More Reasons that Sprinting is Good for You

Perhaps I should issue a disclaimer here: I'm not a doctor, and I'm not giving medical advice here. Indeed, if you're out of shape or have a heart condition, maybe you shouldn't be sprinting at all. Nonetheless, here are a few more reasons that sprinting can be good for your health:

1. Improves learning ability and brain function.
2. Greater improvement in cardiovascular health, as compared to slower running:
3. Improves fat-burning capacity.
4. Improves muscle fitness and endurance.

The supporting studies that I've found:

1. Improves learning ability and brain function.

Winter B, Breitenstein C, Mooren FC, Voelker K, Fobker M, Lechtermann A, Krueger K, Fromme A, Korsukewitz C, Floel A, Knecht S., “High impact running improves learning,” Neurobiol Learn Mem. 87 vol. 4 (May 2007): 597-609.

Regular physical exercise improves cognitive functions and lowers the risk for age-related cognitive decline. Since little is known about the nature and the timing of the underlying mechanisms, we probed whether exercise also has immediate beneficial effects on cognition. Learning performance was assessed directly after high impact anaerobic sprints, low impact aerobic running, or a period of rest in 27 healthy subjects in a randomized cross-over design. Dependent variables comprised learning speed as well as immediate (1 week) and long-term (>8 months) overall success in acquiring a novel vocabulary. Peripheral levels of brain-derived neurotrophic factor (BDNF) and catecholamines (dopamine, epinephrine, norepinephrine) were assessed prior to and after the interventions as well as after learning. We found that vocabulary learning was 20 percent faster after intense physical exercise as compared to the other two conditions. This condition also elicited the strongest increases in BDNF and catecholamine levels. More sustained BDNF levels during learning after intense exercise were related to better short-term learning success, whereas absolute dopamine and epinephrine levels were related to better intermediate (dopamine) and long-term (epinephrine) retentions of the novel vocabulary. Thus, BDNF and two of the catecholamines seem to be mediators by which physical exercise improves learning.

Ferris LT, Williams JS, Shen CL., “The effect of acute exercise on serum brain-derived neurotrophic factor levels and cognitive function,” Med Sci Sports Exerc. 39 no. 4 (April 2007): 728-34.

Brain-derived neurotrophic factor (BDNF) is one of a family of neurotrophic factors that participates in neuronal transmission, modulation and plasticity. Previous studies using animals have demonstrated that acute and chronic exercise leads to increases in BDNF in various brain regions. PURPOSE: To determine the effects of acute exercise on serum BDNF levels in humans, and to determine the relationship between exercise intensity and BDNF responses. Additionally, the relationship between changes in BDNF and cognitive function was examined. METHODS: Fifteen subjects (25.4 +/- 1.01 yr; 11 male, 4 female) performed a graded exercise test (GXT) for the determination of VO2max and ventilatory threshold (VTh) on a cycle ergometer. On separate days, two subsequent 30-min endurance rides were performed at 20% below the VTh (VTh - 20) and at 10% above the VTh (VTh + 10). Serum BDNF and cognitive function were determined before and after the GXT and endurance rides with an enzyme-linked immunosorbent assay (ELISA) and the Stroop tests, respectively. RESULTS: The mean VO2max was 2805.8 +/- 164.3 mL x min(-1) (104.2 +/- 7.0% pred). BDNF values (pg x mL(-1)) increased from baseline (P<0.05) after exercise at the VTh + 10 (13%) and the GXT (30%). There was no significant change in BDNF from baseline after the VTh - 20. Changes in BDNF did not correlate with VO2max during the GXT, but they did correlate with changes in lactate (r=0.57; P<0.05). Cognitive function scores improved after all exercise conditions, but they did not correlate with BDNF changes.

CONCLUSION: BDNF levels in humans are significantly elevated in response to exercise, and the magnitude of increase is exercise intensity dependent. Given that BDNF can transit the blood-brain barrier in both directions, the intensity-dependent findings may aid in designing exercise prescriptions for maintaining or improving neurological health.

2. Greater improvement in cardiovascular health, as compared to slower running:

Kemi, O. J., Haram, P. M., Loennechen, J. P., Osnes, J. B., Skomedal, T., Wisløff, U., and Ellingsen, O., “Moderate vs. high exercise intensity: differential effects on aerobic fitness, cardiomyocyte contractility, and endothelial function,” Cardiovascular Research 67 no. 1 (2005): 161-172.

Abstract:

Current guidelines are controversial regarding exercise intensity in cardiovascular prevention and rehabilitation. Although high-intensity training induces larger increases in fitness and maximal oxygen uptake (VO2max), moderate intensity is often recommended as equally effective. Controlled preclinical studies and randomized clinical trials are required to determine whether regular exercise at moderate versus high intensity is more beneficial. We therefore assessed relative effectiveness of 10-week HIGH versus moderate (MOD) exercise intensity on integrative and cellular functions. Method: Sprague-Dawley rats performed treadmill running intervals at either 85%-90% (HIGH) or 65%-70% (MOD) of VO2max 1 h per day, 5 days per week. Weekly VO2max-testing adjusted exercise intensity. Results: HIGH and MOD increased VO2max by 71% and 28%, respectively. This was paralleled by intensity-dependent cardiomyocyte hypertrophy, 14% and 5% in HIGH and MOD, respectively. Cardiomyocyte function (fractional shortening) increased by 45% and 23%, contraction rate decreased by 43% and 39%, and relaxation rate decreased by 20% and 10%, in HIGH and MOD, respectively. Ca2+ transient time-courses paralleled contraction/relaxation, whereas Ca2+ sensitivity increased 40% and 30% in HIGH and MOD, respectively. Carotid artery endothelial function improved similarly with both intensities. EC50 for acetylcholine-induced relaxation decreased 4.3-fold in HIGH (p<0.05) and 2.8-fold in MOD (p<0.20) as compared to sedentary; difference HIGH versus MOD 1.5-fold (p=0.72). Multiple regression identified rate of systolic Ca2+ increase and diastolic myocyte relengthening as main variables associated with VO2max. Cell hypertrophy, contractility and vasorelaxation also correlated significantly with VO2max.

Conclusions: The present study demonstrates that cardiovascular adaptations to training are intensity-dependent. A close correlation between VO2max, cardiomyocyte dimensions and contractile capacity suggests significantly higher benefit with high intensity, whereas endothelial function appears equivalent at moderate levels. Thus, exercise intensity emerges as an important variable in future preclinical and clinical investigations.

3. Improves fat-burning capacity.

Ethlyn Gail Trapp, “Effect of High Intensity Exercise on Fat Loss in Young Overweight Women,” PhD Diss., University of New South Wales, 2006:

Both exercise groups increased VO2peak. The [sprint] group had a significant loss of total body mass (TBM) and fat mass (FM) when compared to the other groups. There was no change in dietary intake.

Jason L. Talanian, Stuart D. R. Galloway, George J. F. Heigenhauser, Arend Bonen, and Lawrence L. Spriet, “Two weeks of high-intensity aerobic interval training increases the capacity for fat oxidation during exercise in women,” J Appl Physiol 102 (2007): 1439-1447.

Our aim was to examine the effects of seven high-intensity aerobic interval training (HIIT) sessions over 2 wk on skeletal muscle fuel content, mitochondrial enzyme activities, fatty acid transport proteins, peak O2 consumption (VO2 peak), and whole body metabolic, hormonal, and cardiovascular responses to exercise. Eight women (22.1 ± 0.2 yr old, 65.0 ± 2.2 kg body wt, 2.36 ± 0.24 l/min VO2 peak) performed a VO2 peak test and a 60-min cycling trial at ~60% VO2 peak before and after training. Each session consisted of ten 4-min bouts at ~90% VO2 peak with 2 min of rest between intervals. Training increased VO2 peak by 13%. After HIIT, plasma epinephrine and heart rate were lower during the final 30 min of the 60-min cycling trial at ~60% pretraining VO2 peak. Exercise whole body fat oxidation increased by 36% (from 15.0 ± 2.4 to 20.4 ± 2.5 g) after HIIT. Resting muscle glycogen and triacylglycerol contents were unaffected by HIIT, but net glycogen use was reduced during the posttraining 60-min cycling trial. HIIT significantly increased muscle mitochondrial beta-hydroxyacyl-CoA dehydrogenase (15.44 ± 1.57 and 20.35 ± 1.40 mmol•min–1•kg wet mass–1 before and after training, respectively) and citrate synthase (24.45 ± 1.89 and 29.31 ± 1.64 mmol•min–1•kg wet mass–1 before and after training, respectively) maximal activities by 32% and 20%, while cytoplasmic hormone-sensitive lipase protein content was not significantly increased. Total muscle plasma membrane fatty acid-binding protein content increased significantly (25%), whereas fatty acid translocase/CD36 content was unaffected after HIIT.

In summary, seven sessions of HIIT over 2 wk induced marked increases in whole body and skeletal muscle capacity for fatty acid oxidation during exercise in moderately active women.

4. Improves muscle fitness and endurance.

Kirsten A. Burgomaster, Scott C. Hughes, George J. F. Heigenhauser, Suzanne N. Bradwell, and Martin J. Gibala, “Six sessions of sprint interval training increases muscle oxidative potential and cycle endurance capacity in humans,” J Appl Physiol 98 (2005): 1985-1990.

Parra et al. (Acta Physiol. Scand 169: 157–165, 2000) showed that 2 wk of daily sprint interval training (SIT) increased citrate synthase (CS) maximal activity but did not change "anaerobic" work capacity, possibly because of chronic fatigue induced by daily training. The effect of fewer SIT sessions on muscle oxidative potential is unknown, and aside from changes in peak oxygen uptake (O2 peak), no study has examined the effect of SIT on "aerobic" exercise capacity. We tested the hypothesis that six sessions of SIT, performed over 2 wk with 1–2 days rest between sessions to promote recovery, would increase CS maximal activity and endurance capacity during cycling at ~80% O2 peak. Eight recreationally active subjects [age = 22 ± 1 yr; O2 peak = 45 ± 3 ml•kg–1•min–1 (mean ± SE)] were studied before and 3 days after SIT. Each training session consisted of four to seven "all-out" 30-s Wingate tests with 4 min of recovery. After SIT, CS maximal activity increased by 38% (5.5 ± 1.0 vs. 4.0 ± 0.7 mmol•kg protein–1•h–1) and resting muscle glycogen content increased by 26% (614 ± 39 vs. 489 ± 57 mmol/kg dry wt) (both P < 0.05). Most strikingly, cycle endurance capacity increased by 100% after SIT (51 ± 11 vs. 26 ± 5 min; P < 0.05), despite no change in O2 peak. The coefficient of variation for the cycle test was 12.0%, and a control group (n = 8) showed no change in performance when tested ~2 wk apart without SIT. We conclude that short sprint interval training (~15 min of intense exercise over 2 wk) increased muscle oxidative potential and doubled endurance capacity during intense aerobic cycling in recreationally active individuals.

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Rodas G, Ventura JL, Cadefau JA, Cussó R, Parra J., “A short training programme for the rapid improvement of both aerobic and anaerobic metabolism,” Eur J Appl Physiol. 82 vol. 5-6 (Aug. 2000):480-86.

The aim of this study was to evaluate the changes in aerobic and anaerobic metabolism produced by a newly devised short training programme. Five young male volunteers trained daily for 2 weeks on a cycle ergometer. Sessions consisted of 15-s all-out repetitions with 45-s rest periods, plus 30-s all-out repetitions with 12-min rest periods. The number of repetitions was gradually increased up to a maximum of seven. Biopsy samples of the vastus lateralis muscle were taken before and after training. Performance changes were evaluated by two tests, a 30-s all-out test and a maximal progressive test. Significant increases in phosphocreatine (31%) and glycogen (32%) were found at the end of training. In addition, a significant increase was observed in the muscle activity of creatine kinase (44%), phosphofructokinase (106%), lactate dehydrogenase (45%), 3-hydroxy-acyl-CoA dehydrogenase (60%) and citrate synthase (38%). After training, performance of the 30-s all-out test did not increase significantly, while in the maximal progressive test, the maximum oxygen consumption increased from mean (SD) 57.3 (2.6) ml x min(-1) x kg(-1) to 63.8 (3.0) ml min(-1) x kg(-1), and the maximum load from 300 (11) W to 330 (21) W; all changes were significant. In conclusion, this new protocol, which utilises short durations, high loads and long recovery periods, seems to be an effective programme for improving the enzymatic activities of the energetic pathways in a short period of time.

See my previous post: Why Doing Sprints is Great for Your Health.