The effect of brief intermittent stair climbing on glycemic control in people with type 2 diabetes: a pilot study.

We examined the effect of brief intermittent stair climbing exercise on glycemic control using continuous glucose monitoring in people with type 2 diabetes (n = 7, 5 men; 2 women; age, 21-70 years). The protocol involved three 60-s bouts of vigorously ascending and slowly descending a flight of stairs. Mean 24-h blood glucose was unchanged after an acute session (p = 0.43) and following 18 sessions over 6 weeks (p = 0.13). The protocol was well tolerated by participants but seemingly insufficient to alter glycemic control.

Sodium bicarbonate ingestion augments the increase in PGC-1α mRNA expression during recovery from intense interval exercise in human skeletal muscle.

We tested the hypothesis that ingestion of sodium bicarbonate (NaHCO3) prior to an acute session of high-intensity interval training (HIIT) would augment signaling cascades and gene expression linked to mitochondrial biogenesis in human skeletal muscle. On two occasions separated by ∼1 wk, nine men (mean ± SD: age 22 ± 2 yr, weight 78 ± 13 kg, V̇O(2 peak) 48 ± 8 ml·kg(-1)·min(-1)) performed 10 × 60-s cycling efforts at an intensity eliciting ∼90% of maximal heart rate (263 ± 40 W), interspersed with 60 s of recovery. In a double-blind, crossover manner, subjects ingested a total of 0.4 g/kg body weight NaHCO3 before exercise (BICARB) or an equimolar amount of a placebo, sodium chloride (PLAC). Venous blood bicarbonate and pH were elevated at all time points after ingestion (P < 0.05) in BICARB vs. PLAC. During exercise, muscle glycogen utilization (126 ± 47 vs. 53 ± 38 mmol/kg dry weight, P < 0.05) and blood lactate accumulation (12.8 ± 2.6 vs. 10.5 ± 2.8 mmol/liter, P < 0.05) were greater in BICARB vs. PLAC. The acute exercise-induced increase in the phosphorylation of acetyl-CoA carboxylase, a downstream marker of AMP-activated protein kinase activity, and p38 mitogen-activated protein kinase were similar between treatments (P > 0.05). However, the increase in PGC-1α mRNA expression after 3 h of recovery was higher in BICARB vs. PLAC (approximately sevenfold vs. fivefold compared with rest, P < 0.05). We conclude that NaHCO3 before HIIT alters the mRNA expression of this key regulatory protein associated with mitochondrial biogenesis. The elevated PGC-1α mRNA response provides a putative mechanism to explain the enhanced mitochondrial adaptation observed after chronic HIIT supplemented with NaHCO3 in rats.

ß-Alanine Supplementation Does Not Augment the Skeletal Muscle Adaptive Response to 6 Weeks of Sprint Interval Training.

Sprint interval training (SIT), repeated bouts of high-intensity exercise, improves skeletal muscle oxidative capacity and exercise performance. ß-alanine (ß-ALA) supplementation has been shown to enhance exercise performance, which led us to hypothesize that chronic ß-ALA supplementation would augment work capacity during SIT and augment training-induced adaptations in skeletal muscle and performance. Twenty-four active but untrained men (23 ± 2 yr; VO2peak = 50 ± 6 mL · kg(-1) · min(-1)) ingested 3.2 g/day of ß-ALA or a placebo (PLA) for a total of 10 weeks (n = 12 per group). Following 4 weeks of baseline supplementation, participants completed a 6-week SIT intervention. Each of 3 weekly sessions consisted of 4-6 Wingate tests, i.e., 30-s bouts of maximal cycling, interspersed with 4 min of recovery. Before and after the 6-week SIT program, participants completed a 250-kJ time trial and a repeated sprint test. Biopsies (v. lateralis) revealed that skeletal muscle carnosine content increased by 33% and 52%, respectively, after 4 and 10 weeks of ß-ALA supplementation, but was unchanged in PLA. Total work performed during each training session was similar across treatments. SIT increased markers of mitochondrial content, including cytochome c oxidase (40%) and ß-hydroxyacyl-CoA dehydrogenase maximal activities (19%), as well as VO2peak (9%), repeated-sprint capacity (5%), and 250-kJ time trial performance (13%), but there were no differences between treatments for any measure (p < .01, main effects for time; p > .05, interaction effects). The training stimulus may have overwhelmed any potential influence of ß-ALA, or the supplementation protocol was insufficient to alter the variables to a detectable extent.

Manipulating Carbohydrate Availability Between Twice-Daily Sessions of High-Intensity Interval Training Over 2 Weeks Improves Time-Trial Performance.

Commencing some training sessions with reduced carbohydrate (CHO) availability has been shown to enhance skeletal muscle adaptations, but the effect on exercise performance is less clear. We examined whether restricting CHO intake between twice daily sessions of high-intensity interval training (HIIT) augments improvements in exercise performance and mitochondrial content. Eighteen active but not highly trained subjects (peak oxygen uptake [VO2peak] = 44 ± 9 ml/kg/min), matched for age, sex, and fitness, were randomly allocated to two groups. On each of 6 days over 2 weeks, subjects completed two training sessions, each consisting of 5 × 4-min cycling intervals (60% of peak power), interspersed by 2 min of recovery. Subjects ingested either 195 g of CHO (HI-HI group: ~2.3 g/kg) or 17 g of CHO (HI-LO group: ~0.3 g/kg) during the 3-hr period between sessions. The training-induced improvement in 250-kJ time trial performance was greater (p = .02) in the HI-LO group (211 ± 66 W to 244 ± 75 W) compared with the HI-HI group (203 ± 53 W to 219 ± 60 W); however, the increases in mitochondrial content was similar between groups, as reflected by similar increases in citrate synthase maximal activity, citrate synthase protein content and cytochrome c oxidase subunit IV protein content (p > .05 for interaction terms). This is the first study to show that a short-term "train low, compete high" intervention can improve whole-body exercise capacity. Further research is needed to determine whether this type of manipulation can also enhance performance in highly-trained subjects.

Three minutes of all-out intermittent exercise per week increases skeletal muscle oxidative capacity and improves cardiometabolic health.

We investigated whether a training protocol that involved 3 min of intense intermittent exercise per week--within a total training time commitment of 30 min including warm up and cool down--could increase skeletal muscle oxidative capacity and markers of health status. Overweight/obese but otherwise healthy men and women (n = 7 each; age = 29±9 y; BMI = 29.8±2.7 kg/m2) performed 18 training sessions over 6 wk on a cycle ergometer. Each session began with a 2 min warm-up at 50 W, followed by 3×20 s "all-out" sprints against 5.0% body mass (mean power output: ∼450-500 W) interspersed with 2 min of recovery at 50 W, followed by a 3 min cool-down at 50 W. Peak oxygen uptake increased by 12% after training (32.6±4.5 vs. 29.1±4.2 ml/kg/min) and resting mean arterial pressure decreased by 7% (78±10 vs. 83±10 mmHg), with no difference between groups (both p<0.01, main effects for time). Skeletal muscle biopsy samples obtained before and 72 h after training revealed increased maximal activity of citrate synthase and protein content of cytochrome oxidase 4 (p<0.01, main effect), while the maximal activity of ß-hydroxy acyl CoA dehydrogenase increased in men only (p<0.05). Continuous glucose monitoring measured under standard dietary conditions before and 48-72 h following training revealed lower 24 h average blood glucose concentration in men following training (5.4±0.6 vs. 5.9±0.5 mmol/L, p<0.05), but not women (5.5±0.4 vs. 5.5±0.6 mmol/L). This was associated with a greater increase in GLUT4 protein content in men compared to women (138% vs. 23%, p<0.05). Short-term interval training using a 10 min protocol that involved only 1 min of hard exercise, 3x/wk, stimulated physiological changes linked to improved health in overweight adults. Despite the small sample size, potential sex-specific adaptations were apparent that warrant further investigation.

Physiological and health-related adaptations to low-volume interval training: influences of nutrition and sex.

Interval training refers to the basic concept of alternating periods of relatively intense exercise with periods of lower-intensity effort or complete rest for recovery. Low-volume interval training refers to sessions that involve a relatively small total amount of exercise (i.e. ≤10 min of intense exercise), compared with traditional moderate-intensity continuous training (MICT) protocols that are generally reflected in public health guidelines. In an effort to standardize terminology, a classification scheme was recently proposed in which the term 'high-intensity interval training' (HIIT) be used to describe protocols in which the training stimulus is 'near maximal' or the target intensity is between 80 and 100 % of maximal heart rate, and 'sprint interval training' (SIT) be used for protocols that involve 'all out' or 'supramaximal' efforts, in which target intensities correspond to workloads greater than what is required to elicit 100 % of maximal oxygen uptake (VO2max). Both low-volume SIT and HIIT constitute relatively time-efficient training strategies to rapidly enhance the capacity for aerobic energy metabolism and elicit physiological remodeling that resembles changes normally associated with high-volume MICT. Short-term SIT and HIIT protocols have also been shown to improve health-related indices, including cardiorespiratory fitness and markers of glycemic control in both healthy individuals and those at risk for, or afflicted by, cardiometabolic diseases. Recent evidence from a limited number of studies has highlighted potential sex-based differences in the adaptive response to SIT in particular. It has also been suggested that specific nutritional interventions, in particular those that can augment muscle buffering capacity, such as sodium bicarbonate, may enhance the adaptive response to low-volume interval training.

No effect of short-term green tea extract supplementation on metabolism at rest or during exercise in the fed state.

UNLABELLED: Supplementation with green tea extract (GTE) in animals has been reported to induce numerous metabolic adaptations including increased fat oxidation during exercise and improved performance. However, data regarding the metabolic and physiological effects of GTE during exercise in humans are limited and equivocal. PURPOSE: To examine the effects of short-term GTE treatment on resting energy expenditure (REE), wholebody substrate utilization during exercise and time trial performance. METHODS: Fifteen active men (24 ± 3 y; VO(2)peak = 48 ± 7 ml · kg · min(-1); BMI = 26 ± 3 kg · m(2)((-1))) ingested GTE (3x per day = 1,000 mg/d) or placebo (PLA) for 2 day in a double-blind, crossover design (each separated by a 1 week wash-out period). REE was assessed in the fasted state. Subjects then ingested a standardized breakfast (~5.0 kcal · kg(-1)) and 90 min later performed a 60 min cycling bout at an intensity corresponding to individual maximal fat oxidation (44 ± 11% VO(2)peak), followed by a 250 kJ TT. RESULTS: REE, whole-body oxygen consumption (VO2) and substrate oxidation rates during steady-state exercise were not different between treatments. However, mean heart rate (HR) was lower in GTE vs. PLA (115 ± 16 vs. 118 ± 17 beats · min(-1); main effect, p = .049). Mixed venous blood [glycerol] was higher during rest and exercise after GTE vs. PLA (p = .006, main effect for treatment) but glucose, insulin and free-fatty acids were not different. Subsequent time trial performance was not different between treatments (GTE = 25:38 ± 5:32 vs. PLA = 26:08 ± 8:13 min; p = .75). CONCLUSION: GTE had minimal effects on whole-body substrate metabolism but significantly increased plasma glycerol and lowered heart rate during steady-state exercise, suggesting a potential increase in lipolysis and a cardiovascular effect that warrants further investigation.

High-intensity interval exercise induces 24-h energy expenditure similar to traditional endurance exercise despite reduced time commitment.

Subjects performed high-intensity interval training (HIIT) and continuous moderate-intensity training (END) to evaluate 24-h oxygen consumption. Oxygen consumption during HIIT was lower versus END; however, total oxygen consumption over 24 h was similar. These data demonstrate that HIIT and END induce similar 24-h energy expenditure, which may explain the comparable changes in body composition reported despite lower total training volume and time commitment.

Intermittent and continuous high-intensity exercise training induce similar acute but different chronic muscle adaptations.

High-intensity interval training (HIIT) performed in an 'all-out' manner (e.g. repeated Wingate tests) is a time-efficient strategy to induce skeletal muscle remodelling towards a more oxidative phenotype. A fundamental question that remains unclear, however, is whether the intermittent or 'pulsed' nature of the stimulus is critical to the adaptive response. In study 1, we examined whether the activation of signalling cascades linked to mitochondrial biogenesis was dependent on the manner in which an acute high-intensity exercise stimulus was applied. Subjects performed either four 30 s Wingate tests interspersed with 4 min of rest (INT) or a bout of continuous exercise (CONT) that was matched for total work (67 ± 7 kJ) and which required ∼4 min to complete as fast as possible. Both protocols elicited similar increases in markers of adenosine monophosphate-activated protein kinase (AMPK) and p38 mitogen-activated protein kinase activation, as well as Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) mRNA expression (main effects for time, P ≤ 0.05). In study 2, we determined whether 6 weeks of the CONT protocol (3 days per week) would increase skeletal muscle mitochondrial content to a similar extent to what we have previously reported after 6 weeks of INT. Despite similar acute signalling responses to the CONT and INT protocols, training with CONT did not increase the maximal activity or protein content of a range of mitochondrial markers. However, peak oxygen uptake was higher after CONT training (from 45.7 ± 5.4 to 48.3 ± 6.5 ml kg(-1) min(-1); P < 0.05) and 250 kJ time trial performance was improved (from 26:32 ± 4:48 to 23:55 ± 4:16 min:s; P < 0.001) in our recreationally active participants. We conclude that the intermittent nature of the stimulus is important for maximizing skeletal muscle adaptations to low-volume, all-out HIIT. Despite the lack of skeletal muscle mitochondrial adaptations, our data show that a training programme based on a brief bout of high-intensity exercise, which lasted <10 min per session including warm-up, and performed three times per week for 6 weeks, improved peak oxygen uptake in young healthy subjects.

Trophoblast invasion and blood vessel remodeling are altered in a rat model of lifelong maternal obesity.

Maternal obesity is associated with an increased risk of a number of pregnancy complications, including fetal demise, which may be linked to impaired placental development as a result of altered trophoblast invasion and vessel remodeling. Therefore, we examined these parameters in pregnant rats fed a control (normal weight) or high fat (HF) diet (obese) at 2 critical times of rat placental development. Early trophoblast invasion was increased by approximately 2-fold in HF-fed dams with a concomitant increase in the expression of matrix metalloproteinase 9 protein, a mediator of tissue remodeling and invasion. Furthermore, we observed significantly higher levels of smooth muscle actin surrounding the placental spiral arteries of HF-fed dams, suggesting impaired spiral artery remodeling. Taken together, the results of this study suggest that altered placental development is an important contributor to the poor pregnancy outcomes and increased fetal demise in our model of lifelong maternal obesity.

Interval training in the fed or fasted state improves body composition and muscle oxidative capacity in overweight women.

OBJECTIVE: To investigate the effects of low-volume high-intensity interval training (HIT) performed in the fasted (FAST) versus fed (FED) state on body composition, muscle oxidative capacity, and glycemic control in overweight/obese women. DESIGN AND METHODS: Sixteen women (27 ± 8 years, BMI: 29 ± 6 kg/m(2) , VO2peak : 28 ± 3 ml/kg/min) were assigned to either FAST or FED (n = 8 each) and performed 18 sessions of HIT (10× 60-s cycling efforts at ∼90% maximal heart rate, 60-s recovery) over 6 weeks. RESULTS: There was no significant difference between FAST and FED for any measured variable. Body mass was unchanged following training; however, dual energy X-ray absorptiometry revealed lower percent fat in abdominal and leg regions as well as the whole body level (main effects for time, P ≤ 0.05). Fat-free mass increased in leg and gynoid regions (P ≤ 0.05). Resting muscle biopsies revealed a training-induced increase in mitochondrial capacity as evidenced by increased maximal activities of citrate synthase and ß-hydroxyacyl-CoA dehydrogenase (P ≤ 0.05). There was no change in insulin sensitivity, although change in insulin area under the curve was correlated with change in abdominal percent fat (r = 0.54, P ≤ 0.05). CONCLUSION: Short-term low-volume HIT is a time-efficient strategy to improve body composition and muscle oxidative capacity in overweight/obese women, but fed- versus fasted-state training does not alter this response.

Low-volume high-intensity interval training reduces hyperglycemia and increases muscle mitochondrial capacity in patients with type 2 diabetes.

Low-volume high-intensity interval training (HIT) is emerging as a time-efficient exercise strategy for improving health and fitness. This form of exercise has not been tested in type 2 diabetes and thus we examined the effects of low-volume HIT on glucose regulation and skeletal muscle metabolic capacity in patients with type 2 diabetes. Eight patients with type 2 diabetes (63 ± 8 yr, body mass index 32 ± 6 kg/m(2), Hb(A1C) 6.9 ± 0.7%) volunteered to participate in this study. Participants performed six sessions of HIT (10 × 60-s cycling bouts eliciting ∼90% maximal heart rate, interspersed with 60 s rest) over 2 wk. Before training and from ∼48 to 72 h after the last training bout, glucose regulation was assessed using 24-h continuous glucose monitoring under standardized dietary conditions. Markers of skeletal muscle metabolic capacity were measured in biopsy samples (vastus lateralis) before and after (72 h) training. Average 24-h blood glucose concentration was reduced after training (7.6 ± 1.0 vs. 6.6 ± 0.7 mmol/l) as was the sum of the 3-h postprandial areas under the glucose curve for breakfast, lunch, and dinner (both P < 0.05). Training increased muscle mitochondrial capacity as evidenced by higher citrate synthase maximal activity (∼20%) and protein content of Complex II 70 kDa subunit (∼37%), Complex III Core 2 protein (∼51%), and Complex IV subunit IV (∼68%, all P < 0.05). Mitofusin 2 (∼71%) and GLUT4 (∼369%) protein content were also higher after training (both P < 0.05). Our findings indicate that low-volume HIT can rapidly improve glucose control and induce adaptations in skeletal muscle that are linked to improved metabolic health in patients with type 2 diabetes.