Post-exercise leg and forearm flexor muscle cooling in humans attenuates endurance and resistance training effects on muscle performance and on circulatory adaptation

Abstract

The influence of regular post-exercise cold application to exercised muscles trained by ergometer cycling (leg muscles) or handgrip exercise using a weight-loaded handgrip ergometer (forearm flexor muscles) was studied in human volunteers. Muscle loads were applied during exercise programs three to four times a week for 4-6 weeks. Besides measuring parameters characterizing muscle performance, femoral and brachial artery diameters were determined ultrasonographically. Training effects were identified by comparing pre- and post-training parameters in matched groups separately for the trained limbs cooled after exercise by cold-water immersion and the corresponding trained limbs kept at room temperature. Significant training effects were three times more frequent in the control than in the cold group, including increases in artery diameters in the control but not in the cold group. It is concluded that training-induced molecular and humoral adjustments, including muscle hyperthermia, are physiological, transient and essential for training effects (myofiber regeneration, muscle hypertrophy and improved blood supply). Cooling generally attenuates these temperature-dependent processes and, in particular, hyperthermia-induced HSP formation. This seems disadvantageous for training, in contrast to the beneficial combination of rest, ice, compression and elevation in the treatment of macroscopic musculo-tendinous damage.

PGC-1α Mediated Muscle Aerobic Adaptations to Exercise, Heat and Cold Exposure

“…This is indeed unusual, as PGC-1α has been well shown to increase NRF1 expression and transcriptional activity (Wu et al, 1999) and consequently suggests other pathways besides PGC-1α might regulate NRF1 expression following post-exercise cold exposure. Regardless, this study lends some support for the study by Yamane et al (2006), as NRF1 has shown to encode a variety of mitochondrial components (Scarpulla, 2002) and PGC-1α has shown to act through ERRα in inducing VEGF expression (Chinsomboon et al, 2009). A key consideration however, that must be accounted for is that the increase in PGC-1α following cold exposure as demonstrated by Slivka et al (2013; was accompanied by significant elevations in whole body VO2 and shivering thermogenesis, which independently may increase PGC-1α mRNA expression.…”

“…As opposed to passive cold exposure, more studies have investigated the effects of cold exposure following exercise instead Ihsan et al, 2014;Slivka et al, 2013;Slivka et al, 2012;Yamane et al, 2006). In an early study, it was shown that improvements in VO2max and cycling time to exhaustion during single leg cycling following 4 weeks of endurance training were attenuated in the leg subjected to regular post-exercise cooling (2 x 20 min at 5°C) (Yamane et al, 2006).…”

“…In an early study, it was shown that improvements in VO2max and cycling time to exhaustion during single leg cycling following 4 weeks of endurance training were attenuated in the leg subjected to regular post-exercise cooling (2 x 20 min at 5°C) (Yamane et al, 2006). Moreover, it was reported that resting femoral artery diameter in the control limb was significantly increased following endurance training while no such adaptation was observed in the limb subjected to regular cooling, indicating the possibility of attenuated vascular adaptations to training (Yamane et al, 2006).…”

“…In an early study, it was shown that improvements in VO2max and cycling time to exhaustion during single leg cycling following 4 weeks of endurance training were attenuated in the leg subjected to regular post-exercise cooling (2 x 20 min at 5°C) (Yamane et al, 2006). Moreover, it was reported that resting femoral artery diameter in the control limb was significantly increased following endurance training while no such adaptation was observed in the limb subjected to regular cooling, indicating the possibility of attenuated vascular adaptations to training (Yamane et al, 2006). Indeed, cold water immersion could potentially retard vascular adaptations through its ability to decrease postexercise muscle blood flow/perfusion (Gregson et al, 2011;Ihsan et al, 2013a;Mawhinney et al, 2013) and consequently minimising shear stress on the vessel walls, an important stimulus for vascular adaptations (Naylor et al, 2011).…”

“…For instance, in studies using cell culture and animal models, mitochondrial biogenesis has shown to be up-regulated following both heat and cold exposures through PGC-1α dependant mechanisms similar to that observed following exercise (Bruton et al, 2010;Liu & Brooks, 2012;Puigserver et al, 1998;Tamura et al, 2014;Wu et al, 1999). However, when administered following exercise, both heat and cold interventions have demonstrated contradictory results, with some studies showing beneficial, while others detrimental effects on PGC-1α and/or muscle aerobic performance (Ihsan et al, 2014;Slivka et al, 2013;Slivka et al, 2012;Tamura et al, 2014;Yamane et al, 2006). Taken together, these studies highlight the potential of these modalities to both enhance and diminish mitochondrial adaptations to training, as well implicating PGC-1α as a key target in these mechanisms.…”