Lauren E. Skelly

Twelve Weeks of Sprint Interval Training Improves Indices of Cardiometabolic Health Similar to Traditional Endurance Training despite a Five-Fold Lower Exercise Volume and Time Commitment

Aims We investigated whether sprint interval training (SIT) was a time-efficient exercise strategy to improve insulin sensitivity and other indices of cardiometabolic health to the same extent as traditional moderate-intensity continuous training (MICT). SIT involved 1 minute of intense exercise within a 10-minute time commitment, whereas MICT involved 50 minutes of continuous exercise per session. Methods Sedentary men (27±8y; BMI = 26±6kg/m2) performed three weekly sessions of SIT (n = 9) or MICT (n = 10) for 12 weeks or served as non-training controls (n = 6). SIT involved 3x20-second ‘all-out’ cycle sprints (~500W) interspersed with 2 minutes of cycling at 50W, whereas MICT involved 45 minutes of continuous cycling at ~70% maximal heart rate (~110W). Both protocols involved a 2-minute warm-up and 3-minute cool-down at 50W. Results Peak oxygen uptake increased after training by 19% in both groups (SIT: 32±7 to 38±8; MICT: 34±6 to 40±8ml/kg/min; p<0.001 for both). Insulin sensitivity index (CSI), determined by intravenous glucose tolerance tests performed before and 72 hours after training, increased similarly after SIT (4.9±2.5 to 7.5±4.7, p = 0.002) and MICT (5.0±3.3 to 6.7±5.0 x 10−4 min-1 [μU/mL]-1, p = 0.013) (p<0.05). Skeletal muscle mitochondrial content also increased similarly after SIT and MICT, as primarily reflected by the maximal activity of citrate synthase (CS; P<0.001). The corresponding changes in the control group were small for VO2peak (p = 0.99), CSI (p = 0.63) and CS (p = 0.97). Conclusions Twelve weeks of brief intense interval exercise improved indices of cardiometabolic health to the same extent as traditional endurance training in sedentary men, despite a five-fold lower exercise volume and time commitment.

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 β-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.

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.

Superior mitochondrial adaptations in human skeletal muscle after interval compared to continuous single-leg cycling matched for total work.

A classic unresolved issue in human integrative physiology involves the role of exercise intensity, duration and volume in regulating skeletal muscle adaptations to training. We employed counterweighted single‐leg cycling as a unique within‐subject model to investigate the role of exercise intensity in promoting training‐induced increases in skeletal muscle mitochondrial content. Six sessions of high‐intensity interval training performed over 2 weeks elicited greater increases in citrate synthase maximal activity and mitochondrial respiration compared to moderate‐intensity continuous training matched for total work and session duration. These data suggest that exercise intensity, and/or the pattern of contraction, is an important determinant of exercise‐induced skeletal muscle remodelling in humans.

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.

Effect of sex on the acute skeletal muscle response to sprint interval exercise

What is the central question of this study? Are there sex‐based differences in the acute skeletal muscle response to sprint interval training (SIT)? What is the main finding and its importance? In response to a SIT protocol that involved three 20 s bouts of ‘all‐out’ cycling, the expression of multiple genes associated with mitochondrial biogenesis, metabolic control and structural remodelling was largely similar between men and women matched for fitness. Our findings cannot explain previous reports of sex‐based differences in the adaptive response to SIT and suggest that the mechanistic basis for these differences remains to be elucidated.

Short-term green tea extract supplementation attenuates the postprandial blood glucose and insulin response following exercise in overweight men.

Green tea extract (GTE) ingestion improves glucose homeostasis in healthy and diabetic humans, but the interactive effect of GTE and exercise is unknown. The present study examined the effect of short-term GTE supplementation on the glycemic response to an oral glucose load at rest and following an acute bout of exercise, as well as substrate oxidation during exercise. Eleven sedentary, overweight men with fasting plasma glucose (FPG) ≥5.6 mmol·L-1 (age, 34 ± 13 years; body mass index = 32 ± 5 kg·m-2; FPG = 6.8 ± 1.0; mean ± SD) ingested GTE (3× per day, 1050 mg·day-1 total) or placebo (PLA) for 7 days in a double-blind, crossover design. The effects of a 75-g glucose drink were assessed on 4 occasions during both GTE and PLA treatments: On days 1 and 5 at rest, and again following an acute bout of exercise on days 3 and 8. The glycemic response was assessed via an indwelling continuous glucose monitor (CGM) and venous blood draws. At rest, 1-h CGM glucose area under the curve was not different (P > 0.05), but the postexercise response was lower after GTE versus PLA (330 ± 53 and 393 ± 65 mmol·L-1·min-1, main effect of treatment, P < 0.05). The 1-h postprandial peaks in venous blood glucose (8.6 ± 1.6 and 9.8 ± 2.2 mmol·L-1) and insulin (96 ± 59 and 124 ± 68 μIU·ml-1) were also lower postexercise with GTE versus PLA (time × treatment interactions, P < 0.05). In conclusion, short-term GTE supplementation did not affect postprandial glucose at rest; however, GTE was associated with an attenuated glycemic response following a postexercise oral glucose load. These data suggest that GTE might alter skeletal muscle glucose uptake in humans.

Finding the metabolic stress ‘sweet spot’: implications for sprint interval training‐induced muscle remodelling

Exercise-induced homeostatic disturbances initiate the activation of signalling cascades in skeletal muscle that coordinate increases in gene transcription and facilitate cellular remodelling. These acute skeletal muscle responses have been proposed to regulate training-induced increases in mitochondrial proteins. Traditional continuous moderate-intensity training is an effective strategy for inducing mitochondrial biogenesis. Sprint interval training (SIT), characterized by brief intermittent bouts of ‘all-out’ exercise interspersed with recovery periods, is also a potent stimulus for inducing skeletal remodelling despite involving a low total exercise volume. The high metabolic stress associated with low-volume SIT may be an important factor mediating the skeletal muscle adaptive response to this form of training. However, our understanding of how the magnitude of the metabolic disturbance induced by intense intermittent exercise impacts mitochondrial remodelling is limited. A recent article in The Journal of Physiology by Fiorenza et al. (2018) examined the activation of signalling proteins and mitochondrial gene expression in response to two work-matched, low-volume SIT protocols and a higher volume, continuous moderate-intensity protocol. The authors’ findings provide important insight into the relationship between exercise-induced cellular disturbances and the acute skeletal muscle response to low-volume SIT. The study by Fiorenza et al. (2018) involved 12 endurance-trained male cyclists, who completed three experimental trials on separate days in a randomized, counter-balanced manner. Diet and activity were carefully controlled prior to each experimental trial. The protocols involved either intermittent exercise, characterized as ‘repeated-sprint’ (RS) or ‘speed endurance’ (SE), or continuous, moderate-intensity (CM) cycling. RS consisted of 18 × 5 s all-out intervals interspersed with 30 s of passive recovery and SE involved 6 × 20 s all-out sprints interspersed with 2 min of passive recovery. The two SIT protocols were matched for total exercise volume and work to rest ratio but were hypothesized to elicit distinct degrees of intramuscular stress owing to differences in interval duration. The CM protocol involved 50 min of cycling at 70% V̇O2peak and thus was hypothesized to elicit a milder but more prolonged metabolic stress. Mean power output was 902, 669 and 218 W during RS, SE and CM, respectively. Muscle biopsies were obtained from the vastus lateralis prior to, immediately following and 3 h following exercise for analyses of a comprehensive set of metabolites, intracellular signalling proteins and genes associated with mitochondrial biogenesis. The authors also employed multiple linear regression analyses to probe metabolic factors that might predict exercise-induced increases in mitochondrial gene expression. The authors concluded that (1) for a given volume of high-intensity exercise, the initial events associated with mitochondrial biogenesis are dependent on metabolic stress (RS vs. SE), and (2) high-intensity exercise can compensate for reduced exercise volume only when marked metabolic perturbation occurs (SE vs. CM). A strength of the study was the direct comparison between two work-matched low-volume SIT protocols. Consistent with the authors’ hypothesis, SE elicited a greater metabolic stress than RS, as evidenced by a higher exercise-induced increase in muscle lactate and plasma adrenaline, and lower muscle pH. Importantly, the greater metabolic disturbance associated with SE was associated with a higher increase in peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) mRNA expression in post-exercise recovery compared to RS. Moreover, the response between SE and CM was largely comparable, such that both protocols evoked similar increases in mitochondrial gene expression, despite large differences in exercise volume. These findings are noteworthy and serve as a reminder that all low-volume SIT protocols are not equivalent. The greater glycolytic contribution to energy provision associated with 20 s as compared to 5 s sprints may be an important signal for the superior exercise-induced skeletal muscle remodelling in SE. Training using only 3 × 20 s all-out sprints per session is a profound stimulus to induce mitochondrial biogenesis and improve markers of cardiometabolic health, at least in previously inactive adults (Gillen et al. 2014). Interestingly, the protocol by Gillen et al. (2014) evoked large increases in mitochondrial content despite involving half the number of 20 s sprints as Fiorenza and colleagues. Whether reducing the number of 20 s efforts in the SE protocol would provide a sufficient metabolic stress in endurance-trained men is unknown. It is possible that a greater number of intervals is required to initiate mitochondrial responses in well-trained adults compared to the inactive population studied by Gillen et al. (2014). Nonetheless, the findings from Fiorenza et al. (2018) provide further support for the potency of repeated 20 s sprints for inducing skeletal muscle remodelling in a time-efficient manner. The present study advances our understanding of the mechanisms by which brief bursts of intense intermittent exercise may induce skeletal muscle responses, similar to longer bouts of traditional moderate-intensity exercise. While these diverse exercise stimuli have been shown to converge on mutual signalling pathways believed to regulate mitochondrial biogenesis, the present study demonstrates that the initial signalling events that trigger the induction of mitochondrial pathways are distinct. For the low-volume protocols RS and SE, multiple linear regression analyses revealed that exercise-induced increases in plasma adrenaline and muscle H+ concentration, along with muscle glycogen and phosphocreatine utilization during exercise, were important predictors of the post-exercise transcription of mitochondrial genes. The authors were able to manipulate the metabolic perturbation of low-volume interval training by adjusting the interval duration, which evoked a response similar to that

Brachial artery endothelial function is unchanged after acute sprint interval exercise in sedentary men and women

What is the central question of this study? What is the acute brachial artery endothelial function response to sprint interval exercise and are there sex‐based differences? What is the main finding and its importance? Brachial artery endothelial function did not change in either men or women following an acute session of SIT consisting of 3 × 20 s ‘all‐out’ cycling sprints. Our findings suggest this low‐volume protocol may not be sufficient to induce functional changes in the brachial artery of sedentary, but otherwise healthy adults.