-KO) mice display alterations in metabolic and mitochondrial capacity, their severe exercise intolerance suggested a secondary contributor to the observed phenotype. We find that tibialis anterior (TA), but not soleus, muscles of sedentary ß1ß2M-KO mice display a significant myopathy (decreased myofiber areas, increased split and necrotic myofibers, and increased centrally nucleated myofibers. A mitochondrial- and fiber-type-specific etiology to the myopathy was ruled out. However, ß1ß2M-KO TA muscles displayed significant (P<0.05) increases in platelet aggregation and apoptosis within myofibers and surrounding interstitium (P<0.05). These changes correlated with a 45% decrease in capillary density (P<0.05). We hypothesized that the ß1ß2M-KO myopathy in resting muscle resulted from impaired AMPK-nNOSµ signaling, causing increased platelet aggregation, impaired vasodilation, and, ultimately, ischemic injury. Consistent with this hypothesis, AMPK-specific phosphorylation (Ser1446) of nNOSµ was decreased in ß1ß2M-KO compared to wild-type (WT) mice. The AMPK-nNOSµ relationship was further demonstrated by administration of 5-aminoimidazole-4-carboxamide 1-ß-D-ribofuranoside (AICAR) to ß1ß2-MKO muscles and C2C12 myotubes. AICAR significantly increased nNOSµ phosphorylation and nitric oxide production (P<0.05) within minutes of administration in WT muscles and C2C12 myotubes but not in ß1ß2M-KO muscles. These findings highlight the importance of the AMPK-nNOSµ pathway in resting skeletal muscle.

Psychological Resilience in West Point Graduates: Results From a Nationally Representative Study.

Background: The purpose of this study was to examine factors associated with psychological resilience in a nationally representative sample of West Point graduates. Aims: The aims of this study were to (a) employ a dimensional approach to operationalizing psychological resilience in a trauma-exposed population that had been highly trained and educated in persisting in the face of stress, was previously unstudied, and in which we could examine correlates of resilience, (b) identify key psychosocial factors, character traits, health variables, military experiences, and coping strategies as potential correlates of psychological resilience; and (c) examine whether reported gender moderated any of these associations in this population. Methods: A nationally representative sample of 1342 West Point graduates after gender integration from classes 1980 to 2011 were surveyed. Psychological resilience was operationalized using a discrepancy-based approach in which a measure of composite psychological distress (current posttraumatic stress disorder, generalized anxiety and depression symptoms) was regressed on measures of cumulative trauma burden. A multivariable linear regression model was then employed to identify factors that were independently associated with psychological resilience scores. Results: Purpose in life (29.8% of relative variance explained [RVE]), fewer perceived negative experiences in the military (20.6% RVE), social support (9.6% RVE), and grit (9.5% RVE) were the strongest correlates of psychological resilience scores for both women and men. Time in service was positively associated with resilience in women only. Conclusion: This study identifies key correlates of psychological resilience in West Point graduates, individuals who are highly trained to persevere in the face of stress and then were trauma-exposed. Most of these factors are modifiable and can be targeted in stress prevention and treatment interventions, especially for high-stress professions such as the military, frontline health care providers, and first responders.

Initiating treadmill training in late middle age offers modest adaptations in Ca2+ handling but enhances oxidative damage in senescent rat skeletal muscle.

Aging skeletal muscle shows an increased time to peak force and relaxation and a decreased specific force, all of which could relate to changes in muscle Ca(2+) handling. The purpose of this study was to determine if Ca(2+)-handling protein content and function are decreased in senescent gastrocnemius muscle and if initiating a training program in late middle age (LMA, 29 mo old) could improve function in senescent (34- to 36-mo-old) muscle. LMA male Fischer 344 x Brown-Norway rats underwent 5-7 mo of treadmill training. Aging resulted in a decrease in maximal sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA) activity and a decrease in Ca(2+) release rate but no change in Ca(2+) uptake rate. Efficiency of the Ca(2+) pump was increased with age, as was the content of SERCA2a. Training caused a further increase in SERCA2a content. Aging also caused an increase in protein carbonyl and reactive nitrogen species damage accumulation, and both further increased with training. Consistent with the increase in oxidative damage, heat shock protein 70 content was increased with age and further increased with training. Together, these results suggest that while initiating exercise training in LMA augments the age-related increase in expression of heat shock protein 70 and the more efficient SERCA2a isoform, it did not prevent the decrease in SERCA activity and exacerbated oxidative damage in senescent gastrocnemius muscle.

Exercise training from late middle age until senescence does not attenuate the declines in skeletal muscle aerobic function.

We previously showed that 7 wk of treadmill exercise training in late-middle-aged rats can reverse the modest reductions in skeletal muscle aerobic function and enzyme activity relative to values in young adult rats (Exp Physiol 93: 863-871, 2008). The purpose of the present study was to determine whether extending this training program into senescence would attenuate the accelerated decline in the muscle aerobic machinery normally seen at this advanced age. For this purpose, 29-mo-old Fisher 344 Brown-Norway rats underwent 5 or 7 mo of treadmill exercise training. Training resulted in greater exercise capacity during an incremental treadmill exercise test and reduced percent body fat in 34- and 36-mo-old rats and improved survival. Despite these benefits at the whole body level, in situ muscle aerobic capacity and muscle mass were not greater in the trained groups at 34 mo or 36 mo of age. Similarly, the trained groups did not have higher activities of citrate synthase (CS) or Complex IV in homogenates of either the plantaris (fast twitch) or the soleus (slow twitch) muscles at either age. Finally, protein expression of CS (a marker of mitochondrial content) and peroxisome proliferator-activated receptor-gamma coactivator-1 (relating to the drive on mitochondrial biogenesis) were not higher in the trained groups. Therefore, although treadmill training from late middle age into senescence had significant benefits on running capacity, survival, and body fat, it did not prevent the declines in muscle mass, muscle aerobic capacity, or mitochondrial enzyme activities normally seen across this age, revealing a markedly diminished plasticity of the aerobic machinery in response to endurance exercise at advanced age.

Mental and Physical Health Conditions in US Combat Veterans: Results From the National Health and Resilience in Veterans Study.

OBJECTIVE: To identify sociodemographic and military characteristics of combat-exposed and non-combat-exposed veterans in the United States and to compare rates of mental and physical health conditions in these populations. METHODS: Data were analyzed from the National Health and Resilience in Veterans Study (NHRVS), a contemporary, nationally representative survey of 1,480 US veterans conducted September-October 2013. Poststratification weights were applied to analyses to permit generalizability of results to the US veteran population. Outcomes measured included lifetime and current psychiatric disorders and physical health conditions. RESULTS: A total 38% of US veterans reported being exposed to combat. Compared to noncombat veterans, combat veterans were younger, had greater household income, and served a greater number of years in the military; were more likely to be male, to have served in the Marine Corps, and to use the Veterans Affairs Healthcare System as their main source of health care; and reported a greater number of lifetime potentially traumatic events. After adjustment for these sociodemographic and military differences, combat veterans were more than 3 times as likely as noncombat veterans to screen positive for lifetime posttraumatic stress disorder (PTSD) and more than twice as likely for current PTSD and had 82% greater odds of screening positive for current generalized anxiety disorder. After additionally controlling for lifetime diagnoses of PTSD and depression, alcohol or drug use disorder, and nicotine dependence, combat veterans had 68% greater odds of having attempted suicide and 85% and 38% greater odds of being diagnosed with a stroke and chronic pain, respectively. Younger combat veterans were more likely than older combat veterans to screen positive for lifetime (30.6% vs 10.1%) and current PTSD (19.2% vs 4.9%) and suicidal ideation (18.6% vs 6.9%) and to have been diagnosed with migraine headaches (12.8% vs 2.1%), while older combat veterans were more likely than younger combat veterans to report having been diagnosed with heart disease (19.2% vs 2.6%) and heart attack (13.9% vs 2.5%). CONCLUSIONS: Compared to noncombat veterans in the United States, combat veterans have elevated rates of PTSD, suicide attempt, stroke, and chronic pain independent of other sociodemographic, military, and mental health factors. Younger combat veterans have elevated rates of PTSD, suicidal ideation, and migraine headaches, while older combat veterans have elevated rates of heart disease and heart attack. These results characterize the population-based burden of mental and physical health conditions in combat veterans. They further underscore the importance of age- and condition-sensitive screening, monitoring, and treatment efforts in this population.

Voluntary muscle activation is impaired by core temperature rather than local muscle temperature.

Fatigue during hyperthermia may be due in part to a failure of the central nervous system to fully activate the working muscles. We investigated the effects of passive hyperthermia on maximal plantar flexor isometric torque (maximal isometric voluntary contraction) and voluntary activation to determine the roles of local skin temperature, core temperature, and peripheral muscle temperature in fatigue. Nine healthy subjects were passively heated from 37.2 to 39.5 degrees C (core temperature) and then cooled back down to 37.9 degrees C using a liquid-conditioning garment, with the right leg kept at a thermoneutral temperature throughout the protocol, whereas the left leg was allowed to heat and cool. Passive heating resulted in significant decreases in torque from [mean (SD)] 172 N x m (SD 39) to 160 N x m (SD 44) and in voluntary activation from 96% (SD 2) to 91% (SD 5) in the heated leg, and maximal isometric voluntary contraction decreased similarly from 178 N xm (SD 37) to 165 N x m (SD 38) and voluntary activation from 97% (SD 2) to 94% (SD 5) in the thermoneutral leg. The initiation of cooling, which produced a rapid decrease in skin temperature and cardiovascular strain [heart rate reserve decreased from 58% (SD 12) to 31% (SD 12)], did not immediately restore either torque or voluntary activation. However, when core temperature was lowered back to normal, torque and voluntary activation were restored to baseline values. It was concluded that an increase in core temperature is a factor responsible for reducing voluntary activation during brief voluntary isometric contractions and that temperature-induced changes in the contractile properties of muscle and local thermal afferent input from the skin do not contribute significantly to the decrement in torque.

Exercise training initiated in late middle age attenuates cardiac fibrosis and advanced glycation end-product accumulation in senescent rats.

While it has long been postulated that exercise training attenuates the age-related decline in heart function normally associated with increased fibrosis and collagen cross-linking, the potential benefits associated with exercise training initiated later in life are currently unclear. To address this question, Fischer 344 × Brown Norway F1 rats underwent treadmill-based exercise training starting in late middle age and continued into senescence (35 mo) and were compared with age-matched sedentary rats. Hearts were examined for fibrosis and advanced glycation end-products in the subendocardial layer of left ventricular cross-sections. Genes for collagen synthesis and degradation were assessed by polymerase chain reaction, and matrix metalloproteinase (MMP) activity was assessed by EnzChek® Gelatinase/Collagenase Assay Kit. Exercise training of late middle-aged rats attenuated fibrosis and collagen cross-linking, while also reducing age-related mortality between late middle age and senescence. This training was also associated with an attenuated advanced glycation end-product (AGE) accumulation with aging, suggesting a decrease in collagen cross-linking. Conversely, tissue inhibitor of matrix metalloproteinase-1 (TIMP1) gene expression, TIMP and MMP1 protein expression, and MMP activity increased with age but were not significantly impacted by exercise training. While our results demonstrate that exercise training in late middle age attenuates age-related mortality and cardiac fibrosis and is accompanied by attenuated AGE accumulation indicative of less collagen cross-linking, the mechanisms explaining this attenuated replacement fibrosis did not appear to involve altered TIMP1 expression, or MMP protein and activity.

Early oxidative shifts in mouse skeletal muscle morphology with high-fat diet consumption do not lead to functional improvements.

Short-term consumption of a high-fat diet (HFD) can result in an oxidative shift in adult skeletal muscle. However, the impact of HFD on young, growing muscle is largely unknown. Thus, 4-week-old mice were randomly divided into sedentary HFD (60% kcal from fat), sedentary standard chow (control), or exercise-trained standard chow. Tibialis anterior (TA) and soleus muscles were examined for morphological and functional changes after 3 weeks. HFD consumption increased body and epididymal fat mass and induced whole body glucose intolerance versus control mice. Compared to controls, both HFD and exercise-trained TA muscles displayed a greater proportion of oxidative fibers and a trend for an increased succinate dehydrogenase (SDH) content. The soleus also displayed an oxidative shift with increased SDH content in HFD mice. Despite the aforementioned changes, palmitate oxidation rates were not different between groups. To determine if the adaptive changes with HFD manifest as a functional improvement, all groups performed pre- and postexperiment aerobic exercise tests. As expected, exercise-trained mice improved significantly compared to controls, however, no improvement was observed in HFD mice. Interestingly, capillary density was lower in HFD muscles; a finding which may contribute to the lack of functional differences seen with HFD despite the oxidative shift in skeletal muscle morphology. Taken together, our data demonstrate that young, growing muscle exhibits early oxidative shifts in response to a HFD, but these changes do not translate to functional benefits in palmitate oxidation, muscle fatigue resistance, or whole body exercise capacity.

Enhanced lipid oxidation and maintenance of muscle insulin sensitivity despite glucose intolerance in a diet-induced obesity mouse model.

BACKGROUND: Diet-induced obesity is a rising health concern which can lead to the development of glucose intolerance and muscle insulin resistance and, ultimately, type II diabetes mellitus. This research investigates the associations between glucose intolerance or muscle insulin resistance and tissue specific changes during the progression of diet-induced obesity. METHODOLOGY: C57BL/6J mice were fed a normal or high-fat diet (HFD; 60% kcal fat) for 3 or 8 weeks. Disease progression was monitored by measurements of body/tissue mass changes, glucose and insulin tolerance tests, and ex vivo glucose uptake in intact muscles. Lipid metabolism was analyzed using metabolic chambers and ex vivo palmitate assays in intact muscles. Skeletal muscle, liver and adipose tissues were analyzed for changes in inflammatory gene expression. Plasma was analyzed for insulin levels and inflammatory proteins. Histological techniques were used on muscle and liver cryosections to assess metabolic and morphological changes. PRINCIPAL FINDINGS/CONCLUSIONS: A rapid shift in whole body metabolism towards lipids was observed with HFD. Following 3 weeks of HFD, elevated total lipid oxidation and an oxidative fiber type shift had occurred in the skeletal muscle, which we propose was responsible for delaying intramyocellular lipid accumulation and maintaining muscle's insulin sensitivity. Glucose intolerance was present after three weeks of HFD and was associated with an enlarged adipose tissue depot, adipose tissue inflammation and excess hepatic lipids, but not hepatic inflammation. Furthermore, HFD did not significantly increase systemic or muscle inflammation after 3 or 8 weeks of HFD suggesting that early diet-induced obesity does not cause inflammation throughout the whole body. Overall these findings indicate skeletal muscle did not contribute to the development of HFD-induced impairments in whole-body glucose tolerance following 3 weeks of HFD.

Mitochondrial function in permeabilized cardiomyocytes is largely preserved in the senescent rat myocardium.

The aging heart is characterized by a progressive decline in contractile function and diastolic relaxation. Amongst the factors implicated in these changes is a progressive replacement fibrosis secondary to cardiomyocyte death, oxidative damage, and energetic deficit, each of which may be secondary to impaired mitochondrial function. Here, we performed an in-depth examination of mitochondrial function in saponin-permeabilized cardiomyocyte bundles, a preparation where all mitochondria are represented and their structure intact, from young adult (YA) and senescent (SEN) rats (n = 8 per group). When accounting for increased fibrosis (+19%, P<0.01) and proportional decrease in citrate synthase activity in the SEN myocardium (-23%, P<0.05), mitochondrial respiration and reactive oxygen species (H(2)O(2)) emission across a range of energized states was similar between age groups. Accordingly, the abundance of electron transport chain proteins was also unchanged. Likewise, except for CuZnSOD (-37%, P<0.05), the activity of antioxidant enzymes was unaltered with aging. Although time to mitochondrial permeability transition pore (mPTP) opening was decreased (-25%, P<0.05) in the SEN heart, suggesting sensitization to apoptotic stimuli, this was not associated with a difference in apoptotic index measured by ELISA. Collectively, our results suggest that the function of existing cardiac ventricular mitochondria is relatively preserved in SEN rat heart when measured in permeabilized cells.

Alterations in intrinsic mitochondrial function with aging are fiber type-specific and do not explain differential atrophy between muscles.

To determine whether mitochondrial dysfunction is causally related to muscle atrophy with aging, we examined respiratory capacity, H(2) O(2) emission, and function of the mitochondrial permeability transition pore (mPTP) in permeabilized myofibers prepared from four rat muscles that span a range of fiber type and degree of age-related atrophy. Muscle atrophy with aging was greatest in fast-twitch gastrocnemius (Gas) muscle (-38%), intermediate in both the fast-twitch extensor digitorum longus (EDL) and slow-twitch soleus (Sol) muscles (-21%), and non-existent in adductor longus (AL) muscle (+47%). In contrast, indices of mitochondrial dysfunction did not correspond to this differential degree of atrophy. Specifically, despite higher protein expression for oxidative phosphorylation (oxphos) system in fast Gas and EDL, state III respiratory capacity per myofiber wet weight was unchanged with aging, whereas the slow Sol showed proportional decreases in oxphos protein, citrate synthase activity, and state III respiration. Free radical leak (H(2) O(2) emission per O(2) flux) under state III respiration was higher with aging in the fast Gas, whereas state II free radical leak was higher in the slow AL. Only the fast muscles had impaired mPTP function with aging, with lower mitochondrial calcium retention capacity in EDL and shorter time to mPTP opening in Gas and EDL. Collectively, our results underscore that the age-related changes in muscle mitochondrial function depend largely upon fiber type and are unrelated to the severity of muscle atrophy, suggesting that intrinsic changes in mitochondrial function are unlikely to be causally involved in aging muscle atrophy.

Cardiac calcium pump inactivation and nitrosylation in senescent rat myocardium are not attenuated by long-term treadmill training.

The senescent heart has decreased systolic and diastolic functions, both of which could be related to alterations in cardiac sarcoplasmic reticulum (SR) calcium (Ca(2+)) handling. The purpose of this study was to determine if SR protein content and rates of Ca(2+) release and uptake and ATPase activity are lower in the senescent (34-36 mo) Fisher 344×Brown-Norway F1 hybrid rat heart and if a long-term exercise training program could maintain SR function. Late middle aged (29 mo) male rats underwent 5-7 mo of treadmill training. Aging resulted in a decrease in SERCA activity and modest decrease in the rate of Ca(2+) uptake but no change in Ca(2+) release rate. SERCA2a content was not decreased with age but nitrotyrosine accumulation was increased and Ser16 phosphorylated phospholamban (PLN) was decreased. Ryanodine receptor content was not decreased with age but dihydropyridine receptor content was decreased in the senescent heart. Treadmill training had no significant effect on any of the SR properties or protein contents in the senescent rat heart. These results suggest that decreases in Ca(2+) uptake and SERCA activity in the senescent F344BN rat heart are due to increased SERCA2a damage from nitrotyrosine accumulation and inhibition by PLN and that exercise training initiated at late middle age is unable to prevent these age-related changes in cardiac SR function.

Mitochondrial structure and function are disrupted by standard isolation methods.

Mitochondria regulate critical components of cellular function via ATP production, reactive oxygen species production, Ca(2+) handling and apoptotic signaling. Two classical methods exist to study mitochondrial function of skeletal muscles: isolated mitochondria and permeabilized myofibers. Whereas mitochondrial isolation removes a portion of the mitochondria from their cellular environment, myofiber permeabilization preserves mitochondrial morphology and functional interactions with other intracellular components. Despite this, isolated mitochondria remain the most commonly used method to infer in vivo mitochondrial function. In this study, we directly compared measures of several key aspects of mitochondrial function in both isolated mitochondria and permeabilized myofibers of rat gastrocnemius muscle. Here we show that mitochondrial isolation i) induced fragmented organelle morphology; ii) dramatically sensitized the permeability transition pore sensitivity to a Ca(2+) challenge; iii) differentially altered mitochondrial respiration depending upon the respiratory conditions; and iv) dramatically increased H(2)O(2) production. These alterations are qualitatively similar to the changes in mitochondrial structure and function observed in vivo after cellular stress-induced mitochondrial fragmentation, but are generally of much greater magnitude. Furthermore, mitochondrial isolation markedly altered electron transport chain protein stoichiometry. Collectively, our results demonstrate that isolated mitochondria possess functional characteristics that differ fundamentally from those of intact mitochondria in permeabilized myofibers. Our work and that of others underscores the importance of studying mitochondrial function in tissue preparations where mitochondrial structure is preserved and all mitochondria are represented.

Mitochondrial functional impairment with aging is exaggerated in isolated mitochondria compared to permeabilized myofibers.

Mitochondria regulate cellular bioenergetics and apoptosis and have been implicated in aging. However, it remains unclear whether age-related loss of muscle mass, known as sarcopenia, is associated with abnormal mitochondrial function. Two technically different approaches have mainly been used to measure mitochondrial function: isolated mitochondria and permeabilized myofiber bundles, but the reliability of these measures in the context of sarcopenia has not been systematically assessed before. A key difference between these approaches is that contrary to isolated mitochondria, permeabilized bundles contain the totality of fiber mitochondria where normal mitochondrial morphology and intracellular interactions are preserved. Using the gastrocnemius muscle from young adult and senescent rats, we show marked effects of aging on three primary indices of mitochondrial function (respiration, H(2) O(2) emission, sensitivity of permeability transition pore to Ca(2+) ) when measured in isolated mitochondria, but to a much lesser degree when measured in permeabilized bundles. Our results clearly demonstrate that mitochondrial isolation procedures typically employed to study aged muscles expose functional impairments not seen in situ. We conclude that aging is associated with more modest changes in mitochondrial function in sarcopenic muscle than suggested previously from isolated organelle studies.

Initiating exercise training in late middle age minimally protects muscle contractile function and increases myocyte oxidative damage in senescent rats.

Age-related loss of muscle mass and function exhibits a marked acceleration from late middle age to senescence and exercise training is one method that has been proposed to slow this process. The purpose of this study was to determine if long-term treadmill exercise training initiated at late middle age could increase endogenous antioxidant enzyme activity and attenuate the loss of skeletal muscle contractile properties in the gastrocnemius/plantaris (GAS/Plan) and soleus (SOL) muscles of senescent rats (34-36 mo) through a decrease in oxidative damage. Male Fisher 344 × Brown Norway F1-hybrid rats underwent 5-7 mo of treadmill training beginning at late middle age (29 mo). A 7 mo sedentary adult group was used to investigate age-related changes. Aging caused an increase in antioxidant enzyme activities; however, only SOD activity was further increased with exercise training. Exercise training did not attenuate the decrease in twitch or tetanic tension of the GAS/Plan or SOL. It did, however, prevent the increase in twitch half relaxation time of the SOL muscle only. Oxidative damage, as reflected in carbonyl content, was increased with age and even further with exercise training in the GAS muscle. Muscle fibre cross sectional area was decreased with age and even further with exercise training. Interestingly, small muscle fibres showed the highest accumulation of carbonyls. Overall, despite an augmentation of select antioxidant enzyme activities, exercise training from late middle age through to senescence had minimal benefits for muscle contractile properties, perhaps in part due to exacerbated oxidation.