Low Energy Availability and Increased Risk of Relative Energy Deficiency in Sport (RED-S) During a 3767-km Thru-Hike on the Pacific Crest Trail: A Case Study.

Long-distance "thru-hiking" has extraordinary physical demands and has become increasingly popular. This report describes a man (55 y) who thru-hiked the Pacific Crest Trail in 2021 and was at risk of developing the relative energy deficiency in sport (RED-S) syndrome. Hiking distance was 3767 km over 128 d. Eighty-eight days (69%) were full days of hiking, covering 38±8 km/d (mean±SD) in 7.9±1.6 h/d. Exercise energy expenditure above rest (heart rate vs indirect calorimetry regression method) was 2834±1518 kcal/d, total energy expenditure was 5702±1323 kcal/d, and energy intake was 4141 kcal/d. Body mass decreased by 9%, and fat mass (dual-energy X-ray absorptiometry) decreased by 46%. Energy availability (energy intake minus exercise energy expenditure) was 19.3 kcal/d/kg fat-free mass, indicating low energy availability (defined as <30 kcal/d/kg). Dual-energy X-ray absorptiometry-measured spine bone mineral density (BMD) decreased by 8.6%, with little to no decrease in total hip (-1.0%) and femoral neck (-1.5%) BMD. Total cholesterol, low-density lipoprotein cholesterol, and triglycerides increased by 24, 39, and 57%, respectively. Within 8 mo after the hike, BMD and serum lipids nearly or fully returned to baseline. No changes in high-density lipoprotein cholesterol, glycemia, or blood pressure were observed. According to guidelines, these observations are consistent with a moderate risk of RED-S, and a medical evaluation and treatment plan are advisable in order to avoid clinical manifestations (eg, stress fractures, anemia, psychological disturbances). To minimize RED-S risk, it may be prudent for thru-hikers to optimize energy availability by moderating daily hiking distances and/or increasing food intake.

Effect of Huperzine A on Cognitive Function and Perception of Effort during Exercise: A Randomized Double-Blind Crossover Trial.

Huperzine A has shown the ability to acutely improve cognitive function in certain populations, and therefore is commonly added to pre-workout supplements. However, its effects have not been studied in exercise-trained individuals. OBJECTIVE: We hypothesized that acute consumption of huperzine A would improve cognitive function during exercise, which may be beneficial for exercise performance. METHODS: From January to April, 2018, 15 exercise-trained individuals (11 women [height 166 ± 2 cm, weight 60.5 ± 3.0 kg] and 4 men [height 173 ± 4 cm, weight 82.0 ± 11.0 kg], BMI 23.5 ± 1.4 kg/m2, age 30.4 ± 3.6 years) were studied in a double blind randomized-sequence cross-over study, in which they underwent tests for cognitive function (digit span, verbal/word fluency, and Stroop), neuromuscular performance (sharpened Romberg and dart throwing), and exercise performance (estimated aerobic capacity, hand-grip strength, vertical jump, and push-up) after acute ingestion of huperzine A (200 mcg) or placebo. One week separated the two trials. RESULTS: No measures of cognitive function differed between placebo and huperzine A trials (all p ≥ 0.296). Heart rates (157 ± 4 vs. 158 ± 4 bpm; p = 0.518) and ratings of perceived exertion (13.7 ± 0.56 vs. 13.9 ± 0.61; p = 0.582) did not differ between placebo and huperzine A trials, respectively. Ratings of subjective difficulty post-exercise (0-10 scale) were significantly higher (5.7 ± 0.38 vs. 6.8 ± 0.38; p = 0.002) in the huperzine A trial than the placebo trial. No differences were observed for neuromuscular or exercise performance measures between groups (all p ≥ 0.497). CONCLUSIONS: Huperzine A does not enhance cognitive function during exercise despite it being marketed as a cognitive enhancer. Because of its inability to enhance cognitive function, its inclusion in pre-workout supplements warrants reconsideration. Other more practical and effective strategies should be considered.

Correction: The Effect of Protandim® Supplementation on Athletic Performance and Oxidative Blood Markers in Runners.

[This corrects the article DOI: 10.1371/journal.pone.0160559.].

Short Term High-Repetition Back Squat Protocol Does Not Improve 5-km Run Performance.

The purpose of this study was to evaluate the hypothesis that a novel high-repetition, low-resistance back squat training protocol, designed to stimulate high-intensity interval training, improves 5-km run performance. Fifteen runners [4 male, 11 female; 150 + minutes of endurance exercise/week; age = 22.7 ± 2.0 y; 21.5 ± 2.2 kg/m2 BMI] in this single-group test-retest design completed two weeks of back squats consisting of three sets of 15-24 repetitions at 60% of estimated one-repetition max (1RM), three times per week (1-2 days of rest between sessions). Outcome tests included a 5-km outdoor timed run, laboratory indirect calorimetry to quantify substrate oxidation rates during steady-state submaximal exercise (60% and 70% heart rate max (HRmax)), and estimated 1RM for back squats. Back squat estimated 1RM increased by 20% (58.3 ± 18.5 to 70.2 ± 16.7 kg, P < 0.001). However, 5-km run times due to the back squat protocol did not significantly change (Pre-Squats: 23.9 ± 5.0 vs. Post-Squats: 23.7 ± 4.3 minutes, P = 0.71). Likewise, the squat training program did not significantly alter carbohydrate or lipid oxidation rates during steady-state submaximal exercise at 60% or 70% of HRmax (P values ranged from 0.36 - 0.99). Short term high-repetition back squat training does not appear to impact 5-km run performance or substrate utilization during submaximal exercise.

Short-Term Mediterranean Diet Improves Endurance Exercise Performance: A Randomized-Sequence Crossover Trial.

Objective: Healthful dietary patterns have constituents that are known to improve exercise performance, such as antioxidants, nitrates, and alkalizing effects. However, ergogenic effects of such diets have not been evaluated. We hypothesized that a short-term Mediterranean diet results in better exercise performance, as compared to a typical Western diet. Methods: Eleven recreationally active women (n = 7) and men (n = 4) (body mass index, 24.6 ± 3.2 kg/m2; age 28 ± 3 years) were studied in a randomized-sequence crossover study, in which they underwent exercise performance testing on one occasion after 4 days of a Mediterranean diet and on another occasion after 4 days of a Western diet. A 9- to 16-day washout period separated the two trials. Endurance exercise performance was evaluated with a 5-km treadmill time trial. Anaerobic exercise performance tests included a Wingate cycle test, a vertical jump test, and hand grip dynamometry. Results: Five-kilometer run time was 6% ± 3% shorter (faster) in the Mediterranean diet trial than in the Western diet trial (27.09 ± 3.55 vs 28.59 ± 3.21 minutes; p = 0.030) despite similar heart rates (160 ± 5 vs 160 ± 4 beats/min; p = 0.941) and ratings of perceived exertion (14.6 ± 0.5 vs 15.0 ± 0.5; p = 0.356). No differences between the diet conditions were observed for anaerobic exercise tests, including peak and mean power from the Wingate test (both p ≥ 0.05), the vertical jump test (p = 0.19), and the hand grip strength test (p = 0.69). Conclusions: Our findings extend existing evidence of the health benefits of the Mediterranean diet by showing that this diet is also effective for improving endurance exercise performance in as little as 4 days. Further studies are warranted to determine whether a longer-term Mediterranean diet provides greater benefits and whether it might also be beneficial for anaerobic exercise performance and muscle strength and power.

The historical context and scientific legacy of John O. Holloszy.

John O. Holloszy, as perhaps the world's preeminent exercise biochemist/physiologist, published >400 papers over his 50+ year career, and they have been cited >41,000 times. In 1965 Holloszy showed for the first time that exercise training in rodents resulted in a doubling of skeletal muscle mitochondria, ushering in a very active era of skeletal muscle plasticity research. He subsequently went on to describe the consequences of and the mechanisms underlying these adaptations. Holloszy was first to show that muscle contractions increase muscle glucose transport independent of insulin, and he studied the mechanisms underlying this response throughout his career. He published important papers assessing the impact of training on glucose and insulin metabolism in healthy and diseased humans. Holloszy was at the forefront of rodent studies of caloric restriction and longevity in the 1980s, following these studies with important cross-sectional and longitudinal caloric restriction studies in humans. Holloszy was influential in the discipline of cardiovascular physiology, showing that older healthy and diseased populations could still elicit beneficial cardiovascular adaptations with exercise training. Holloszy and his group made important contributions to exercise physiology on the effects of training on numerous metabolic, hormonal, and cardiovascular adaptations. Holloszy's outstanding productivity was made possible by his mentoring of ~100 postdoctoral fellows and substantial NIH grant funding over his entire career. Many of these fellows have also played critical roles in the exercise physiology/biochemistry discipline. Thus it is clear that exercise biochemistry and physiology will be influenced by John Holloszy for numerous years to come.

Low-carbohydrate, ketogenic diet impairs anaerobic exercise performance in exercise-trained women and men: a randomized-sequence crossover trial.

BACKGROUND: Low-carbohydrate, ketogenic diets cause mild, subclinical systemic acidosis. Anaerobic exercise performance is limited by acidosis. Therefore, we evaluated the hypothesis that a low-carbohydrate, ketogenic diet impairs anaerobic exercise performance, as compared to a high-carbohydrate diet. METHODS: Sixteen men and women (BMI, 23±1 kg/m2, age 23±1 years) participated in a randomized-sequence, counterbalanced crossover study in which they underwent exercise testing after 4 days of either a low-carbohydrate, ketogenic diet (LC; <50 g/day and <10% of energy from carbohydrates) or a high-carbohydrate diet (HC; 6-10 g/kg/day carbohydrate). Dietary compliance was assessed with nutrient analysis of diet records, and with measures of urine pH and ketones. Anaerobic exercise performance was evaluated with the Wingate anaerobic cycling test and the yo-yo intermittent recovery test. RESULTS: The diets were matched for total energy (LC: 2333±158 kcal/d; HC: 2280±160 kcal/d; P=0.65) but differed in carbohydrate content (9±1% vs. 63±2% of energy intake; P<0.001). LC resulted in lower urine pH (5.9±0.1 vs. 6.3±0.2, P=0.004) and the appearance of urine ketones in every participant. LC resulted in 7% lower peak power (801±58 watts vs. 857±61 watts, P=0.008) and 6% lower mean power (564±50 watts vs. 598±51 watts, P=0.01) during the Wingate Test. Total distance ran in the yo-yo intermittent recovery test was 15% less after LC diet (887±139 vs. 1045±145 meters, P=0.02). CONCLUSIONS: Short-term low-carbohydrate, ketogenic diets reduce exercise performance in activities that are heavily dependent on anaerobic energy systems. These findings have clear performance implications for athletes, especially for high-intensity, short duration activities and sports.

Sex-specific effects of dehydroepiandrosterone (DHEA) on bone mineral density and body composition: A pooled analysis of four clinical trials.

OBJECTIVE: Studies of dehydroepiandrosterone (DHEA) therapy in older adults suggest sex-specific effects on bone mineral density (BMD) and body composition, but the ability of a single study to reach this conclusion was limited. We evaluated the effects of DHEA on sex hormones, BMD, fat mass and fat-free mass in older women and men enrolled in four similar clinical trials. DESIGN: Pooled analyses of data from four double-blinded, randomized controlled trials. PARTICIPANTS: Women (n = 295) and men (n = 290) aged 55 years or older who took DHEA or placebo tablet daily for 12 months. MEASUREMENTS: Twelve-month changes in BMD, fat mass, fat-free mass and serum DHEA sulphate (DHEAS), (17)estradiol, testosterone and insulin-like growth factor-1 (IGF-1). RESULTS: Women on DHEA had increases (mean ± SD; all P < 0.001 vs placebo) in DHEAS (231 ± 164 µg/dL), testosterone (18.6 ± 20.9 µg/dL), (17)estradiol (8.7 ± 11.0 pg/mL) and IGF-1 (25.1 ± 52.3 ng/mL), and men had increases in DHEAS (269.0 ± 177 µg/dL; P < 0.01), (17)estradiol (4.8 ± 12.2 pg/m; P < 0.01) and IGF-1 (6.3 ± 41.4 ng/mL; P < 0.05). Women on DHEA had increases in lumbar spine (1.0% ± 3.4%) and trochanter (0.5% ± 3.8%) BMD and maintained total hip BMD (0.0% ± 2.8%); men had no BMD benefit and a decrease in fat mass (-0.4 ± 2.6 kg; all P < 0.01 vs placebo). CONCLUSIONS: Dehydroepiandrosterone therapy may be an effective approach for preserving bone and muscle mass in women. Key questions are (a) the extent to which longer duration DHEA can attenuate the loss of bone and muscle in women, and (b) whether DHEA has a more favourable benefit-to-risk profile for women than oestrogen therapy.

Adropin: An endocrine link between the biological clock and cholesterol homeostasis.

OBJECTIVE: Identify determinants of plasma adropin concentrations, a secreted peptide translated from the Energy Homeostasis Associated (ENHO) gene linked to metabolic control and vascular function. METHODS: Associations between plasma adropin concentrations, demographics (sex, age, BMI) and circulating biomarkers of lipid and glucose metabolism were assessed in plasma obtained after an overnight fast in humans. The regulation of adropin expression was then assessed in silico, in cultured human cells, and in animal models. RESULTS: In humans, plasma adropin concentrations are inversely related to atherogenic LDL-cholesterol (LDL-C) levels in men (n = 349), but not in women (n = 401). Analysis of hepatic Enho expression in male mice suggests control by the biological clock. Expression is rhythmic, peaking during maximal food consumption in the dark correlating with transcriptional activation by RORα/γ. The nadir in the light phase coincides with the rest phase and repression by Rev-erb. Plasma adropin concentrations in nonhuman primates (rhesus monkeys) also exhibit peaks coinciding with feeding times (07:00 h, 15:00 h). The ROR inverse agonists SR1001 and the 7-oxygenated sterols 7-ß-hydroxysterol and 7-ketocholesterol, or the Rev-erb agonist SR9009, suppress ENHO expression in cultured human HepG2 cells. Consumption of high-cholesterol diets suppress expression of the adropin transcript in mouse liver. However, adropin over expression does not prevent hypercholesterolemia resulting from a high cholesterol diet and/or LDL receptor mutations. CONCLUSIONS: In humans, associations between plasma adropin concentrations and LDL-C suggest a link with hepatic lipid metabolism. Mouse studies suggest that the relationship between adropin and cholesterol metabolism is unidirectional, and predominantly involves suppression of adropin expression by cholesterol and 7-oxygenated sterols. Sensing of fatty acids, cholesterol and oxysterols by the RORα/γ ligand-binding domain suggests a plausible functional link between adropin expression and cellular lipid metabolism. Furthermore, the nuclear receptors RORα/γ and Rev-erb may couple adropin synthesis with circadian rhythms in carbohydrate and lipid metabolism.

Endurance exercise improves function in individuals with Parkinson's disease: A meta-analysis.

Current evidence has shown that exercise can reduce symptoms of Parkinson's disease (PD). However, previous studies indicated mixed results, possibly because of variability in terms of the nature of the exercise interventions. The purpose of this study was to perform a metaanalysis of current evidence from endurance exercise intervention studies for effects on the United Parkinson's Disease Rating Scale (UPDRS) in individuals with PD. A systematic literature search in six electronic databases was performed and two independent reviewers screened the title and abstract of 1106 records captured by the initial search. Inclusion criteria for full-text review were (A) peer-reviewed English-language publications, (B) randomized controlled trials that compared an endurance exercise intervention group to a non-exercising control group, and (C) an outcome measure which included the UPDRS total score or section III (motor) subscore. From the title/abstract screening, the same independent reviewers assessed 245 full-text articles for eligibility. Of the fulltext articles reviewed 7 articles were included in our meta-analysis, 238 were excluded for the following reasons: 147 did not meet endurance exercise criteria, 53 were review/systematic reviews, 34 were conference abstracts or posters, 2 were editorial or commentary, 1 was a study protocol, and 1 was unpublished. The d index was used to calculate the difference between means of different groups within individual studies, and a weighting factor or w was used to calculate the effect size across studies. Overall, d index was found to be -0.32 with 95% confidence interval, CI (-0.09, -0.56) found to be statistically significant indicating a positive effect of endurance exercise in UPDRS scores. In conclusion, this meta-analysis supports integrating endurance exercise training, as defined by ACSM, into treatment of PD.

Effects of Weight Loss on Lean Mass, Strength, Bone, and Aerobic Capacity.

PURPOSE: This study aimed to evaluate the hypothesis that exercise attenuates the reductions in lean mass, muscle strength, bone mineral density, and V˙O2max that accompany modest weight loss induced by calorie restriction (CR). METHODS: Overweight, sedentary women and men (n = 52, 45-65 yr) were randomized to 6%-8% weight loss by using CR, endurance exercise training (EX), or both (CREX). The CR and the CREX groups underwent counseling to reduce energy intake by 20% and 10%, respectively. The EX and the CREX groups exercised 7.4 ± 0.5 and 4.4 ± 0.5 h·wk, respectively. Before and after 16.8 ± 1.1 wk of weight loss, lean mass and bone mineral density were measured with dual-energy x-ray absorptiometry, strength was measured with dynamometry, and aerobic capacity (V˙O2max) was measured with indirect calorimetry during maximal-intensity treadmill exercise. RESULTS: Weight loss was ~7% in all groups. Decreases in whole-body (~2%, P = 0.003) and lower extremity (~4%, P < 0.0001) lean mass occurred in the CR group (both P < 0.05). Despite similar weight loss, these reductions were attenuated in the CREX group (~1%, P = 0.44 and ~2%, P = 0.05, respectively) and absent in the EX group. Absolute aerobic capacity decreased ~6% in the CR group (P = 0.04), was unchanged in the CREX group (P = 0.28), and increased ~15% in the EX group (P < 0.0001). No changes in muscle strength or bone were observed. CONCLUSIONS: Modest weight loss (~7%) induced by 20% CR in overweight women and men decreases lean mass and reduces absolute V˙O2max. Exercise protects against these effects. Although the CR-induced changes might be considered physiologically appropriate for a reduced body weight, exercise preserves and/or improves these parameters during weight loss, which likely improves physical function. These findings support the notion of using exercise as an important component of weight loss programs.

Circulating cytokines as determinants of weight loss-induced improvements in insulin sensitivity.

Dietary calorie restriction and exercise promote weight loss and may have additive effects for improving insulin sensitivity, independent of weight loss. It is not known if these effects are attributable to changes in circulating cytokines. We evaluated the hypothesis that modest, matched weight loss induced by calorie restriction and exercise have additive effects on circulating cytokines and these changes correlate with improvements in insulin sensitivity. Overweight and sedentary women and men (n = 52, 45-65 years) were randomized to undergo 7 % weight loss by using 3-6 months of calorie restriction, exercise, or a combination of both calorie restriction and exercise. Concentrations of cytokines and hormones were measured in fasting and oral glucose tolerance test blood samples. Insulin sensitivity was estimated based on oral glucose tolerance test for glucose and insulin. With all groups combined, fasting leptin (p < 0.0001) and high molecular weight adiponectin (p = 0.04) decreased and pentraxin-3 increased (p < 0.0001), in a manner that correlated with improvements in insulin sensitivity (all p ≤ 0.0002). These changes, combined with decreases in glucose-dependent insulinotropic polypeptide from the oral glucose tolerance test, explained 63 % of the variance (p < 0.0001) in insulin sensitivity improvements. Exercise and calorie restriction had additive effects on leptin, with a similar trend for high molecular weight adiponectin. Monocyte chemoattractant protein-1 and C-reactive protein concentrations did not change. Calorie restriction and exercise had opposite effects on soluble tumor necrosis factor receptor-1. Modest weight loss in overweight adults decreases serum leptin and high molecular weight adiponectin, and increases pentraxin-3 concentrations in a manner that correlates with increased insulin sensitivity. Exercise has additive effects to those induced by calorie restriction for reductions in leptin and possibly adiponectin. These changes may contribute to the additive effects of calorie restriction and exercise for improving insulin sensitivity.

Exercise as an Adjunctive Treatment for Substance Use Disorders: Rationale and Intervention Description.

Substance use disorders (SUDs) are maladaptive patterns of substance use that are associated with psychiatric comorbidity, unhealthy lifestyle choices, and high rates of relapse. Exercise is associated with a wide range of acute and long-term benefits for both mental and physical health and is presently being investigated as a promising adjunctive treatment for SUD. Despite positive effects of regular physical activity on treatment outcomes and risk factors for relapse, low adherence and high attrition rates limit the benefits derived from exercise interventions. Lack of motivation is one of many perceived barriers to initiating exercise that contributes to poor adherence to interventions. In the present article, we describe the protocol for a novel, integrated exercise intervention that combines motivational interviewing (MI), a client-centered approach designed to enhance intrinsic motivation and resolve ambivalence toward change, and contingency management (CM), a behavioral treatment that provides monetary incentives for the completion of target behaviors. The protocol seeks to address the challenges surrounding initiation and maintenance of an exercise program at a level consistent with public health guidelines, particularly for sedentary patients. We conclude with considerations for the implementation of the intervention in SUD specific clinics.

The Effect of Protandim® Supplementation on Athletic Performance and Oxidative Blood Markers in Runners.

UNLABELLED: The purpose of this study determined if oral supplementation of Protandim® (a nutraceutical) for 90 days improved 5-km running performance and reduced serum thiobarbituric acid-reacting substances (TBARS) at rest, an indicator of oxidative stress. Secondary objectives were to measure whole blood superoxide dismutase (SOD), glutathione (GSH), and glutathione peroxidase (GPX), at rest and 10 minutes after completion of the race before and after supplementation as well as quality of life. In a double-blind, randomized, placebo controlled trial, 38 runners [mean (SD) = 34 (7) yrs; BMI = 22 (2) kg/m2] received either 90 days of Protandim® [1 pill a day, n = 19)] or placebo (n = 19). Randomization was done in blocks of two controlling for sex and 5-km baseline performance. A 5-km race was performed at baseline and after 90 days of supplementation, with blood samples taken before and 10-min after each race. Fasting blood samples were acquired at baseline, after 30, 60, and 90 days of supplementation. TBARS, SOD, GPX, and GSH were assayed in an out-of-state accredited lab. Running performance was not altered by Protandim® or placebo [20.3 (2.1) minutes, with an -8 (33) seconds change in 5-km time regardless of group]. There was no change in TBARS, SOD, or GPX (at rest) after three months of Protandim® supplementation compared to placebo. However, in a subgroup ≥ 35 years of age, there was a 2-fold higher increase in SOD in those taking Protandim® for three months compared to those on placebo (p = 0.038). The mean post-race change in TBARS (compared to pre-race) increased by about 20% in half of the subjects, but was not altered between groups, even after three months of supplementation. Quality of life was also not different between the two conditions. In conclusion, Protandim® did not (1) alter 5-km running time, (2) lower TBARS at rest (3) raise antioxidant enzyme concentrations compared to placebo (with exception of SOD in those ≥ 35 years old) or, (4) affect quality of life compared to placebo. TRIAL REGISTRATION: ClinicalTrials.gov NCT02172625.

Effects of matched weight loss from calorie restriction, exercise, or both on cardiovascular disease risk factors: a randomized intervention trial.

BACKGROUND: Weight loss from calorie restriction (CR) and/or endurance exercise training (EX) is cardioprotective. However CR and EX also have weight loss-independent benefits. OBJECTIVE: We tested the hypothesis that weight loss from calorie restriction and exercise combined (CREX) improves cardiovascular disease (CVD) risk factors more so than similar weight loss from CR or EX alone. DESIGN: Overweight, sedentary men and women (n = 52; aged 45-65 y) were randomly assigned to undergo 6-8% weight loss by using CR, EX, or CREX. Outcomes were measured before and after weight loss and included maximal oxygen consumption (VO2max), resting blood pressure, fasting plasma lipids, glucose, C-reactive protein, and arterial stiffness [carotid-femoral pulse wave velocity (PWV) and carotid augmentation index (AI)]. Values are means ± SEs. RESULTS: Reductions in body weight (∼7%) were similar in all groups. VO2max changed in proportion to the amount of exercise performed (CR, -1% ± 3%; EX, +22% ± 3%; and CREX, +11% ± 3%). None of the changes in CVD risk factors differed between groups. For all groups combined, decreases were observed for systolic and diastolic blood pressure (-5 ± 1 and -4 ± 1 mm Hg, respectively; both P < 0.0008), total cholesterol (-17 ± 4 mg/dL; P < 0.0001), non-HDL cholesterol (-16 ± 3 mg/dL; P < 0.0001), triglycerides (-18 ± 8 mg/dL; P = 0.03), and glucose (-3 ± 1 mg/dL; P = 0.0003). No changes were observed for HDL cholesterol (P = 0.30), C-reactive protein (P = 0.10), PWV (P = 0.30), or AI (P = 0.84). These changes would be expected to decrease the lifetime risk of CVD from 46% to 36%. CONCLUSION: Matched weight losses from CR, EX, and CREX have substantial beneficial effects on CVD risk factors. However, the effects are not additive when weight loss is matched. This trial was registered at clinicaltrials.gov as NCT00777621.

Inverse association between carbohydrate consumption and plasma adropin concentrations in humans.

OBJECTIVE: The role of metabolic condition and diet in regulating circulating levels of adropin, a peptide hormone linked to cardiometabolic control, is not well understood. In this study, weight loss and diet effects on plasma adropin concentrations were examined. METHODS: This report includes data from (1) a weight loss trial, (2) an evaluation of acute exercise effects on mixed-meal (60% kcal from carbohydrates) tolerance test responses, and (3) a meta-analysis to determine normal fasting adropin concentrations. RESULTS: Distribution of plasma adropin concentrations exhibited positive skew and kurtosis. The effect of weight loss on plasma adropin concentrations was dependent on baseline plasma adropin concentrations, with an inverse association between baseline and a decline in concentrations after weight loss (Spearman's ρ = -0.575; P < 0.001). When ranked by baseline plasma adropin concentrations, only values in the upper quartile declined with weight loss. Plasma adropin concentrations under the main area of the bell curve correlated negatively with habitual carbohydrate intake and plasma lipids. There was a negative correlation between baseline values and a transient decline in plasma adropin during the mixed-meal tolerance test. CONCLUSIONS: Plasma adropin concentrations in humans are sensitive to dietary macronutrients, perhaps due to habitual consumption of carbohydrate-rich diets suppressing circulating levels. Very high adropin levels may indicate cardiometabolic conditions sensitive to weight loss.

Effects of Short-Term Docosahexaenoic Acid Supplementation on Markers of Inflammation after Eccentric Strength Exercise in Women.

The omega-3 fatty acid docosahexaenoic acid (DHA) has anti-inflammatory and anti-nociceptive (pain inhibiting) effects. Because strenuous exercise often results in local inflammation and pain, we hypothesized that DHA supplementation attenuates the rise in markers of local muscle inflammation and delayed onset muscle soreness (DOMS) that occur after eccentric strength exercise. Twenty-seven, healthy women (33 ± 2 y, BMI 23.1±1.0 kg·m(-2)) were randomized to receive 9d of 3000 mg/d DHA or placebo in a double-blind fashion. On day 7 of the supplementation period, the participants performed 4 sets of maximal-effort eccentric biceps curl exercise. Before and 48h after the eccentric exercise, markers of inflammation were measured including measures of muscle soreness (10-point visual analog pain scale, VAS), swelling (arm circumference), muscle stiffness (active and passive elbow extension), skin temperature, and salivary C-reactive protein (CRP) concentrations. As expected, muscle soreness and arm circumference increased while active and passive elbow extension decreased. The increase in soreness was 23% less in the DHA group (48h increase in VAS soreness ratings: 4.380.4 vs. 5.600.5, p=0.02). Furthermore, the number of subjects who were able to achieve full active elbow extension 48h after eccentric exercise was greater in the DHA group (71% vs. 15%, p = 0.006), indicating significantly less muscle stiffness. No between-group differences were observed for passive elbow extension (p = 0.78) or arm swelling (p = 0.75). Skin temperature and salivary CRP concentrations did not change from baseline to 48h after exercise in either group. These findings indicate that short-term DHA supplementation reduces exercise-induced muscle soreness and stiffness. Therefore, in addition to other health benefits that n-3 fatty acids have been associated with, DHA supplementation could be beneficial for improving tolerance to new and/or strenuous exercise programs and thereby might facilitate better training adaptations and exercise adherence. Key pointsSeven days of 3000 mg/day supplementation with algae-derived docosahexaenoic acid (DHA) attenuates the delayed onset muscle soreness and stiffness, and protects against the loss of joint range of motion that is caused by strenuous eccentric exercise.This benefit was observed in women, and supports the findings from other studies that were conducted on men or a combination of men and womenThe benefits from algae-derived DHA appear to be similar to those reported in other studies that used a combination of DHA and eicosapentaenoic acid (EPA) derived from fish oilThe findings of better recovery from strenuous exercise with DHA supplementation, paired with other research which demonstrated that DHA and EPA protect against chronic diseases suggest that DHA is an attractive optionThese findings have relevance to athletic populations, in that DHA would be expected to facilitate recovery and allow for better performance during training and competition. However, DHA supplementation might also benefit non-athletic populations, such as individuals starting new exercise programs and patient populations that are prone to muscle soreness (e.g. physical therapy patients).

Micronutrient Deficiencies in Patients With Heart Failure: Relationships With Body Mass Index and Age.

BACKGROUND: It is conceivable that lean patients (body mass index 18.5-24.9 kg/m(2)) with heart failure (HF) have low body weight due to low food consumption and that this may contribute to micronutrient deficiencies and to their poorer prognosis compared with overweight/obese patients. We hypothesized that lean patients have a greater number of inadequate micronutrient intakes (<50% of recommendations) than overweight/obese patients and that this also depends on age. METHODS AND RESULTS: Lean (n = 15) and overweight/obese (n = 49) patients underwent 24-hour diet and physical activity recall interviews. Inadequate essential micronutrient intakes were ubiquitous (intakes of 13 ± 1 of 27 micronutrients were inadequate) and did not depend on race, status, or access to supermarkets. Younger (40-64 y) lean patients had inadequate intakes of 20 ± 2 micronutrients, which was more than the other weight/age subgroups (all P < .01). Physical activity levels did not differ across weight and age groups. CONCLUSIONS: Patients with HF may be at risk of malnutrition due to numerous inadequate micronutrient intakes; younger lean patients may have an especially high risk. Future studies are needed to confirm these preliminary findings and to investigate the possibility that incorporating a micronutrient-dense meal plan will improve patient outcomes.

Effects of dietary Acid load on exercise metabolism and anaerobic exercise performance.

Dietary acid load, quantified as the potential renal acid load (PRAL) of the diet, affects systemic pH and acid-base regulation. In a previous cross-sectional study, we reported that a low dietary PRAL (i.e. alkaline promoting diet) is associated with higher respiratory exchange ratio (RER) values during maximal exercise. The purpose of the present study was to confirm the previous findings with a short-term dietary intervention study. Additionally, we sought to determine if changes in PRAL affects submaximal exercise RER (as a reflection of substrate utilization) and anaerobic exercise performance. Subjects underwent a graded treadmill exercise test (GXT) to exhaustion and an anaerobic exercise performance test on two occasions, once after following a low-PRAL diet and on a separate occasion, after a high-PRAL diet. The diets were continued as long as needed to achieve an alkaline or acid fasted morning urine pH, respectively, with all being 4-9 days in duration. RER was measured during the GXT with indirect calorimetry. The anaerobic performance test was a running time-to-exhaustion test lasting 1-4 min. Maximal exercise RER was lower in the low-PRAL trial compared to the high-PRAL trial (1.10 ± 0.02 vs. 1.20 ± 0.05, p = 0.037). The low-PRAL diet also resulted in a 21% greater time to exhaustion during anaerobic exercise (2.56 ± 0.36 vs. 2.11 ± 0.31 sec, p = 0.044) and a strong tendency for lower RER values during submaximal exercise at 70% VO2max (0.88 ± 0.02 vs. 0.96 ± 0.04, p = 0.060). Contrary to our expectations, a short-term low-PRAL (alkaline promoting) diet resulted in lower RER values during maximal-intensity exercise. However, the low-PRAL diet also increased anaerobic exercise time to exhaustion and appears to have shifted submaximal exercise substrate utilization to favor lipid oxidation and spare carbohydrate, both of which would be considered favorable effects in the context of exercise performance. Key pointsShort-term (4-9 days) changes in the acid or alkaline promoting qualities of the diet, quantified as potential renal acid load (PRAL), alter systemic pH, as evidenced in the present study by changes in fasted morning urine pH. Low-PRAL (alkaline promoting) diets are characterized by high intakes of vegetables and fruits with limited consumption of meats, cheeses, and grains while high-PRAL diets are characterized by the opposite dietary pattern.An alkaline promoting (low-PRAL) diet increases anaerobic exercise performance, as evidenced by greater time-to-exhaustion during high-intensity treadmill running.Preliminary evidence suggests that an alkaline promoting (low-PRAL) diet increases lipid oxidation and may have a carbohydrate-sparing effect during submaximal endurance exercise, although further studies are needed.In contrast to what has been observed in response to habitual/long-term dietary patterns, a short-term low-PRAL diet does not increase maximal exercise respiratory exchange ratio and even appears to lower it. This suggests that short-term and long-term alterations in PRAL have different physiologic effects on this parameter.