Martin J. Gibala

Similar metabolic adaptations during exercise after low volume sprint interval and traditional endurance training in humans

Low‐volume ‘sprint’ interval training (SIT) stimulates rapid improvements in muscle oxidative capacity that are comparable to levels reached following traditional endurance training (ET) but no study has examined metabolic adaptations during exercise after these different training strategies. We hypothesized that SIT and ET would induce similar adaptations in markers of skeletal muscle carbohydrate (CHO) and lipid metabolism and metabolic control during exercise despite large differences in training volume and time commitment. Active but untrained subjects (23 ± 1 years) performed a constant‐load cycling challenge (1 h at 65% of peak oxygen uptake before and after 6 weeks of either SIT or ET (n= 5 men and 5 women per group). SIT consisted of four to six repeats of a 30 s ‘all out’ Wingate Test (mean power output ∼500 W) with 4.5 min recovery between repeats, 3 days per week. ET consisted of 40–60 min of continuous cycling at a workload that elicited ∼65% (mean power output ∼150 W) per day, 5 days per week. Weekly time commitment (∼1.5 versus∼4.5 h) and total training volume (∼225 versus∼2250 kJ week−1) were substantially lower in SIT versus ET. Despite these differences, both protocols induced similar increases (P < 0.05) in mitochondrial markers for skeletal muscle CHO (pyruvate dehydrogenase E1α protein content) and lipid oxidation (3‐hydroxyacyl CoA dehydrogenase maximal activity) and protein content of peroxisome proliferator‐activated receptor‐γ coactivator‐1α. Glycogen and phosphocreatine utilization during exercise were reduced after training, and calculated rates of whole‐body CHO and lipid oxidation were decreased and increased, respectively, with no differences between groups (all main effects, P < 0.05). Given the markedly lower training volume in the SIT group, these data suggest that high‐intensity interval training is a time‐efficient strategy to increase skeletal muscle oxidative capacity and induce specific metabolic adaptations during exercise that are comparable to traditional ET.

Short‐term sprint interval versus traditional endurance training: similar initial adaptations in human skeletal muscle and exercise performance

Brief, intense exercise training may induce metabolic and performance adaptations comparable to traditional endurance training. However, no study has directly compared these diverse training strategies in a standardized manner. We therefore examined changes in exercise capacity and molecular and cellular adaptations in skeletal muscle after low volume sprint‐interval training (SIT) and high volume endurance training (ET). Sixteen active men (21 ± 1 years, ) were assigned to a SIT or ET group (n= 8 each) and performed six training sessions over 14 days. Each session consisted of either four to six repeats of 30 s ‘all out’ cycling at ∼250% with 4 min recovery (SIT) or 90–120 min continuous cycling at ∼65% (ET). Training time commitment over 2 weeks was ∼2.5 h for SIT and ∼10.5 h for ET, and total training volume was ∼90% lower for SIT versus ET (∼630 versus∼6500 kJ). Training decreased the time required to complete 50 and 750 kJ cycling time trials, with no difference between groups (main effects, P≤ 0.05). Biopsy samples obtained before and after training revealed similar increases in muscle oxidative capacity, as reflected by the maximal activity of cytochrome c oxidase (COX) and COX subunits II and IV protein content (main effects, P≤ 0.05), but COX II and IV mRNAs were unchanged. Training‐induced increases in muscle buffering capacity and glycogen content were also similar between groups (main effects, P≤ 0.05). Given the large difference in training volume, these data demonstrate that SIT is a time‐efficient strategy to induce rapid adaptations in skeletal muscle and exercise performance that are comparable to ET in young active men.

Physiological adaptations to low‐volume, high‐intensity interval training in health and disease

Abstract  Exercise training is a clinically proven, cost‐effective, primary intervention that delays and in many cases prevents the health burdens associated with many chronic diseases. However, the precise type and dose of exercise needed to accrue health benefits is a contentious issue with no clear consensus recommendations for the prevention of inactivity‐related disorders and chronic diseases. A growing body of evidence demonstrates that high‐intensity interval training (HIT) can serve as an effective alternate to traditional endurance‐based training, inducing similar or even superior physiological adaptations in healthy individuals and diseased populations, at least when compared on a matched‐work basis. While less well studied, low‐volume HIT can also stimulate physiological remodelling comparable to moderate‐intensity continuous training despite a substantially lower time commitment and reduced total exercise volume. Such findings are important given that ‘lack of time’ remains the most commonly cited barrier to regular exercise participation. Here we review some of the mechanisms responsible for improved skeletal muscle metabolic control and changes in cardiovascular function in response to low‐volume HIT. We also consider the limited evidence regarding the potential application of HIT to people with, or at risk for, cardiometabolic disorders including type 2 diabetes. Finally, we provide insight on the utility of low‐volume HIT for improving performance in athletes and highlight suggestions for future research.

A practical model of low-volume high-intensity interval training induces mitochondrial biogenesis in human skeletal muscle: potential mechanisms

High‐intensity interval training (HIT) induces skeletal muscle metabolic and performance adaptations that resemble traditional endurance training despite a low total exercise volume. Most HIT studies have employed ‘all out’, variable‐load exercise interventions (e.g. repeated Wingate tests) that may not be safe, practical and/or well tolerated by certain individuals. Our purpose was to determine the performance, metabolic and molecular adaptations to a more practical model of low‐volume HIT. Seven men (21 ± 0.4 years, ml kg−1 min−1) performed six training sessions over 2 weeks. Each session consisted of 8–12 × 60 s intervals at ∼100% of peak power output elicited during a ramp peak test (355 ± 10 W) separated by 75 s of recovery. Training increased exercise capacity, as assessed by significant improvements on both 50 kJ and 750 kJ cycling time trials (P < 0.05 for both). Skeletal muscle (vastus lateralis) biopsy samples obtained before and after training revealed increased maximal activity of citrate synthase (CS) and cytochrome c oxidase (COX) as well as total protein content of CS, COX subunits II and IV, and the mitochondrial transcription factor A (Tfam) (P < 0.05 for all). Nuclear abundance of peroxisome proliferator‐activated receptor γ co‐activator 1α (PGC‐1α) was ∼25% higher after training (P < 0.05), but total PGC‐1α protein content remained unchanged. Total SIRT1 content, a proposed activator of PGC‐1α and mitochondrial biogenesis, was increased by ∼56% following training (P < 0.05). Training also increased resting muscle glycogen and total GLUT4 protein content (both P < 0.05). This study demonstrates that a practical model of low volume HIT is a potent stimulus for increasing skeletal muscle mitochondrial capacity and improving exercise performance. The results also suggest that increases in SIRT1, nuclear PGC‐1α, and Tfam may be involved in coordinating mitochondrial adaptations in response to HIT in human skeletal muscle.

Metabolic Adaptations to Short-term High-intensity Interval Training: A Little Pain for a Lot of Gain?

High-intensity interval training (HIT) is a potent time-efficient strategy to induce numerous metabolic adaptations usually associated with traditional endurance training. As little as six sessions of HIT over 2 wk or a total of only approximately 15 min of very intense exercise (~600 kJ), can increase skeletal muscle oxidative capacity and endurance performance and alter metabolic control during aerobic-based exercise.

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.

An acute bout of high-intensity interval training increases the nuclear abundance of PGC-1α and activates mitochondrial biogenesis in human skeletal muscle

Low-volume, high-intensity interval training (HIT) increases skeletal muscle mitochondrial capacity, yet little is known regarding potential mechanisms promoting this adaptive response. Our purpose was to examine molecular processes involved in mitochondrial biogenesis in human skeletal muscle in response to an acute bout of HIT. Eight healthy men performed 4 × 30-s bursts of all-out maximal intensity cycling interspersed with 4 min of rest. Muscle biopsy samples (vastus lateralis) were obtained immediately before and after exercise, and after 3 and 24 h of recovery. At rest, the majority of peroxisome proliferator-activated receptor γ coactivator (PGC)-1α, a master regulator of mitochondrial biogenesis, was detected in cytosolic fractions. Exercise activated p38 MAPK and AMPK in the cytosol. Nuclear PGC-1α protein increased 3 h into recovery from exercise, a time point that coincided with increased mRNA expression of mitochondrial genes. This was followed by an increase in mitochondrial protein content and enzyme activity after 24 h of recovery. These findings support the hypothesis that an acute bout of low-volume HIT activates mitochondrial biogenesis through a mechanism involving increased nuclear abundance of PGC-1α.

Coingestion of protein with carbohydrate during recovery from endurance exercise stimulates skeletal muscle protein synthesis in humans

Coingestion of protein with carbohydrate (CHO) during recovery from exercise can affect muscle glycogen synthesis, particularly if CHO intake is suboptimal. Another potential benefit of protein feeding is an increased synthesis rate of muscle proteins, as is well documented after resistance exercise. In contrast, the effect of nutrient manipulation on muscle protein kinetics after aerobic exercise remains largely unexplored. We tested the hypothesis that ingesting protein with CHO after a standardized 2-h bout of cycle exercise would increase mixed muscle fractional synthetic rate (FSR) and whole body net protein balance (WBNB) vs. trials matched for total CHO or total energy intake. We also examined whether postexercise glycogen synthesis could be enhanced by adding protein or additional CHO to a feeding protocol that provided 1.2 g CHO x kg(-1) x h(-1), which is the rate generally recommended to maximize this process. Six active men ingested drinks during the first 3 h of recovery that provided either 1.2 g CHO.kg(-1).h(-1) (L-CHO), 1.2 g CHO + 0.4 g protein x kg(-1) x h(-1) (PRO-CHO), or 1.6 g CHO x kg(-1) x h(-1) (H-CHO) in random order. Based on a primed constant infusion of l-[ring-(2)H(5)]phenylalanine, analysis of biopsies (vastus lateralis) obtained at 0 and 4 h of recovery showed that muscle FSR was higher (P < 0.05) in PRO-CHO (0.09 +/- 0.01%/h) vs. both L-CHO (0.07 +/- 0.01%/h) and H-CHO (0.06 +/- 0.01%/h). WBNB assessed using [1-(13)C]leucine was positive only during PRO-CHO, and this was mainly attributable to a reduced rate of protein breakdown. Glycogen synthesis rate was not different between trials. We conclude that ingesting protein with CHO during recovery from aerobic exercise increased muscle FSR and improved WBNB, compared with feeding strategies that provided CHO only and were matched for total CHO or total energy intake. However, adding protein or additional CHO to a feeding strategy that provided 1.2 g CHO x kg(-1) x h(-1) did not further enhance glycogen resynthesis during recovery.

Muscle time under tension during resistance exercise stimulates differential muscle protein sub-fractional synthetic responses in men

Non‐technical summary  A single bout of resistance exercise stimulates the synthesis of new muscle proteins. Chronic performance of resistance exercise (i.e. weight training) is what makes your muscles grow bigger; a process known as hypertrophy. However, it is unknown if increasing the time that muscle is under tension will lead to greater increases in muscle protein synthesis. We report that leg extension exercise at 30% of the best effort (which is a load that is comparatively light), with a slow lifting movement (6 s up and 6 s down) performed to fatigue produces greater increases in rates of muscle protein synthesis than the same movement performed rapidly (1 s up and 1 s down). These results suggest that the time the muscle is under tension during exercise may be important in optimizing muscle growth; this understanding enables us to better prescribe exercise to those wishing to build bigger muscles and/or to prevent muscle loss that occurs with ageing or disease.

Acute high‐intensity interval exercise reduces the postprandial glucose response and prevalence of hyperglycaemia in patients with type 2 diabetes

High‐volume endurance exercise (END) improves glycaemic control in type 2 diabetes (T2D) but many individuals cite ‘lack of time’ as a barrier to regular participation. High‐intensity interval training (HIT) is a time‐efficient method to induce physiological adaptations similar to END, but little is known regarding the effect of HIT in T2D. Using continuous glucose monitoring (CGM), we examined the 24‐h blood glucose response to one session of HIT consisting of 10 × 60 s cycling efforts at ∼90% maximal heart rate, interspersed with 60 s rest. Seven adults with T2D underwent CGM for 24‐h on two occasions under standard dietary conditions: following acute HIT and on a non‐exercise control day (CTL). HIT reduced hyperglycaemia measured as proportion of time spent above 10 mmol/l (HIT: 4.5 ± 4.4 vs. CTL: 15.2 ± 12.3%, p = 0.04). Postprandial hyperglycaemia, measured as the sum of post‐meal areas under the glucose curve, was also lower after HIT vs. CTL (728 ± 331 vs. 1142 ± 556 mmol/l·9 h, p = 0.01). These findings highlight the potential for HIT to improve glycaemic control in T2D.