Mitochondrial-targeted antioxidant ingestion acutely blunts VO2max in physically inactive females.

PURPOSE: To determine the acute effects of a mitochondrial targeting antioxidant (MitoQ) on the metabolic response during exercise. METHODS: Nine (n = 9) physically inactive females (age 47 ± 22 years) performed two trials (Placebo and MitoQ) in a double-blind randomized cross-over design. In both trials, participants performed an exercise protocol consisting of 3-min stages at submaximal workloads followed by a ramp protocol to volitional exhaustion. Participants received either Placebo or MitoQ (80 mg) 1 h prior to exercise. Indirect calorimetry and cardiovascular measurements were collected throughout the duration of the exercise bout. RESULTS: Submaximal metabolic and cardiovascular variables were not different between trials (p > 0.05). VO2max was higher (p = 0.03) during Placebo (23.5 ± 5.7 mL kg min-1 ) compared to MitoQ (21.0 ± 6.6 mL kg min-1 ). Maximal ventilation was also higher (p = 0.02) in Placebo (82.4 ± 17.7 L/min) compared to MitoQ (75.0 ± 16.8 L/min). Maximal cardiovascular variables and blood lactate were not different between trials (p > 0.05). CONCLUSION: An acute dose of MitoQ blunted VO2max , which was primarily mediated by impairment of ventilatory function. These data suggest that the acute accumulation of exercise-induced mitochondrial reactive oxygen species (mtROS) are necessary for maximal aerobic capacity. Further research is warranted on mtROS-antioxidant cell signaling cascades, and how they relate to mitochondrial function during exercise.

High Cardiorespiratory Optimal Point Values Are Related to Cardiovascular Mortality in Men Aged 46 to 70 Years: a Prospective Cohort Study

Abstract Background: Several hemodynamic and respiratory variables measured during cardiopulmonary exercise testing (CPX) have been shown to predict survival. One such measure is the cardiorespiratory optimal point (COP) that reflects the best possible circulation-respiration interaction, but there are still limited data on its relationship with adverse outcomes. Objective: To assess the association between COP and cardiovascular mortality in men aged 46 to 70 years. Methods: A sample of 2201 men who had anthropometric, clinical, and COP data obtained during cycling CPX between 1995 and 2022 was extracted from the CLINIMEX Exercise cohort. COP was identified as the minimal minute-to-minute VE/VO2 during CPX. Vital data were censored on October 31, 2022 for ICD-10-identified cardiovascular deaths. Cox proportional hazard models were used to estimate hazard ratios (HRs) with 95% confidence intervals (95% CIs). Results: The mean ± standard deviation age was 57 ± 6 years and the median COP value was 24 (interquartile range = 21.2 to 27.4). During a mean follow-up of 4688 ± 2416 days, 129 (5.6%) patients died from cardiovascular causes. The death rates for low (< 28), high (28 to 30), and very high (> 30) categories of COP were 3.2%, 9.6%, and 18.7%, respectively. Following adjustment for age, history of myocardial infarction, diagnosis of coronary artery disease, and diabetes mellitus, the HR (95% CI) for cardiovascular mortality comparing very high versus low COP was 2.76 (1.87 to 4.07; p < 0.001). Conclusions: Our data indicate that, for a general population-based sample of men, COP > 30 represents a considerably higher risk for cardiovascular death. Information on COP could assist cardiovascular risk assessment in men.

A Nonexercise Prediction of Peak Oxygen Uptake for Patients With Cardiovascular Disease: DATA FROM THE FITNESS REGISTRY AND THE IMPORTANCE OF EXERCISE INTERNATIONAL DATABASE (FRIEND).

PURPOSE: Nonexercise predictions of peak oxygen uptake (V˙ o2peak ) are used clinically, yet current equations were developed from cohorts of apparently healthy individuals and may not be applicable to individuals with cardiovascular disease (CVD). Our purpose was to develop a CVD-specific nonexercise prediction equation for V˙ o2peak . METHODS: Participants were from the Fitness Registry and Importance of Exercise International Database (FRIEND) with a diagnosis of coronary artery bypass surgery (CABG), myocardial infarction (MI), percutaneous coronary intervention (PCI), or heart failure (HF) who met maximal effort criteria during a cardiopulmonary exercise test (n = 15 997; 83% male; age 63.1 ± 10.4 yr). The cohort was split into development (n = 12 798) and validation groups (n = 3199). The prediction equation was developed using regression analysis and compared with a previous equation developed on a healthy cohort. RESULTS: Age, sex, height, weight, exercise mode, and CVD diagnosis were all significant predictors of V˙ o2peak . The regression equation was:V˙ o2peak (mL · kg -1 · min -1 ) = 16.18 - (0.22 × age [yr]) + (3.63 × sex [male = 1; female = 0]) + (0.14 × height [cm]) - (0.12 × weight [kg]) + (3.62 × mode [treadmill = 1; cycle = 0]) - (2.70 × CABG [yes = 1, no = 0]) - (0.31 × MI [yes = 1, no = 0]) + (0.37 × PCI [yes = 1, no = 0]) - (4.47 × HF [yes = 1, no = 0]). Adjusted R 2 = 0.43; SEE = 4.75 mL · kg -1 · min -1 .Compared with measured V˙ o2peak in the validation group, percent predicted V˙ o2peak was 141% for the healthy cohort equation and 100% for the CVD-specific equation. CONCLUSIONS: The new equation for individuals with CVD had lower error between measured and predicted V˙ o2peak than the healthy cohort equation, suggesting population-specific equations are needed for predicting V˙ o2peak ; however, errors associated with nonexercise prediction equations suggest V˙ o2peak should be directly measured whenever feasible.

Trends in cardiorespiratory fitness among apparently healthy adults from the Ball State Adult Fitness Longitudinal Lifestyle STudy (BALL ST) cohort from 1970-2019.

INTRODUCTION: Cardiorespiratory fitness (CRF) is a strong independent predictor of cardiovascular disease (CVD) and CVD mortality. However, little is known in regards to how CRF has trended in apparently healthy adults over the past several decades. PURPOSE: To analyze trends in CRF and CVD risk factors over the last 50 years in a population of apparently healthy adult men and women. METHODS: Participants were 4,214 apparently healthy adults (2,390 men and 1,824 women) from the Ball State Adult Fitness Longitudinal Lifestyle STudy (BALL ST) that performed maximal cardiopulmonary exercise testing between 1970-2019 for the assessment of CRF defined as VO2max (ml/kg/min). Participants were self-referred either to a community-based exercise program, fitness testing, or were research subjects in exercise related studies and were placed into groups by decade based on testing date. RESULTS: CRF showed a general trend to decline (P<0.05) from the 1970s to the 2000s with an increase (P<0.05) from the 2000s to the 2010s for both men and women. This pattern persisted for age and sex-adjusted CRF level, determined by Fitness Registry and the Importance of Exercise: A National Data Base (FRIEND). For both women and men, CRF across the decades was associated (P<0.05) with the prevalence of physical inactivity, smoking, obesity, dyslipidemia and hypertension, and with diabetes in men only. CONCLUSION: CRF declined from 1970 through the 2000s in a cohort of apparently healthy men and women which was associated with worsening CVD risk profiles. However, the decline in CRF was attenuated over the past decade which may have a positive impact on future CVD in the population. Promoting physical activity to increase CRF should be a primary aspect of CVD prevention programs.

The Journal of Cardiopulmonary Rehabilitation and Prevention at 40 yr and Its Role in Promoting Preventive Cardiology: Part 2.

Aggressive risk factor modification, including smoking cessation, blood pressure management, and more intensive efforts to control hyperlipidemia, as well as stress management training, are associated with improved cardiovascular outcomes and impressive mortality reductions. This commentary addresses these topics, with specific reference to lifestyle modification and complementary cardioprotective medications.

Cardiorespiratory Fitness Normalized to Fat-Free Mass and Mortality Risk.

PURPOSE: Cardiorespiratory fitness (CRF) is known to be directly related to fat-free mass (FFM), therefore, it has been suggested that normalizing CRF to FFM (V˙O2peakFFM) may be the most accurate expression of CRF as related to exercise performance and cardiorespiratory function. However, the influence of V˙O2peakFFM (mL·kg FFM·min) on predicting mortality has been largely unexplored. This study aimed to primarily assess the relationship between V˙O2peakFFM and all-cause and disease-specific mortality risk in apparently healthy adults. Further, this study sought to compare the predictive ability of V˙O2peakFFM to V˙O2peak normalized to total body weight (V˙O2peakTBW) for mortality outcomes. METHODS: Participants included 2905 adults (1555 men, 1350 women) who completed a cardiopulmonary exercise test between 1970 and 2016 to determine CRF. Body composition was assessed using the skinfold method to estimate FFM. Cardiorespiratory fitness was expressed as V˙O2peakTBW and V˙O2peakFFM. Participants were followed for 19.0 ± 11.7 yr after their cardiopulmonary exercise test for mortality outcomes. Cox-proportional hazard models were performed to determine the relationship of V˙O2peakFFM with mortality outcomes. Parameter estimates were assessed to compare the predictive ability of CRF expressed as V˙O2peakTBW and V˙O2peakFFM. RESULTS: Overall, V˙O2peakFFM was inversely related to all-cause, cardiovascular disease, and cancer mortality, with a 16.2%, 8.4%, and 8.0% lower risk per 1 mL·kg FFM·min improvement, respectively (P < 0.01). Further, assessment of the parameter estimates showed V˙O2peakFFM to be a significantly stronger predictor of all-cause mortality than V˙O2peakTBW (parameter estimates, -0.49 vs -0.16). CONCLUSIONS: Body composition is an important factor when considering the relationship between CRF and mortality risk. Clinicians should consider normalizing CRF to FFM when feasible, because it will strengthen the predictive power of the measure.

The Association between the Change in Directly Measured Cardiorespiratory Fitness across Time and Mortality Risk.

BACKGROUND: The relationship between cardiorespiratory fitness (CRF) and mortality risk has typically been assessed using a single measurement, though some evidence suggests the change in CRF over time influences risk. This evidence is predominantly based on studies using estimated CRF (CRFe). The strength of this relationship using change in directly measured CRF over time in apparently healthy men and women is not well understood. PURPOSE: To examine the association of change in CRF over time, measured using cardiopulmonary exercise testing (CPX), with all-cause and disease-specific mortality and to compare baseline and subsequent CRF measurements as predictors of all-cause mortality. METHODS: Participants included 833 apparently healthy men and women (42.9 ±â€¯10.8 years) who underwent two maximal CPXs, the second CPX being ≥1 year following the baseline assessment (mean 8.6 years, range 1.0 to 40.3 years). Participants were followed for up to 17.7 (SD 11.8) years for all-cause-, cardiovascular disease- (CVD), and cancer mortality. Cox-proportional hazard models were performed to determine the association between the change in CRF, computed as visit 1 (CPX1) peak oxygen consumption (VO2peak [mL·kg-1·min-1]) - visit 2 (CPX2) VO2peak, and mortality outcomes. A Wald-Chi square test of equality was used to compare the strength of CPX1 to CPX2 VO2peak in predicting mortality. RESULTS: During follow-up, 172 participants died. Overall, the change in CPX-CRF was inversely related to all-cause, CVD, and cancer mortality (p < 0.05). Each 1 mL·kg-1·min-1 increase was associated with a ~11, 15, and 16% (all p < 0.001) reduction in all-cause, CVD, and cancer mortality, respectively. The inverse relationship between CRF and all-cause mortality was significant (p < 0.05) when men and women were examined independently, after adjusting for years since first CPX, baseline VO2peak, and age. Further, the Wald Chi-square test of equality found CPX2 VO2peak to be a significantly stronger predictor of all-cause mortality than CPX1 VO2peak (p < 0.05). CONCLUSION: The change in CRF over time was inversely related to mortality outcomes, and mortality was better predicted by CRF measured at subsequent test than CPX1 CRF. These findings emphasize the importance of adopting lifestyle behaviors that promote CRF, as well as support the need for routine assessment of CRF in clinical practice to better assess risk.

Cardiorespiratory Fitness and Mortality in Healthy Men and Women.

BACKGROUND: There is a well-established inverse relationship between cardiorespiratory fitness (CRF) and mortality. However, this relationship has almost exclusively been studied using estimated CRF. OBJECTIVES: This study aimed to assess the association of directly measured CRF, obtained using cardiopulmonary exercise (CPX) testing with all-cause, cardiovascular disease (CVD), and cancer mortality in apparently healthy men and women. METHODS: Participants included 4,137 self-referred apparently healthy adults (2,326 men, 1,811 women; mean age: 42.8 ± 12.2 years) who underwent CPX testing to determine baseline CRF. Participants were followed for 24.2 ± 11.7 years (1.1 to 49.3 years) for mortality. Cox-proportional hazard models were performed to determine the relationship of CRF (ml·kg-1·min-1) and CRF level (low, moderate, and high) with mortality outcomes. RESULTS: During follow-up, 727 participants died (524 men, 203 women). CPX-derived CRF was inversely related to all-cause, CVD, and cancer mortality. Low CRF was associated with higher risk for all-cause (hazard ratio [HR]: 1.73; 95% confidence interval [CI]: 1.20 to 3.50), CVD (HR: 2.27; 95% CI: 1.20 to 3.49), and cancer (HR: 2.07; 95% CI: 1.18 to 3.36) mortality compared with high CRF. Further, each metabolic equivalent increment increase in CRF was associated with a 11.6%, 16.1%, and 14.0% reductions in all-cause, CVD, and cancer mortality, respectively. CONCLUSIONS: Given the prognostic ability of CPX-derived CRF for all-cause and disease-specific mortality outcomes, its use should be highly considered for apparently healthy populations as it may help to improve the efficacy of the individualized patient risk assessment and guide clinical decisions.

Relationship between intermuscular adipose tissue infiltration and myostatin before and after aerobic exercise training.

Intermuscular adipose tissue (IMAT) is associated with impaired skeletal muscle contractile and metabolic function. Myostatin and downstream signaling proteins such as cyclin-dependent kinase 2 (CDK2) contribute to the regulation of adipose and skeletal muscle mass in cell culture and animals models, but this relationship remains incompletely understood in humans. The purpose of this study was to determine if the infiltration of IMAT was associated with skeletal muscle myostatin and downstream proteins before and after 12 wk of aerobic exercise training (AET) in healthy older women (OW; 69 ± 2 yr), older men (OM; 74 ± 3 yr), and young men (YM; 20 ± 1 yr). We found that the infiltration of IMAT was correlated with myostatin and phosphorylated CDK2 at tyrosine 15 [P-CDK2(Tyr15)]. IMAT infiltration was greater in the older subjects and was associated with lower skeletal muscle function and exercise capacity. After 12 wk of AET, there was no change in body weight. Myostatin and P-CDK2(Tyr15) were both decreased after AET, and the reduction in myostatin was associated with decreased IMAT infiltration. The decrease in myostatin and IMAT occurred concomitantly with increased exercise capacity, skeletal muscle size, and function after AET. These findings demonstrate that the reduction in IMAT infiltration after AET in weight stable individuals was accompanied by improvements in skeletal muscle function and exercise capacity. Moreover, the association between myostatin and IMAT was present in the untrained state and in response to exercise training, strengthening the potential regulatory role of myostatin on IMAT.

The effect of feeding during recovery from aerobic exercise on skeletal muscle intracellular signaling.

We previously reported an increase in skeletal muscle protein synthesis during fasted and fed recovery from nonexhaustive aerobic exercise (Harber et al., 2010). The current study examined skeletal muscle intracellular signaling in the same subjects to further investigate mechanisms of skeletal muscle protein metabolism with and without feeding following aerobic exercise. Eight males (VO2peak: 52 ± 2 ml⁻¹·kg⁻¹·min⁻¹) performed 60-min of cycle ergometry at 72 ± 1% VO2peak on two occasions in a counter-balanced design. Exercise trials differed only in the postexercise nutritional intervention: EX-FED (5 kcal, 0.83 g carbohydrate, 0.37 g protein, 0.03 g fat per kg body weight) and EX-FAST (noncaloric, isovolumic placebo) ingested immediately and one hour after exercise. Muscle biopsies were obtained from the vastus lateralis at rest (on a separate day) and two hours postexercise to assess intracellular signaling via western blotting of p70S6K1, eEF2, 4EBP1, AMPKα and p38 MAPK. p70S6K1 phosphorylation was elevated (p < .05) in EX-FED relative to REST and EX-FAST. eEF2, 4EBP1, AMPKα and p38 MAPK signaling were unaltered at 2 h after exercise independent of feeding status when expressed as the ratio of phosphorylated to total protein normalized to actin. These data demonstrate that feeding after a nonexhaustive bout of aerobic exercise stimulates skeletal muscle p70S6K1 intracellular signaling favorable for promoting protein synthesis which may, as recent literature has suggested, better prepare the muscle for subsequent exercise bouts. These data provide further support into the role of feeding on mechanisms regulating muscle protein metabolism during recovery from aerobic exercise.

Amino acid infusion alters the expression of growth-related genes in multiple skeletal muscles.

BACKGROUND: Exercise and nutritional interventions have been examined independently as countermeasures to offset the loss of skeletal muscle mass with unloading, yet a protocol to completely preserve the soleus has not been identified. Little is known regarding the combined effect of exercise and nutrition on factors regulating skeletal muscle growth. The purpose of this investigation was to evaluate the influence of amino acid (AA) infusion on myogenic (MRF-4, MyoD, and Myogenin), proteolytic (MuRF-1, Atrogin-1, FOXO3A, Calpain-1, Calpain-2, Caspase-3, Cathepsin L1), and cytokine (IL-6, IL-8, and IL-15) mRNA transcripts in two skeletal muscles that respond distinctly to microgravity unloading. METHODS: Muscle biopsies were obtained from the vastus lateralis (VL) and soleus of eight male subjects prior to and after 4 h of AA infusion for analysis of mRNA expression. All subjects performed a standardized exercise bout (45-min treadmill run) 24 h prior to the AA infusion. RESULTS: In the VL, proteolytic factors MuRF-1 and FOXO3A were reduced (44 +/- 9 and 28 +/- 6%, respectively) in response toAA infusion. In the soleus, mRNA transcripts of myogenic factor MRF-4 (91 +/- 36%) and cytokines IL-6, IL-8, and IL-15 were elevated while the proteolytic marker FOXO3A mRNA was reduced by 19 +/- 9%. DISCUSSION: These data suggest that the expression of genes related to skeletal muscle remodeling is altered during acute AA infusion 24 h post-exercise. It appears that increased amino acid availability in concert with exercise may create an intramuscular environment favorable for the prevention of muscle atrophy associated with unloading, which may be particularly beneficial for the soleus.

Local anesthetic effects on gene transcription in human skeletal muscle biopsies.

INTRODUCTION: We examined if epinephrine in the local anesthetic to help control incision-related bleeding interferes with molecular measurements obtained with the Duchenne-Bergström percutaneous needle biopsy technique for sampling human skeletal muscle. METHODS: Three groups received 2.5-3.0 ml of 1% lidocaine in 2 injections: (1) 0.5-1.0 ml superficially, which varied among the groups according to (i) -Epi; intra- and subcutaneous without epinephrine, (ii) +Epi -Fascia; intra- and subcutaneous with epinephrine, avoiding the fascia, and (iii) +Epi +Fascia; intra- and subcutaneous with epinephrine, directing a small amount (∽0.2 ml) into the fascia area; and (2) ∽2.0 ml without epinephrine into the fascia area for all subjects. A muscle biopsy was obtained 5-10 min later for IL-6 and MuRF-1 mRNA levels. RESULTS: IL-6 mRNA levels were low in -Epi and +Epi -Fascia, but ∽300-fold higher in +Epi +Fascia. MuRF-1 mRNA levels were similar among the groups. CONCLUSIONS: Lidocaine with epinephrine can confound intramuscular measurements from needle biopsies, but this can be avoided with a careful injection approach.

Muscle protein synthesis and gene expression during recovery from aerobic exercise in the fasted and fed states.

The purpose of this investigation was to assess mixed-muscle fractional synthesis rate (FSR) and the expression of genes involved in skeletal muscle remodeling after aerobic exercise in the fasted and fed states. Eight recreationally active males (25 ± 1 yr; Vo(2 max): 52 ± 2 ml·kg(-1)·min(-1)) performed 60-min of cycle ergometry at 72 ± 1% Vo(2 max) on two occasions in a counter-balanced design. Subjects ingested a noncaloric placebo (EX-FAST) or a beverage containing (per kg body wt): 5 kcal, 0.83 g carbohydrate, 0.37 g protein, and 0.03 g fat (EX-FED) immediately and 1 h after exercise. FSR was assessed at rest and following exercise with the use of a l-[ring (2)H(5)]-phenylalanine infusion combined with muscle biopsies at 2 and 6 h postexercise. mRNA expression was assessed at 2 and 6 h postexercise via real-time RT-PCR. FSR was higher (P < 0.05) after exercise in both EX-FAST (0.112 ± 0.010%·h(-1)) and EX-FED (0.129 ± 0.014%·h(-1)) compared with rest (0.071 ± 0.005%·h(-1)). Feeding attenuated the mRNA expression (P < 0.05) of proteolytic factors MuRF-1 (6 h) and calpain-2 (2 and 6 h) postexercise but did not alter FOXO3A, calpain-1, caspase3, or myostatin mRNA expression compared with EX-FAST. Myogenic regulatory factor (MRF4) mRNA was also attenuated (P < 0.05) at 2 and 6 h postexercise in EX-FED compared with EX-FAST. These data demonstrate that a nonexhaustive bout of aerobic exercise stimulates skeletal muscle FSR in the fasted state and that feeding does not measurably enhance FSR between 2 and 6 h after aerobic exercise. Additionally, postexercise nutrient intake attenuates the expression of factors involved in the ubiquitin-proteosome and Ca(2+)-dependent protein degradation pathways. These data provide insight into the role of feeding on muscle protein metabolism during recovery from aerobic exercise.

Molecular adaptations to aerobic exercise training in skeletal muscle of older women.

BACKGROUND: We have recently shown that 12 weeks of progressive aerobic exercise training improves whole-muscle size and function in older women. The purpose of this investigation was to evaluate molecular markers that may be associated with muscle hypertrophy after aerobic training in aging skeletal muscle. METHODS: Muscle biopsies were obtained before and after 12 weeks of aerobic exercise training on a cycle ergometer in nine older women (70 ± 2 years) to determine basal levels of messenger RNA and protein content of select myogenic, proteolytic, and mitochondrial factors. RESULTS: The training program increased (p < .05) aerobic capacity 30 ± 9%, whole-muscle cross-sectional area 11 ± 2%, and whole-muscle force production 29 ± 8%. Basal messenger RNA levels of FOXO3A, myostatin, HSP70, and MRF4 were lower (p < .05) after aerobic training. FOXO3A, FOXO3A phosphorylation, and HSP70 protein content were unaltered after training. Mitochondrial protein COX IV was elevated (p < .05) 33 ± 7% after aerobic training, whereas PGC-1α protein content was 20 ± 5% lower (p < .05). CONCLUSIONS: These data suggest that reductions in FOXO3A and myostatin messenger RNA are potentially associated with exercise-induced muscle hypertrophy. Additionally, it appears that mitochondrial biogenesis can occur with aerobic training in older women independent of increased PGC-1α protein. Aerobic exercise training alters molecular factors related to the regulation of skeletal muscle, which supports the beneficial role of aerobic training for improving muscle health in older women.

Energy deficit after exercise augments lipid mobilization but does not contribute to the exercise-induced increase in insulin sensitivity.

The content of meals consumed after exercise can impact metabolic responses for hours and even days after the exercise session. The purpose of this study was to compare the effect of low dietary carbohydrate (CHO) vs. low energy intake in meals after exercise on insulin sensitivity and lipid metabolism the next day. Nine healthy men participated in four randomized trials. During the control trial (CON) subjects remained sedentary. During the other three trials, subjects exercised [65% peak oxygen consumption (Vo(2 peak)); cycle ergometer and treadmill exercise] until they expended approximately 800 kcal. Dietary intake during CON and one exercise trial (BAL) was designed to provide sufficient energy and carbohydrate to maintain nutrient balance. In contrast, the diets after the other two exercise trials were low in either CHO (LOW-CHO) or energy (LOW-EN). The morning after exercise we obtained a muscle biopsy, assessed insulin sensitivity (S(i); intravenous glucose tolerance test) and measured lipid kinetics (isotope tracers). Although subjects were in energy balance during both LOW-CHO and CON, the lower muscle glycogen concentration during LOW-CHO vs. CON (402 +/- 29 vs. 540 +/- 33 mmol/kg dry wt, P < 0.01) coincided with a significant increase in S(i) [5.2 +/- 0.7 vs. 3.8 +/- 0.7 (mU/l)(-1) x min(-1); P < 0.05]. Conversely, despite ingesting several hundred fewer kilocalories after exercise during LOW-EN compared with BAL, this energy deficit did not affect S(i) the next day [4.9 +/- 0.9, and 5.0 +/- 0.8 (mU/l)(-1) x min(-1)]. Maintaining an energy deficit after exercise had the most potent effect on lipid metabolism, as measured by a higher plasma triacylglycerol concentration, and increased plasma fatty acid mobilization and oxidation compared with when in nutrient balance. Carbohydrate deficit after exercise, but not energy deficit, contributed to the insulin-sensitizing effects of acute aerobic exercise, whereas maintaining an energy deficit after exercise augmented lipid mobilization.

Aerobic exercise training improves whole muscle and single myofiber size and function in older women.

To comprehensively assess the influence of aerobic training on muscle size and function, we examined seven older women (71 +/- 2 yr) before and after 12 wk of cycle ergometer training. The training program increased (P < 0.05) aerobic capacity by 30 +/- 6%. Quadriceps muscle volume, determined by magnetic resonance imaging (MRI), was 12 +/- 2% greater (P < 0.05) after training and knee extensor power increased 55 +/- 7% (P < 0.05). Muscle biopsies were obtained from the vastus lateralis to determine size and contractile properties of individual slow (MHC I) and fast (MHC IIa) myofibers, myosin light chain (MLC) composition, and muscle protein concentration. Aerobic training increased (P < 0.05) MHC I fiber size 16 +/- 5%, while MHC IIa fiber size was unchanged. MHC I peak power was elevated 21 +/- 8% (P < 0.05) after training, while MHC IIa peak power was unaltered. Peak force (Po) was unchanged in both fiber types, while normalized force (Po/cross-sectional area) was 10% lower (P < 0.05) for both MHC I and MHC IIa fibers after training. The decrease in normalized force was likely related to a reduction (P < 0.05) in myofibrillar protein concentration after training. In the absence of an increase in Po, the increase in MHC I peak power was mediated through an increased (P < 0.05) maximum contraction velocity (Vo) of MHC I fibers only. The relative proportion of MLC(1s) (Pre: 0.62 +/- 0.01; Post: 0.58 +/- 0.01) was lower (P < 0.05) in MHC I myofibers after training, while no differences were present for MLC(2s) and MLC(3f) isoforms. These data indicate that aerobic exercise training improves muscle function through remodeling the contractile properties at the myofiber level, in addition to pronounced muscle hypertrophy. Progressive aerobic exercise training should be considered a viable exercise modality to combat sarcopenia in the elderly population.

Single muscle fibre contractile properties in young and old men and women.

The purpose of this study was to determine whether there was an age-related decline in the isometric and isotonic contractile function of permeabilized slow (MHC I) and fast (MHC IIa) single muscle fibres. Vastus lateralis muscle fibres from six young men (YM; 25 +/- 1 years), six young women (YW; 25 +/- 1 years), six old men (OM; 80 +/- 4 years) and six old women (OW; 78 +/- 2 years) were studied at 15 degrees C for in vitro force-velocity properties, peak force and contractile velocity. Peak power was 23-28 % lower (P < 0.05) in MHC I fibres of YW compared to the other three groups. MHC IIa peak power was 25-40 % lower (P < 0.05) in OW compared to the other three groups. No difference was found in MHC I and IIa normalized peak power among any of the groups. Peak force was lower (P < 0.05) in the YW (MHC I fibres) and OW (MHC IIa fibres) compared to the other groups. Differences in peak force with ageing were negated when normalized to cell size. No age-related differences were observed in single fibre contractile velocity of MHC I and IIa fibres. These data show that YW (MHC I) and OW (MHC IIa) have lower single fibre absolute peak power and peak force compared to men; however, these differences are negated when normalized to cell size. General muscle protein concentrations (i.e. total, sarcoplasmic and myofibrillar) from the same biopsies were lower (4-9 %, P < 0.05) in the OM and OW. However, myosin and actin concentrations were not different (P > 0.05) among the four groups. These data suggest that differences in whole muscle strength and function that are often observed with ageing appear to be regulated by quantitative rather than qualitative parameters of single muscle fibre contractile function.

Muscle fiber characteristics of competitive power lifters.

To examine the skeletal muscle characteristics of power lifters, 5 competitive power lifters (PL; X +/- SE; age = 31.0 +/- 1.5 years, squat = 287.7 +/- 15.7 kg, bench press = 170.5 +/- 17.7 kg, and deadlift = 284.2 +/- 7.5 kg) and 5 untrained control subjects (CON; age = 27.3 +/- 3.3 years) served as subjects. Isokinetic squat force and power was greater (p < 0.05) for the PL at all bar velocities (0.20, 0.82, and 1.43 m;pd s(-1)), as was vertical jump height and estimated power. Muscle biopsies from the vastus lateralis m. revealed significant differences for percent fiber type (PL, IIA = 45.5 +/- 1.6%, IIB = 1.3 +/- 0.8%; CON, IIA = 33.4 +/- 3.1%, IIB = 12.0 +/- 2.4%); percent fiber type area (PL, IIA = 51.8 +/- 1.6%, IIB = 1.3 +/- 0.8%; CON, IIA = 43.5 +/- 3.4%, IIB = 12.4 +/- 2.6%); and percent myosin heavy chain isoform (PL, IIa = 59.5 +/- 6.1%; CON, 46.5 +/- 2.5%). Muscle fiber characteristics were significantly correlated (r = +/- 0.61) with numerous strength and power measures for the PL. These data illustrate the muscle fiber characteristics necessary for the maximal force production requirements of power lifting.